F.D.A. TO PLACE NEW LIMITS ON PRESCRIPTIONS OF NARCOTICS

From the News Desk of Jeanne Hambleton

By GARDINER HARRIS -Published: February 9, 2009

WASHINGTON — Many doctors may lose their ability to prescribe 24 popular narcotics as part of a new effort to reduce the deaths and injuries that result from these medicines’ inappropriate use, federal drug officials announced Monday.

A new control program will result in further restrictions on the prescribing, dispensing and distribution of extended-release opioids like OxyContin, fentanyl patches, methadone tablets and some morphine tablets.

These products are classified as Schedule II narcotics and already are restricted according to rules jointly administered by the Food and Drug Administration and the Drug Enforcement Agency. But the current restrictions have failed to “fully meet the goals we want to achieve,” said Dr. John K. Jenkins, director of the F.D.A.’s new drug center.

“What we’re talking about is putting in place a program to try to ensure that physicians prescribing these products are properly trained in their safe use, and that only those physicians are prescribing those products,” Dr. Jenkins said in a news conference on Monday. “This is going to be a massive program.”

Hundreds of patients die and thousands are injured every year in the United States because they were inappropriately prescribed drugs like OxyContin or Duragesic or they took the medicines when they should not have or in ways that made the drugs dangerous. The agency has issued increasingly urgent warnings about the risks, but the toll has only worsened in recent years.

The blame for this is shared among doctors who prescribe poorly, patients who pay little attention to instructions or get access to the medicines inappropriately, and companies that have marketed their products illegally.

The F.D.A. this year will hold meetings with manufacturers, patient and consumer advocates, and the public to ask for advice on how to carry out the new control program, officials announced. The first meeting will be on March 3, and no immediate changes in access to the drugs is planned.

The 24 medicines under review had 21 million prescriptions written for them in 2007, to 3.7 million patients, Dr. Jenkins said. They are extremely effective in reducing pain, which many medical studies suggest is widely undertreated in patients suffering serious illness. (A complete list of the drugs is at www.fda.gov/cder.)

But many doctors prescribe the drugs far too cavalierly, Dr. Jenkins said. The F.D.A. has received reports of patients’ being prescribed such medicines to treat something as simple as a sprained ankle, he said. In such patients, the medicines can be dangerous.

Part of the problem is marketing. Several reports, for instance, have suggested that Purdue Pharma, the maker of OxyContin, helped fuel widespread abuse of the drug by aggressively promoting it to general practitioners not skilled in either pain treatment or in recognizing drug abuse.

The company has denied such a connection, but a holding company connected with Purdue and three top Purdue executives pleaded guilty last year to criminal charges that the company had misled doctors and patients by claiming for five years that OxyContin was less prone to abuse because it was a long-acting narcotic.

Doctors are also to blame. A common reason for disciplinary actions at state medical boards is the use of narcotics in patients who show clear signs of addiction or for whom the drugs are obviously inappropriate.

The F.D.A. generally avoids interfering with the practice of medicine because doctor behavior is governed by state medical boards. Instead, the agency usually tries to provide doctors with the best and most current information, and then allows them to decide how to use it.

Most of the drugs withdrawn over the last 20 years, however, were taken off the market because doctors continued to use the medicines in ways that the F.D.A. warned against.

For decades, the agency’s armory in these battles held only a popgun and a cannon — the popgun being the issuance of widely ignored warnings; the cannon being its ability to force a medicine’s withdrawal. But a law passed in 2007 gave the agency a new, intermediate weapon — Risk Evaluation and Mitigation Strategies. Known as REMS, these programs allow the agency to place strong restrictions on the distribution of certain drugs.

 

Courtesy New York Times (Money & Policy – Health Alert) Copyright  & All Rights Reserved 

(http://www.nytimes.com/2009/02/10/health/policy/10fda.html?_r=1&emc=tnt&tntemail1=y)

 

 

New insights into inflammation in osteoarthritis

Contact: Amy Molnar
amolnar@wiley.com
John Wiley & Sons, Inc.

Study indicates role of inflammatory mechanism distinct from joint cartilage

The most common degenerative joint disease, osteoarthritis (OA) is marked by the breakdown of articular cartilage, which is the type of cartilage that lines the ends of most limb bones. It can afflict any joint—fingers, toes, wrists, ankles, elbows, shoulders, and the spine, as well as the weight-bearing knees and hips. As OA progresses, sufferers often experience inflammation around the affected joint. This inflammation has been attributed to bits of cartilage breaking off and aggravating the synovium, the thin, smooth membrane lining a joint. Yet, MRI detection of prominent synovitis in early OA—when joint cartilage appears normal—suggests that other joint structures may be involved in triggering this inflammation. Recent studies of inflammation in spinal arthritis implicate the enthesis, which is the attachment site of ligament or tendon to bone as being a potential driving factor in joint inflammation.

Intrigued by the potential role of tendon or ligament attachment sites in synovitis, Professors Michael Benjamin of Cardiff University and Dennis McGonagle of the University of Leeds decided to investigate the extent to which different entheses could contribute to inflammation by forming a functional unit and destructive partnership with adjacent synovium. Featured in the November 2007 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), their findings shed light on a potential novel mechanism for synovial inflammation in degenerative arthritis. This is based on a structure that the authors have called the “synovial-entheseal complex” (SEC). Basically insertions have a different type of cartilage called fibrocartilage near the bone. Although this is different from articular cartilage that lines the ends of bones, the authors speculated that this type of cartilage could also derive nourishment from synovium. However, this close integration although desirable in health could have unfortunate consequences if the enthesis was damaged.

To validate the widespread formation and to explore further, the possible inflammatory function of SECs, researchers collected ligament and tendon attachment samples from 60 cadavers, 35 male and 25 female, with a mean age of 84 years at death. 49 different entheses—19 from the arms, 26 from the legs, and 4 from the spinal column—were preserved for examination. To exclude cartilage degeneration as a trigger for synovial inflammation, 17 of the selected entheses were not immediately adjacent to joint cartilage. Each sample was studied for evidence of inflammatory cells and soft tissue microdamage, as well as for the composition of SECs.

At 82 percent of the entheses, the formation of a SEC was found. As expected, this occurred in entheses very close to joint cartilage, where the synovium was often part of the joint itself. However, a SEC was also detected in 47 percent of the sites separated from joint cartilage. For example, the SEC found at the Achilles tendon was formed with synovium that protruded from a cavity called a “bursa”, located a considerable distance from the ankle joint.

Joint insertions are sites of high mechanical stressing and the authors speculated that this could lead to damage within them, including their fibrocartilage This is exactly what the authors found. Degenerative changes—at least one and sometimes several—were detected on the soft tissue side of attachment sites. Most notably, cell clustering and/or fissuring was found in 76 percent of entheses. In 85 percent of SECs, the synovial component also showed evidence of mild inflammatory change. Finally, in 73 percent of the attachments, small numbers of inflammatory cells were present in the enthesis itself. Therefore the authors suggest that joint degeneration of fibrocartilage at insertions could trigger inflammation within SECs.

As Professors Benjamin and McGonagle note, one their most striking findings was the large number of attachment sites with evidence of changes in the entheses mirroring those typically seen in joint cartilage in OA—fibrocartilage cell clusters, cell hypertrophy, and fissuring among them. “Such changes at certain entheses could be directly relevant to older subjects with joint symptoms due to degenerative disease,” Professor McGonagle observes, “and some of the symptoms could be emanating from the SEC.”

Affirming the concept of a “synovio-etheseal complex” as widely applicable at many sites in the body, both right next to and removed from joint cartilage, this study also supports the idea that biomechanical factors related to the enthesis could play an important role in synovial inflammation in both degenerative and inflammatory arthritis.

###

Article: “Histopathologic Changes at ‘Synovio-Entheseal Complexes’ Suggesting a Novel Mechanism for Synovitis in Osteoarthritis and Spondylarthritis,” Michael Benjamin and Dennis McGonagle, Arthritis & Rheumatism, November 2007; (DOI: 10.1002/art.23078).

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