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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rheumatoid arthritis is a debilitating, chronic, systemic, autoimmune disease of unknown etiology that causes destruction of joint cartilage and bone. It generally occurs between the fourth and sixth decades of life, and affects two to three times more women than men. It is characterized by joint stiffness, pain, and swelling, and is accompanied by a loss of body cell mass. This loss of cell mass, known as rheumatoid cachexia, predominates in skeletal muscle, but also occurs in the viscera and immune system. Thus, rheumatoid cachexia leads to muscle weakness and a loss of functional capacity, and is believed to accelerate morbidity and mortality in rheumatoid arthritis. Currently there is no established mechanism for rheumatoid cachexia, but it is accompanied by elevated resting energy expenditure, accelerated whole-body protein catabolism, and excess production of the inflammatory cytokines, tumor necrosis factor-alpha and interleukin-1beta. Tumor necrosis factor-alpha is probably the central mediator of muscle wasting in rheumatoid arthritis, and is known to act synergistically with interleukin-1beta to promote cachexia. In general, tumor necrosis factor-alpha and interleukin-1beta are thought to alter the balance between protein degradation and protein synthesis in rheumatoid arthritis to cause muscle wasting. The precise mechanism by which they do this is not known. Reduced peripheral insulin action and low habitual physical activity are important consequences of rheumatoid arthritis, and have also been implicated as mediators of rheumatoid cachexia. Insulin inhibits muscle protein degradation. Consequently, reduced peripheral insulin action in rheumatoid arthritis is thought to be permissive to cytokine-driven muscle loss. The cause of reduced peripheral insulin action in rheumatoid arthritis is not known, but tumor necrosis factor-alpha has been shown to interfere with insulin receptor signaling and is probably an important contributor. Low habitual physical activity has consistently been observed in rheumatoid arthritis and is an important consequence of, and contributor to, muscle wasting. In addition, low physical activity predisposes to fat gain and is believed to precipitate a negative reinforcing cycle of muscle loss, reduced physical function, and fat gain in rheumatoid arthritis, which leads to 'cachectic obesity'. To date, there is no standard treatment for rheumatoid cachexia. However, physical exercise is currently believed to be the most important and clinically relevant countermeasure against rheumatoid cachexia. In general, a combination of skeletal muscle strength training and aerobic exercise is recommended, but must be prescribed with the patient's disease status, overall health, and safety in mind. Future studies should investigate the safety, efficacy, and required dose of anti-cytokine therapy for the treatment of rheumatoid cachexia. In this review, we outline the current definition of rheumatoid cachexia, and discuss the etiology, pathogenesis, and treatment of rheumatoid cachexia.
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PMID:Cachexia in rheumatoid arthritis. 1216 13

Ideally, treatment is based on etiology, if possible on pathophysiology, and in practice on anatomical and clinical findings. A systematic search for the etiological factors of osteoarthritis (OA) shows that the various mechanisms are frequently associated. Etiological treatments are rare. We may mention acetabular tectoplasty in hip dysplasia with minimal joint space narrowing. Valgus osteotomy would also be indicated for early medial tibiofemoral OA in genu varum if we had definite proof that, if left untreated, this deformity inevitably leads to clinically severe OA. This is not the case. One of the limitations of this etiological treatment lies in the fact that we do not know which patients are at risk of developing painful OA. Instead, certain risk factors for OA are known, so that primary and secondary prevention of the disease is possible. While age, sex and genetic predisposition are not amenable to preventive action, the same does not apply to the following factors: obesity, sports, and occupational activity. Thanks to in vitro studies of cultured normal and osteoarthritic chondrocytes and to experimental models of OA in animals, the pathophysiological mechanisms of OA are beginning to be better known. The prospect thus arises of "therapeutic manipulations" of precise pharmacological targets, even if it is still too soon to speak of true pathophysiological treatment of this disease. For instance, various interventions along the IL-1 pathway can be envisaged and have all been tested in animals. In practice, treating OA means taking into consideration its various signs: pain which appears to be mechanical and more or less chronic, joint stiffness, instability, effusion, and--the consequence of these symptoms--the professional, social and personal handicap of the patient. The treatment of OA must be approached from a global perspective, associating whenever possible symptomatic treatment, disease-modifying treatment, education and rehabilitation. In other words, the treatment of OA requires an overall approach, associating pharmacological and non-pharmacological modalities.
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PMID:The therapeutic approach to osteoarthritis. 1470 6

Osteo-arthritis is the chronic degenerative disease associated with joint pain and loss of joint function. It is caused by 'wear and tear' on a joint. Knee is the most commonly Involved joint. Disease is so crippling that patient is unable to walk independently from bed to bathroom. The major causes of osteo-arthritis are age, gender, obesity, medical condition and hereditary. The signs and symptoms of osteo-arthritis are pain, joint stiffness, joint swelling, and loss of function. No blood tests are helpful in diagnosing osteo-arthritis. Management of osteo-arthritis includes non-pharmacological, pharmacological and surgical. A relatively new procedure is viscosupplementation, in which a preparation of hyaluronic acid is injected into the knee joint. Hyaluronic acid is a naturally occurring substance found in the synovial fluid. It acts as a lubricant to enable bones to move smoothly over each other and a shock absorber for joint loads. The decrease in the elastic and viscous properties of synovial fluid in osteo-arthritis results from both a reduced molecular size and a reduced concentration of hyaluronic acid in the synovial fluid. Viscosupplementation may be a therapeutic option for individuals with osteo-arthritis of the knee. Viscosupplementation has been shown to relieve pain in many patients who cannot get relief from non-medicinal measures or analgesic drugs. This article is to know the mechanism of action, patients' selection criteria, rationale and efficacy of viscosupplimentation in the management of osteo-arthritis of knee.
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PMID:Role of viscosupplementation in osteo-arthritis of knee joint. 2476 95

In individuals with Down syndrome (DS), the prevalence of obesity is widespread; despite this, there are no experimental studies on the effect of obesity on gait strategy in DS individuals. The aim of this study is to assess the clinical gait analysis of a group of obese individuals with DS and a group of nonobese individuals with DS to determine whether obesity produces a different gait pattern in these participants. In addition, although females and males share a similar mass, they are characterized by different fat distribution and/or accumulation; thus, the presence of differences between females and males within the two DS groups was investigated. Gait analysis data of a group of 78 young individuals with DS and 20 normal-weight participants in the 5-18-year age range were considered. Among DS individuals, 40 were classified as obese (obese DS group), whereas 38 were classified as normal weight (nonobese groups). A three-dimensional gait analysis was carried out using an optoelectronic system, force platforms and video recording. Spatiotemporal, kinematic and kinetic parameters were identified and calculated for each participant. Our results show that most of the parameters were similar in the two groups of DS participants; the only differences were in terms of stance duration, longer in the obese DS group and dorsiflexion ability during the swing phase, which was limited in the obese DS group. The two DS groups were significantly different in terms of ankle stiffness (Ka index): both groups were characterized by reduced values compared with the control group, but the obese group presented lower values with respect to nonobese participants. The data showed that females were characterized by significant modifications of gait pattern compared with males in both groups, in particular, at proximal levels, such as the hip and the pelvis. Our findings indicate that the presence of obesity exerts effects on gait pattern in DS individuals and in particular on ankle joint stiffness. These results may have special clinical relevance; the biomechanical comparison of gait in young obese and nonobese DS individuals may provide a basis for developing either specific or common rehabilitative strategies.
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PMID:Effects of obesity on gait pattern in young individuals with Down syndrome. 2541 90