Northwestern University researchers are the first to design a bioactive nanomaterial that promotes the growth of new cartilage in vivo and without the use of expensive growth factors. Minimally invasive, the therapy activates the bone marrow stem cells and produces natural cartilage. No conventional therapy can do this.
The results will be published online the week of Feb. 1 by the Proceedings of the National Academy of Sciences (PNAS).
"Unlike bone, cartilage does not grow back, and therefore clinical strategies to regenerate this tissue are of great interest," said Samuel I. Stupp, senior author, Board of Trustees Professor of Chemistry, Materials Science and Engineering, and Medicine, and director of the Institute for BioNanotechnology in Medicine. Countless people - amateur athletes, professional athletes and people whose joints have just worn out -- learn this all too well when they bring their bad knees, shoulders and elbows to an orthopaedic surgeon.
Damaged cartilage can lead to joint pain and loss of physical function and eventually to osteoarthritis, a disorder with an estimated economic impact approaching $65 billion in the United States. With an aging and increasingly active population, this figure is expected to grow.
"Cartilage does not regenerate in adults. Once you are fully grown you have all the cartilage you'll ever have," said first author Ramille N. Shah, assistant professor of materials science and engineering at the McCormick School of Engineering and Applied Science and assistant professor of orthopaedic surgery at the Feinberg School of Medicine. Shah is also a resident faculty member at the Institute for BioNanotechnology in Medicine.
Type II collagen is the major protein in articular cartilage, the smooth, white connective tissue that covers the ends of bones where they come together to form joints.
"Our material of nanoscopic fibers stimulates stem cells present in bone marrow to produce cartilage containing type II collagen and repair the damaged joint," Shah said. "A procedure called microfracture is the most common technique currently used by doctors, but it tends to produce a cartilage having predominantly type I collagen which is more like scar tissue."
The Northwestern gel is injected as a liquid to the area of the damaged joint, where it then self-assembles and forms a solid. This extracellular matrix, which mimics what cells usually see, binds by molecular design one of the most important growth factors for the repair and regeneration of cartilage. By keeping the growth factor concentrated and localized, the cartilage cells have the opportunity to regenerate.
Together with Nirav A. Shah, a sports medicine orthopaedic surgeon and former orthopaedic resident at Northwestern, the researchers implanted their nanofiber gel in an animal model with cartilage defects.
The animals were treated with microfracture, where tiny holes are made in the bone beneath the damaged cartilage to create a new blood supply to stimulate the growth of new cartilage. The researchers tested various combinations: microfracture alone; microfracture and the nanofiber gel with growth factor added; and microfracture and the nanofiber gel without growth factor added.
They found their technique produced much better results than the microfracture procedure alone and, more importantly, found that addition of the expensive growth factor was not required to get the best results. Instead, because of the molecular design of the gel material, growth factor already present in the body is enough to regenerate cartilage.
The matrix only needed to be present for a month to produce cartilage growth. The matrix, based on self-assembling molecules known as peptide amphiphiles, biodegrades into nutrients and is replaced by natural cartilage.
The PNAS paper is titled "Supramolecular Design of Self-assembling Nanofibers for Cartilage Regeneration." In addition to Stupp, Ramille Shah and Nirav Shah, other authors of the paper are Marc M. Del Rosario Lim, Caleb Hsieh and Gordon Nuber, all from Northwestern.
The National Institutes of Health and the company Nanotope supported the research.
Source:
Wendy Leopold
Northwestern University
воскресенье, 19 июня 2011 г.
суббота, 18 июня 2011 г.
Arthritis Foundation Convenes Country's Top Researchers For Biennial Conference
More than 200 leading
researchers committed to discovering new technologies and therapies to
prevent and treat arthritis will meet April 20 - 23 in Atlanta, GA, for the
2007 Arthritis Research Conference, organized by the Arthritis Foundation.
Some of the most promising and innovative research to be presented at the
conference pertains to using stem cells to advance cartilage regeneration
for patients with osteoarthritis. Other exciting developments include new
approaches to manipulating a special type of white blood cell known as the
B lymphocyte in ways that can diminish inflammation in diseases such as
rheumatoid arthritis.
"As the nation's largest private, not-for-profit funder of arthritis
research, this conference is very exciting for all of us here at the
Arthritis Foundation," said John H. Klippel, M.D., president and CEO of the
Arthritis Foundation. "The three-day event is an opportunity for the best
and brightest minds in arthritis research to develop research
collaborations that will pave the way to a cure."
Scientists predict that recent revelations in the area of stem cell
research will lead to treatments that heal damaged cartilage and tissue,
thereby greatly reducing or eliminating the number of joint replacement
surgeries. Scientists hope introducing stem cells into areas where
cartilage and tissue are already damaged may initiate a process of
rebuilding healthy tissue and preventing further joint degradation. Many
are optimistic that treatments using stem cells to 'jump-start' tissue
regeneration will be available within the next decade.
One of the most significant advances in recent years has been the
development of biologics -- drugs which are based on substances produced by
living cells. This is an important and very successful example of a class
of biologic drugs that are now a common treatment for several types of
arthritis. The class of biologics known as TNF inhibitors, block the action
of one of the major mediators of inflammation in the body and have become
important treatments for diseases such as rheumatoid arthritis, psoriatic
arthritis, and juvenile arthritis. TNF release results in inflammation of
the joints in patients with the diseases noted above. Research sponsored by
the Foundation is leading to therapies that can halt the chemical cascade
that leads to TNF production at very early stages of these diseases. This
approach can prevent the appearance of arthritis before any tissue damage
can occur.
"Combining the best and brightest minds in arthritis research and
advanced technologies for studying the cause of disease at its most basic
levels is enabling great advances," said Dr. John H. Hardin, chief
scientific officer of the Arthritis Foundation.
The three-day conference begins at 10:00 a.m. Friday, April 20.
Researchers from across the country will share research, best practices and
theories that will propel the next generation of arthritis research. The
conference consists of three primary sessions:
-- Plenary Session: Translation in Arthritis Medicine
-- Basic Science Symposium: Signaling and Regulation in the Joint
-- Clinical Science Symposium: New Perspectives on Inflammatory Disease
About The Arthritis Foundation
The Arthritis Foundation is the leading health organization addressing
the needs of some 46 million Americans living with arthritis, the nation's
number- one cause of disability. Founded in 1948, with headquarters in
Atlanta, the Arthritis Foundation has chapters and 150 community service
points located throughout the country.
The Arthritis Foundation is the largest private, not-for-profit
contributor to arthritis research in the world, funding more than $380
million in research grants since 1948. The foundation helps individuals
take control of arthritis by providing public health education; pursuing
public policy and legislation; and conducting evidence-based programs to
improve the quality of life for those living with arthritis.
Arthritis Foundation
arthritis
researchers committed to discovering new technologies and therapies to
prevent and treat arthritis will meet April 20 - 23 in Atlanta, GA, for the
2007 Arthritis Research Conference, organized by the Arthritis Foundation.
Some of the most promising and innovative research to be presented at the
conference pertains to using stem cells to advance cartilage regeneration
for patients with osteoarthritis. Other exciting developments include new
approaches to manipulating a special type of white blood cell known as the
B lymphocyte in ways that can diminish inflammation in diseases such as
rheumatoid arthritis.
"As the nation's largest private, not-for-profit funder of arthritis
research, this conference is very exciting for all of us here at the
Arthritis Foundation," said John H. Klippel, M.D., president and CEO of the
Arthritis Foundation. "The three-day event is an opportunity for the best
and brightest minds in arthritis research to develop research
collaborations that will pave the way to a cure."
Scientists predict that recent revelations in the area of stem cell
research will lead to treatments that heal damaged cartilage and tissue,
thereby greatly reducing or eliminating the number of joint replacement
surgeries. Scientists hope introducing stem cells into areas where
cartilage and tissue are already damaged may initiate a process of
rebuilding healthy tissue and preventing further joint degradation. Many
are optimistic that treatments using stem cells to 'jump-start' tissue
regeneration will be available within the next decade.
One of the most significant advances in recent years has been the
development of biologics -- drugs which are based on substances produced by
living cells. This is an important and very successful example of a class
of biologic drugs that are now a common treatment for several types of
arthritis. The class of biologics known as TNF inhibitors, block the action
of one of the major mediators of inflammation in the body and have become
important treatments for diseases such as rheumatoid arthritis, psoriatic
arthritis, and juvenile arthritis. TNF release results in inflammation of
the joints in patients with the diseases noted above. Research sponsored by
the Foundation is leading to therapies that can halt the chemical cascade
that leads to TNF production at very early stages of these diseases. This
approach can prevent the appearance of arthritis before any tissue damage
can occur.
"Combining the best and brightest minds in arthritis research and
advanced technologies for studying the cause of disease at its most basic
levels is enabling great advances," said Dr. John H. Hardin, chief
scientific officer of the Arthritis Foundation.
The three-day conference begins at 10:00 a.m. Friday, April 20.
Researchers from across the country will share research, best practices and
theories that will propel the next generation of arthritis research. The
conference consists of three primary sessions:
-- Plenary Session: Translation in Arthritis Medicine
-- Basic Science Symposium: Signaling and Regulation in the Joint
-- Clinical Science Symposium: New Perspectives on Inflammatory Disease
About The Arthritis Foundation
The Arthritis Foundation is the leading health organization addressing
the needs of some 46 million Americans living with arthritis, the nation's
number- one cause of disability. Founded in 1948, with headquarters in
Atlanta, the Arthritis Foundation has chapters and 150 community service
points located throughout the country.
The Arthritis Foundation is the largest private, not-for-profit
contributor to arthritis research in the world, funding more than $380
million in research grants since 1948. The foundation helps individuals
take control of arthritis by providing public health education; pursuing
public policy and legislation; and conducting evidence-based programs to
improve the quality of life for those living with arthritis.
Arthritis Foundation
arthritis
пятница, 17 июня 2011 г.
Centocor, Inc. Submits Application To FDA Requesting Approval Of Golimumab For The Treatment Of Rheumatoid Arthritis
Centocor, Inc. announced
that a Biologics License Application (BLA) has been submitted to the U.S.
Food and Drug Administration (FDA) requesting the approval of golimumab
(CNTO 148) as a monthly subcutaneous treatment for adults with active forms
of rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis.
Golimumab, Centocor's next-generation human anti-TNF-alpha monoclonal
antibody, is being studied as an every four week subcutaneous injection and
is also being studied as an intravenous (IV) infusion therapy. In February
2008, Centocor submitted a Marketing Authorization Application (MAA) to the
European Medicines Agency (EMEA) requesting the approval of golimumab as a
monthly subcutaneous treatment for the same indications.
"This submission marks a major milestone in the clinical development
program of golimumab, and we look forward to working with the FDA to bring
golimumab to market," said Jerome A. Boscia, M.D., senior vice president,
Clinical R&D, Centocor, Inc. "We remain focused on our commitment to
innovation in the field of biomedicines, to addressing the ongoing needs of
patients living with these debilitating diseases and to physicians in need
of additional therapeutic options to effectively treat their patients."
Five pivotal Phase 3 trials support the BLA, which include the
GOlimumab Before Employing methotrexate as the First-line Option in the
treatment of Rheumatoid arthritis of Early onset (GO-BEFORE) study; the
GOlimumab FOR subjects With Active RA Despite MTX (GO-FORWARD) study; and A
Multicenter, Randomized, Double-blind, Placebo-controlled Trial of
Golimumab, a Human Anti-TNF-alpha Monoclonal Antibody, Administered
Subcutaneously in Subjects with Active Rheumatoid Arthritis and Previously
Treated with Biologic Anti-TNF-alpha Agent(s) (GO-AFTER) study were
recently presented at the European League Against Rheumatism Annual
Congress. In November 2007, primary endpoint study findings from the
Golimumab - A Randomized Evaluation of Safety and Efficacy in Subjects with
Psoriatic Arthritis Using a Human Anti-TNF Monoclonal Antibody (GO-REVEAL)
trial and the Golimumab - A Randomized Study in Ankylosing Spondylitis
Subjects of a Novel Anti-TNF mAB Injection (SC) Given Every Four Weeks
(GO-RAISE) trial were reported at the American College of Rheumatology
Annual Scientific Meeting.
About Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic and debilitating disease that
affects approximately 1.3 million people in the United States and more than
three million people in Europe. Signs and symptoms of RA include pain,
stiffness and motion restriction in multiple joints. Because RA is a
progressive disease, it can cause permanent joint deformity and severe
disability if not diagnosed early or if initial treatment is delayed. RA
can occur at any age, but is most common in adults 30-50 years old and is
two-to-three times more prevalent in women than in men. The cause of RA is
unknown, although genetic factors may contribute to the disease.
About Psoriatic Arthritis
Psoriatic arthritis is a chronic inflammatory arthropathy manifesting
with joint pain and swelling that can lead to joint destruction and
debilitation. It is frequently associated with inflamed, scaly, red patches
of skin psoriasis and psoriasis nail involvement. Symptoms may include
stiffness and tenderness of the joints and surrounding tissue and reduced
range of motion. Joints of the hands, wrists, knees, ankles, feet, lower
back and neck are commonly affected. Psoriasis affects an estimated two to
three percent of the world's population, and approximately one out of three
patients affected by psoriasis may develop psoriatic arthritis. Both men
and women are equally affected by psoriatic arthritis, most commonly
between the ages 30 and 50, in the peak of their productive years.
About Ankylosing Spondylitis
Ankylosing spondylitis (AS) is a painful and progressive form of spinal
arthritis and symptoms of inflammatory back pain often first present in
people before age 35. It typically begins in the late teens and early
twenties and in severe cases may result in fusing spinal vertebrae and may
cause structural damage to hips and other joints. Often misdiagnosed as
"just back pain" or undifferentiated arthritis, AS is a systemic
inflammatory disease that, in addition to its effect on the spine, can
affect internal organs, peripheral joints and vision. The Arthritis
Research Campaign estimates that on the European continent, AS prevalence
ranges from 0.2 to 1 percent of the entire population. The Spondylitis
Association of America estimates that between 350,000 and one million
people in the U.S. suffer from ankylosing spondylitis.
About Golimumab
Golimumab, Centocor, Inc.'s next-generation human anti-tumor necrosis
factor (TNF)-alpha monoclonal antibody, is currently in the most
comprehensive Phase 3 development program to date for an anti-TNF-alpha
biologic therapy. With ongoing studies for the treatment of rheumatoid
arthritis, psoriatic arthritis and ankylosing spondylitis, golimumab is
being studied as an every four week subcutaneous injection and an
intravenous (IV) infusion therapy. Golimumab targets and neutralizes both
the soluble and membrane-bound forms of TNF-alpha.
Centocor discovered golimumab and has exclusive marketing rights to the
product in the United States. Pending regulatory approval, Schering-Plough
will assume exclusive marketing rights outside the United States except in
Japan, Indonesia and Taiwan where golimumab will be co-marketed by
Mitsubishi Tanabe Pharma Corporation and Janssen Pharmaceutical Kabushiki
Kaisha; Hong Kong, where golimumab will be exclusively marketed by
Janssen-Cilag; and China where golimumab will be exclusively marketed by
Xian-Janssen.
About Centocor, Inc.
Centocor is harnessing the power of world-leading research and
biomanufacturing to deliver innovative biomedicines that transform
patients' lives. Centocor has already brought innovation to the treatment
of adult and pediatric Crohn's disease, rheumatoid arthritis, ankylosing
spondylitis, psoriatic arthritis, ulcerative colitis and psoriasis.
The world leader in monoclonal antibody production and technology,
Centocor has brought critical biologic therapies to patients suffering from
debilitating immune disorders. Centocor is a wholly-owned subsidiary of
Johnson & Johnson.
CENTOCOR DISCLOSURE NOTICE: This press release contains
"forward-looking statements" as defined in the Private Securities
Litigation Reform Act of 1995. These statements are based on current
expectations of future events. If underlying assumptions prove inaccurate
or unknown risks or uncertainties materialize, actual results could vary
materially from Centocor's expectations and projections. Risks and
uncertainties include general industry conditions and competition; economic
conditions, such as interest rate and currency exchange rate fluctuations;
technological advances and patents attained by competitors; challenges
inherent in new product development, including obtaining regulatory
approvals; domestic and foreign health care reforms and governmental laws
and regulations; and trends toward health care cost containment. A further
list and description of these risks, uncertainties and other factors can be
found in Exhibit 99 of Johnson & Johnson's Annual Report on Form 10-K for
the fiscal year ended December 30, 2007. Copies of this Form 10-K, as well
as subsequent filings, are available online at sec, jnj or
on request from Johnson & Johnson. Centocor does not undertake to update
any forward-looking statements as a result of new information or future
events or developments.
Centocor, Inc.
jnj
that a Biologics License Application (BLA) has been submitted to the U.S.
Food and Drug Administration (FDA) requesting the approval of golimumab
(CNTO 148) as a monthly subcutaneous treatment for adults with active forms
of rheumatoid arthritis, psoriatic arthritis and ankylosing spondylitis.
Golimumab, Centocor's next-generation human anti-TNF-alpha monoclonal
antibody, is being studied as an every four week subcutaneous injection and
is also being studied as an intravenous (IV) infusion therapy. In February
2008, Centocor submitted a Marketing Authorization Application (MAA) to the
European Medicines Agency (EMEA) requesting the approval of golimumab as a
monthly subcutaneous treatment for the same indications.
"This submission marks a major milestone in the clinical development
program of golimumab, and we look forward to working with the FDA to bring
golimumab to market," said Jerome A. Boscia, M.D., senior vice president,
Clinical R&D, Centocor, Inc. "We remain focused on our commitment to
innovation in the field of biomedicines, to addressing the ongoing needs of
patients living with these debilitating diseases and to physicians in need
of additional therapeutic options to effectively treat their patients."
Five pivotal Phase 3 trials support the BLA, which include the
GOlimumab Before Employing methotrexate as the First-line Option in the
treatment of Rheumatoid arthritis of Early onset (GO-BEFORE) study; the
GOlimumab FOR subjects With Active RA Despite MTX (GO-FORWARD) study; and A
Multicenter, Randomized, Double-blind, Placebo-controlled Trial of
Golimumab, a Human Anti-TNF-alpha Monoclonal Antibody, Administered
Subcutaneously in Subjects with Active Rheumatoid Arthritis and Previously
Treated with Biologic Anti-TNF-alpha Agent(s) (GO-AFTER) study were
recently presented at the European League Against Rheumatism Annual
Congress. In November 2007, primary endpoint study findings from the
Golimumab - A Randomized Evaluation of Safety and Efficacy in Subjects with
Psoriatic Arthritis Using a Human Anti-TNF Monoclonal Antibody (GO-REVEAL)
trial and the Golimumab - A Randomized Study in Ankylosing Spondylitis
Subjects of a Novel Anti-TNF mAB Injection (SC) Given Every Four Weeks
(GO-RAISE) trial were reported at the American College of Rheumatology
Annual Scientific Meeting.
About Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic and debilitating disease that
affects approximately 1.3 million people in the United States and more than
three million people in Europe. Signs and symptoms of RA include pain,
stiffness and motion restriction in multiple joints. Because RA is a
progressive disease, it can cause permanent joint deformity and severe
disability if not diagnosed early or if initial treatment is delayed. RA
can occur at any age, but is most common in adults 30-50 years old and is
two-to-three times more prevalent in women than in men. The cause of RA is
unknown, although genetic factors may contribute to the disease.
About Psoriatic Arthritis
Psoriatic arthritis is a chronic inflammatory arthropathy manifesting
with joint pain and swelling that can lead to joint destruction and
debilitation. It is frequently associated with inflamed, scaly, red patches
of skin psoriasis and psoriasis nail involvement. Symptoms may include
stiffness and tenderness of the joints and surrounding tissue and reduced
range of motion. Joints of the hands, wrists, knees, ankles, feet, lower
back and neck are commonly affected. Psoriasis affects an estimated two to
three percent of the world's population, and approximately one out of three
patients affected by psoriasis may develop psoriatic arthritis. Both men
and women are equally affected by psoriatic arthritis, most commonly
between the ages 30 and 50, in the peak of their productive years.
About Ankylosing Spondylitis
Ankylosing spondylitis (AS) is a painful and progressive form of spinal
arthritis and symptoms of inflammatory back pain often first present in
people before age 35. It typically begins in the late teens and early
twenties and in severe cases may result in fusing spinal vertebrae and may
cause structural damage to hips and other joints. Often misdiagnosed as
"just back pain" or undifferentiated arthritis, AS is a systemic
inflammatory disease that, in addition to its effect on the spine, can
affect internal organs, peripheral joints and vision. The Arthritis
Research Campaign estimates that on the European continent, AS prevalence
ranges from 0.2 to 1 percent of the entire population. The Spondylitis
Association of America estimates that between 350,000 and one million
people in the U.S. suffer from ankylosing spondylitis.
About Golimumab
Golimumab, Centocor, Inc.'s next-generation human anti-tumor necrosis
factor (TNF)-alpha monoclonal antibody, is currently in the most
comprehensive Phase 3 development program to date for an anti-TNF-alpha
biologic therapy. With ongoing studies for the treatment of rheumatoid
arthritis, psoriatic arthritis and ankylosing spondylitis, golimumab is
being studied as an every four week subcutaneous injection and an
intravenous (IV) infusion therapy. Golimumab targets and neutralizes both
the soluble and membrane-bound forms of TNF-alpha.
Centocor discovered golimumab and has exclusive marketing rights to the
product in the United States. Pending regulatory approval, Schering-Plough
will assume exclusive marketing rights outside the United States except in
Japan, Indonesia and Taiwan where golimumab will be co-marketed by
Mitsubishi Tanabe Pharma Corporation and Janssen Pharmaceutical Kabushiki
Kaisha; Hong Kong, where golimumab will be exclusively marketed by
Janssen-Cilag; and China where golimumab will be exclusively marketed by
Xian-Janssen.
About Centocor, Inc.
Centocor is harnessing the power of world-leading research and
biomanufacturing to deliver innovative biomedicines that transform
patients' lives. Centocor has already brought innovation to the treatment
of adult and pediatric Crohn's disease, rheumatoid arthritis, ankylosing
spondylitis, psoriatic arthritis, ulcerative colitis and psoriasis.
The world leader in monoclonal antibody production and technology,
Centocor has brought critical biologic therapies to patients suffering from
debilitating immune disorders. Centocor is a wholly-owned subsidiary of
Johnson & Johnson.
CENTOCOR DISCLOSURE NOTICE: This press release contains
"forward-looking statements" as defined in the Private Securities
Litigation Reform Act of 1995. These statements are based on current
expectations of future events. If underlying assumptions prove inaccurate
or unknown risks or uncertainties materialize, actual results could vary
materially from Centocor's expectations and projections. Risks and
uncertainties include general industry conditions and competition; economic
conditions, such as interest rate and currency exchange rate fluctuations;
technological advances and patents attained by competitors; challenges
inherent in new product development, including obtaining regulatory
approvals; domestic and foreign health care reforms and governmental laws
and regulations; and trends toward health care cost containment. A further
list and description of these risks, uncertainties and other factors can be
found in Exhibit 99 of Johnson & Johnson's Annual Report on Form 10-K for
the fiscal year ended December 30, 2007. Copies of this Form 10-K, as well
as subsequent filings, are available online at sec, jnj or
on request from Johnson & Johnson. Centocor does not undertake to update
any forward-looking statements as a result of new information or future
events or developments.
Centocor, Inc.
jnj
четверг, 16 июня 2011 г.
RCGP Comment On MHRA Announcemnet Re: NSAIDs And Coxibs
RCGP comment on the announcement made by the Medicines and Healthcare Products Regulatory Agency (MHRA) on the safety of selective and non-selective NSAIDs.
"The Royal College of General Practitioners (RCGP) would like to reassure patients who are on a small dose of non-selective NSAIDs and coxibs for a short period of time that this study indicates little risk. For patients on a high dosage for a long period of time, there is a small increase in risk but they should discuss this or any other concerns with their GP at their next routine appointment or with their pharmacist. GPs will work with patients to select a drug and a dosage that is right for them based on this latest information and on the patient's clinical history.
"The RCGP would like to reiterate its longstanding advice to restrain the use of NSAIDs and coxibs for definite clinical indications to the lowest possible dose and for the shortest period of time. If long term treatment is needed, then that need must be reviewed periodically."
Professor Mayur Lakhani, RCGP Chairman
For further information please go to:
Royal College of General Practitioners
"The Royal College of General Practitioners (RCGP) would like to reassure patients who are on a small dose of non-selective NSAIDs and coxibs for a short period of time that this study indicates little risk. For patients on a high dosage for a long period of time, there is a small increase in risk but they should discuss this or any other concerns with their GP at their next routine appointment or with their pharmacist. GPs will work with patients to select a drug and a dosage that is right for them based on this latest information and on the patient's clinical history.
"The RCGP would like to reiterate its longstanding advice to restrain the use of NSAIDs and coxibs for definite clinical indications to the lowest possible dose and for the shortest period of time. If long term treatment is needed, then that need must be reviewed periodically."
Professor Mayur Lakhani, RCGP Chairman
For further information please go to:
Royal College of General Practitioners
среда, 15 июня 2011 г.
FDA Expands REMICADE(R) Psoriatic Arthritis Indication: Anti-TNF Shown To Inhibit Joint Damage And Improve Physical Function
Centocor, Inc. announced today
that the U.S. Food and Drug Administration (FDA) has extended its approval
for REMICADE(R) (infliximab) for inhibiting progression of structural
damage and improving physical function in patients with psoriatic
arthritis, in addition to reducing signs and symptoms of active arthritis.
The approval is based on one-year data from the double-blind,
placebo-controlled trial IMPACT 2 and two-year data from the double-blind,
placebo-controlled trial IMPACT. Findings from IMPACT 2 showed that at week
24, REMICADE-treated patients had less structural damage as assessed
radiographically compared with patients receiving placebo (mean change
-0.70 vs. 0.82, P < 0.001), and REMICADE- treated patients were more than
twice as likely to achieve a clinically meaningful improvement in physical
function compared with patients receiving placebo (54 percent vs. 22
percent, respectively).
An immune-mediated inflammatory disease, psoriatic arthritis affects
approximately one million men and women in the U.S.(i) and is often
characterized by symptoms of joint inflammation and skin lesions. First
approved in 1998 for Crohn's disease, REMICADE has been used to treat over
770,000 patients worldwide living with gastroenterologic, rheumatologic and
dermatologic inflammatory diseases.
"The study findings supporting this approval show that treatment with
infliximab can slow the progression in joint destruction often associated
with this disease," said Arthur Kavanaugh, MD, Professor of Medicine at the
University of California at San Diego and lead study investigator. "A
significant proportion of infliximab-treated patients showed improvement in
physical function in addition to improvement in both joint and skin
symptoms, an important treatment outcome in a potentially debilitating
inflammatory disease like psoriatic arthritis."
One-year radiographic analyses from IMPACT 2 showed that treatment with
REMICADE resulted in significant inhibition of the progression of
structural damage, compared with placebo (as measured by the change from
baseline in van der Heijde-Sharp [vdH-S] score modified for psoriatic
arthritis by adding measurement for distal interphalangeal joints of the
hands). In this method, a higher change in score indicates greater
progression of structural damage, while lower change in score indicates
less progression of structural damage. At 24 weeks of treatment,
REMICADE-treated patients experienced a mean change (+/- standard
deviation) in vdH-S score of -0.70 (+/- 2.53) from baseline, compared with
an average change of 0.82 (+/- 2.62) in the placebo group (P < 0.001). At
week 54, patients who received a full 54-week regimen of REMICADE
experienced a mean change of -0.94 (+/- 3.40) from baseline, compared with
an average change of 0.53 (+/- 2.60) in patients who crossed over from
placebo to REMICADE (P = 0.001) at week 16 or 24.
In terms of the skin component of the disease, 50 percent of REMICADE-
treated patients in IMPACT 2 maintained at least 75 percent improvement
from baseline, as assessed by Psoriasis Area Severity Index (PASI 75), in
psoriasis at one year, and 64 percent of REMICADE-treated patients in
IMPACT maintained PASI 75 through two years. Moreover, 42 percent of
REMICADE-treated patients in IMPACT 2 achieved PASI 90, or near total skin
clearance, at one year, and 48 percent in IMPACT achieved PASI 90 through
two years.
REMICADE-treated patients demonstrated significant improvement in
physical function as measured by the Health Assessment
Questionnaire-Disability Index (HAQ-DI). The HAQ-DI assesses the difficulty
a patient has accomplishing tasks in eight functional areas (dressing,
arising, eating, walking, hygiene, reaching, gripping and other activities
of daily living). By week 14 of the IMPACT 2 trial, patients in the
REMICADE group experienced a median improvement of 43 percent, compared
with zero percent in the placebo group (P < 0.001), and results were
maintained through one year. At week 54 of IMPACT 2, there was a median 50
percent improvement in HAQ-DI score from baseline in the group randomized
to REMICADE, and a 46 percent improvement in placebo patients who switched
to REMICADE. At week 16 of the IMPACT trial, REMICADE- treated patients
demonstrated a median improvement in HAQ-DI score of 50 percent versus two
percent in the placebo group (P < 0.01); these responses were generally
sustained through two years.
In May 2005, REMICADE was approved in the United States for reducing
signs and symptoms of active arthritis in patients with psoriatic
arthritis. In September 2004, REMICADE received European Union (EU)
approval, in combination with methotrexate, for the treatment of active and
progressive psoriatic arthritis in patients who have responded inadequately
to disease-modifying anti-rheumatic drugs (DMARDs). Additionally, in July
2006, the European Commission approved the use of REMICADE for the
treatment of active and progressive psoriatic arthritis in patients who
have responded inadequately to DMARDs to be used in combination with
methotrexate or alone in patients who show intolerance to methotrexate or
in whom methotrexate is contraindicated.
About IMPACT/IMPACT 2
The Infliximab Multinational Psoriatic Arthritis Controlled Trial
(IMPACT) was a Phase 2b randomized, double-blind, placebo-controlled study
that involved 104 patients with active psoriatic arthritis (defined as
affecting at least five joints) who failed at least one DMARD. Patients
received either REMICADE (5 mg/kg) or placebo, administered at weeks 0, 2,
6 and 14. The REMICADE group continued on maintenance treatments every
eight weeks through week 94. Beginning at week 16, patients randomized to
the placebo group received an induction regimen of REMICADE followed by
maintenance treatment every eight weeks through week 94. Hands and feet
radiographs were taken at screening and at weeks 50 and 98. Physical
function was measured at multiple visits including screening and at weeks
16, 22, 50 and 94.
REMICADE was generally well tolerated in this study, with one REMICADE
and one placebo patient experiencing serious adverse events (AEs) in the
placebo- controlled portion of the study through week 16. Fourteen patients
out of 104 experienced serious AEs from week 16 through 50 in
placebo/REMICADE crossover and REMICADE groups together. In the second year
of IMPACT, seven patients out of 78 treated with REMICADE were reported
with serious AEs. No deaths, cases of tuberculosis or other opportunistic
infections were reported and serious infections were uncommon. There were
no serious infusion reactions. One patient had a serious AE relating to
malignancy: a ductal adenocarcinoma of the pancreas three months after week
98. See "Important Safety Information" below.
The Induction and Maintenance of Psoriatic Arthritis Clinical Trial 2
(IMPACT 2) was a Phase 3, randomized, double-blind, placebo-controlled
study of 200 patients with active psoriatic arthritis (defined as affecting
at least five joints). The study evaluated the safety and efficacy of
REMICADE in patients who had an inadequate response to DMARDs or
nonsteroidal anti- inflammatory drugs (NSAIDs). Patients received REMICADE
(5 mg/kg) at weeks 0, 2, 6 and every 8 weeks until week 46 or placebo at
weeks 0, 2, 6, 14 and 22. Placebo patients with less than 10 percent
improvement in both swollen and tender joints at week 16 entered early
escape and received REMICADE at weeks 16, 18 and 22 (n=47). At week 24,
placebo patients who did not qualify for early escape received REMICADE at
weeks 24, 26, 30, 38 and 46. Patients randomized to REMICADE who had less
than 20 percent improvement in combined swollen and tender joint count at
week 38 received REMICADE 10 mg/kg at weeks 38 and 46 (n=15). Patients were
allowed concomitant methotrexate use at a stable dose. Hand and foot
radiographs were taken at weeks 0, 24 and 54. Physical function was
measured at multiple visits including weeks 0, 14, 24 and 54.
Through 54 weeks, 12 percent of patients in combined REMICADE treatment
groups experienced serious AEs (during average follow-up of 42.8 weeks) as
compared to 6 percent of placebo patients (average follow-up 20.2 weeks).
No deaths, cases of tuberculosis or other opportunistic infections or
serious infusion reactions were reported; serious infections were uncommon.
Two patients reported an AE of malignancy: one case of basal cell carcinoma
in the placebo group and one case of stage I Hodgkin lymphoma in the
REMICADE group. The only laboratory abnormalities that occurred more
frequently with REMICADE compared with placebo were asymptomatic liver
enzyme test elevations. See "Important Safety Information" below.
About Psoriatic Arthritis
Psoriatic arthritis is a chronic inflammatory arthropathy manifesting
with joint pain and swelling that can lead to joint destruction and
debilitation. It is frequently associated with inflamed, scaly, red patches
of skin psoriasis. Symptoms may include stiffness and tenderness of the
joints and surrounding tissue, reduced range of motion, nail changes and
redness and pain of the eye (uveitis). Joints of the hands, wrists, knees,
ankles, feet, lower back and neck are commonly affected. Psoriasis affects
an estimated two to three percent of the world's population, and
approximately one out of three patients affected by psoriasis may develop
psoriatic arthritis. Both men and women are equally affected by psoriatic
arthritis, most commonly between the ages of 30 and 50, in the peak of
their productive years.
About REMICADE
REMICADE is the global market leader among anti-tumor necrosis factor
alpha (TNF-alpha) therapies and has demonstrated broad clinical utility in
Crohn's disease (CD), rheumatoid arthritis (RA), ankylosing spondylitis
(AS), psoriatic arthritis (PsA), ulcerative colitis (UC), and pediatric
Crohn's disease (PCD). The safety and efficacy of REMICADE have been well
established in clinical trials over the past 14 years and with more than
770,000 patients treated worldwide through commercial experience.
In the U.S., REMICADE, in combination with methotrexate, is indicated
for reducing signs and symptoms, inhibiting the progression of structural
damage and improving physical function in patients with moderately to
severely active RA. REMICADE is the only biologic indicated for reducing
signs and symptoms and inducing and maintaining clinical remission in adult
and pediatric patients with moderately to severely active CD who have had
an inadequate response to conventional therapy. REMICADE is also indicated
for reducing the number of draining enterocutaneous and rectovaginal
fistulas and maintaining fistula closure in patients with fistulizing CD.
In December 2004, REMICADE was approved for reducing signs and symptoms in
patients with active AS. In May 2005, REMICADE was approved for reducing
signs and symptoms of active arthritis in patients with PsA. Additionally,
in September 2005, REMICADE was approved for reducing signs and symptoms,
achieving clinical remission and mucosal healing, and eliminating
corticosteroid use in patients with moderately to severely active UC who
have had an inadequate response to conventional therapy. This approval
makes REMICADE the first and only biologic approved for the treatment of
moderate to severe UC. In addition, on May 19, 2006, REMICADE was approved
for reducing signs and symptoms and inducing and maintaining clinical
remission in pediatric patients with moderately to severely active Crohn's
disease who have had an inadequate response to conventional therapy. This
approval establishes REMICADE as the first and only biologic therapy
approved for the treatment of PCD.
REMICADE is unique among available anti-TNF biologic therapies. Unlike
self-administered therapies that require patients to inject themselves
frequently, REMICADE is the only anti-TNF biologic administered directly by
caregivers in the clinic or office setting. In RA (3 mg/kg), CD (5 mg/kg),
PsA (5 mg/kg), UC (5 mg/kg), and PCD (5 mg/kg) REMICADE is a two-hour
infusion administered every 8 weeks, following a standard induction regimen
that requires treatment at weeks 0, 2 and 6. As a result, REMICADE patients
may require as few as six treatments each year. In AS (5 mg/kg), REMICADE
is a two-hour infusion administered every 6 weeks, following a standard
induction regimen that requires treatment at weeks 0, 2 and 6.
Important Safety Information
Many people with heart failure should not take REMICADE; so prior to
treatment you should discuss any heart condition with your doctor. Tell
your doctor right away if you develop new or worsening symptoms of heart
failure (such as shortness of breath or swelling of your ankles or feet).
There are reports of serious infections, including tuberculosis (TB),
sepsis and pneumonia. Some of these infections have been fatal. Tell your
doctor if you have had recent or past exposure to people with TB. Your
doctor will evaluate you for TB and perform a skin test. If you have latent
(inactive) TB, your doctor should begin TB treatment before you start
REMICADE. REMICADE can lower your ability to fight infections, so if you
are prone to or have a history of infections, or develop any signs of an
infection such as fever, fatigue, cough, or the flu while taking REMICADE,
tell your doctor right away. Also tell your doctor if you have lived in a
region where histoplasmosis or coccidioidomycosis is common.
Reports of a type of blood cancer called lymphoma in patients on
REMICADE or other TNF blockers are rare but occur more often than expected
for people in general. People who have been treated for rheumatoid
arthritis, Crohn's disease, ankylosing spondylitis, or psoriatic arthritis
for a long time, particularly those with highly active disease may be more
prone to develop lymphoma. Cancers, other than lymphoma, have also been
reported. Children and young adults who have been treated for Crohn's
disease with REMICADE have developed a rare type of lymphoma that often
results in death. These patients also were receiving drugs known as
azathioprine or 6-mercaptopurine. If you take REMICADE or other TNF
blockers, your risk for developing lymphoma or other cancers may increase.
You should also tell your doctor if you have had or develop lymphoma or
other cancers or if you have a lung disease called chronic obstructive
pulmonary disease (COPD). Reactivation of hepatitis B virus has been
reported in patients who are carriers of this virus and are taking TNF
blockers, such as REMICADE. Some of these cases have been fatal. Tell your
doctor if you know or think you may be a carrier of hepatitis B virus.
There have been rare cases of serious liver injury in people taking
REMICADE, some fatal. Contact your doctor immediately if you develop
symptoms such as jaundice (yellow skin and eyes), dark brown urine,
right-sided abdominal pain, fever, or severe fatigue.
Blood disorders have been reported, some fatal. Tell your doctor if you
develop possible signs of blood disorders such as persistent fever,
bruising, bleeding, or paleness while taking REMICADE. Nervous system
disorders have also been reported. Tell your doctor if you have or have had
a disease that affects the nervous system, or if you experience any
numbness, weakness, tingling, or visual disturbances while taking REMICADE.
Serious infusion reactions have been reported with REMICADE, including
hives, difficulty breathing, and low blood pressure. Reactions have
occurred during or after infusions. In clinical studies, some people
experienced the following common side effects: respiratory infections (that
may include sinus infections and sore throat), coughing, and stomach pain
or mild reactions to infusion such as rash or itchy skin.
Please read important information about REMICADE, including full U.S.
prescribing information, at remicade.
About Centocor
Centocor is harnessing the power of world-leading research and
biomanufacturing to deliver innovative biomedicines that transform
patients' lives. Centocor has already brought innovation to the treatment
of Crohn's disease, rheumatoid arthritis, ankylosing spondylitis, psoriatic
arthritis, ulcerative colitis and pediatric Crohn's disease.
The world leader in monoclonal antibody production and technology,
Centocor has brought critical biologic therapies to patients suffering from
debilitating immune disorders. Centocor, Inc. is a wholly owned subsidiary
of Johnson & Johnson.
(i) National Institute of Arthritis and Musculoskeletal and Skin
Disorders. Questions and Answers About Psoriasis. U.S. Department of Health
and Human Services, National Institutes of Health; 2003. NIH Publication
No. 03-5040.
Centocor, Inc.
remicade
View drug information on Remicade.
that the U.S. Food and Drug Administration (FDA) has extended its approval
for REMICADE(R) (infliximab) for inhibiting progression of structural
damage and improving physical function in patients with psoriatic
arthritis, in addition to reducing signs and symptoms of active arthritis.
The approval is based on one-year data from the double-blind,
placebo-controlled trial IMPACT 2 and two-year data from the double-blind,
placebo-controlled trial IMPACT. Findings from IMPACT 2 showed that at week
24, REMICADE-treated patients had less structural damage as assessed
radiographically compared with patients receiving placebo (mean change
-0.70 vs. 0.82, P < 0.001), and REMICADE- treated patients were more than
twice as likely to achieve a clinically meaningful improvement in physical
function compared with patients receiving placebo (54 percent vs. 22
percent, respectively).
An immune-mediated inflammatory disease, psoriatic arthritis affects
approximately one million men and women in the U.S.(i) and is often
characterized by symptoms of joint inflammation and skin lesions. First
approved in 1998 for Crohn's disease, REMICADE has been used to treat over
770,000 patients worldwide living with gastroenterologic, rheumatologic and
dermatologic inflammatory diseases.
"The study findings supporting this approval show that treatment with
infliximab can slow the progression in joint destruction often associated
with this disease," said Arthur Kavanaugh, MD, Professor of Medicine at the
University of California at San Diego and lead study investigator. "A
significant proportion of infliximab-treated patients showed improvement in
physical function in addition to improvement in both joint and skin
symptoms, an important treatment outcome in a potentially debilitating
inflammatory disease like psoriatic arthritis."
One-year radiographic analyses from IMPACT 2 showed that treatment with
REMICADE resulted in significant inhibition of the progression of
structural damage, compared with placebo (as measured by the change from
baseline in van der Heijde-Sharp [vdH-S] score modified for psoriatic
arthritis by adding measurement for distal interphalangeal joints of the
hands). In this method, a higher change in score indicates greater
progression of structural damage, while lower change in score indicates
less progression of structural damage. At 24 weeks of treatment,
REMICADE-treated patients experienced a mean change (+/- standard
deviation) in vdH-S score of -0.70 (+/- 2.53) from baseline, compared with
an average change of 0.82 (+/- 2.62) in the placebo group (P < 0.001). At
week 54, patients who received a full 54-week regimen of REMICADE
experienced a mean change of -0.94 (+/- 3.40) from baseline, compared with
an average change of 0.53 (+/- 2.60) in patients who crossed over from
placebo to REMICADE (P = 0.001) at week 16 or 24.
In terms of the skin component of the disease, 50 percent of REMICADE-
treated patients in IMPACT 2 maintained at least 75 percent improvement
from baseline, as assessed by Psoriasis Area Severity Index (PASI 75), in
psoriasis at one year, and 64 percent of REMICADE-treated patients in
IMPACT maintained PASI 75 through two years. Moreover, 42 percent of
REMICADE-treated patients in IMPACT 2 achieved PASI 90, or near total skin
clearance, at one year, and 48 percent in IMPACT achieved PASI 90 through
two years.
REMICADE-treated patients demonstrated significant improvement in
physical function as measured by the Health Assessment
Questionnaire-Disability Index (HAQ-DI). The HAQ-DI assesses the difficulty
a patient has accomplishing tasks in eight functional areas (dressing,
arising, eating, walking, hygiene, reaching, gripping and other activities
of daily living). By week 14 of the IMPACT 2 trial, patients in the
REMICADE group experienced a median improvement of 43 percent, compared
with zero percent in the placebo group (P < 0.001), and results were
maintained through one year. At week 54 of IMPACT 2, there was a median 50
percent improvement in HAQ-DI score from baseline in the group randomized
to REMICADE, and a 46 percent improvement in placebo patients who switched
to REMICADE. At week 16 of the IMPACT trial, REMICADE- treated patients
demonstrated a median improvement in HAQ-DI score of 50 percent versus two
percent in the placebo group (P < 0.01); these responses were generally
sustained through two years.
In May 2005, REMICADE was approved in the United States for reducing
signs and symptoms of active arthritis in patients with psoriatic
arthritis. In September 2004, REMICADE received European Union (EU)
approval, in combination with methotrexate, for the treatment of active and
progressive psoriatic arthritis in patients who have responded inadequately
to disease-modifying anti-rheumatic drugs (DMARDs). Additionally, in July
2006, the European Commission approved the use of REMICADE for the
treatment of active and progressive psoriatic arthritis in patients who
have responded inadequately to DMARDs to be used in combination with
methotrexate or alone in patients who show intolerance to methotrexate or
in whom methotrexate is contraindicated.
About IMPACT/IMPACT 2
The Infliximab Multinational Psoriatic Arthritis Controlled Trial
(IMPACT) was a Phase 2b randomized, double-blind, placebo-controlled study
that involved 104 patients with active psoriatic arthritis (defined as
affecting at least five joints) who failed at least one DMARD. Patients
received either REMICADE (5 mg/kg) or placebo, administered at weeks 0, 2,
6 and 14. The REMICADE group continued on maintenance treatments every
eight weeks through week 94. Beginning at week 16, patients randomized to
the placebo group received an induction regimen of REMICADE followed by
maintenance treatment every eight weeks through week 94. Hands and feet
radiographs were taken at screening and at weeks 50 and 98. Physical
function was measured at multiple visits including screening and at weeks
16, 22, 50 and 94.
REMICADE was generally well tolerated in this study, with one REMICADE
and one placebo patient experiencing serious adverse events (AEs) in the
placebo- controlled portion of the study through week 16. Fourteen patients
out of 104 experienced serious AEs from week 16 through 50 in
placebo/REMICADE crossover and REMICADE groups together. In the second year
of IMPACT, seven patients out of 78 treated with REMICADE were reported
with serious AEs. No deaths, cases of tuberculosis or other opportunistic
infections were reported and serious infections were uncommon. There were
no serious infusion reactions. One patient had a serious AE relating to
malignancy: a ductal adenocarcinoma of the pancreas three months after week
98. See "Important Safety Information" below.
The Induction and Maintenance of Psoriatic Arthritis Clinical Trial 2
(IMPACT 2) was a Phase 3, randomized, double-blind, placebo-controlled
study of 200 patients with active psoriatic arthritis (defined as affecting
at least five joints). The study evaluated the safety and efficacy of
REMICADE in patients who had an inadequate response to DMARDs or
nonsteroidal anti- inflammatory drugs (NSAIDs). Patients received REMICADE
(5 mg/kg) at weeks 0, 2, 6 and every 8 weeks until week 46 or placebo at
weeks 0, 2, 6, 14 and 22. Placebo patients with less than 10 percent
improvement in both swollen and tender joints at week 16 entered early
escape and received REMICADE at weeks 16, 18 and 22 (n=47). At week 24,
placebo patients who did not qualify for early escape received REMICADE at
weeks 24, 26, 30, 38 and 46. Patients randomized to REMICADE who had less
than 20 percent improvement in combined swollen and tender joint count at
week 38 received REMICADE 10 mg/kg at weeks 38 and 46 (n=15). Patients were
allowed concomitant methotrexate use at a stable dose. Hand and foot
radiographs were taken at weeks 0, 24 and 54. Physical function was
measured at multiple visits including weeks 0, 14, 24 and 54.
Through 54 weeks, 12 percent of patients in combined REMICADE treatment
groups experienced serious AEs (during average follow-up of 42.8 weeks) as
compared to 6 percent of placebo patients (average follow-up 20.2 weeks).
No deaths, cases of tuberculosis or other opportunistic infections or
serious infusion reactions were reported; serious infections were uncommon.
Two patients reported an AE of malignancy: one case of basal cell carcinoma
in the placebo group and one case of stage I Hodgkin lymphoma in the
REMICADE group. The only laboratory abnormalities that occurred more
frequently with REMICADE compared with placebo were asymptomatic liver
enzyme test elevations. See "Important Safety Information" below.
About Psoriatic Arthritis
Psoriatic arthritis is a chronic inflammatory arthropathy manifesting
with joint pain and swelling that can lead to joint destruction and
debilitation. It is frequently associated with inflamed, scaly, red patches
of skin psoriasis. Symptoms may include stiffness and tenderness of the
joints and surrounding tissue, reduced range of motion, nail changes and
redness and pain of the eye (uveitis). Joints of the hands, wrists, knees,
ankles, feet, lower back and neck are commonly affected. Psoriasis affects
an estimated two to three percent of the world's population, and
approximately one out of three patients affected by psoriasis may develop
psoriatic arthritis. Both men and women are equally affected by psoriatic
arthritis, most commonly between the ages of 30 and 50, in the peak of
their productive years.
About REMICADE
REMICADE is the global market leader among anti-tumor necrosis factor
alpha (TNF-alpha) therapies and has demonstrated broad clinical utility in
Crohn's disease (CD), rheumatoid arthritis (RA), ankylosing spondylitis
(AS), psoriatic arthritis (PsA), ulcerative colitis (UC), and pediatric
Crohn's disease (PCD). The safety and efficacy of REMICADE have been well
established in clinical trials over the past 14 years and with more than
770,000 patients treated worldwide through commercial experience.
In the U.S., REMICADE, in combination with methotrexate, is indicated
for reducing signs and symptoms, inhibiting the progression of structural
damage and improving physical function in patients with moderately to
severely active RA. REMICADE is the only biologic indicated for reducing
signs and symptoms and inducing and maintaining clinical remission in adult
and pediatric patients with moderately to severely active CD who have had
an inadequate response to conventional therapy. REMICADE is also indicated
for reducing the number of draining enterocutaneous and rectovaginal
fistulas and maintaining fistula closure in patients with fistulizing CD.
In December 2004, REMICADE was approved for reducing signs and symptoms in
patients with active AS. In May 2005, REMICADE was approved for reducing
signs and symptoms of active arthritis in patients with PsA. Additionally,
in September 2005, REMICADE was approved for reducing signs and symptoms,
achieving clinical remission and mucosal healing, and eliminating
corticosteroid use in patients with moderately to severely active UC who
have had an inadequate response to conventional therapy. This approval
makes REMICADE the first and only biologic approved for the treatment of
moderate to severe UC. In addition, on May 19, 2006, REMICADE was approved
for reducing signs and symptoms and inducing and maintaining clinical
remission in pediatric patients with moderately to severely active Crohn's
disease who have had an inadequate response to conventional therapy. This
approval establishes REMICADE as the first and only biologic therapy
approved for the treatment of PCD.
REMICADE is unique among available anti-TNF biologic therapies. Unlike
self-administered therapies that require patients to inject themselves
frequently, REMICADE is the only anti-TNF biologic administered directly by
caregivers in the clinic or office setting. In RA (3 mg/kg), CD (5 mg/kg),
PsA (5 mg/kg), UC (5 mg/kg), and PCD (5 mg/kg) REMICADE is a two-hour
infusion administered every 8 weeks, following a standard induction regimen
that requires treatment at weeks 0, 2 and 6. As a result, REMICADE patients
may require as few as six treatments each year. In AS (5 mg/kg), REMICADE
is a two-hour infusion administered every 6 weeks, following a standard
induction regimen that requires treatment at weeks 0, 2 and 6.
Important Safety Information
Many people with heart failure should not take REMICADE; so prior to
treatment you should discuss any heart condition with your doctor. Tell
your doctor right away if you develop new or worsening symptoms of heart
failure (such as shortness of breath or swelling of your ankles or feet).
There are reports of serious infections, including tuberculosis (TB),
sepsis and pneumonia. Some of these infections have been fatal. Tell your
doctor if you have had recent or past exposure to people with TB. Your
doctor will evaluate you for TB and perform a skin test. If you have latent
(inactive) TB, your doctor should begin TB treatment before you start
REMICADE. REMICADE can lower your ability to fight infections, so if you
are prone to or have a history of infections, or develop any signs of an
infection such as fever, fatigue, cough, or the flu while taking REMICADE,
tell your doctor right away. Also tell your doctor if you have lived in a
region where histoplasmosis or coccidioidomycosis is common.
Reports of a type of blood cancer called lymphoma in patients on
REMICADE or other TNF blockers are rare but occur more often than expected
for people in general. People who have been treated for rheumatoid
arthritis, Crohn's disease, ankylosing spondylitis, or psoriatic arthritis
for a long time, particularly those with highly active disease may be more
prone to develop lymphoma. Cancers, other than lymphoma, have also been
reported. Children and young adults who have been treated for Crohn's
disease with REMICADE have developed a rare type of lymphoma that often
results in death. These patients also were receiving drugs known as
azathioprine or 6-mercaptopurine. If you take REMICADE or other TNF
blockers, your risk for developing lymphoma or other cancers may increase.
You should also tell your doctor if you have had or develop lymphoma or
other cancers or if you have a lung disease called chronic obstructive
pulmonary disease (COPD). Reactivation of hepatitis B virus has been
reported in patients who are carriers of this virus and are taking TNF
blockers, such as REMICADE. Some of these cases have been fatal. Tell your
doctor if you know or think you may be a carrier of hepatitis B virus.
There have been rare cases of serious liver injury in people taking
REMICADE, some fatal. Contact your doctor immediately if you develop
symptoms such as jaundice (yellow skin and eyes), dark brown urine,
right-sided abdominal pain, fever, or severe fatigue.
Blood disorders have been reported, some fatal. Tell your doctor if you
develop possible signs of blood disorders such as persistent fever,
bruising, bleeding, or paleness while taking REMICADE. Nervous system
disorders have also been reported. Tell your doctor if you have or have had
a disease that affects the nervous system, or if you experience any
numbness, weakness, tingling, or visual disturbances while taking REMICADE.
Serious infusion reactions have been reported with REMICADE, including
hives, difficulty breathing, and low blood pressure. Reactions have
occurred during or after infusions. In clinical studies, some people
experienced the following common side effects: respiratory infections (that
may include sinus infections and sore throat), coughing, and stomach pain
or mild reactions to infusion such as rash or itchy skin.
Please read important information about REMICADE, including full U.S.
prescribing information, at remicade.
About Centocor
Centocor is harnessing the power of world-leading research and
biomanufacturing to deliver innovative biomedicines that transform
patients' lives. Centocor has already brought innovation to the treatment
of Crohn's disease, rheumatoid arthritis, ankylosing spondylitis, psoriatic
arthritis, ulcerative colitis and pediatric Crohn's disease.
The world leader in monoclonal antibody production and technology,
Centocor has brought critical biologic therapies to patients suffering from
debilitating immune disorders. Centocor, Inc. is a wholly owned subsidiary
of Johnson & Johnson.
(i) National Institute of Arthritis and Musculoskeletal and Skin
Disorders. Questions and Answers About Psoriasis. U.S. Department of Health
and Human Services, National Institutes of Health; 2003. NIH Publication
No. 03-5040.
Centocor, Inc.
remicade
View drug information on Remicade.
вторник, 14 июня 2011 г.
Moderate Weight Loss Helps Reduce Risk Of Osteoarthritis In The Knee, Maintaining Weight Provides No Benefit
Here's another good reason to lose even a moderate amount of weight: it could reduce your risk of developing osteoarthritis in your knees.
People who are overweight and lose just 5 percent of their weight are less likely to develop osteoarthritis of the knee, or knee OA, compared to people who gain weight, according to data from a large ongoing study by the Thurston Arthritis Research Center at the University of North Carolina at Chapel Hill School of Medicine.
"We hear a lot of messages about how obesity affects cardiovascular disease and diabetes, but arthritis is often overlooked," says Lauren Abbate, a third-year medical student at UNC and lead investigator of the knee OA paper, presented Monday, Oct. 19, 2009, at the American College of Rheumatology scientific meeting in Philadelphia.
"OA is painful and debilitating. Effective treatments are limited and there's not a cure. But if we can get people to lose weight we may reduce their risk and reduce the pain and disability associated with this condition," Abbate says.
More than 27 million Americans have OA, the most common joint disease affecting middle-aged and older people. OA causes progressive damage to the joint cartilage and changes in the structures around the joint, which can include fluid accumulation, bony overgrowth and loosening and weakness of muscles and tendons, all of which may limit movement and cause pain and swelling.
Abbate and her colleagues used data from the Johnston County Osteoarthritis Project, one of the largest ongoing population-based studies of arthritis in the world. It began at Thurston in 1990 and is funded by the Centers for Disease Control and Prevention and the National Institutes of Health.
The researchers included 1,480 men and women 45 and older who were disease-free in at least one knee and followed them for approximately six years to see who developed radiographic OA - disease confirmed by X-rays; almost two-thirds were women, and more than 25 percent were African Americans.
They then divided people into categories based on weight change: people who lost 5 percent or more of their total body weight, people who maintained within 3 percent above or below their weight and those who gained at least 5 percent more than their weight.
"It was our hope that people who maintained weight would have reduced risk, but obesity is such a strong risk factor for OA, that maintaining weight showed no significant benefit," says Abbate, who recently finished her doctoral degree in epidemiology from the UNC Gillings School of Global Public Health. She also has a master's of science in public health from the school.
Weight loss can be difficult to achieve. But, Abbate says, people can aim for losing a certain percentage of their weight instead of shooting for an ideal number. "For someone who weighs 200 pounds, losing 5 percent just means losing 10 pounds," she says.
Abbate's paper was one of several research highlights at the ACR meeting for UNC's Thurston Arthritis Research Center. Abbate and two other UNC medical students, Joshua Knight, a second-year student, and Shelby Addison, a third-year student, won research awards. Amanda Nelson, M.D., a fellow at Thurston, won a fellowship award.
"We have placed a high priority on working with medical and graduate students and being open to collaborating," says Joanne Jordan, M.D., the center director and Herman and Louise Smith Distinguished Professor of Medicine at UNC's School of Medicine. Jordan received the ACR's Award of Distinction for Excellence in Investigative Mentoring.
"We take our role as the arthritis research center for the people of North Carolina very seriously," Jordan said. "That is why we are always looking for ways to bring our research findings to the community and to learn from the community."
Source
University of North Carolina at Chapel Hill School of Medicine
People who are overweight and lose just 5 percent of their weight are less likely to develop osteoarthritis of the knee, or knee OA, compared to people who gain weight, according to data from a large ongoing study by the Thurston Arthritis Research Center at the University of North Carolina at Chapel Hill School of Medicine.
"We hear a lot of messages about how obesity affects cardiovascular disease and diabetes, but arthritis is often overlooked," says Lauren Abbate, a third-year medical student at UNC and lead investigator of the knee OA paper, presented Monday, Oct. 19, 2009, at the American College of Rheumatology scientific meeting in Philadelphia.
"OA is painful and debilitating. Effective treatments are limited and there's not a cure. But if we can get people to lose weight we may reduce their risk and reduce the pain and disability associated with this condition," Abbate says.
More than 27 million Americans have OA, the most common joint disease affecting middle-aged and older people. OA causes progressive damage to the joint cartilage and changes in the structures around the joint, which can include fluid accumulation, bony overgrowth and loosening and weakness of muscles and tendons, all of which may limit movement and cause pain and swelling.
Abbate and her colleagues used data from the Johnston County Osteoarthritis Project, one of the largest ongoing population-based studies of arthritis in the world. It began at Thurston in 1990 and is funded by the Centers for Disease Control and Prevention and the National Institutes of Health.
The researchers included 1,480 men and women 45 and older who were disease-free in at least one knee and followed them for approximately six years to see who developed radiographic OA - disease confirmed by X-rays; almost two-thirds were women, and more than 25 percent were African Americans.
They then divided people into categories based on weight change: people who lost 5 percent or more of their total body weight, people who maintained within 3 percent above or below their weight and those who gained at least 5 percent more than their weight.
"It was our hope that people who maintained weight would have reduced risk, but obesity is such a strong risk factor for OA, that maintaining weight showed no significant benefit," says Abbate, who recently finished her doctoral degree in epidemiology from the UNC Gillings School of Global Public Health. She also has a master's of science in public health from the school.
Weight loss can be difficult to achieve. But, Abbate says, people can aim for losing a certain percentage of their weight instead of shooting for an ideal number. "For someone who weighs 200 pounds, losing 5 percent just means losing 10 pounds," she says.
Abbate's paper was one of several research highlights at the ACR meeting for UNC's Thurston Arthritis Research Center. Abbate and two other UNC medical students, Joshua Knight, a second-year student, and Shelby Addison, a third-year student, won research awards. Amanda Nelson, M.D., a fellow at Thurston, won a fellowship award.
"We have placed a high priority on working with medical and graduate students and being open to collaborating," says Joanne Jordan, M.D., the center director and Herman and Louise Smith Distinguished Professor of Medicine at UNC's School of Medicine. Jordan received the ACR's Award of Distinction for Excellence in Investigative Mentoring.
"We take our role as the arthritis research center for the people of North Carolina very seriously," Jordan said. "That is why we are always looking for ways to bring our research findings to the community and to learn from the community."
Source
University of North Carolina at Chapel Hill School of Medicine
понедельник, 13 июня 2011 г.
Vioxx Successor Arcoxia May Have Similar Heart Attack Risks
Arcoxia, a new experimental painkiller Merck & Co hope will become the successor of Vioxx, which was taken off the market because of its heart attack risks, may have similar risks, say scientists who looked at 23 clinical trials comparing several painkillers.
You can read about this new report in JAMA (the Journal of the American Medical Association).
In fact, the report showed that Vioxx and diclofenac carried similar cardiovascular risks (diclofenac is a much older painkiller). According to a Merck study, Arcoxia and diclofenac (Voltaren) have the same risks.
Vioxx raises cardiovascular risk by approximately 35%, diclofenac raises cardiovascular risk by about 40%. Voltaren (diclofenac) is currently sold in 62 countries.
By arguing that Arcoxia is no worse than diclofenac will not logically get it approved by the FDA if Vioxx and diclofenac carried similar risks. Arcoxia has already been turned down by the FDA (2004) because of insufficient safety data.
If you found the information above confusing, perhaps the alternative explanation below may make it clearer.
1. Vioxx was taken off the market some time ago because of heart attack and stroke risk.
2. Voltaren (diclofenac) is still sold in 62 countries and has similar risks to Vioxx.
3. Merck compares Arcoxia, a new experimental drug, to diclofenac, saying Arcoxia has similar risks. As the drug is still on the market it is saying Arcoxia is not more dangerous than a drug which is still on the market.
4. Why would the FDA approve Arcoxia if it has similar risks to diclofenac, which has similar risks to Vioxx?
"COX-2 Inhibitors, Other NSAIDs, and Cardiovascular Risk"
"The Seduction of Common Sense"
David J. Graham, MD, MPH
JAMA. 2006;296:(doi:10.1001/jama.296.13.jed60058).
Click Here To Read Article Online
Written by:
View drug information on Vioxx.
You can read about this new report in JAMA (the Journal of the American Medical Association).
In fact, the report showed that Vioxx and diclofenac carried similar cardiovascular risks (diclofenac is a much older painkiller). According to a Merck study, Arcoxia and diclofenac (Voltaren) have the same risks.
Vioxx raises cardiovascular risk by approximately 35%, diclofenac raises cardiovascular risk by about 40%. Voltaren (diclofenac) is currently sold in 62 countries.
By arguing that Arcoxia is no worse than diclofenac will not logically get it approved by the FDA if Vioxx and diclofenac carried similar risks. Arcoxia has already been turned down by the FDA (2004) because of insufficient safety data.
If you found the information above confusing, perhaps the alternative explanation below may make it clearer.
1. Vioxx was taken off the market some time ago because of heart attack and stroke risk.
2. Voltaren (diclofenac) is still sold in 62 countries and has similar risks to Vioxx.
3. Merck compares Arcoxia, a new experimental drug, to diclofenac, saying Arcoxia has similar risks. As the drug is still on the market it is saying Arcoxia is not more dangerous than a drug which is still on the market.
4. Why would the FDA approve Arcoxia if it has similar risks to diclofenac, which has similar risks to Vioxx?
"COX-2 Inhibitors, Other NSAIDs, and Cardiovascular Risk"
"The Seduction of Common Sense"
David J. Graham, MD, MPH
JAMA. 2006;296:(doi:10.1001/jama.296.13.jed60058).
Click Here To Read Article Online
Written by:
View drug information on Vioxx.
воскресенье, 12 июня 2011 г.
Key Clinical Studies Of Regeneron's ARCALYST (rilonacept) For Treatment Of CAPS Published
Regeneron Pharmaceuticals, Inc. (Nasdaq: REGN) announced the publication of the results of three studies which supported the U.S. Food and Drug Administration (FDA) regulatory submission for ARCALYST® (rilonacept) Injection for Subcutaneous Use for the treatment of Cryopyrin-Associated Periodic Syndromes (CAPS).
Two studies were published in the August 2008 issue of Arthritis and Rheumatism, the flagship publication of the American College of Rheumatology. The first study was the preliminary trial to evaluate the impact of ARCALYST on markers of inflammation, clinical response, and safety and the second was the pivotal efficacy and safety clinical trial of ARCALYST. A third study, conducted to develop and validate a key symptoms assessment scale for CAPS patients and subsequently utilized as the primary endpoint measure in the pivotal clinical study of ARCALYST, was published online in the August 2008 issue of Current Medical Research and Opinion.
ARCALYST, also known as interleukin-1 (IL-1) Trap, is a targeted inhibitor of IL-1, which is the key driver of inflammation in CAPS. ARCALYST is the only therapy approved for patients with CAPS, including Familial Cold Auto-inflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS) in adults and children 12 and older. CAPS represent a group of rare, inherited, auto-inflammatory conditions characterized by life-long, recurrent symptoms of rash, fever/chills, joint pain, eye redness/pain, and fatigue. Intermittent, disruptive exacerbations or flares can be triggered at any time by exposure to cooling temperatures, stress, exercise, or other unknown stimuli. The incidence of CAPS has been reported to be approximately one in 1,000,000 people in the United States.
"The ultimate goal of our work over the last ten years has been to find an effective therapy for Cryopyrin-Associated Periodic Syndromes. We began by characterizing the unusual clinical features and debilitating impact of CAPS and then discovered the underlying genetic basis of the disease. A major concern was whether a pharmaceutical company would expend the significant resources necessary to develop a treatment for a disease that has been diagnosed in only a few hundred patients in the United States," stated Hal Hoffman, M.D., Associate Professor, University of California, San Diego and a leading expert on CAPS. "These publications highlight that scientists, clinicians, and industry can collaborate to efficiently, yet rigorously, develop therapies for rare diseases with significant unmet medical need. As a result of this collaboration, patients with CAPS now have an approved treatment available that can help them to effectively manage their disease."
In the initial, open-label pilot evaluation of ARCALYST® (rilonacept), five patients with the Familial Cold Auto-inflammatory Syndrome (FCAS) sub-type of CAPS experienced a marked improvement in symptoms with a corresponding reduction in markers of inflammation. Based upon these convincing findings, a pivotal clinical program was designed to support a registration filing. In order to develop a basis for measuring symptom severity as reported by CAPS patients in a disease that waxes and wanes from day to day, an observational, non-pharmacologic study was conducted in 48 patients with either FCAS or Muckle-Wells Syndrome (MWS). Systematic evaluation of a series of patient-reported outcomes tools resulted in the development of a validated CAPS symptoms measurement instrument with high internal consistency and reliability.
In the pivotal, randomized, double-blind clinical study, 47 patients with FCAS or MWS were randomized to receive either ARCALYST or placebo for six weeks. Patients treated with ARCALYST experienced an 84 percent statistically significant improvement in overall symptom scores versus baseline, whereas those treated with placebo did not experience a significant improvement in their symptoms (13 percent improvement). Ninety-six percent of patients receiving ARCALYST experienced at least a 30 percent improvement in symptoms during this six-week phase of the study. All patients were subsequently given single-blind ARCALYST for nine weeks. Patients were then re-randomized to either ARCALYST or placebo and evaluated over a subsequent nine-week period. Patients remaining on ARCALYST continued to experience symptom control, whereas those receiving placebo experienced a statistically significant worsening of their CAPS symptoms. The most commonly reported adverse reactions reported with ARCALYST were injection-site reaction and upper respiratory tract infection.
"The development process for ARCALYST for the treatment of CAPS highlights Regeneron's overall approach to drug development - to develop drugs targeted at well-documented mediators of disease, focus clinical development on diseases in which those biologic mediators play a primary underlying role, establish clinical proof of concept, and then strive to conduct efficient, pivotal studies with well-validated clinical endpoints," stated George D. Yancopoulos, M.D., Ph.D., President of Regeneron Research Laboratories. "In this case, recognizing that IL-1 is an active mediator of inflammatory disease, we developed ARCALYST to potently inhibit IL-1 in the bloodstream before it can bind to its receptors. Once it was recognized that the genetic mutation associated with CAPS is associated with IL-1 overproduction, we rapidly initiated a pilot study to determine the clinical impact of IL-1 inhibition with ARCALYST. Based upon the clear-cut responses experienced by the CAPS patients in the pilot study, we then developed a validated instrument to assess the severity of CAPS symptoms over time and introduced that instrument into two randomized, placebo-controlled pivotal study phases."
About Cryopyrin-Associated Periodic Syndromes (CAPS)
Recently, medical researchers have identified and described a group of rare, inherited, auto-inflammatory disorders, known as Cryopyrin-Associated Periodic Syndromes or CAPS. Three related conditions make up the broader disease known as CAPS: Familial Cold Auto-inflammatory Syndrome (FCAS), Muckle-Wells Syndrome (MWS), and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). ARCALYST has not been studied in patients with NOMID.
CAPS are characterized by life-long, recurrent symptoms of rash, fever/chills, joint pain, eye redness/pain, and fatigue. Intermittent, disruptive exacerbations or flares can be triggered at any time by exposure to cooling temperatures, stress, exercise, or other unknown stimuli.
CAPS are generally caused by autosomal-dominant mutations (changes) in the NLRP-3 (previously known as CIAS1) gene and resultant alterations in the protein, cryopyrin, which it encodes. Cryopyrin, active in circulating infection-fighting white blood cells, controls the production of a protein called interleukin-1 (IL-1). As part of the body's infection-fighting defense system, IL-1 circulates throughout the body and can trigger inflammatory reactions when it binds to inflammatory cells. Researchers have found that alterations in the cryopyrin protein lead to over-production of IL-1, resulting in an inflammatory response and the symptoms of CAPS. Most, but not all, patients with CAPS have the NLRP-3 gene mutation.
Important Information About ARCALYST® (rilonacept)
ARCALYST is indicated for the treatment of Cryopyrin-Associated Periodic Syndromes (CAPS), including Familial Cold Auto-inflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS) in adults and children 12 and older. IL-1 blockade may interfere with immune response to infections. Serious, life-threatening infections have been reported in patients taking ARCALYST. ARCALYST should be discontinued if a patient develops a serious infection. Taking ARCALYST with tumor necrosis factor inhibitors is not recommended because this may increase the risk of serious infections. Treatment with ARCALYST should not be initiated in patients with active or chronic infections. Patients should not receive a live vaccine while taking ARCALYST. It is recommended that patients receive all recommended vaccinations prior to initiation of treatment with ARCALYST. Patients should be monitored for changes in their lipid profiles and provided with medical treatment if warranted. Hypersensitivity reactions associated with ARCALYST administration have been rare. Please see the full Prescribing Information for ARCALYST, available online at regeneron/ARCALYST-fpi.pdf.
About Regeneron Pharmaceuticals, Inc.
Regeneron is a fully integrated biopharmaceutical company that discovers, develops, and commercializes medicines for the treatment of serious medical conditions. In addition to ARCALYST® (rilonacept) Injection for Subcutaneous Use, its first commercialized product, Regeneron has therapeutic candidates in clinical trials for the potential treatment of cancer, eye diseases, and inflammatory diseases, and has preclinical programs in other diseases and disorders. Additional information about Regeneron and recent news releases are available on Regeneron's web site at regeneron.
Forward Looking Statement
This news release discusses historical information and includes forward-looking statements about Regeneron and its products, development programs, finances, and business, all of which involve a number of risks and uncertainties, such as risks associated with preclinical and clinical development of Regeneron's drug candidates, determinations by regulatory and administrative governmental authorities which may delay or restrict Regeneron's ability to continue to develop or commercialize its product and drug candidates, competing drugs that are superior to Regeneron's product and drug candidates, uncertainty of market acceptance of Regeneron's product and drug candidates, unanticipated expenses, the availability and cost of capital, the costs of developing, producing, and selling products, the potential for any collaboration agreement, including Regeneron's agreements with the sanofi-aventis Group and Bayer HealthCare, to be canceled or to terminate without any product success, risks associated with third party intellectual property, and other material risks. A more complete description of these and other material risks can be found in Regeneron's filings with the United States Securities and Exchange Commission (SEC), including its Form 10-K for the year ended December 31, 2007 and Form 10-Q for the quarter ending June 30, 2008. Regeneron does not undertake any obligation to update publicly any forward-looking statement, whether as a result of new information, future events, or otherwise unless required by law.
Biosector 2
Two studies were published in the August 2008 issue of Arthritis and Rheumatism, the flagship publication of the American College of Rheumatology. The first study was the preliminary trial to evaluate the impact of ARCALYST on markers of inflammation, clinical response, and safety and the second was the pivotal efficacy and safety clinical trial of ARCALYST. A third study, conducted to develop and validate a key symptoms assessment scale for CAPS patients and subsequently utilized as the primary endpoint measure in the pivotal clinical study of ARCALYST, was published online in the August 2008 issue of Current Medical Research and Opinion.
ARCALYST, also known as interleukin-1 (IL-1) Trap, is a targeted inhibitor of IL-1, which is the key driver of inflammation in CAPS. ARCALYST is the only therapy approved for patients with CAPS, including Familial Cold Auto-inflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS) in adults and children 12 and older. CAPS represent a group of rare, inherited, auto-inflammatory conditions characterized by life-long, recurrent symptoms of rash, fever/chills, joint pain, eye redness/pain, and fatigue. Intermittent, disruptive exacerbations or flares can be triggered at any time by exposure to cooling temperatures, stress, exercise, or other unknown stimuli. The incidence of CAPS has been reported to be approximately one in 1,000,000 people in the United States.
"The ultimate goal of our work over the last ten years has been to find an effective therapy for Cryopyrin-Associated Periodic Syndromes. We began by characterizing the unusual clinical features and debilitating impact of CAPS and then discovered the underlying genetic basis of the disease. A major concern was whether a pharmaceutical company would expend the significant resources necessary to develop a treatment for a disease that has been diagnosed in only a few hundred patients in the United States," stated Hal Hoffman, M.D., Associate Professor, University of California, San Diego and a leading expert on CAPS. "These publications highlight that scientists, clinicians, and industry can collaborate to efficiently, yet rigorously, develop therapies for rare diseases with significant unmet medical need. As a result of this collaboration, patients with CAPS now have an approved treatment available that can help them to effectively manage their disease."
In the initial, open-label pilot evaluation of ARCALYST® (rilonacept), five patients with the Familial Cold Auto-inflammatory Syndrome (FCAS) sub-type of CAPS experienced a marked improvement in symptoms with a corresponding reduction in markers of inflammation. Based upon these convincing findings, a pivotal clinical program was designed to support a registration filing. In order to develop a basis for measuring symptom severity as reported by CAPS patients in a disease that waxes and wanes from day to day, an observational, non-pharmacologic study was conducted in 48 patients with either FCAS or Muckle-Wells Syndrome (MWS). Systematic evaluation of a series of patient-reported outcomes tools resulted in the development of a validated CAPS symptoms measurement instrument with high internal consistency and reliability.
In the pivotal, randomized, double-blind clinical study, 47 patients with FCAS or MWS were randomized to receive either ARCALYST or placebo for six weeks. Patients treated with ARCALYST experienced an 84 percent statistically significant improvement in overall symptom scores versus baseline, whereas those treated with placebo did not experience a significant improvement in their symptoms (13 percent improvement). Ninety-six percent of patients receiving ARCALYST experienced at least a 30 percent improvement in symptoms during this six-week phase of the study. All patients were subsequently given single-blind ARCALYST for nine weeks. Patients were then re-randomized to either ARCALYST or placebo and evaluated over a subsequent nine-week period. Patients remaining on ARCALYST continued to experience symptom control, whereas those receiving placebo experienced a statistically significant worsening of their CAPS symptoms. The most commonly reported adverse reactions reported with ARCALYST were injection-site reaction and upper respiratory tract infection.
"The development process for ARCALYST for the treatment of CAPS highlights Regeneron's overall approach to drug development - to develop drugs targeted at well-documented mediators of disease, focus clinical development on diseases in which those biologic mediators play a primary underlying role, establish clinical proof of concept, and then strive to conduct efficient, pivotal studies with well-validated clinical endpoints," stated George D. Yancopoulos, M.D., Ph.D., President of Regeneron Research Laboratories. "In this case, recognizing that IL-1 is an active mediator of inflammatory disease, we developed ARCALYST to potently inhibit IL-1 in the bloodstream before it can bind to its receptors. Once it was recognized that the genetic mutation associated with CAPS is associated with IL-1 overproduction, we rapidly initiated a pilot study to determine the clinical impact of IL-1 inhibition with ARCALYST. Based upon the clear-cut responses experienced by the CAPS patients in the pilot study, we then developed a validated instrument to assess the severity of CAPS symptoms over time and introduced that instrument into two randomized, placebo-controlled pivotal study phases."
About Cryopyrin-Associated Periodic Syndromes (CAPS)
Recently, medical researchers have identified and described a group of rare, inherited, auto-inflammatory disorders, known as Cryopyrin-Associated Periodic Syndromes or CAPS. Three related conditions make up the broader disease known as CAPS: Familial Cold Auto-inflammatory Syndrome (FCAS), Muckle-Wells Syndrome (MWS), and Neonatal-Onset Multisystem Inflammatory Disease (NOMID). ARCALYST has not been studied in patients with NOMID.
CAPS are characterized by life-long, recurrent symptoms of rash, fever/chills, joint pain, eye redness/pain, and fatigue. Intermittent, disruptive exacerbations or flares can be triggered at any time by exposure to cooling temperatures, stress, exercise, or other unknown stimuli.
CAPS are generally caused by autosomal-dominant mutations (changes) in the NLRP-3 (previously known as CIAS1) gene and resultant alterations in the protein, cryopyrin, which it encodes. Cryopyrin, active in circulating infection-fighting white blood cells, controls the production of a protein called interleukin-1 (IL-1). As part of the body's infection-fighting defense system, IL-1 circulates throughout the body and can trigger inflammatory reactions when it binds to inflammatory cells. Researchers have found that alterations in the cryopyrin protein lead to over-production of IL-1, resulting in an inflammatory response and the symptoms of CAPS. Most, but not all, patients with CAPS have the NLRP-3 gene mutation.
Important Information About ARCALYST® (rilonacept)
ARCALYST is indicated for the treatment of Cryopyrin-Associated Periodic Syndromes (CAPS), including Familial Cold Auto-inflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS) in adults and children 12 and older. IL-1 blockade may interfere with immune response to infections. Serious, life-threatening infections have been reported in patients taking ARCALYST. ARCALYST should be discontinued if a patient develops a serious infection. Taking ARCALYST with tumor necrosis factor inhibitors is not recommended because this may increase the risk of serious infections. Treatment with ARCALYST should not be initiated in patients with active or chronic infections. Patients should not receive a live vaccine while taking ARCALYST. It is recommended that patients receive all recommended vaccinations prior to initiation of treatment with ARCALYST. Patients should be monitored for changes in their lipid profiles and provided with medical treatment if warranted. Hypersensitivity reactions associated with ARCALYST administration have been rare. Please see the full Prescribing Information for ARCALYST, available online at regeneron/ARCALYST-fpi.pdf.
About Regeneron Pharmaceuticals, Inc.
Regeneron is a fully integrated biopharmaceutical company that discovers, develops, and commercializes medicines for the treatment of serious medical conditions. In addition to ARCALYST® (rilonacept) Injection for Subcutaneous Use, its first commercialized product, Regeneron has therapeutic candidates in clinical trials for the potential treatment of cancer, eye diseases, and inflammatory diseases, and has preclinical programs in other diseases and disorders. Additional information about Regeneron and recent news releases are available on Regeneron's web site at regeneron.
Forward Looking Statement
This news release discusses historical information and includes forward-looking statements about Regeneron and its products, development programs, finances, and business, all of which involve a number of risks and uncertainties, such as risks associated with preclinical and clinical development of Regeneron's drug candidates, determinations by regulatory and administrative governmental authorities which may delay or restrict Regeneron's ability to continue to develop or commercialize its product and drug candidates, competing drugs that are superior to Regeneron's product and drug candidates, uncertainty of market acceptance of Regeneron's product and drug candidates, unanticipated expenses, the availability and cost of capital, the costs of developing, producing, and selling products, the potential for any collaboration agreement, including Regeneron's agreements with the sanofi-aventis Group and Bayer HealthCare, to be canceled or to terminate without any product success, risks associated with third party intellectual property, and other material risks. A more complete description of these and other material risks can be found in Regeneron's filings with the United States Securities and Exchange Commission (SEC), including its Form 10-K for the year ended December 31, 2007 and Form 10-Q for the quarter ending June 30, 2008. Regeneron does not undertake any obligation to update publicly any forward-looking statement, whether as a result of new information, future events, or otherwise unless required by law.
Biosector 2
суббота, 11 июня 2011 г.
Scientists Implicate Gene In Vitiligo And Other Autoimmune Diseases
In a study appearing in the March 22 New England Journal of Medicine, scientists supported by the National Institutes of Health's National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS) have discovered a connection between a specific gene and the inflammatory skin condition vitiligo, as well as a possible host of autoimmune diseases.
Vitiligo is a chronic condition in which melanocytes (the cells that make pigment) in the skin are destroyed. As a result, white patches appear on the skin in different parts of the body. Similar patches also appear on both the mucous membranes (tissues that line the inside of the mouth and nose), and perhaps in the retina (inner layer of the eyeball). The hair that grows on areas affected by vitiligo sometimes turns white.
The researchers began a search for genes involved in vitiligo almost a decade ago with the help of the Vitiligo Society in the United Kingdom. "In the beginning we were looking for multiple family members with vitiligo," says Richard Spritz, M.D., director of the Human Medical Genetics Program at the University of Colorado at Denver and Health Sciences Center and lead investigator for the study. The researchers sent a questionnaire to members of the society, asking them about their own vitiligo and whether other family members were affected. As part of the questionnaire, they also asked about other autoimmune diseases. What they learned was that vitiligo was "very highly associated" with a number of other autoimmune diseases, mostly thyroid disease, but also pernicious anemia, rheumatoid arthritis, psoriasis, lupus, Addison's disease, and adult-onset autoimmune diabetes.
That finding prompted the researchers to study families with multiple affected members and to look for similarities in genes among those who were affected. By searching the genome, they discovered a gene, NALP1, that was key to predisposing people to vitiligo and other autoimmune diseases, particularly autoimmune thyroid disease, says Dr. Spritz. "We know that about 20 percent of people with vitiligo also get autoimmune thyroid disease, and this gene may be involved in mediating both of those," he says.
Dr. Spritz says the implications of this finding are exciting. The identified gene controls part of what is called the innate immune system, which is our body's first defense against infection, he says. "When we are attacked by viruses or bacteria, the innate immune system stimulates the inflammatory pathways and calls the rest of the immune system to action. NALP1 is probably a receptor for bacterial or viral signals. We don't know what these signals are, but now that we know what the gene is, we can use that knowledge to search for the signals that trigger autoimmune disease."
"All autoimmune diseases involve the interaction of multiple genes and environmental triggers," he continues. "You are born with your genes, but you are not born with these diseases. Something happens. We don't know what the triggers are that start these diseases, but if we did, maybe we could avoid them or even block the process. In fact, it may even be possible to actually stop the autoimmune disease," he says.
The most immediate application of this research might be for the disease that began the research: vitiligo. Doctors usually treat vitiligo with ultraviolet (UV) light to stimulate skin repigmentation. Scientists also know that there is one medication available (approved for treating rheumatoid arthritis) that blocks an inflammatory pathway thought to be controlled by NALP1. The possibility of combining a drug with UV light to improve vitiligo treatment is intriguing, and Dr. Spritz is now interested in finding out more about how the medication might affect people with vitiligo.
NIAMS Director Stephen I. Katz, M.D., Ph.D., calls the discovery of the NALP1-autoimmunity connection an important advance in the understanding of autoimmune diseases that collectively affect an estimated 15 million to 25 million Americans. "The more we understand about these diseases, including the genes that predispose to them and the environmental factors that trigger them, the closer we come to better treatments and even preventive measures," he says.
Additional support for this research was provided by the National Institute of Allergy and Infectious Diseases, the National Institute of Diabetes and Digestive and Kidney Diseases, the U.K. Vitiligo Society and the National Vitiligo Foundation.
The mission of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), a part of the Department of Health and Human Services' National Institutes of Health, is to support research into the causes, treatment and prevention of arthritis and musculoskeletal and skin diseases; the training of basic and clinical scientists to carry out this research; and the dissemination of information on research progress in these diseases. For more information about NIAMS, call the information clearinghouse at (301) 495-4484 or (877) 22-NIAMS (free call) or visit the NIAMS Web site at niams.nih/.
The National Institutes of Health (NIH) - The Nation's Medical Research Agency - includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit nih/. Jin Y, et al. NAPL1 in vitiligo-associated multiple autoimmune disease. NEJM 2007;365:10-18.
Contact: Ray Fleming
niams.nih/
NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases
Vitiligo is a chronic condition in which melanocytes (the cells that make pigment) in the skin are destroyed. As a result, white patches appear on the skin in different parts of the body. Similar patches also appear on both the mucous membranes (tissues that line the inside of the mouth and nose), and perhaps in the retina (inner layer of the eyeball). The hair that grows on areas affected by vitiligo sometimes turns white.
The researchers began a search for genes involved in vitiligo almost a decade ago with the help of the Vitiligo Society in the United Kingdom. "In the beginning we were looking for multiple family members with vitiligo," says Richard Spritz, M.D., director of the Human Medical Genetics Program at the University of Colorado at Denver and Health Sciences Center and lead investigator for the study. The researchers sent a questionnaire to members of the society, asking them about their own vitiligo and whether other family members were affected. As part of the questionnaire, they also asked about other autoimmune diseases. What they learned was that vitiligo was "very highly associated" with a number of other autoimmune diseases, mostly thyroid disease, but also pernicious anemia, rheumatoid arthritis, psoriasis, lupus, Addison's disease, and adult-onset autoimmune diabetes.
That finding prompted the researchers to study families with multiple affected members and to look for similarities in genes among those who were affected. By searching the genome, they discovered a gene, NALP1, that was key to predisposing people to vitiligo and other autoimmune diseases, particularly autoimmune thyroid disease, says Dr. Spritz. "We know that about 20 percent of people with vitiligo also get autoimmune thyroid disease, and this gene may be involved in mediating both of those," he says.
Dr. Spritz says the implications of this finding are exciting. The identified gene controls part of what is called the innate immune system, which is our body's first defense against infection, he says. "When we are attacked by viruses or bacteria, the innate immune system stimulates the inflammatory pathways and calls the rest of the immune system to action. NALP1 is probably a receptor for bacterial or viral signals. We don't know what these signals are, but now that we know what the gene is, we can use that knowledge to search for the signals that trigger autoimmune disease."
"All autoimmune diseases involve the interaction of multiple genes and environmental triggers," he continues. "You are born with your genes, but you are not born with these diseases. Something happens. We don't know what the triggers are that start these diseases, but if we did, maybe we could avoid them or even block the process. In fact, it may even be possible to actually stop the autoimmune disease," he says.
The most immediate application of this research might be for the disease that began the research: vitiligo. Doctors usually treat vitiligo with ultraviolet (UV) light to stimulate skin repigmentation. Scientists also know that there is one medication available (approved for treating rheumatoid arthritis) that blocks an inflammatory pathway thought to be controlled by NALP1. The possibility of combining a drug with UV light to improve vitiligo treatment is intriguing, and Dr. Spritz is now interested in finding out more about how the medication might affect people with vitiligo.
NIAMS Director Stephen I. Katz, M.D., Ph.D., calls the discovery of the NALP1-autoimmunity connection an important advance in the understanding of autoimmune diseases that collectively affect an estimated 15 million to 25 million Americans. "The more we understand about these diseases, including the genes that predispose to them and the environmental factors that trigger them, the closer we come to better treatments and even preventive measures," he says.
Additional support for this research was provided by the National Institute of Allergy and Infectious Diseases, the National Institute of Diabetes and Digestive and Kidney Diseases, the U.K. Vitiligo Society and the National Vitiligo Foundation.
The mission of the National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS), a part of the Department of Health and Human Services' National Institutes of Health, is to support research into the causes, treatment and prevention of arthritis and musculoskeletal and skin diseases; the training of basic and clinical scientists to carry out this research; and the dissemination of information on research progress in these diseases. For more information about NIAMS, call the information clearinghouse at (301) 495-4484 or (877) 22-NIAMS (free call) or visit the NIAMS Web site at niams.nih/.
The National Institutes of Health (NIH) - The Nation's Medical Research Agency - includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit nih/. Jin Y, et al. NAPL1 in vitiligo-associated multiple autoimmune disease. NEJM 2007;365:10-18.
Contact: Ray Fleming
niams.nih/
NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases
пятница, 10 июня 2011 г.
Comparison Of Latest Rheumatoid Arthritis Drugs
Findings published in the open access journal BMC Musculoskeletal Disorders shows that the latest class of drugs used to treat rheumatoid arthritis (RA) are better than standard anti-inflammatories.
RA is a chronic, debilitating, inflammatory disease of the joints, which is usually treated with anti-inflammatory drugs such as methotrexate or steroids. However, the discovery that a protein from white blood cells, known as tumour necrosis factor alpha (TNF?±), caused some of the symptoms of RA, led to the development of novel drugs which block TNF?±. This group of drugs, known as anti-TNF?± drugs (which include infliximab, etanercept and adalimumab), are now commonly used to treat RA.
However, there have been no 'head-to-head' comparisons of the new anti-TNF?± drugs in terms of safety or efficacy for the treatment of RA.
Alberto Alonso-Ruiz of the Cruces Hospital in Barakaldo, Vizcaya, Spain and colleagues at the Donostia Hospital and the University of the Basque Country, systematically searched for research on the use of anti-TNF?± drugs in RA patients. They found thirteen clinical trials including over 7000 patients. The researchers then analyzed the trial results, systematically logging patient benefits and side effects for different doses of the three main anti-TNF?± drugs.
Analysis of the combined results of all thirteen trials showed that anti-TNF?± drugs, given at recommended doses, were better than the usual treatments, such as methotrexate, for treating RA. Patients who had previously seen little benefit from methotrexate alone showed a better response with combined anti-TNF?± plus methotrexate therapy.
The team found that all three drugs were very similar in their benefits even at doses higher than those recommended by the drug manufacturer. This class of drugs, while very effective, does have a higher frequency of adverse side-effects. Patients on infliximab were most likely to drop out of a trial because of these side effects. In contrast, patients using etanercept had the lowest withdrawal rate. The researchers point out that this could be because this drug was not reported as being used at higher than recommended dosage in the trials.
"Anti-TNF?± drugs such as infliximab, adalimumab and etanercept all appear to be effective in the treatment of RA" said Alonso-Ruiz. "Performing comparisons of new drugs is vital for measuring safety/efficacy relationships and monitoring adverse side-effects"
1. Tumor necrosis factor drugs in rheumatoid arthritis: systematic review and meta-analysis of efficacy and safety
Alberto Alonso-Ruiz, Jose Ignacio Pijoan, Eukene Ansuategui, Arantxa Urkaregi, Marcelo Calabozo and Antonio Quintana
BMC Musculoskeletal Disorders (in press)
Article available at the journal website: biomedcentral/bmcmusculoskeletdisord/
All articles are available free of charge, according to BioMed Central's open access policy.
2. BMC Musculoskeletal Disorders is an open access journal publishing original peer-reviewed research articles in all aspects of the prevention, diagnosis and management of musculoskeletal and associated disorders, as well as related molecular genetics, pathophysiology, and epidemiology. BMC Musculoskeletal Disorders (ISSN 1471-2474) is indexed/tracked/covered by PubMed, MEDLINE, CAS, Scopus, EMBASE, Thomson Scientific (ISI) and Google Scholar.
3. BioMed Central (biomedcentral/) is an independent online publishing house
committed to providing immediate access without charge to the peer-reviewed biological and medical research it publishes. This commitment is based on the view that open
access to research is essential to the rapid and efficient communication of science.
Source: Charlotte Webber
BioMed Central
RA is a chronic, debilitating, inflammatory disease of the joints, which is usually treated with anti-inflammatory drugs such as methotrexate or steroids. However, the discovery that a protein from white blood cells, known as tumour necrosis factor alpha (TNF?±), caused some of the symptoms of RA, led to the development of novel drugs which block TNF?±. This group of drugs, known as anti-TNF?± drugs (which include infliximab, etanercept and adalimumab), are now commonly used to treat RA.
However, there have been no 'head-to-head' comparisons of the new anti-TNF?± drugs in terms of safety or efficacy for the treatment of RA.
Alberto Alonso-Ruiz of the Cruces Hospital in Barakaldo, Vizcaya, Spain and colleagues at the Donostia Hospital and the University of the Basque Country, systematically searched for research on the use of anti-TNF?± drugs in RA patients. They found thirteen clinical trials including over 7000 patients. The researchers then analyzed the trial results, systematically logging patient benefits and side effects for different doses of the three main anti-TNF?± drugs.
Analysis of the combined results of all thirteen trials showed that anti-TNF?± drugs, given at recommended doses, were better than the usual treatments, such as methotrexate, for treating RA. Patients who had previously seen little benefit from methotrexate alone showed a better response with combined anti-TNF?± plus methotrexate therapy.
The team found that all three drugs were very similar in their benefits even at doses higher than those recommended by the drug manufacturer. This class of drugs, while very effective, does have a higher frequency of adverse side-effects. Patients on infliximab were most likely to drop out of a trial because of these side effects. In contrast, patients using etanercept had the lowest withdrawal rate. The researchers point out that this could be because this drug was not reported as being used at higher than recommended dosage in the trials.
"Anti-TNF?± drugs such as infliximab, adalimumab and etanercept all appear to be effective in the treatment of RA" said Alonso-Ruiz. "Performing comparisons of new drugs is vital for measuring safety/efficacy relationships and monitoring adverse side-effects"
1. Tumor necrosis factor drugs in rheumatoid arthritis: systematic review and meta-analysis of efficacy and safety
Alberto Alonso-Ruiz, Jose Ignacio Pijoan, Eukene Ansuategui, Arantxa Urkaregi, Marcelo Calabozo and Antonio Quintana
BMC Musculoskeletal Disorders (in press)
Article available at the journal website: biomedcentral/bmcmusculoskeletdisord/
All articles are available free of charge, according to BioMed Central's open access policy.
2. BMC Musculoskeletal Disorders is an open access journal publishing original peer-reviewed research articles in all aspects of the prevention, diagnosis and management of musculoskeletal and associated disorders, as well as related molecular genetics, pathophysiology, and epidemiology. BMC Musculoskeletal Disorders (ISSN 1471-2474) is indexed/tracked/covered by PubMed, MEDLINE, CAS, Scopus, EMBASE, Thomson Scientific (ISI) and Google Scholar.
3. BioMed Central (biomedcentral/) is an independent online publishing house
committed to providing immediate access without charge to the peer-reviewed biological and medical research it publishes. This commitment is based on the view that open
access to research is essential to the rapid and efficient communication of science.
Source: Charlotte Webber
BioMed Central
четверг, 9 июня 2011 г.
Disabling gene defuses rheumatoid arthritis in mice
Scientists studying mice have identified a gene that allows immune cells known as neutrophils to protect themselves from
the inflammatory chemicals they secrete.
Researchers at Washington University School of Medicine in St. Louis showed that knocking the gene out in mice prevented the
development of an arthritis-like disorder by making the neutrophils victims of their own damaging secretions.
The newly identified role for the gene, Foxo3a, may open a new window for treating arthritic conditions caused by immune
dysfunction. Currently, most treatments in development for these disorders focus either on preventing wayward immune cells
from attacking the joints or on reducing the ability of these cells to open fire. The new results suggest it may be just as
helpful to let these cells kill themselves and each other.
"We already know a great deal about Foxo3a from studies of its role in some cancers, and hopefully that puts us in a good
position to devise ways to manipulate its activity," says senior author Stanford Peng, M.D., Ph.D., assistant professor of
medicine and of pathology and immunology. "If the human version of this gene functions in a similar fashion, modifying its
activity may be a useful approach for arthritis therapy even when the disease is already well underway."
Peng and colleagues will publish their results in the June issue of Nature Medicine.
Rheumatoid arthritis, the most prevalent autoimmune form of arthritis, afflicts approximately 2.1 million Americans or about
1 percent of the population. Women are two to three times more likely to develop the disorder than men. Symptoms often occur
in episodic bursts and may include morning stiffness, fatigue and joint and muscle pain. In severe cases, rheumatoid
arthritis can damage cartilage, tendons, ligaments and bone, leading to joint deformity and instability.
Rheumatoid arthritis has long been recognized as a condition that involves defensive cells from the body's immune system
mistakenly attacking healthy joint tissues. Scientists once thought the cells that were most active in these attacks were
adaptive immune cells including T cells. Most of these cells are like guided missiles: they get a fix on a specific target,
pursue it and attack it.
"Classically, everyone thought that the T cells somehow recognized something specific in the joint like collagen or some
other protein and attacked it," Peng explains. "In recent years, though, it's become more accepted that rheumatoid arthritis
is also the result of a less specific but still harmful inflammation generated by cells from the other branch of the immune
system, the innate immune system."
Innate immune cells such as neutrophils respond rapidly to invaders and normally comprise the body's frontline defenses
against bacterial infection.
Peng became interested in Foxo3a because of prior studies his research team had conducted on a related gene, Foxj1. Both
genes belong to the forkhead family of genes, which regulates the activity of other genes and has been connected to cancer
and longevity. Last year Peng found that knocking out Foxj1 produced a lupus-like condition in mice.
Foxj1 and Foxo3a are thought to play similar roles in immune T cells. To get a better sense for Foxo3a's activities, Peng's
group created a line of mice where Foxo3a had been disabled and studied the effects this change had on T cells.
As a follow-up, Peng decided to inject the new line of mice with antibodies that normally induce a condition like rheumatoid
arthritis. But the mice remained healthy even after the injections.
"It was a surprise finding," Peng says. "We really didn't expect to see this kind of response."
Further study revealed that neutrophils in the mice were killing themselves through a cellular self-destruct process known as
apoptosis. Damaged or highly stressed cells can pull their own plug in this or a similar manner to prevent themselves from
becoming cancerous.
"It seems that evolution has somehow provided protective mechanisms for innate immune cells when they go into the hazardous
inflammatory environments they create," Peng notes. "They need ways to keep themselves alive, and Foxo3a is one of those
ways."
Peng's group is currently trying to discern more details of Foxo3a's activities in neutrophils, including the pathways the
gene activates to block apoptosis. They will also be looking for drugs that inhibit Foxo3a and testing them in the mice as
potential anti-arthritis drugs.
Jonsson H, Allen P, Peng SL. "Inflammatory arthritis requires Foxo3a to prevent Fas ligand-induced neutrophil apoptosis."
Nature Medicine, June 2005.
Funding from Washington University School of Medicine, the National Institutes of Health, the Arthritis Foundation, and the
Lupus Research Institute supported this research.
Washington University School of Medicine's full-time and volunteer faculty physicians also are the medical staff of
Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and
patient care institutions in the nation, currently ranked third in the nation by U.S. News & World Report. Through its
affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
Contact: Michael C. Purdy
purdymwustl
314-286-0122
Washington University School of Medicine
medinfo.wustl
the inflammatory chemicals they secrete.
Researchers at Washington University School of Medicine in St. Louis showed that knocking the gene out in mice prevented the
development of an arthritis-like disorder by making the neutrophils victims of their own damaging secretions.
The newly identified role for the gene, Foxo3a, may open a new window for treating arthritic conditions caused by immune
dysfunction. Currently, most treatments in development for these disorders focus either on preventing wayward immune cells
from attacking the joints or on reducing the ability of these cells to open fire. The new results suggest it may be just as
helpful to let these cells kill themselves and each other.
"We already know a great deal about Foxo3a from studies of its role in some cancers, and hopefully that puts us in a good
position to devise ways to manipulate its activity," says senior author Stanford Peng, M.D., Ph.D., assistant professor of
medicine and of pathology and immunology. "If the human version of this gene functions in a similar fashion, modifying its
activity may be a useful approach for arthritis therapy even when the disease is already well underway."
Peng and colleagues will publish their results in the June issue of Nature Medicine.
Rheumatoid arthritis, the most prevalent autoimmune form of arthritis, afflicts approximately 2.1 million Americans or about
1 percent of the population. Women are two to three times more likely to develop the disorder than men. Symptoms often occur
in episodic bursts and may include morning stiffness, fatigue and joint and muscle pain. In severe cases, rheumatoid
arthritis can damage cartilage, tendons, ligaments and bone, leading to joint deformity and instability.
Rheumatoid arthritis has long been recognized as a condition that involves defensive cells from the body's immune system
mistakenly attacking healthy joint tissues. Scientists once thought the cells that were most active in these attacks were
adaptive immune cells including T cells. Most of these cells are like guided missiles: they get a fix on a specific target,
pursue it and attack it.
"Classically, everyone thought that the T cells somehow recognized something specific in the joint like collagen or some
other protein and attacked it," Peng explains. "In recent years, though, it's become more accepted that rheumatoid arthritis
is also the result of a less specific but still harmful inflammation generated by cells from the other branch of the immune
system, the innate immune system."
Innate immune cells such as neutrophils respond rapidly to invaders and normally comprise the body's frontline defenses
against bacterial infection.
Peng became interested in Foxo3a because of prior studies his research team had conducted on a related gene, Foxj1. Both
genes belong to the forkhead family of genes, which regulates the activity of other genes and has been connected to cancer
and longevity. Last year Peng found that knocking out Foxj1 produced a lupus-like condition in mice.
Foxj1 and Foxo3a are thought to play similar roles in immune T cells. To get a better sense for Foxo3a's activities, Peng's
group created a line of mice where Foxo3a had been disabled and studied the effects this change had on T cells.
As a follow-up, Peng decided to inject the new line of mice with antibodies that normally induce a condition like rheumatoid
arthritis. But the mice remained healthy even after the injections.
"It was a surprise finding," Peng says. "We really didn't expect to see this kind of response."
Further study revealed that neutrophils in the mice were killing themselves through a cellular self-destruct process known as
apoptosis. Damaged or highly stressed cells can pull their own plug in this or a similar manner to prevent themselves from
becoming cancerous.
"It seems that evolution has somehow provided protective mechanisms for innate immune cells when they go into the hazardous
inflammatory environments they create," Peng notes. "They need ways to keep themselves alive, and Foxo3a is one of those
ways."
Peng's group is currently trying to discern more details of Foxo3a's activities in neutrophils, including the pathways the
gene activates to block apoptosis. They will also be looking for drugs that inhibit Foxo3a and testing them in the mice as
potential anti-arthritis drugs.
Jonsson H, Allen P, Peng SL. "Inflammatory arthritis requires Foxo3a to prevent Fas ligand-induced neutrophil apoptosis."
Nature Medicine, June 2005.
Funding from Washington University School of Medicine, the National Institutes of Health, the Arthritis Foundation, and the
Lupus Research Institute supported this research.
Washington University School of Medicine's full-time and volunteer faculty physicians also are the medical staff of
Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine is one of the leading medical research, teaching and
patient care institutions in the nation, currently ranked third in the nation by U.S. News & World Report. Through its
affiliations with Barnes-Jewish and St. Louis Children's hospitals, the School of Medicine is linked to BJC HealthCare.
Contact: Michael C. Purdy
purdymwustl
314-286-0122
Washington University School of Medicine
medinfo.wustl
среда, 8 июня 2011 г.
Can Psychosocial Stress At Work Put At Risk Of Developing Rheumatoid Arthritis?
A Swedish study published in one of the latest issue of Psychotherapy and Psychosomatics discloses new relationships between stress at work and development of rheumatoid arthritis.
Psychosocial work stress, in terms of high psychological demands, low decision latitude or the combination of these stressors (job strain), is associated with an increased risk of several diseases (e.g. cardiovascular disease), but it has not been studied in relation to rheumatoid arthritis (RA). However, research on the relationship between psychosocial work stress and immunological parameters also suggests a possible association with inflammatory conditions, including RA. In order to investigate whether high psychological job demands, low decision latitude and job strain are associated with the risk of developing RA, a group of Swedish investigators used data from EIRA, a large population-based case-control study with incident cases of RA. The study base comprised the population, aged 18 - 65 years, in middle and southern parts of Sweden during 1996 - 2003. In total, 1,221 cases and 1,454 controls participated.
Psychological job demands and job decision latitude were measured according to questions developed by Karasek and Theorell. Questions were posed about participants' present work situations; both demands and decision latitude were categorized using the quartiles among the controls (each gender separately) as cut-off points. High psychological job demands, as well as high decision latitude, were defined as a score above the upper quartile. Low psychological job demands, as well as low decision latitude, were defined as a score below the lower quartile. Job strain was defined as the combination of high demands and low decision latitude.
The investigators also performed a classification of psychological job demands and decision latitude based on a job exposure matrix (JEM), in order to avoid potential bias due to differential recall between cases and controls. Among the controls, mean scores of demands and decision latitude were calculated for each latest reported occupation (each gender separately) where the number of controls was at least 3. Both cases and controls were then given the mean scores according to their latest reported occupation. Cut-off points of psychological job demands and decision latitude were calculated in the same way as described above. The odds ratios (OR) of developing RA with 95% confidence intervals (CI) were calculated for high compared with low psychological job demands and low compared with high decision latitude. Job strain was compared with relaxed working conditions (low psychological job demands and high decision latitude) and with conditions without job strain. OR were interpreted as relative risks, as the study was population-based, and were adjusted for age, sex, residential area, smoking and social class.
High psychological job demands tended to be associated with a decreased risk of RA, especially in the JEM-derived data (OR = 0.8, 95% CI = 0.6 - 1.0). Low decision latitude was associated with an increased risk of RA (selfreported data: OR = 1.6, 95% CI = 1.2 - 2.2, JEM-derived data: OR = 1.3, 95% CI = 1.0 - 1.7). Self-reported job strain was associated with a 30% higher risk of RA, compared with relaxed working conditions, but the CI was wide and the result was not confirmed by JEM-derived data.
To summarize few methodological considerations, the investigators conclude that the observed association between low decision latitude and risk of developing RA is most likely real, and that the influence of various biases is of limited magnitude. The main new finding of this study was that low decision latitude was associated with an increased risk of developing RA, according to both self-reported and JEM-derived information. Low decision latitude is also the component in the demand-control model that has most consistently been related to risk of cardiovascular disease. Furthermore, some evidence that those with high psychological job demands had a decreased risk of RA was found.
Source: Psychotherapy and Psychosomatics
Psychosocial work stress, in terms of high psychological demands, low decision latitude or the combination of these stressors (job strain), is associated with an increased risk of several diseases (e.g. cardiovascular disease), but it has not been studied in relation to rheumatoid arthritis (RA). However, research on the relationship between psychosocial work stress and immunological parameters also suggests a possible association with inflammatory conditions, including RA. In order to investigate whether high psychological job demands, low decision latitude and job strain are associated with the risk of developing RA, a group of Swedish investigators used data from EIRA, a large population-based case-control study with incident cases of RA. The study base comprised the population, aged 18 - 65 years, in middle and southern parts of Sweden during 1996 - 2003. In total, 1,221 cases and 1,454 controls participated.
Psychological job demands and job decision latitude were measured according to questions developed by Karasek and Theorell. Questions were posed about participants' present work situations; both demands and decision latitude were categorized using the quartiles among the controls (each gender separately) as cut-off points. High psychological job demands, as well as high decision latitude, were defined as a score above the upper quartile. Low psychological job demands, as well as low decision latitude, were defined as a score below the lower quartile. Job strain was defined as the combination of high demands and low decision latitude.
The investigators also performed a classification of psychological job demands and decision latitude based on a job exposure matrix (JEM), in order to avoid potential bias due to differential recall between cases and controls. Among the controls, mean scores of demands and decision latitude were calculated for each latest reported occupation (each gender separately) where the number of controls was at least 3. Both cases and controls were then given the mean scores according to their latest reported occupation. Cut-off points of psychological job demands and decision latitude were calculated in the same way as described above. The odds ratios (OR) of developing RA with 95% confidence intervals (CI) were calculated for high compared with low psychological job demands and low compared with high decision latitude. Job strain was compared with relaxed working conditions (low psychological job demands and high decision latitude) and with conditions without job strain. OR were interpreted as relative risks, as the study was population-based, and were adjusted for age, sex, residential area, smoking and social class.
High psychological job demands tended to be associated with a decreased risk of RA, especially in the JEM-derived data (OR = 0.8, 95% CI = 0.6 - 1.0). Low decision latitude was associated with an increased risk of RA (selfreported data: OR = 1.6, 95% CI = 1.2 - 2.2, JEM-derived data: OR = 1.3, 95% CI = 1.0 - 1.7). Self-reported job strain was associated with a 30% higher risk of RA, compared with relaxed working conditions, but the CI was wide and the result was not confirmed by JEM-derived data.
To summarize few methodological considerations, the investigators conclude that the observed association between low decision latitude and risk of developing RA is most likely real, and that the influence of various biases is of limited magnitude. The main new finding of this study was that low decision latitude was associated with an increased risk of developing RA, according to both self-reported and JEM-derived information. Low decision latitude is also the component in the demand-control model that has most consistently been related to risk of cardiovascular disease. Furthermore, some evidence that those with high psychological job demands had a decreased risk of RA was found.
Source: Psychotherapy and Psychosomatics
вторник, 7 июня 2011 г.
Identification Of Role For Proteins In Children's Muscle Disease Could Open Up New Treatment Options
A study presented by Mrs. Elisabeth Elst today shows for the first time that a protein - heat shock protein 60 (HSP60) - that is present in chronic inflammations, triggers a response by T-cells (a type of white blood cells that plays a part in the body's own immune response) in children with juvenile dermatomyositis (JDM).
The specific response has earlier been observed in juvenile idiopathic arthritis, but to date, little is known about the role of HSP60 in inflammatory myositis. Inflammatory myositis (IM) is the name given to a group of diseases that cause inflammation in the muscles of the body, which is mediated by the immune system of the body. The main symptoms are pain and weakness and can cause patient disability because of damage to the muscles. The main types of IM are dermatomyositis and polymyositis.
For children, the conditions of myositis are complex and are characterized by muscle damage due to an inflammatory process of the blood vessels that lie under the skin and muscles. Some of the symptoms include skin changes around the eyelids and over the knuckles and finger joints, as well as weakness in muscles, mainly affecting the large muscles around the hips and shoulders resulting in increased difficulty with walking, climbing stairs, getting up from the floor and lifting the arms. The children also often become uncharacteristically miserable and fractious and they may complain of tummy pain.
Heat shock proteins (HSP) are a group of proteins whose expression is increased when the cells are exposed to elevated temperatures. Production of high levels of heat shock proteins can also be triggered by exposure to different kinds of environmental stress conditions, such as infection, inflammation, exposure of the cell to toxins (e.g. ethanol, arsenic, and ultraviolet light), or water deprivation.
Mrs. Elst, pediatric immunologist at the University Medical Centre Utrecht, said, "We have shown for the first time that HSP60 plays an active part in the control of the inflammatory process in JDM. Thus, therapy aimed at the expansion of T-cells with regulatory capacities reacting to HSP60 could contribute to disease remission in patients with JDM. This conclusion opens up new perspectives for the understanding and approach for antigens in immunotherapy."
Jim Baxter - Onsite tel: +44 (0) 7900 605652
Jo Spadaccino - Onsite tel: +44 (0) 7773 271930
Mia Gannedahl - Office tel: +44 (0) 20 7331 2325
Abstract number: OP0060
About EULAR
* The European League Against Rheumatism (EULAR) is the organization which represents the patient, health professional and scientific societies of rheumatology of all the European nations.
* The aims of EULAR are to reduce the burden of rheumatic diseases on the individual and society and to improve the treatment, prevention and rehabilitation of musculoskeletal diseases. To this end, EULAR fosters excellence in education and research in the field of rheumatology. It promotes the translation of research advances into daily care and fights for the recognition of the needs of people with musculoskeletal diseases by the governing bodies in Europe.
* Diseases of bones and joints, such as rheumatoid arthritis and osteoarthritis cause disability in 4 - 5 % of the adult population and are predicted to rise as people live longer.
* As new treatments emerge and cellular mechanisms are discovered, the 7th Annual European Congress of Rheumatology in Amsterdam (EULAR 2006) brings together more than 10,000 experts - scientists, clinicians, healthcare workers, pharmaceutical companies and patients - to share their knowledge in a global endeavour to challenge the pain and disability caused by musculo-skeletal disorders.
* To find out more information about the activities of EULAR, visit: eular/.
Contact: Mia Gannedahl
European League Against Rheumatism
The specific response has earlier been observed in juvenile idiopathic arthritis, but to date, little is known about the role of HSP60 in inflammatory myositis. Inflammatory myositis (IM) is the name given to a group of diseases that cause inflammation in the muscles of the body, which is mediated by the immune system of the body. The main symptoms are pain and weakness and can cause patient disability because of damage to the muscles. The main types of IM are dermatomyositis and polymyositis.
For children, the conditions of myositis are complex and are characterized by muscle damage due to an inflammatory process of the blood vessels that lie under the skin and muscles. Some of the symptoms include skin changes around the eyelids and over the knuckles and finger joints, as well as weakness in muscles, mainly affecting the large muscles around the hips and shoulders resulting in increased difficulty with walking, climbing stairs, getting up from the floor and lifting the arms. The children also often become uncharacteristically miserable and fractious and they may complain of tummy pain.
Heat shock proteins (HSP) are a group of proteins whose expression is increased when the cells are exposed to elevated temperatures. Production of high levels of heat shock proteins can also be triggered by exposure to different kinds of environmental stress conditions, such as infection, inflammation, exposure of the cell to toxins (e.g. ethanol, arsenic, and ultraviolet light), or water deprivation.
Mrs. Elst, pediatric immunologist at the University Medical Centre Utrecht, said, "We have shown for the first time that HSP60 plays an active part in the control of the inflammatory process in JDM. Thus, therapy aimed at the expansion of T-cells with regulatory capacities reacting to HSP60 could contribute to disease remission in patients with JDM. This conclusion opens up new perspectives for the understanding and approach for antigens in immunotherapy."
Jim Baxter - Onsite tel: +44 (0) 7900 605652
Jo Spadaccino - Onsite tel: +44 (0) 7773 271930
Mia Gannedahl - Office tel: +44 (0) 20 7331 2325
Abstract number: OP0060
About EULAR
* The European League Against Rheumatism (EULAR) is the organization which represents the patient, health professional and scientific societies of rheumatology of all the European nations.
* The aims of EULAR are to reduce the burden of rheumatic diseases on the individual and society and to improve the treatment, prevention and rehabilitation of musculoskeletal diseases. To this end, EULAR fosters excellence in education and research in the field of rheumatology. It promotes the translation of research advances into daily care and fights for the recognition of the needs of people with musculoskeletal diseases by the governing bodies in Europe.
* Diseases of bones and joints, such as rheumatoid arthritis and osteoarthritis cause disability in 4 - 5 % of the adult population and are predicted to rise as people live longer.
* As new treatments emerge and cellular mechanisms are discovered, the 7th Annual European Congress of Rheumatology in Amsterdam (EULAR 2006) brings together more than 10,000 experts - scientists, clinicians, healthcare workers, pharmaceutical companies and patients - to share their knowledge in a global endeavour to challenge the pain and disability caused by musculo-skeletal disorders.
* To find out more information about the activities of EULAR, visit: eular/.
Contact: Mia Gannedahl
European League Against Rheumatism
понедельник, 6 июня 2011 г.
Abbott Announces HUMIRA® (adalimumab) Approved In Japan For The Treatment Of Rheumatoid Arthritis
Abbott announced that it has received approval from the Japanese Ministry of Health, Labour and Welfare for HUMIRA® (adalimumab) for the treatment of rheumatoid arthritis in patients with inadequate response to conventional therapy. This approval is the first for HUMIRA in Japan, where Abbott co-developed and will co-market HUMIRA with Eisai Co., Ltd. HUMIRA is now approved in 75 countries for rheumatoid arthritis and other autoimmune disease indications.
"The approval of HUMIRA in Japan is a significant milestone for Abbott," said Glenn Warner, vice president, Pharmaceuticals, Japan, Abbott. "This approval is both good news for Japanese patients and a significant step forward for Abbott in Japan."
HUMIRA is expected to become available to patients in Japan in the coming months, following the standard pricing approval process.
"The clinical studies of HUMIRA in Japanese patients demonstrated the efficacy and safety of this medicine," said Prof. Nobuyuki Miyasaka, M.D., Department of Collagen Disease and Rheumatology, Tokyo Medical and Dental University Graduate School of Medicine, who was involved in the development of HUMIRA for the treatment of rheumatoid arthritis in Japan.
Abbott has submitted an application for approval of HUMIRA for plaque psoriasis, and is also developing HUMIRA in Japan for Crohn's disease, ankylosing spondylitis, juvenile rheumatoid arthritis and ulcerative colitis. Eisai is co-developing and will jointly market these indications with Abbott.
More Information About Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation, joint pain and stiffness, which can lead to long-term joint damage. The joints most commonly affected early in the disease are the smaller joints of the fingers, feet and wrists. The elbows, knees, ankles and hips can also be affected. Although there is no cure for RA, people continue to seek treatments that help alleviate pain and inflammation and slow disease progression.
More information on RA and current treatment options can be found at RA.
Important Safety Information
Globally, prescribing information varies; refer to the individual country product label for complete information.
Serious infections, sepsis, rare cases of tuberculosis (TB), and opportunistic infections, including fatalities, have been reported with the use of TNF antagonists, including HUMIRA. Many of the serious infections have occurred in patients on concomitant immunosuppressive therapy that, in addition to their underlying disease could predispose them to infections. Patients must be monitored closely for infections, including tuberculosis, before, during and after treatment with HUMIRA. Treatment should not be initiated in patients with active infections until infections are controlled. HUMIRA should not be used by patients with active TB or other severe infections such as sepsis and opportunistic infections. Patients who develop new infections while using HUMIRA should be monitored closely. HUMIRA should be discontinued if a patient develops a new serious infection until infections are controlled. Physicians should exercise caution when considering use of HUMIRA in patients with a history of recurring infection or with underlying conditions that may predispose patients to infections.
TNF-blocking agents have been associated with reactivation of hepatitis B (HBV) in patients who are chronic carriers of the virus. Some cases have been fatal. Patients at risk for HBV infection should be evaluated for prior evidence of HBV infection before initiating HUMIRA.
The combinations of HUMIRA and anakinra as well as HUMIRA and abatacept is not recommended.
TNF antagonists, including HUMIRA, have been associated in rare cases with demyelinating disease and serious allergic reactions. Rare reports of pancytopenia including aplastic anemia have been reported with TNF-blocking agents. Adverse events of the haematologic system, including medically significant cytopenia have been infrequently reported with HUMIRA.
More cases of malignancies including lymphoma have been observed among patients receiving a TNF antagonist compared with control patients in clinical trials. The size of the control group and limited duration of the controlled portions of studies precludes the ability to draw firm conclusions. Furthermore, there is an increased background lymphoma risk in rheumatoid arthritis patients with long-standing, highly active, inflammatory disease, which complicates the risk estimation. During the long-term open-label trials with HUMIRA, the overall rate of malignancies was similar to what would be expected for an age-, gender- and race-matched general population. With the current knowledge, a possible risk for the development of lymphomas or other malignancies in patients treated with a TNF antagonist cannot be excluded. All patients, and in particular patients with a medical history of extensive immunosuppressant therapy or psoriasis patients with a history of PUVA treatment, should be examined for the presence of non-melanoma skin cancer prior to and during treatment with HUMIRA.
In clinical studies with another TNF antagonist, a higher rate of serious congestive heart failure (CHF) related adverse events including worsening CHF and new onset CHF have been reported. Cases of worsening CHF have also been reported in patients receiving HUMIRA. Physicians should exercise caution when using HUMIRA in patients who have heart failure and monitor them carefully. HUMIRA should not be used in patients with moderate or severe heart failure.
The most frequently reported adverse event (?‰?1/10 patients) at least possibly causally related to HUMIRA is injection site reaction (including pain, swelling, redness or pruritus). Other common adverse events (?‰?1/100 patients) at least possibly causally related to HUMIRA include lower respiratory infections (including pneumonia, bronchitis), viral infections (including influenza, herpes infections), candidiasis, bacterial infection (including urinary tract infections), upper respiratory infection, dizziness (including vertigo), headache, neurologic sensation disorders (including paraesthesias), cough, nasopharyngeal pain, diarrhea, abdominal pain, stomatitis and mouth ulceration, nausea, hepatic enzymes increased, rash, pruritus, musculoskeletal pain, pyrexia and fatigue (including asthenia and malaise).
About HUMIRA
HUMIRA is the only fully human monoclonal antibody approved for the treatment of rheumatoid arthritis (RA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), Crohn???s disease and plaque psoriasis (Ps) in the United States and Europe. HUMIRA is also approved for the treatment of juvenile idiopathic arthritis (JIA) in the United States, and review for JIA in Europe is ongoing. Clinical trials are underway evaluating the potential of HUMIRA in ulcerative colitis. To date, HUMIRA has been approved in 75 countries and more than 250,000 people worldwide are currently being treated with HUMIRA.
HUMIRA resembles antibodies normally found in the body. It works by blocking tumor necrosis factor alpha (TNF-?±), a protein that, when produced in excess, plays a central role in the inflammatory responses of many immune-mediated diseases.
In the United States, HUMIRA is approved by the FDA for reducing signs and symptoms, inducing major clinical response, inhibiting the progression of structural damage, and improving physical function in adult patients with moderately to severely active rheumatoid arthritis (RA). HUMIRA can be used alone or in combination with methotrexate (MTX) or other disease-modifying anti-rheumatic drugs (DMARDs). HUMIRA is indicated for reducing signs and symptoms of moderately to severely active polyarticular juvenile idiopathic arthritis in patients 4 years of age and older. HUMIRA can be used alone or in combination with MTX. HUMIRA is indicated for reducing the signs and symptoms of active arthritis, inhibiting the progression of structural damage and improving physical function in patients with psoriatic arthritis. HUMIRA can be used alone or in combination with MTX or other DMARDs. HUMIRA is indicted for reducing signs and symptoms in patients with active ankylosing spondylitis. HUMIRA is indicated for reducing the signs and symptoms and inducing and maintaining clinical remission in adults with moderately to severely active Crohn's disease who have had an inadequate response to conventional therapy. HUMIRA is indicated for reducing signs and symptoms and inducing clinical remission in these patients if they have also lost response to or are intolerant to infliximab. HUMIRA is indicated for the treatment of adult patients with moderate to severe chronic plaque psoriasis who are candidates for systemic therapy of phototherapy, and when other systemic therapies are medically less appropriate. HUMIRA should only be administered to patients who will be closely monitored and have regular follow-up visits with a physician.
In Europe, HUMIRA, in combination with MTX, is indicated for the treatment of moderate to severe, active RA in adult patients when the response to DMARDs including MTX has been inadequate, and for the treatment of severe, active and progressive RA in adults not previously treated with MTX. HUMIRA can be given as monotherapy in case of intolerance to MTX or when continued treatment with MTX is inappropriate. HUMIRA has been shown to reduce the rate of progression of joint damage as measured by x-ray and to improve physical function, when given in combination with MTX.
Also in Europe, HUMIRA is indicated for the treatment of active and progressive PsA in adults when the response to previous DMARD therapy has been inadequate and for the treatment of severe, active AS in adults who have had an inadequate response to conventional therapy. HUMIRA is indicated for treatment of severe, active Crohn's disease, in patients who have not responded despite a full and adequate course of therapy with a corticosteroid and/or an immunosuppressant; or who are intolerant to or have medical contraindications for such therapies. For induction treatment, HUMIRA should be given in combination with corticosteroids. HUMIRA can be given as monotherapy in case of intolerance to corticosteroids or when continued treatment with corticosteroids is inappropriate. HUMIRA is indicated for the treatment of moderate-to-severe chronic plaque psoriasis in adult patients who failed to respond to or who have a contraindication to, or are intolerant to other systemic therapy including cyclosporine, methotrexate or PUVA.
Abbott's Commitment to Immunology
Abbott is focused on the discovery and development of innovative treatments for immunologic diseases.
About Abbott
Abbott ( NYSE: ABT) is a global, broad-based health care company devoted to the discovery, development, manufacture and marketing of pharmaceuticals and medical products, including nutritionals, devices and diagnostics. The company employs more than 68,000 people and markets its products in more than 130 countries. Abbott employs 2,100 people in Japan with offices in Tokyo, Osaka, Fukui, and Chiba.
Abbott
abbott
View drug information on Humira.
"The approval of HUMIRA in Japan is a significant milestone for Abbott," said Glenn Warner, vice president, Pharmaceuticals, Japan, Abbott. "This approval is both good news for Japanese patients and a significant step forward for Abbott in Japan."
HUMIRA is expected to become available to patients in Japan in the coming months, following the standard pricing approval process.
"The clinical studies of HUMIRA in Japanese patients demonstrated the efficacy and safety of this medicine," said Prof. Nobuyuki Miyasaka, M.D., Department of Collagen Disease and Rheumatology, Tokyo Medical and Dental University Graduate School of Medicine, who was involved in the development of HUMIRA for the treatment of rheumatoid arthritis in Japan.
Abbott has submitted an application for approval of HUMIRA for plaque psoriasis, and is also developing HUMIRA in Japan for Crohn's disease, ankylosing spondylitis, juvenile rheumatoid arthritis and ulcerative colitis. Eisai is co-developing and will jointly market these indications with Abbott.
More Information About Rheumatoid Arthritis
Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by joint inflammation, joint pain and stiffness, which can lead to long-term joint damage. The joints most commonly affected early in the disease are the smaller joints of the fingers, feet and wrists. The elbows, knees, ankles and hips can also be affected. Although there is no cure for RA, people continue to seek treatments that help alleviate pain and inflammation and slow disease progression.
More information on RA and current treatment options can be found at RA.
Important Safety Information
Globally, prescribing information varies; refer to the individual country product label for complete information.
Serious infections, sepsis, rare cases of tuberculosis (TB), and opportunistic infections, including fatalities, have been reported with the use of TNF antagonists, including HUMIRA. Many of the serious infections have occurred in patients on concomitant immunosuppressive therapy that, in addition to their underlying disease could predispose them to infections. Patients must be monitored closely for infections, including tuberculosis, before, during and after treatment with HUMIRA. Treatment should not be initiated in patients with active infections until infections are controlled. HUMIRA should not be used by patients with active TB or other severe infections such as sepsis and opportunistic infections. Patients who develop new infections while using HUMIRA should be monitored closely. HUMIRA should be discontinued if a patient develops a new serious infection until infections are controlled. Physicians should exercise caution when considering use of HUMIRA in patients with a history of recurring infection or with underlying conditions that may predispose patients to infections.
TNF-blocking agents have been associated with reactivation of hepatitis B (HBV) in patients who are chronic carriers of the virus. Some cases have been fatal. Patients at risk for HBV infection should be evaluated for prior evidence of HBV infection before initiating HUMIRA.
The combinations of HUMIRA and anakinra as well as HUMIRA and abatacept is not recommended.
TNF antagonists, including HUMIRA, have been associated in rare cases with demyelinating disease and serious allergic reactions. Rare reports of pancytopenia including aplastic anemia have been reported with TNF-blocking agents. Adverse events of the haematologic system, including medically significant cytopenia have been infrequently reported with HUMIRA.
More cases of malignancies including lymphoma have been observed among patients receiving a TNF antagonist compared with control patients in clinical trials. The size of the control group and limited duration of the controlled portions of studies precludes the ability to draw firm conclusions. Furthermore, there is an increased background lymphoma risk in rheumatoid arthritis patients with long-standing, highly active, inflammatory disease, which complicates the risk estimation. During the long-term open-label trials with HUMIRA, the overall rate of malignancies was similar to what would be expected for an age-, gender- and race-matched general population. With the current knowledge, a possible risk for the development of lymphomas or other malignancies in patients treated with a TNF antagonist cannot be excluded. All patients, and in particular patients with a medical history of extensive immunosuppressant therapy or psoriasis patients with a history of PUVA treatment, should be examined for the presence of non-melanoma skin cancer prior to and during treatment with HUMIRA.
In clinical studies with another TNF antagonist, a higher rate of serious congestive heart failure (CHF) related adverse events including worsening CHF and new onset CHF have been reported. Cases of worsening CHF have also been reported in patients receiving HUMIRA. Physicians should exercise caution when using HUMIRA in patients who have heart failure and monitor them carefully. HUMIRA should not be used in patients with moderate or severe heart failure.
The most frequently reported adverse event (?‰?1/10 patients) at least possibly causally related to HUMIRA is injection site reaction (including pain, swelling, redness or pruritus). Other common adverse events (?‰?1/100 patients) at least possibly causally related to HUMIRA include lower respiratory infections (including pneumonia, bronchitis), viral infections (including influenza, herpes infections), candidiasis, bacterial infection (including urinary tract infections), upper respiratory infection, dizziness (including vertigo), headache, neurologic sensation disorders (including paraesthesias), cough, nasopharyngeal pain, diarrhea, abdominal pain, stomatitis and mouth ulceration, nausea, hepatic enzymes increased, rash, pruritus, musculoskeletal pain, pyrexia and fatigue (including asthenia and malaise).
About HUMIRA
HUMIRA is the only fully human monoclonal antibody approved for the treatment of rheumatoid arthritis (RA), psoriatic arthritis (PsA), ankylosing spondylitis (AS), Crohn???s disease and plaque psoriasis (Ps) in the United States and Europe. HUMIRA is also approved for the treatment of juvenile idiopathic arthritis (JIA) in the United States, and review for JIA in Europe is ongoing. Clinical trials are underway evaluating the potential of HUMIRA in ulcerative colitis. To date, HUMIRA has been approved in 75 countries and more than 250,000 people worldwide are currently being treated with HUMIRA.
HUMIRA resembles antibodies normally found in the body. It works by blocking tumor necrosis factor alpha (TNF-?±), a protein that, when produced in excess, plays a central role in the inflammatory responses of many immune-mediated diseases.
In the United States, HUMIRA is approved by the FDA for reducing signs and symptoms, inducing major clinical response, inhibiting the progression of structural damage, and improving physical function in adult patients with moderately to severely active rheumatoid arthritis (RA). HUMIRA can be used alone or in combination with methotrexate (MTX) or other disease-modifying anti-rheumatic drugs (DMARDs). HUMIRA is indicated for reducing signs and symptoms of moderately to severely active polyarticular juvenile idiopathic arthritis in patients 4 years of age and older. HUMIRA can be used alone or in combination with MTX. HUMIRA is indicated for reducing the signs and symptoms of active arthritis, inhibiting the progression of structural damage and improving physical function in patients with psoriatic arthritis. HUMIRA can be used alone or in combination with MTX or other DMARDs. HUMIRA is indicted for reducing signs and symptoms in patients with active ankylosing spondylitis. HUMIRA is indicated for reducing the signs and symptoms and inducing and maintaining clinical remission in adults with moderately to severely active Crohn's disease who have had an inadequate response to conventional therapy. HUMIRA is indicated for reducing signs and symptoms and inducing clinical remission in these patients if they have also lost response to or are intolerant to infliximab. HUMIRA is indicated for the treatment of adult patients with moderate to severe chronic plaque psoriasis who are candidates for systemic therapy of phototherapy, and when other systemic therapies are medically less appropriate. HUMIRA should only be administered to patients who will be closely monitored and have regular follow-up visits with a physician.
In Europe, HUMIRA, in combination with MTX, is indicated for the treatment of moderate to severe, active RA in adult patients when the response to DMARDs including MTX has been inadequate, and for the treatment of severe, active and progressive RA in adults not previously treated with MTX. HUMIRA can be given as monotherapy in case of intolerance to MTX or when continued treatment with MTX is inappropriate. HUMIRA has been shown to reduce the rate of progression of joint damage as measured by x-ray and to improve physical function, when given in combination with MTX.
Also in Europe, HUMIRA is indicated for the treatment of active and progressive PsA in adults when the response to previous DMARD therapy has been inadequate and for the treatment of severe, active AS in adults who have had an inadequate response to conventional therapy. HUMIRA is indicated for treatment of severe, active Crohn's disease, in patients who have not responded despite a full and adequate course of therapy with a corticosteroid and/or an immunosuppressant; or who are intolerant to or have medical contraindications for such therapies. For induction treatment, HUMIRA should be given in combination with corticosteroids. HUMIRA can be given as monotherapy in case of intolerance to corticosteroids or when continued treatment with corticosteroids is inappropriate. HUMIRA is indicated for the treatment of moderate-to-severe chronic plaque psoriasis in adult patients who failed to respond to or who have a contraindication to, or are intolerant to other systemic therapy including cyclosporine, methotrexate or PUVA.
Abbott's Commitment to Immunology
Abbott is focused on the discovery and development of innovative treatments for immunologic diseases.
About Abbott
Abbott ( NYSE: ABT) is a global, broad-based health care company devoted to the discovery, development, manufacture and marketing of pharmaceuticals and medical products, including nutritionals, devices and diagnostics. The company employs more than 68,000 people and markets its products in more than 130 countries. Abbott employs 2,100 people in Japan with offices in Tokyo, Osaka, Fukui, and Chiba.
Abbott
abbott
View drug information on Humira.
воскресенье, 5 июня 2011 г.
Can Blood Samples Predict Arthritic Rheumatism?
Levels of inflammatory proteins, so-called cytokines, are elevated in the blood even before the onset of arthritic rheumatism. This means that such blood samples could be used to predict the development of the disease and thereby make it possible to prevent the pathological process, according to an article by Umea researcher Solbritt Rantapaa Dahlqvist and her associates in the journal Arthritis and Rheumatism.
The research team analyzed blood samples from 86 individuals who donated samples to the Medical Biobank before they developed arthritic rheumatism. Of these, 69 had submitted samples at the time they were developing the disease. Moreover, blood samples were analyzed from 256 population-based matched controls from the Medical Biobank. The concentrations of 30 different cytokines and cytokine-related factors in plasma were measured using a so-called multiplex system.
The results show that individuals that later developed arthritic rheumatism had significantly elevated levels of most cytokines and that these cytokine patterns distinguished them from the control individuals. There was a connection with several different parts of the immune defense and also with specific auto-antibodies, so-called anti-cyclic citrullinated peptide antibodies. The results indicate that several years before individuals develop symptoms of arthritic rheumatism, the immune system is activated and the process that leads to arthritic rheumatism has started.
"Our findings point to the possibility of better predicting the development of arthritic rheumatism and perhaps also of preventing the development of the disease," says Solbritt Rantapaa Dahlqvist.
Arthritic rheumatism is a chronic autoimmune disorder characterized by joint inflammation that ultimately leads to the breakdown of cartilage and bone. The disease is difficult to diagnose early since its symptoms can often be diffuse at first. However, studies have shown that it is important to diagnose and treat the disease early in order to prevent severe joint damage.
Source: Expertanswer
The research team analyzed blood samples from 86 individuals who donated samples to the Medical Biobank before they developed arthritic rheumatism. Of these, 69 had submitted samples at the time they were developing the disease. Moreover, blood samples were analyzed from 256 population-based matched controls from the Medical Biobank. The concentrations of 30 different cytokines and cytokine-related factors in plasma were measured using a so-called multiplex system.
The results show that individuals that later developed arthritic rheumatism had significantly elevated levels of most cytokines and that these cytokine patterns distinguished them from the control individuals. There was a connection with several different parts of the immune defense and also with specific auto-antibodies, so-called anti-cyclic citrullinated peptide antibodies. The results indicate that several years before individuals develop symptoms of arthritic rheumatism, the immune system is activated and the process that leads to arthritic rheumatism has started.
"Our findings point to the possibility of better predicting the development of arthritic rheumatism and perhaps also of preventing the development of the disease," says Solbritt Rantapaa Dahlqvist.
Arthritic rheumatism is a chronic autoimmune disorder characterized by joint inflammation that ultimately leads to the breakdown of cartilage and bone. The disease is difficult to diagnose early since its symptoms can often be diffuse at first. However, studies have shown that it is important to diagnose and treat the disease early in order to prevent severe joint damage.
Source: Expertanswer
суббота, 4 июня 2011 г.
Over 200 Genes Influenced By Vitamin D, Highlighting Links To Disease
The extent to which vitamin D deficiency may increase susceptibility to a wide range of diseases is dramatically highlighted in research just published. Scientists have mapped the points at which vitamin D interacts with our DNA - and identified over two hundred genes that it directly influences. The results are published in the journal Genome Research.
It is estimated that one billion people worldwide do not have sufficient vitamin D. This deficiency is thought to be largely due to insufficient exposure to the sun and in some cases to poor diet. As well as being a well-known risk factor for rickets, there is a growing body of evidence that vitamin D deficiency also increases an individual's susceptibility to autoimmune conditions such as multiple sclerosis (MS), rheumatoid arthritis and type 1 diabetes, as well as certain cancers and even dementia.
Now, in a study whose funders include the Medical Research Council (MRC), the MS Society, the Wellcome Trust and the MS Society of Canada, researchers at the University of Oxford have shown the extent to which vitamin D interacts with our DNA. They used new DNA sequencing technology to create a map of vitamin D receptor binding across the genome. The vitamin D receptor is a protein activated by vitamin D, which attaches itself to DNA and thus influences what proteins are made from our genetic code.
The researchers found 2,776 binding sites for the vitamin D receptor along the length of the genome. These were unusually concentrated near a number of genes associated with susceptibility to autoimmune conditions such as MS, Crohn's disease, systemic lupus erythematosus (or 'lupus') and rheumatoid arthritis, and to cancers such as chronic lymphocytic leukaemia and colorectal cancer.
They also showed that vitamin D had a significant effect on the activity of 229 genes including IRF8, previously associated with MS, and PTPN2, associated with Crohn's disease and type 1 diabetes.
"Our study shows quite dramatically the wide-ranging influence that vitamin D exerts over our health," says Dr Andreas Heger from the MRC Functional Genomics Unit at Oxford, one of the lead authors of the study.
The first author of the paper, Dr Sreeram Ramagopalan from the Wellcome Trust Centre for Human Genetics, adds: "There is now evidence supporting a role for vitamin D in susceptibility to a host of diseases. Vitamin D supplements during pregnancy and the early years could have a beneficial effect on a child's health in later life. Some countries such as France have instituted this as a routine public health measure."
The main source of vitamin D in the body comes from exposing the skin to sunlight, although a diet of oily fish can provide some of the vitamin. Research has previously suggested that lighter skin colour and hair colour evolved in populations moving to parts of the globe with less sun to optimise production of vitamin D in the body. A lack of vitamin D can affect bone development, leading to rickets; in pregnant mothers, poor bone health can be fatal to both mother and child at birth, hence there are selective pressures in favour of people who are able to produce adequate vitamin D.
This new study supports this hypothesis, having found a significant number of vitamin D receptor binding sites in regions of the genome with genetic changes more commonly found in people of European and Asian descent. It is probable that skin lightening as we migrated out of Africa resulted from the necessity to be able to make more vitamin D and prevent rickets: vitamin D deficiency led to pelvic contraction resulting in increased risk of fatality of both mother and unborn child, effectively ending maternal lineages unable to find ways of increasing availability of the vitamin.
"Vitamin D status is potentially one of the most powerful selective pressures on the genome in relatively recent times," says Professor George Ebers, Action Medical Research Professor of Clinical Neurology and one of the senior authors of the paper. "Our study appears to support this interpretation and it may be we have not had enough time to make all the adaptations we have needed to cope with our northern circumstances."
Source:
Wellcome Trust
It is estimated that one billion people worldwide do not have sufficient vitamin D. This deficiency is thought to be largely due to insufficient exposure to the sun and in some cases to poor diet. As well as being a well-known risk factor for rickets, there is a growing body of evidence that vitamin D deficiency also increases an individual's susceptibility to autoimmune conditions such as multiple sclerosis (MS), rheumatoid arthritis and type 1 diabetes, as well as certain cancers and even dementia.
Now, in a study whose funders include the Medical Research Council (MRC), the MS Society, the Wellcome Trust and the MS Society of Canada, researchers at the University of Oxford have shown the extent to which vitamin D interacts with our DNA. They used new DNA sequencing technology to create a map of vitamin D receptor binding across the genome. The vitamin D receptor is a protein activated by vitamin D, which attaches itself to DNA and thus influences what proteins are made from our genetic code.
The researchers found 2,776 binding sites for the vitamin D receptor along the length of the genome. These were unusually concentrated near a number of genes associated with susceptibility to autoimmune conditions such as MS, Crohn's disease, systemic lupus erythematosus (or 'lupus') and rheumatoid arthritis, and to cancers such as chronic lymphocytic leukaemia and colorectal cancer.
They also showed that vitamin D had a significant effect on the activity of 229 genes including IRF8, previously associated with MS, and PTPN2, associated with Crohn's disease and type 1 diabetes.
"Our study shows quite dramatically the wide-ranging influence that vitamin D exerts over our health," says Dr Andreas Heger from the MRC Functional Genomics Unit at Oxford, one of the lead authors of the study.
The first author of the paper, Dr Sreeram Ramagopalan from the Wellcome Trust Centre for Human Genetics, adds: "There is now evidence supporting a role for vitamin D in susceptibility to a host of diseases. Vitamin D supplements during pregnancy and the early years could have a beneficial effect on a child's health in later life. Some countries such as France have instituted this as a routine public health measure."
The main source of vitamin D in the body comes from exposing the skin to sunlight, although a diet of oily fish can provide some of the vitamin. Research has previously suggested that lighter skin colour and hair colour evolved in populations moving to parts of the globe with less sun to optimise production of vitamin D in the body. A lack of vitamin D can affect bone development, leading to rickets; in pregnant mothers, poor bone health can be fatal to both mother and child at birth, hence there are selective pressures in favour of people who are able to produce adequate vitamin D.
This new study supports this hypothesis, having found a significant number of vitamin D receptor binding sites in regions of the genome with genetic changes more commonly found in people of European and Asian descent. It is probable that skin lightening as we migrated out of Africa resulted from the necessity to be able to make more vitamin D and prevent rickets: vitamin D deficiency led to pelvic contraction resulting in increased risk of fatality of both mother and unborn child, effectively ending maternal lineages unable to find ways of increasing availability of the vitamin.
"Vitamin D status is potentially one of the most powerful selective pressures on the genome in relatively recent times," says Professor George Ebers, Action Medical Research Professor of Clinical Neurology and one of the senior authors of the paper. "Our study appears to support this interpretation and it may be we have not had enough time to make all the adaptations we have needed to cope with our northern circumstances."
Source:
Wellcome Trust
пятница, 3 июня 2011 г.
Sex -- A Major Predictor Of Remission In Early Rheumatoid Arthritis?
Women with rheumatoid arthritis have significantly less chance of remission than men, finds research published ahead of print in the Annals of the Rheumatic Diseases.
The authors base their findings on almost 700 adults who had been recently diagnosed with rheumatoid arthritis.
Their average age was 58, and they had had their disease for an average of six months. Two thirds of study participants were women, and they tended to be younger than the men.
After two years, the disease had gone into remission in just under four out of 10 study participants. After five years, the proportion in remission was similar, at 38.5%. But only around one in five were in remission at both time points.
Gender was a significant factor in the progress of the disease. At two years, just under a third of the women (32%) were in remission compared with almost half of the men (48%).
By five years, the gap had widened, with just under 31% of women in remission compared with 52% of the men.
Men were more than twice as likely to be in remission as women at both time points.
Women did not have more severe disease than the men initially, but it quickly became more severe and progressed more rapidly than it did among the men.
Differences in how long a person had had the disease, their age, or their drug treatment could not explain the discrepancy in remission rate, say the authors.
Contact: Emma Dickinson
BMJ Specialty Journals
The authors base their findings on almost 700 adults who had been recently diagnosed with rheumatoid arthritis.
Their average age was 58, and they had had their disease for an average of six months. Two thirds of study participants were women, and they tended to be younger than the men.
After two years, the disease had gone into remission in just under four out of 10 study participants. After five years, the proportion in remission was similar, at 38.5%. But only around one in five were in remission at both time points.
Gender was a significant factor in the progress of the disease. At two years, just under a third of the women (32%) were in remission compared with almost half of the men (48%).
By five years, the gap had widened, with just under 31% of women in remission compared with 52% of the men.
Men were more than twice as likely to be in remission as women at both time points.
Women did not have more severe disease than the men initially, but it quickly became more severe and progressed more rapidly than it did among the men.
Differences in how long a person had had the disease, their age, or their drug treatment could not explain the discrepancy in remission rate, say the authors.
Contact: Emma Dickinson
BMJ Specialty Journals
четверг, 2 июня 2011 г.
Popular Painkillers Linked To Hospital Admissions For Heart Failure
A British study has shown that nonsteroidal anti-inflammatory (NSAID) drugs raise older patients' risk of a first hospital admission for heart failure by 30%. The study looked at people aged 60-84.
Popular painkillers, such as Nurofen and Voltaren are NSAIDs. This is the third study in less than one year that links NSAIDs to heart risks.
The study found, predictably, that those who had a history of heart failure, obesity, smoking, recent specialist appointments and recent hospital stays, had a higher risk of being admitted to hospital for heart failure for the first time.
You can read about this study in the journal Heart.
The study also found, however, that 14% of those being admitted for heart failure were at the time taking NSAIDs. This compares to 10% of people who would normally be taking an NSAID for that age group.
Older patients who take indomethacin (indocin), a NSAID, are three times as likely to be admitted to hospital for heart failure for the first time.
NSAIDs are most commonly taken by patients with osteoarthritis.
What does this mean in numbers of patients being admitted into hospital? For the 60-84 age group, for every 1000 people taking NSAIDs, it means one extra hospital admission for heart failure. For those over 70 taking NSAIDs, if they have diabetes or hypertension, it could mean an extra three per thousand.
The researchers said that even a small increase in risk can mean an important increase in the workload for public health services.
Their conclusion was that not only do NSAIDs raise the risk for patients with a history of cardiovascular disease, but also people without any history of heart disease.
Many health experts wonder whether NSAIDs should be available so readily in supermarkets.
The FDA is currently reviewing NSAIDs.
With Cox-2 inhibitors, such as Vioxx, taken off the market, patients suffering from osteoarthritis and in need of painkillers will be concerned at these latest findings.
Web site with information on NSAIDs
Written by:
View drug information on Vioxx.
Popular painkillers, such as Nurofen and Voltaren are NSAIDs. This is the third study in less than one year that links NSAIDs to heart risks.
The study found, predictably, that those who had a history of heart failure, obesity, smoking, recent specialist appointments and recent hospital stays, had a higher risk of being admitted to hospital for heart failure for the first time.
You can read about this study in the journal Heart.
The study also found, however, that 14% of those being admitted for heart failure were at the time taking NSAIDs. This compares to 10% of people who would normally be taking an NSAID for that age group.
Older patients who take indomethacin (indocin), a NSAID, are three times as likely to be admitted to hospital for heart failure for the first time.
NSAIDs are most commonly taken by patients with osteoarthritis.
What does this mean in numbers of patients being admitted into hospital? For the 60-84 age group, for every 1000 people taking NSAIDs, it means one extra hospital admission for heart failure. For those over 70 taking NSAIDs, if they have diabetes or hypertension, it could mean an extra three per thousand.
The researchers said that even a small increase in risk can mean an important increase in the workload for public health services.
Their conclusion was that not only do NSAIDs raise the risk for patients with a history of cardiovascular disease, but also people without any history of heart disease.
Many health experts wonder whether NSAIDs should be available so readily in supermarkets.
The FDA is currently reviewing NSAIDs.
With Cox-2 inhibitors, such as Vioxx, taken off the market, patients suffering from osteoarthritis and in need of painkillers will be concerned at these latest findings.
Web site with information on NSAIDs
Written by:
View drug information on Vioxx.
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