Targeting The Inflammatory Processes That Occur Early On In The Development Of Osteoarthritis

Main Category: Arthritis / Rheumatology
Also Included In: Immune System / Vaccines
Article Date: 09 Nov 2011 – 0:00 PST

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In a study published online in Nature Medicine, investigators at the Stanford University School of Medicine have shown that the development of osteoarthritis is in great part driven by low-grade inflammatory processes. This is at odds with the prevailing view attributing the condition to a lifetime of wear and tear on long-suffering joints.

“It’s a paradigm change,” said William Robinson, MD, PhD, the study’s senior author, of the implication of the findings. “People in the field predominantly view osteoarthritis as a matter of simple wear and tear, like tires gradually wearing out on a car.” It also is commonly associated with blow-outs, he added, such as a tear in the meniscus – a cartilage-rich, crescent-shaped pad that serves as a shock-absorber in joints – or some other traumatic damage to a joint.

But Robinson’s paper suggests a different way of understanding the disease. Its findings offer hope that by targeting the inflammatory processes that occur early on in the development of osteoarthritis – well before it progresses to the point where symptoms appear – the condition might someday be preventable.

Robinson is an associate professor of immunology and rheumatology at Stanford and a staff physician with the Veterans Affairs Palo Alto Health Care System. The first authorship of the study is shared by research associate Qian Wang, MD, PhD, and Andrew Rozelle, MD, a former Stanford rheumatology fellow now at the Palo Alto Medical Foundation.

Osteoarthritis is the most common joint disease, afflicting some 27 million people in the United States alone. It is characterized by breakdown of cartilage, most often in the knees, hips, fingers and spine. Drugs commonly used to treat osteoarthritis, such as acetaminophen and ibuprofen, relieve pain but do not slow the disease’s progression.

It has long been known that osteoarthritic joint tissues host a heightened number of migratory inflammatory cells and of some of the substances these cells secrete – “not nearly as much as in the case of rheumatoid arthritis, which is clearly an autoimmune disease, but enough to make us wonder if inflammation is also a major player in osteoarthritis as well,” Robinson said. His team’s observation of increased numbers of certain specialized inflammatory proteins early in the progress of osteoarthritis, before it becomes symptomatic, suggested that inflammation might be a driver, rather than a secondary consequence, of the disease.

The new study showed that, indeed, initial damage to the joint sets in motion a chain of molecular events that escalates into an attack upon the damaged joint by one of the body’s key defense systems against bacterial and viral infections, the so-called complement system. This sequence of events involves activation of a chain reaction called the “complement cascade,” and begins early in the development of osteoarthritis.

The complement system consists of an orchestra of proteins present in blood. Upon activation of the complement cascade – typically, in response to the presence of bacterial or viral infection – these proteins engage in a complex interplay, variously enhancing or inhibiting one another’s actions at certain points and culminating in the activation of a protein cluster called the MAC (for “membrane attack complex”). By punching holes in the membranes of bacterial or virally infected human cells, the MAC helps to clear the body of infections.

An early clue regarding the complement system’s key role in osteoarthritis came when Robinson and his colleagues, employing advanced lab techniques, compared the levels of large numbers of proteins present in the joint fluid taken from osteoarthritis patients with levels present in fluid from healthy individuals. They found that the patients’ tissues had a relative overabundance of proteins that act as accelerators in the complement cascade, along with a dearth of proteins that act as brakes.

Robinson’s group also examined the activity level of genes (which are recipes for proteins) in joint-lining tissues of osteoarthritic versus healthy subjects, and observed a similar result: more expression of genes encoding complement-activating and related inflammatory proteins, and less expression of genes encoding complement- and inflammation-inhibiting ones, in the osteoarthritic patients’ joint tissues.

To further explore the complement system’s role in osteoarthritis, the researchers induced the equivalent of meniscal tears or removal in mice who (like humans) are much more prone to getting osteoarthritis in joints that have suffered such damage. The procedure was performed on normal mice and on three separate strains of bioengineered lab mice, each strain missing a different protein component of the complement system. In two cases, the missing protein was one that ordinarily acts as an accelerator within the complement cascade, and in the third case one that acts as a brake.

The normal mice developed osteoarthritis as expected. But in comparison with these mice, the two strains of bioengineered mice lacking a complement-cascade-accelerating protein developed less-severe arthritis, while the mice lacking the complement-inhibiting protein got worse, faster. Thus, mice with impaired complement activation were protected against the development of osteoarthritis in response to meniscal damage.

Next, Robinson’s team asked how complement was causing osteoarthritis. Further experiments in mice and with human tissue showed that the MAC, the heavy artillery of the complement system, was damaging joint-tissue cells, but not by punching holes in them. Instead, it was binding to cartilage-producing cells in these tissues and causing them to secrete, on their own, still more complement-component proteins as well as other inflammatory chemicals, and other specialized proteins, or enzymes, that chew up the matrix of cartilage occupying the spaces between cells. They demonstrated that breakdown products of cartilage destruction, including one called fibromodulin, can directly activate the complement system, fostering a continuing cycle of joint-tissue damage.

Finally, the investigators showed that all these insults inflicted by the complement system – measured by microscopic examination of mouse joints – were mirrored by functional impairment. Bioengineered mice lacking a key complement-component protein, without which the complement system fails to activate, maintained their ability to walk normally, while normal mice developed a hindered gait due to severe osteoarthritis following meniscal injury.

“Recent findings suggest that low-grade complement activation contributes to the development of degenerative diseases including Alzheimer’s disease and macular degeneration. Our results suggest that osteoarthritis can be added to this list of diseases,” said Robinson.

Drugs that target the complement system may someday prove useful in preventing the onset of osteoarthritis in people who have suffered joint injuries, Robinson said, though he cautioned that this system is so crucial to our defense against microbial infection that systemic delivery of complement inhibitors would likely not be safe. But it is possible that a brief period of local administration of a complement inhibitor might provide benefit to patients developing osteoarthritis, while minimizing their risk for the development of infections.

“Right now we don’t have anything to offer osteoarthritis patients to treat their underlying disease,” Robinson said. “It would be incredible, for the one-third of humans over 60 who have it, to find a way to slow it down.”

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Some Rheumatoid Arthritis Drugs Not Linked To Serious Infections

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Main Category: Arthritis / Rheumatology
Also Included In: Infectious Diseases / Bacteria / Viruses
Article Date: 08 Nov 2011 – 10:00 PST

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According to a study published early in JAMA to coincide with its presentation at the American College of Rheumatology/Association of Rheumatology Health Professionals Annual Scientific Meeting, researchers have discovered that overall tumor necrosis factor-α antagonists medication is not linked to an increased risk of hospitalization for serious infections in comparison to using nonbiologic medications. Although tumor necrosis factor (TNF)-α antagonists have revolutionized the treatment of autoimmune diseases, safety concerns remain regarding their use for treating autoimmune disease, such as rheumatoid arthritis and psoriasis.

Background information of the article says that:

“Several studies reported serious infections in users of TNF-α antagonists. However, whether the risk of serious infections with TNF-α antagonists is greater than that with comparator nonbiologic medications is unclear.”

Carlos G. Grijalva, M.D., M.P.H., of the Vanderbilt University in Nashville, Tenn., and his team decided to establish whether initiation of TNF-α antagonists was linked to an increased risk of serious infections in patients suffering from autoimmune diseases, and if risk varies depending on a specific TNF-α antagonist.

In order to compare the use and outcomes of TNF-α antagonists and nonbiologic treatments, researchers conducted a retrospective cohort study within the SABER project, a U.S. multi-institutional collaboration from 1998 to 2007 of patients suffering from inflammatory bowel disease (IBD), rheumatoid arthritis (RA), psoriasis and psoriatic arthritis, or ankylosing spondylitis (psoriasis and spondyloarthropathies, a disease affecting the spinal joints.

The researchers established baseline glucocorticoid use as a separate covariate and measured primary outcome as serious infections that needed hospitalization during the first year after starting TNF-α antagonists or nonbiologic treatments.

From the study cohorts consisting of 10,484 patients with RA, 2,323 with IBD, and 3,215 patients suffering from psoriasis and spondyloarthropathies matched pairs of patients using TNF-α antagonists and comparator medications, the researchers reported 1,172 serious infections. Most of these infections (53%) consisted of pneumonia, skin and soft tissue infections. 30 of 823 RA patients (3.6%) died of their serious infection during hospitalization, as well as 4 patients of 194 IBD patients (2.1%) and 11 of 155 psoriasis patients (7.1%) respectively.

After researchers analyzed the data, they discovered that serious infection hospitalization rates were not substantially different between the overall TNF-α antagonists compared with comparative treatment for RA, IBD and psoriasis, psoriatic arthritis, or ankylosing spondylitis. However, they did discover that in patients suffering from RA, infliximab was linked to a substantial increase in serious infections in comparison to etanercept and adalimumab. Patients’ baseline glucocorticoid use was linked to a dose-dependent increase in infections.

The authors summarize:

“In conclusion, in this large retrospective cohort study of predominantly low-income and vulnerable U.S. patients with autoimmune diseases, we observed higher absolute rates of infection compared with previously published cohort studies and randomized controlled trials. We found no increased risk of hospitalizations for serious infections among patients initiating a TNF-α antagonist (as a group) compared with those taking comparator nonbiologic therapies.”

Editorial: Is Anti-TNF Therapy Safer Than Previously Thought?

In an accompanying editorial, Will Dixon, M.R.C.P., Ph.D., of the University of Manchester, England, and David T. Felson, M.D., M.P.H., of the Boston University School of Medicine comment on the findings of this study, saying:

“Given its large and comprehensive information about drug use and outcomes, the SABER project will certainly contribute to the understanding of the risks of biologic therapy. Conflicting findings between large pharma-coepidemiology studies are to be expected, and exploring reasons for discrepant results can yield helpful insights. From existing knowledge plus this recent study by Grijalva et al, one conclusion is that when compared with ongoing nonbiologic disease-modifying antirheumatic drug (DMARD) use, infection rates are increased in patients who started treatment with anti-TNF agents. However, this study suggests that serious infection risk may be no higher in those initiating anti-TNF therapy than in those starting a new DMARD, perhaps in combination with methotrexate. These intriguing findings need replication in other studies. Nevertheless, the report by Grijalva et al raises important questions about the comparative safety of immunosuppressant and biologic therapy and may prompt a re-evaluation of anti-TNF safety.”

Written by Petra Rattue

Copyright: Medical News Today

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Juvenile Arthritis

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Main Category: Pediatrics / Children’s Health
Also Included In: Arthritis / Rheumatology
Article Date: 08 Nov 2011 – 10:00 PST

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According to JAMA, one third of patients with juvenile idiopathic arthritis (JIA) starting receiving etanercept treatment demonstrated excellent responses. Etanercept, approved 10 years ago by the U.S. FDA and European Agency for the treatment of JIA, is linked to younger age at the onset of JIA, low measures of disability at study entry and fewer disease-modifying antirheumatic drug use before starting etanercept therapy. The study will be presented at the American College of Rheumatology/Association of Rheumatology Health Professionals Annual Scientific Meeting.

Background information in the article says:

“Since the development of biological agents, the pharmacological treatment approach of JIA is changing rapidly, and synthetic disease-modifying antirheumatic agents (DMARDs) are used earlier in the disease course, which seem to provide better long-term outcomes. As a result of these treatment successes, a treatment goal of reaching inactive disease now seems realistic. However, inactive disease is still not achieved in a substantial proportion of cases, and current approaches need to be optimized even more. The ability to identify patients who are more likely to respond to etanercept treatment would be an important step toward tailored patient-specific treatment and subsequently could improve current treatment approaches.”

Lead author Marieke H. Otten, M.D., M.Sc., of the Erasmus MC Sophia Children’s Hospital in Rotterdam, The Netherlands and her team decided to assess JIA disease activity after initiating etanercept treatment and to establish characteristics linked to responses in treatment. They utilized data from the Arthritis and Biologicals in Children Register, an ongoing prospective observational study since 1999 that contains all Dutch JIA patients who received biologic agents. The study included all biologically naïve, i.e. patients who had not previously received a biological agent, who started etanercept therapy before October 2009 and follow-up data to January 2011. The total number of 262 patients included 185 (71%) female patients and 46 (18%) with systemic-onset of the disease with an average age of 12.4 years at the start of etanercept treatment.

Researchers assessed the participants’ responses to the treatment 15 months after the start of treatment with etanercept. They defined ‘excellent response’ as inactive disease or discontinuation earlier due to disease remission, and ‘intermediate response’ as more than 50% improvement from baseline, but no inactive disease, whilst ‘poor response’ was defined as less than 50% improvement from baseline or discontinuation earlier due to ineffectiveness or intolerance.

After 15 months, researchers established that 85 (32%) of the total of 262 patients responded ‘excellent’, whilst 85 patients (32 percent) demonstrated ‘poor responders’ and the other 92 patients showed ‘intermediate response’.
The findings revealed that those who demonstrated ‘excellent response’ were linked to lower scores on disability measures at study entry, a younger age at disease onset and a low number of DMARDs, including methotrexate before being introduced to etanercept compared with those who achieved intermediate or poor responses. They also established that poor response was linked to systemic JIA and females in comparison to those with intermediate or excellent response.

199 patients developed 1 or more adverse events, such as infectious, non-infectious or serious AEs. 37 of these patients were in the ‘excellent response’ group, with 36 in the ‘intermediate group’ and 46 in the ‘poor response group’. 53 patients reported at least 1 infectious adverse event or an infectious serious adverse event.

A total of 61% participants discontinued etanercept therapy within the first 15 months of treatment, of which 4 had an excellent response and 57 a poor response. All participants with intermediate response finished their treatment.
The authors comment:

“In a secondary analysis of 262 patients with a median follow-up of 35.6 months after initiation of etanercept, a range of 37% to 49% of patients reached inactive disease. [Average] drug survival [i.e., average duration from start until first discontinuation due to ineffectiveness or adverse events] was 49.2 months for patients with an excellent response after 15 months, 47.5 months for patients with an intermediate response, and 17.4 months for patients with a poor response.”

During the overall etanercept treatment the researchers noted 31 serious, 99 infectious and 179 non-infectious adverse events.

Written by Petra Rattue

Copyright: Medical News Today

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Everyday Health Network

Dark, Cold Weather Derails Physical Activity Routines Of Older Arthritis Sufferers

Main Category: Arthritis / Rheumatology
Also Included In: Seniors / Aging
Article Date: 07 Nov 2011 – 0:00 PST

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As cold winter weather sets in and daylight hours dwindle, many older Chicagoans with arthritis tend to sit idle, missing out on the daily dose of physical activity they need to improve their health, according to a Northwestern Medicine study.

“We found that there’s a huge difference in trying to get these patients to be active in the winter and trying to get them to be active in the summer,” said Joe Feinglass, a research professor of medicine at Northwestern University Feinberg School of Medicine.

Results of the study, published in the September issue of the Journal of Physical Activity and Health, also highlight a lack of indoor recreational facilities for elderly, lower-income people in urban areas that experience extreme weather, Feinglass said.

“Chicago has indoor ‘exercise deserts,’ just like we have food deserts, making it difficult for low-income seniors, like many in our study, to get the physical activity they need,” said Feinglass, lead author of the study. “Even modest reductions in activity can have serious health consequences for people with arthritis.”

Researchers analyzed Chicago’s daily weather conditions and the amount of daylight from sunrise to sunset every day, over the three-year period of the study. They tracked the nearly 250 participants’ physical activity with an accelerometer, a small, sophisticated device that looks like a pedometer.

The participants, most over 60, all with documented knee osteoarthritis or a rheumatoid arthritis diagnosis, wore the accelerometer during waking hours, up to six times a week, at three to six months intervals, in all different types of Chicago weather.

Weather extremes, such as cold days with average daily temperature below 20 degrees or hot days, with daily average temperature over 75, kept participants inside and inactive for an additional hour a day, but the amount of daylight hours played the most significant role in derailing physical activity routines.

“The lack of daylight hours in the winter had a huge effect on the participants,” Feinglass said. “There’s more than a three-hour difference in the amount of completely sedentary time each day, where people are just sitting around doing nothing, during the months with less daylight, such as November, versus June.”

The federal guidelines recommend that adults with arthritis participate in 150 minutes per week of moderate-intensity, low-impact activity. That amounts to an average of slightly more than 20 minutes per day. It’s not the kind of physical activity that requires an expensive gym membership, but, unless they engage in TV or taped exercise programs, it usually means a brisk walk, not something many want to do outdoors in the dead of winter, Feinglass said.

“We spend an enormous amount of money on outdoor activities in the summer months for younger and healthier people,” he said. “We need to design more public access opportunities for older people to be more physically active indoors, in the winter.”

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American College Of Rheumatology 2011 Annual Meeting: Presentations By NYU Langone Experts

Main Category: Arthritis / Rheumatology
Also Included In: Bones / Orthopedics;  Lupus;  Gout
Article Date: 07 Nov 2011 – 0:00 PST

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Experts from NYU Langone Medical Center will present new research findings and clinical insight into the treatment of rheumatic and bone diseases in a variety of presentations at the American College of Rheumatology (ACR) 2011 Annual Scientific Meeting in Chicago, November 5-9, 2011.

Press Conferences

Osteoarthritis and Bone – Unintended Consequences: Increased Prescription of Narcotic Analgesics for OA in the Elderly is Associated with Increased Falls and Fractures in the Post-Vioxx Era
Lydia Rolita, MD and Bruce N. Cronstein, MD
Monday, November 7 at 8:30AM
Following the removal of Vioxx from the market there was a marked increase in the prescription of narcotic analgesics. Subsequently, the number of falls and fractures among the elderly population with osteoarthritis also went up – which was attributed to patients prescribed narcotic analgesics. The findings strongly indicate that recommendations for the treatment of chronic pain be re-evaluated.

Lupus, Gout and Vaccines – Favorable Prognosis in a Large, Prospective Multicenter Study of Lupus Pregnancies
Jill P. Buyon, MD
Tuesday, November 8 at 8:30AM
A study of pregnant women with systemic lupus erythematosus found eighty percent (80%) of women had positive outcomes, with adverse outcomes associated with an increase in lupus activity during pregnancy, high titer aPL antibody, and higher levels of uric acid at baseline. This large, prospective study provides reassurances to those patients with stable lupus considering pregnancy – and suggests guidelines for those at-risk patients.

Presentations, Demonstrations Panel Discussion

A Distinctive Oral Microbiome Characterizes Periodontitis in Patients with Early Rheumatoid Arthritis
Jose U. Scher, MD
Tuesday, November 8 at 4:45PM
This presentation investigates the abundance of a unique subgingival oral microbiota in patients with new-onset, never-treated rheumatoid arthritis, compared to those with chronic-established RA and healthy individuals. The study suggests that further identification and characterization of Porphyromonas species as well as other bacteria may help explain the reported link between RA and periodontal disease.

Successes in Rheumatology Comparative Effectiveness – Research Registries/Cohorts That Have Made a Difference in Rheumatology
Jeffrey Greenberg, MPH, MD
Saturday, November 5 at 3:00PM
This presentation highlights the value of comparative effectiveness research and how it enables the evaluation and comparison of the health outcomes, risks and benefits of established, commonly used treatments without the expense and limitations of randomized, controlled clinical trials.

ACR State of the Art Lecture – Biomarkers in Systemic Lupus Erythematosus: Where Do We Stand?
Jill P. Buyon, MD and Anca D. Askanase, MD
Monday November 7 at 1:00PM
This lecture will provide an understanding of the ongoing efforts to identify and validate biomarkers needed to advance the diagnosis, monitoring and treatment of systemic lupus erythematosus.

Rheumatic Disease Update – Paraneoplastic Rheumatic Disorders
Yusef Yazici, MD
Monday, November 7 at 2:30PM
The presentation will look at rheumatologic disorders known to be associated with a variety of malignancies – and the challenge clinicians’ face in identifying a malignancy that may not be apparent when rheumatic disease first appears.

Leveraging Existing Resources for Your Research – Introduction to the Clinical and Translational Science Award
Bruce N. Cronstein, MD
Monday, November 7 at 4:30PM
This session will introduce early career investigators to CTSA research resources and alternatives when a CTSA center is not available.

ACR Clinical Symposia – Hyperuricemia and Gout: Mechanisms and Morbidity
Michael H. Pillinger, MD
Tuesday, November 8 at 1:00PM
This discussion offers clinicians an update on recent findings on the pathogenesis and consequences of hyperuricemia and gout, one of the most common forms of inflammatory arthritis in men over the age of 50.

ACR Workshops – Patient Questionnaires to Monitor Status and Document Improvement in Standard Care: Practical Considerations
Theodore Pincus, MD
Tuesday, November 8 at 4:00PM
During this workshop, attendees will learn about the significance of patient questionnaire data in the prognosis of long-term care, how a rheumatology practice can use patient questionnaires to monitor and document patient status, identify incomplete responses to therapies or a need for changes in tight control of inflammation.

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MAP Kinase Resolved Well Enough To Spot Potentially Unique Drug Target

Main Category: Alzheimer’s / Dementia
Also Included In: Arthritis / Rheumatology;  Pharma Industry / Biotech Industry
Article Date: 07 Nov 2011 – 1:00 PST

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In many pharmaceutical company and university laboratories, scientists are looking closely at kinase complexes because the enzymes play key roles in essential cell functions. By taking unusual steps to examine a kinase complex, researchers at Brown University and the National Institutes of Health have found a sought-after prize: an unprecedentedly detailed description of its structure complete with a rare location on its structure that could be a target for new therapeutic drugs.

“Disregulation always leads to disease,” said Wolfgang Peti, associate professor of medicine and chemistry at Brown University and senior author of a paper published online in Nature Chemical Biology. “To make better drugs, what we want to do is look for individual things that are different between different complexes. The problem is we didn’t know where those non-common spots are. We didn’t have the structures that tell us the story. We were the first to get one of those structures.”

The complex that Peti, Brown colleague Rebecca Page, and their team has now characterized is hardly a household name: p38alpha:HePTP. It does however, matter in millions of households around the world. It is a member of the MAP kinase family, enzymes that regulate cell functions such as growth and inflammation. Diseases that correlate with disruptions to MAP kinase signaling include Alzheimer’s disease, rheumatoid arthritis, and cancer.

To determine the structure, the group took the rare step of combining techniques including nuclear magnetic resonance spectroscopy and small-angle X-ray scattering, using the National Synchrotron Light Source at Brookhaven National Laboratory on Long Island. The result was the clearest picture yet of a MAP kinase complex, which turns out to measure a mere 108 Angstroms (tenths of billionths of a meter) long by 30 Angstroms wide. The resolution of their resulting model is on the scale of individual atoms.

To elucidate their model, they probed the complex to discover areas where p38alpha binds to different HePTP-derived peptides. They found a specific area called “KIS” that is responsible for how the p38alpha:HePTP complex forms in its unique way.

“That really showed there are these areas outside the common sites that are likely unique between different complexes,” Peti said.

The next step is to learn more about KIS and the role it could ultimately play in disregulation and disease. In their paper, the authors expressed optimism that their newfound knowledge will have clinical relevance: “These results provide novel insights into the molecular interactions that regulate the strength and duration of MAP kinase signaling and, in turn, provide novel avenues for therapeutic interventions of MAP kinase-related diseases.”

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Investigating Link Between Autoimmune Diseases And Wounds That Don’t Heal

Main Category: Immune System / Vaccines
Also Included In: Dermatology;  Vascular;  Arthritis / Rheumatology
Article Date: 07 Nov 2011 – 1:00 PST

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Millions of Americans suffer from wounds that don’t heal, and while most are typically associated with diabetes, new research has identified another possible underlying cause – autoimmune diseases. The finding represents an unappreciated link that could lead to important new insights in wound healing, say researchers at Georgetown University Medical Center.

The research will be presented during a poster session on Tuesday, Nov. 8, 2011, at the annual meeting of the American College of Rheumatology in Chicago.

The study was sparked by the keen observation of Georgetown rheumatologist Victoria Shanmugam, M.D., who began noticing something rather unusual in her patients with autoimmune diseases – any open wound they had was very slow to heal. Their recovery was even more protracted than in patients with wounds who have diabetes, a disease that is notoriously damaging to blood vessels and to normal skin repair.

So Shanmugam and her colleagues conducted a chart review of people who sought care at a high-volume wound clinic at Georgetown University Hospital to determine the prevalence of autoimmune diseases. The study included patients with open wounds – usually leg ulcers who were treated during a three-month period in 2009. Of the 340 patients, 49 percent had diabetes, which she says is a typical rate.

“But what was surprising is that 23 percent had underlying autoimmune diseases, and the connection between these relatively rare disorders and wounds that don’t heal is under-recognized,” she says.

Of the 78 patients in the cohort who had autoimmune disease, most had rheumatoid arthritis, lupus or livedoid vasculopathy, a type of vascular disease.

Shanmugam says her findings also show that autoimmune disease-associated wounds were significantly larger at the patient’s first visit. These non-healing wounds can be “incredibly emotionally draining and financially costly,” Shanmugam says, because they require doctor visits over many months as well as an ever-present risk of serious infections. Sometimes, infections can lead to surgery and the amputation of limbs. More often, they require skin grafts or use of skin substitutes, which may still not solve the problem.

In fact, Shanmugam’s study found that skin grafts were more likely to fail in patients with autoimmune disease-associated wounds.

Shanmugam hopes the link she has made between autoimmune diseases and wound healing will make its way into the consciousness of the general practitioner. While it is much too invasive and costly to recommend that all patients with wounds be tested for autoimmune diseases, she says, “If a doctor has a patient with a leg ulcer that won’t heal after three or four months and they have done all the appropriate treatments, I hope they will look for the presence of an autoimmune disorder.”

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Young Women With Rheumatoid Arthritis At Increased Risk For Broken Bones

Main Category: Arthritis / Rheumatology
Also Included In: Bones / Orthopedics;  Women’s Health / Gynecology
Article Date: 07 Nov 2011 – 1:00 PST

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Women under 50 with rheumatoid arthritis are at greater risk of breaking bones than women without the condition, according to a Mayo Clinic study being presented at the American College of Rheumatology annual scientific meeting in Chicago. Men with rheumatoid arthritis also are in more danger of fractures, but that risk seems to surface when they are older, researchers found.

Rheumatoid arthritis (http://www.mayoclinic.com/health/rheumatoid-arthritis/DS00020) can lead to chronic, debilitating inflammation of the joints and other parts of the body. People over 50 with the condition are more likely to break a bone from a fall or sometimes even mild stress such as coughing. However, little has been known about the fracture risk among rheumatoid arthritis patients under 50.

Researchers studied two groups of 1,155 adults each, all from the same community: one set with a new diagnosis of rheumatoid arthritis, the other without the condition. Based on gender and birth year, each person was paired with someone from the other group, and the medical records of each duo were examined over time for new fractures unrelated to cancer or severe trauma. In women and men with rheumatoid arthritis, new fractures were more likely than in their counterparts, regardless of their age when they were diagnosed with rheumatoid arthritis.

Women under 50 when diagnosed with rheumatoid arthritis were more likely than their counterparts without the condition to have their first new fracture even before age 50. While men with rheumatoid arthritis were also more vulnerable to fractures, that danger didn’t grow until they got older.

“Understanding what contributes to the risk for fractures for all with rheumatoid arthritis, including young women, would help us better prevent them,” says lead researcher Shreyasee Amin, M.D., a rheumatologist at Mayo Clinic in Rochester, Minn. Women under 50 with rheumatoid arthritis need to know that even though they are young, they need to take greater care to prevent fractures, she says.

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Affordable Care Act Saves Over $1.2 Billion For Seniors, USA

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Main Category: Seniors / Aging
Also Included In: Medicare / Medicaid / SCHIP
Article Date: 07 Nov 2011 – 6:00 PST

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The Centers for Medicare Medicaid Services announced that until now, over 2.2 million people with Medicare have saved over $1.2 billion on their prescriptions, an average saving of $550 per person. It also reports that over 22.6 million seniors and people with disabilities have taken advantage of at least one free Medicare preventive benefit, such as the new Annual Wellness Visit made possible by the Affordable Care Act.

CMS Administrator Donald M. Berwick, MD said: “Thanks to the Affordable Care Act, seniors are getting cheaper prescription drugs and free preventive care.”

People with Medicare can take advantage of many preventive services free of charge under the Affordable Care Act, such as diabetes screening, some cancer screenings and help to quit smoking.

Across the country those with Medicare also receive cheaper prescription drugs. The Affordable Care Act, also gives seniors and people with disabilities a 50% discount on covered brand name drugs in the Medicare Part D coverage gap, also known as the ‘donut hole’. This will be continued throughout 2012 and progressively increase each year until the coverage gap closes in 2020.

In addition, the average premiums for Medicare Part D prescription drug plans will remain virtually unchanged in 2012. Medicare also recently announced a 4% decrease for 2012 in average Medicare Advantage premiums whilst Part B premiums, covering outpatient services including doctor visits, will increase by $3.50 monthly for most beneficiaries in 2012, with some seeing a decrease. According to Medicare, these changes will be more than offset by the average Social Security cost of living increase of $43 per month for retired workers.


Medicare open enrollment: From October 15 – December 7

As part of the annual Medicare Open Enrollment Period, Medicare clients can now review their drug and health plan coverage options for 2012. Cover plans that have achieved an overall quality rating of five stars with a high performer or “gold star” icon is highlighted by the CMS on Medicare’s Plan Finder at www.medicare.gov/find-a-plan.

The Enrollment Period for this year is early and has been extended by one week from October 15 to December 7 allowing Medicare beneficiaries more time to find the best plan for their needs by being able to switch to any available five-star plan at any time during the year without having to wait for the next open season.

Written by Petra Rattue

Copyright: Medical News Today

Not to be reproduced without permission of Medical News Today

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Medical Equipment for Hospitals and Research Laboratories

The accuracy of medical tests and experiments largely depends on the kind of equipment used. Medical equipment> manufactured by top names in the industry comes with advanced features and functionalities to ensure quality output. Hospitals and research laboratories can source such equipment from established CCR (Central Contractor Registration) certified medical laboratory equipment suppliers that offer both brand new and recertified models of various medical lab devices at reasonable prices.

Equipment to Ensure Flawless Performance

Hospitals and research laboratories require medical equipment such as blood gas analyzers, autoclaves, coagulation analyzers, immunology analyzers, microscopes, hematology analyzers, incubators, DNA analyzers, differential counters, gamma counters, urinalysis analyzers, microbiological systems, and more. New equipment comes with the latest technology and functions efficiently.

Though expensive, brand new models of medical laboratory equipment ensure many advantages:

  • Speed and accuracy: New devices come with advanced technology and specifications so that complex applications can be done accurately and quickly.
  • Flawless performance: Brand new medical laboratory appliances are stringently evaluated to ensure quality performance. This ensures there are no technical flaws and that the device works smoothly.
  • Manufacturer warranty: New medical equipment comes with manufacturer warranty of up to one or two years for the parts or for the device as a whole. So research facilities can easily claim for the replacement of parts or the device as a whole if it malfunctions.

Recertified Equipment: A Money Saving Option

Based on their budget specifications, research labs and hospitals can also go in for used and recertified devices.

Recertified medical lab equipment is a perfect option for research facilities operating on tight budgets. Most established distributors offer used and recertified devices at reasonable prices. Though priced low, there is no compromise when it comes to quality. They ensure excellent performance and durability. Before being put up for sale, used laboratory devices are thoroughly evaluated. If malfunctions are detected, the devices are revamped by factory-trained technicians. The reconditioning procedures performed include disassembling, replacement of parts, and repair in strict accordance with the specifications of the original manufacturer. Reconditioned devices are retested and if the performance is satisfactory, they are cleaned, packed, recertified, and offered for sale with extended warranty and proper service contracts.

Established Distributor for Quality Equipment

Hospitals and research laboratories should purchase the medical equipment they need from reliable CCR-certified lab equipment suppliers. Most online laboratory equipment suppliers maintain a wide product inventory that features medical lab devices from well-known brands. So labs can choose the equipment they need after comparing brands, features, technical specifications, warranty options, and prices. Purchasing from an established distributor ensures premium devices at competitive prices, efficient post-sales support and safe product delivery.