Impact of different types of exercise programs on ankylosing spondylitis: a systematic review and meta-analysis.

PURPOSE: This systematic review and meta-analysis of controlled studies aimed to assess the efficacy of different types of exercise programs (EP) on ankylosing spondylitis (AS) activity, function and mobility. METHODS: We searched PubMed/Medline, Cochrane Library and Embase databases for reports of controlled trials of patients with AS published up to May 2022. The studies were classified by intervention into categories defined by the 4 exercise domains established by the American College of Sports Medicine and then adopted by the European League Against Rheumatism: aerobic, muscle strength, flexibility, neuromotor performance. RESULTS: We found a moderate effect of EP as a whole on BASDAI (Bath Ankylosing Spondylitis Disease Activity Index) (-0.60, 95% CI -0.95, -0.25, p < 0.001), BASFI (Functional) (-0.63, 95% CI -0.84, -0.42, p < 0.0001) and BASMI (Metrology) (-0.52, 95% CI -0.88, -0.15, p < 0.01). The effect of "flexibility + muscle strength" EP was large for BASMI, moderate for BASDAI and BASFI. The effect of "flexibility + muscle strength + aerobic" EP was large for BASFI, moderate for BASDAI. CONCLUSIONS: EP, regardless of the specific type of exercise, have a moderate effect on AS activity, function and mobility. EP including flexibility and muscle strength exercises may have a large effect, especially for mobility. Programs including aerobic exercise showed significant efficacy for function.IMPLICATIONS FOR REHABILITATIONIn ankylosing spondylitis (AS), any exercise program (EP), regardless of the type of exercises involved, showed a moderate effect on disease activity, function and spinal mobility.In AS, EP combining flexibility and strength exercises showed the largest effect on spinal mobility and should be encouraged.In AS, EP combining flexibility, muscle strength and aerobic exercises may be particularly effective on patient function.

Vaginal microbiota as an unusual cause of spondylodiscitis.

The incidence of extra pelvic infections due to vaginal microflora bacteria has increased as growth media and methods of isolation have improved. However, bone infections seem to be still relatively rare, and little is known about their risk factors, clinical presentation, treatment and final outcome. We describe here a spondylodiscitis due to Gardnerella vaginalis, Atopobium vaginae, Peptostreptococcus indolicus and Prevotella amnii, anaerobic bacteria from vaginal microbiota. Our patient had no obvious predisposing factor and recovered after antibiotic treatment. To our knowledge, this case is the first reported spondylodiscitis caused by polymicrobial vaginal flora in a healthy, immunocompetent woman.

Cachexia and adiposity in rheumatoid arthritis. Relevance for disease management and clinical outcomes.

Altered body composition is a frequent finding in rheumatoid arthritis and is associated with the two major outcomes of the disease: disability and cardiovascular mortality. It is estimated that up to two thirds of patients may be affected by loss of lean mass, the so-called rheumatoid cachexia. Hence, body weight being equal, the relative amount of lean mass is lower and that of body fat is higher in rheumatoid arthritis patients vs. healthy controls. Both disease-related factors and other factors, like drug treatments, physical activity and nutrition contribute to modify body composition in rheumatoid arthritis. The effect of pharmacological treatments, and notably of anti-TNF drugs, on body composition is controversial. Conversely, training programs to stimulate muscle growth can restore lean mass and reduce adiposity. There is good evidence that amelioration of body composition ameliorates function and reduces disability. Currently, there is no evidence that interventions that modify body composition can reduce cardiovascular morbidity and mortality in rheumatoid arthritis.

Teriparatide for osteoporosis in patients with sarcoidosis: Report on risk-benefit ratio in four cases.

OBJECTIVES: For patients with sarcoidosis, no consensus exists about the management of osteoporosis, whether related or unrelated to glucocorticoid therapy. METHODS: We report the first series of 4patients with histologically documented sarcoidosis who received teriparatide therapy for severe osteoporosis manifesting as a fracture cascade with multilevel vertebral fractures. When teriparatide was started, 1patient was receiving 10mg of prednisone equivalents per day, 1 was progressively tapering glucocorticoid dose, 2 had never received any glucocorticoid treatment. RESULTS: In all 4patients, teriparatide was effective in halting the fracture cascade, including in the 2patients who remained on long-term glucocorticoid therapy. None of the patients developed hypercalcemia. During teriparatide therapy, 3patients underwent a flare or a complication of sarcoidosis. Only the patient on stable glucocorticoid treatment did not present any adverse event. Before teriparatide initiation, sarcoidosis had been well controlled in all 3patients for several years. CONCLUSIONS: Even if the implication of teriparatide is unclear, the appearance of adverse events in 3 out of 4patients in this small series suggest caution in the use of teriparatide in patients with sarcoidosis.

Rheumatoid arthritis: from autoimmunity to synovitis and joint destruction.

Rheumatoid arthritis is an autoimmune disease characterized by the production of two known antibodies - rheumatoid factor and anti-citrullinated peptide antibody (ACPA) - against common autoantigens that are widely expressed within and outside the joints. The interactions between genes and environment are crucial in all stages of the disease, involving namely genes from major histocompatibility complex locus, and antigens such as tobacco or microbes (e.g. Porphyromonas gingivalis). T and B cells are activated as soon as the earliest phases of the disease, rheumatoid arthritis appearing as a Th1 and Th17 disease. Inflammatory cytokines have a considerable importance in the hierarchy of the processes involved in RA. The joint destruction seen in RA is caused not only by cytokine imbalances, but also by specific effects of the Wnt system and osteoprotegerin on osteoclasts and by matrix production dysregulation responsible for cartilage damage. Both innate and adaptative immunity demonstrated their respective cornerstone position in rheumatoid arthritis, since targeted treatments has been efficiently developed against TNF-α, IL-6 receptor, IL-1ß, CD20 B cells and T-cell/Dendritic cell interactions.