Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The pathogenesis of acne fulminans remains obscure despite extensive investigations discussed in this review, but evidence points toward an immune mediated phenomenon (eg, hypergammaglobulinemia, depressed complement, circulating immune complexes, hematuria, lytic bone lesions, or inflammatory myositis). Whether acne fulminans begins as an autoimmune process de novo, or whether the process is somehow triggered by minimal inflammation in susceptible individuals remains to be elucidated. Acne fulminans is a rare, disfiguring, and disabling disease. It is associated with many problems, including abnormalities revealed in the laboratory or on roentgenogram. We have reviewed past and present therapies. In conclusion, we emphasize the importance of early diagnosis and treatment to decrease the significant morbidity of acne fulminans.
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PMID:Acne fulminans. 214 35

Fibrodysplasia (myositis) ossificans progressiva is a rare but severely disabling disease in which ossification forms within muscle and leads to progressive restriction of the movements of the jaw, neck, shoulders and hips. Shortening of the big toes is usually present. It is important to recognise this disease as avoidance of intra-muscular injections, surgery and trauma reduces the risk of further ossification.
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PMID:Fibrodysplasia (myositis) ossificans progressiva in Dominica. 272 35

The lungs are frequently involved in systemic sclerosis ('scleroderma'), a rare, disabling disease of unknown origin, characterised by skin thickening and Raynaud's phenomenon. The pathogenesis of scleroderma is complex, but signs and symptoms of excessive fibrosis, vasculopathy and inflammation are almost universally present. Dyspnoea in scleroderma patients can be due to chest wall tightening from skin thickening, pleural disease, cardiac involvement, myositis of intercostal muscles, or so-called scleroderma lung disease. Scleroderma lung disease encompasses vascular (pulmonary artery hypertension) or interstitial lung disease, or both. A comprehensive work-up is required to delineate the underlying cause of dyspnoea in a scleroderma patient, and to establish the contribution of each component to the symptoms. This should include a 6-minute walk test, pulmonary function testing, high-resolution thoracic CT scanning, ECG, echocardiography and, if pulmonary artery hypertension is suspected, right-heart catheterisation; bronchoalveolar lavage is optional. Lung disease in scleroderma contributes significantly to excess morbidity and early mortality, especially when diffusion capacity drops below 40% and/or forced vital capacity below 50%. However, recent clinical studies have unequivocally demonstrated that scleroderma lung disease is amenable to treatment with new vasodilatory drugs that target specific pathways involved in vasoconstriction, or with cyclophosphamide for interstitial lung disease. Uncontrolled studies have suggested that these therapies also have an impact on survival, but controlled studies with a long follow-up are needed to corroborate this point.
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PMID:Scleroderma lung: pathogenesis, evaluation and current therapy. 1748 44

Sporadic inclusion-body myositis (sIBM) presents in average at the sixth decade of life and affects three men for one woman. It is a non-lethal, slowly progressive but disabling disease. Except the striated muscles, no other organs (such as the interstitial lung) are involved. The phenotype of this myopathy is particular since it involves the axial muscles (camptocormia, swallowing dysfunction) and limb girdle (notably the quadriceps) but also the distal muscles (in particular the fingers' and wrists' flexors) in a bilateral but non-symmetrical manner. The clinical presentation is then very suggestive of the diagnosis, which remains to be proven by a muscle biopsy. Histological features defining the diagnosis associate endomysial inflammatory infiltrates with frequent invaded fibres (the myositis) and amyloid deposits generally accompanying rimmed vacuoles (the inclusions). There is still today a debate to know if this disease is at its beginning a degenerative or an auto-immune condition. Nonetheless, usual immunosuppressive drugs (corticosteroids, azathioprine, methotrexate) or polyvalent immunoglobulines remain ineffective and even may worsen the handicap. Some controlled randomized trials will soon be launched for this condition, but for now, the best therapeutic approach to slow down the rapidity of progression of the disease is to maintain muscle exercise with the help of the physiotherapists.
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PMID:[Inclusion-body myositis]. 2412 35