There is no known cause or cure for Still’s Disease but there is research into treatment options. One such study was reported in the January, 2011 issue of Arthritis Care & Research.

This was a small cohort study which included only 14 patients with Still’s Disease. The study participants had failed all available therapies, which in some cases included three TNF inhibitors, abatacept, and rituximab. Eight of the patient’s had suffered irreversible joint damage as a result of their arthritis. Recurrent systemic symptoms were present in seven of the patients.

The 14 study participants were treated with the anti-interleukin (IL)-6 receptor antibody tocilizumab (Actermra). The dosages varied in the study, but the most common was the recommended dose for rheumatoid arthritis – 8mg/kg every 4 weeks.

The average disease activity score in 28 joints (DAS28) decreased from 5.61 at the beginning of the study to 3.21 after three months and decreased further, to 2.91 after six months.

Based on the European League Against Rheumatism (EULAR), a good response to treatment requires a DAS28 score or 3.2 or lower. 64% of the patients achieved this level. In addition, EULAR describes remission as a DAS28 score below 2.6, which was achieved by 57% of the patients.

Concurrent with the treatment with tocilizumab the patient’s average dosage of prednisone fell from 23.3 mg/day and the beginning of the study to 13 mg/day after three months and to 10.3 mg/day after six months.

A 60% improvement was seen in number of tender and swollen joints and in patient global health rating at six months and systemic symptoms resolved in 86% by three months.

The study was conducted by Xavier Puéchal, MD, PhD, of Le Mans General Hospital in Le Mans, France, and colleagues.

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More than half of the participants had rheumatoid arthritis while the non-RA group were selected randomly from the general population and had a similar distribution of age, sex and residence.

The study groups completed surveys related to lifestyle, including alcohol consumption and smoking. They also had blood samples taken to test for genetic risk factors.

The results revealed that alcohol consumption was associated with a substantially reduced risk of development of rheumatoid arthritis. It also showed that the risk decreased as the amount of alcohol consumed increased.

Among the regular drinkers, the top 25% in terms of alcohol consumed were 50% less likely to develop RA. This was true for both women and men. The highest reduction in risk was in those who smoked and also had risk factors for rheumatoid arthritis.

The researchers stated that these studies reinforce the idea that lifestyle factors have a significant impact in the development of rheumatoid arthritis, and that quitting smoking is still the most importance step in reducing risk.

These studies were also compatible with previous studies that showed that alcohol consumption helps protect against the development and the severity of rheumatoid arthritis, as well as other inflammatory diseases, such as cardiovascular disease.

This research was published in the June 5th issue of Annals of the Rheumatic Diseases.

Originally posted 2008-08-12 17:36:10. Republished by Blog Post Promoter

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There were several other interesting findings in the report about the emotional impacts of RA:

• Impairments in cognitive function were found more frequently in patients that were over 50 years old (39% vs. 9%)
• One third (33%) of RA patients suffer from sleep disorders
• Cognitive dysfunction was diagnosed in 23% of patients, with 16% of these ascribed to depression
• The age of rheumatoid arthritis patients when they first used prednisone was significantly higher in those with depression (48 years) compared to those without (30 years)
• Those RA patients with depression also displayed more severe symptoms as measured by X-ray, greater loss of function and pain than patients without depression. In addition, rheumatoid arthritis patients with depression received less aggressive treatment than patients without depression.

Dr Tatiana Lisitsyna from the State Institute of Rheumatology RAMS, Russian Federation, who conducted the study, said: “Psychiatric disorders are a very common comorbidity for people with RA, and they tend to be stress-related and associated with disease activity and chronic pain. Evaluating and addressing the mental health of those with RA should be a regular feature of rheumatology practice to improve quality of life and reduce the potentially distressing psychological burden of RA.”

The study included 75 RA patients, 72 of whom were women, with a median age of 52, with diagnosis based on the American College of Rheumatology definition. Psychiatric disorders were diagnosed in accordance with the ICD-10 (International Classification of Disease) scale, and other psychiatric and psychological scales.

The results were presented on June 12, 2009.

Originally posted 2009-06-12 12:39:49. Republished by Blog Post Promoter

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A new study conducted by researchers at the Medical Research Council’s Laboratory of Molecular Biology in Cambridge has resulted in a breakthrough in the understanding of how autoimmune responses can be controlled.

In a normal immune system, the body develops immune cells to recognize foreign material, like bacteria. Once encountered, the immune cells respond to eliminate the foreign material. Any rogue immune cells that would attack the body itself are destroyed during development or are regulated by special cell. A key gene in these regulatory cells is called Foxp3. Those people that either lack the Foxp3 gene or have a mutated version of the gene have dysfunctional immune regulation which can result in autoimmune diseases.

As a part of the study, scientists created a genetically engineered form of Foxp3 that can change developing immune cells into regulatory cells that have the ability to suppress immune response. They then injected the engineered gene into animals that were missing the Foxp3 gene.

Said group leader Dr. Alexander Betz: “When administered to and activated in animal models of arthritis, the modified cells inhibit or even reverse the disease process.”

The scientists are now working on determining the molecular mechanisms involved in the functioning of the Foxp3 gene and applying that to human cells. In that research they need to ensure that the human form of the gene does not negatively impact the body’s immune system.

“If Foxp3 functions as a key developmental switch in human immune cells, there is potential for a new avenue of therapy development that could transform arthritis treatment” — Dr. Betz.

The study was published in the current issue of the journal PLoS Biology.

Originally posted 2008-11-14 12:00:58. Republished by Blog Post Promoter

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