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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe a patient who developed fever, fatigue, muscle weakness, dyspnea, skin rash, and eosinophilia after taking "high doses" of tryptophan for insomnia for two years. A gallium-67 scan revealed diffuse increased uptake in the lung and no abnormal uptake in the muscular distribution. Bronchoscopy and biopsy confirmed inflammatory reactions with infiltration by eosinophils, mast cells, and lymphocytes. CT scan showed an interstitial alveolar pattern without fibrosis. EMG demonstrated diffuse myopathy. Muscle biopsy from the right thigh showed an inflammatory myositis with eosinophilic and lymphocytic infiltrations.
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PMID:Gallium uptake in tryptophan-related pulmonary disease. 199 38

Acute compartment syndrome of the thigh has been reported infrequently. To date, only eight cases from isolated blunt trauma without fracture have been reported. Two additional cases caused by intramuscular hematomas following blunt, low-energy trauma, which were treated successfully with emergency fasciotomies, are presented. The morbidity from this syndrome varies from mild, with quadriceps weakness, fatigue, and myositis ossificans, to severe, with limb-threatening vascular compromise. Morbidity can be avoided if a high level of suspicion is maintained, compartment pressures are measured, fasciotomies are performed, and hematomas are drained. Postoperatively, patients can expect a dramatic decrease in pain and a quick return of quadriceps function with aggressive physical rehabilitation.
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PMID:Acute anterior thigh compartment syndrome complicating quadriceps hematoma. Two case reports and review of the literature. 218 98

A young, previously healthy woman presented with increasing muscle pain, lower limb swelling, fatigue and eosinophilia. She had consumed L-tryptophan tablets (one to two at night) over the preceding five months for management of her insomnia. Her condition slowly deteriorated and she developed generalised oedema and severe lethargy. A white blood cell count was 21.3 x 10(9)/L with 43% eosinophils (Normal range: 4.0-11.0 x 10(9)/L with 1-6% eosinophils. A biopsy specimen of the deep fascia and gastrocnemius muscle demonstrated fasciitis and myositis. The patient failed to recover after cessation of L-tryptophan use but her condition improved rapidly without significant sequelae after systemic treatment with corticosteroids.
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PMID:Eosinophilia-myalgia syndrome associated with L-tryptophan use. 199 19

Eight patients who became ill while taking tryptophan had myalgia, fatigue, rash, fever, edema, alopecia, arthralgias, diminished joint motion, skin tightening, muscle cramping, and distal paresthesias. Three had shortness of breath, and one had pulmonary hypertension. Laboratory abnormalities included peripheral eosinophilia, leukocytosis, thrombocytosis, raised erythrocyte sedimentation rate, and elevated serum levels of aldolase, lactate dehydrogenase, and liver enzymes. Of 4 chest radiographs, 3 were abnormal. Of 5 skin and muscle biopsies, 4 showed sclerosis or mixed inflammatory cell infiltration of the dermis, subcutis, and fascia. Eosinophils were often present, but vasculitis was absent. Muscle inflammation was minimal. We conclude that the "eosinophilia-myalgia syndrome" is related to the ingestion of tryptophan and that abnormalities in the secretion of lymphokines may be important in its pathogenesis.
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PMID:Tryptophan-induced eosinophilia-myalgia syndrome. 221 1

This paper represents a philosophical shift in thinking. The authors propose that heel spur syndrome is not a primary soft tissue injury (i.e., enthesiopathy with concomitant bruising of the bursae and fat pad, and eventually the formation of a traction spur by the pull of the plantar fascia), but rather a primary bone injury. A microtrabecular stress failure (fatigue perturbation) of the os calcis occurs with secondary soft tissue involvement such as enthesiopathy, periostitis, myositis, bursitis, and finally the formation of a buttress callous (bone spur) to stabilize a microcortical crack. This study describes four stages in a progressive, sequential, pattern of fatigue failure of the os calcis. Clinical symptoms for each stage, along with supporting data such as x-rays, bone scans, and MRIs will be presented, as well as a suggested treatment plan for the chronic resistant cases.
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PMID:Fatigue perturbation of the os calcis. 795 Nov 94

The first known human case of Trichinella pseudospiralis myositis is described. A 33 years old woman reported 5 years of relatively mild symptoms of tiredness, muscle fatigue and muscle pain after exercise. She had minimal proximal weakness. Creatinine kinase was significantly elevated, and muscle biopsy showed polymyositis and Trichinella larvae. Steroid treatment dramatically worsened the weakness. Treatment with albendazole led to complete resolution of symptoms and laboratory abnormalities. Diagnosis and identification of the parasite were based on the distinctive appearance of the unencapsulated larvae and their movement in fresh muscle, plus clinical and laboratory findings.
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PMID:Trichinella pseudospiralis in humans: description of a case and its treatment. 803 73

This study was a 12-week, double-blind, placebo-controlled, multinational trial of fosinopril in 308 patients with mild to moderately severe heart failure (New York Heart Association [NYHA] functional class IIS 17%, IIM 48%, and III 35%; mean ejection fraction [+/-SD] 26.5% [+/-6.9%]; bicycle exercise duration 1 to 11 min). An initial dose of 10 mg once daily was titrated as tolerated to 40 mg once daily. Patients all received diuretic therapy; digoxin was optional. The primary endpoint was maximal bicycle exercise time; a secondary endpoint was occurrence of the following prospectively defined, ordered clinical events indicative of worsening heart failure: death, study discontinuation, hospitalization, emergency room visits, and need for supplemental diuretic. At study endpoint (last value obtained for each patient), bicycle exercise time increased more with fosinopril (38.1 s) than with placebo (23.5 s) (P = 0.101 by ANCOVA and 0.010 by prospectively defined dropout-adjusted endpoint analysis). More patients remained free of clinical events indicative of worsening heart failure when treated with fosinopril (89%) than with placebo (75%), and the worst events of fosinopril-treated patients tended to be less severe than those of placebo patients (P = 0.001). Analysis of the occurrence of individual clinical events showed that the need for supplemental diuretic was markedly reduced with fosinopril (8% vs 20%, of patients, P = 0.002), as were hospitalizations (3% vs 12% of patients, P = 0.002) and study discontinuations (2% vs 12% of patients, P < 0.001) for worsening heart failure; the two groups had similar incidences of death (3% of patients in the fosinopril group vs 2% in the placebo group, P = 0.723). In addition, symptoms of dyspnoea (P = 0.017), fatigue (P = 0.019), and NYHA functional class (P = 0.008) improved with fosinopril relative to placebo. In conclusion, fosinopril, at an initial dose of 10 mg once daily, subsequently titrated as tolerated to 40 mg once daily, increased exercise tolerance and reduced the frequency of clinical events indicative of worsening heart failure.
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PMID:Fosinopril attenuates clinical deterioration and improves exercise tolerance in patients with heart failure. Fosinopril Efficacy/Safety Trial (FEST) Study Group. 868 23

A 69-year-old woman was admitted to our hospital because of slight fever, general fatigue, joint pain and proximal muscle weakness. Severe elevation of serum enzyme levels of CPK, transaminase and aldolase was noted. The chest roentgengram showed diffuse reticular and nodular infiltrates. Histological examination of the transbronchial lung biopsy specimens revealed alveolitis and organizing pneumonia. Daily administration of 80 mg predonisolone was effective for both lung findings and myositis.
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PMID:[A case of polymyositis presenting histological picture of bronchiolitis obliterans organizing pneumonia with transbronchial lung biopsy specimens]. 872 Feb 70

Simvastatin belongs to a class of lipid-lowering drugs which completely inhibit 3-hydroxy-3-methylglutaryl co-enzyme A (HMG CoA) reductase. The commonest adverse effects of therapy with simvastatin HMG CoA reductase inhibitors are gastro-intestinal disturbance, myositis and myopathy. Rhabdomyolysis leading to renal failure has been reported, but it appears to be very rare, except in patients also receiving cyclosporin, nicotinic acid or gemfibrozil. Here we report the case of an elderly lady who was known to have chronic renal failure, but who developed rhabdomyolysis following simvastatin therapy. Her symptoms of muscle pain, fatigue, myoglobulinuria, oliguria and pulmonary oedema appeared 48 h after the first dose of simvastatin. Simvastatin was immediately stopped, and the patient was dialysed for 1 week. Her renal function improved and came back. We suggest that extreme care should be exercised in prescribing this drug, particularly for the elderly with renal impairment.
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PMID:Simvastatin-induced rhabdomyolysis in a patient with chronic renal failure. 1127 41

Sarcoidosis is a systemic granulomatous disorder of unknown cause. It has protean manifestations and can affect any organ, including bones, joints, muscles, and vessels. This article reviews the most recent information on the immunologic and inflammatory pathogenesis of sarcoidosis and its implications for therapy. Sarcoidosis results from an overexuberant T cell-mediated immune response to the unknown antigen. This antigen presentation/T cell antigen recognition event occurs in a microenvironment that is suffused in proinflammatory cytokines and growth factors that promote cell attraction, adhesion, permeability changes, further cytokine production, and release. An amplified cellular immune response ensues, leading to granuloma formation and fibrosis. The article summarizes the new developments in the medical literature related to the rheumatologic manifestations and their detection and management in sarcoidosis patients. Osseous involvement in sarcoidosis is often underdiagnosed because it can be asymptomatic. New imaging techniques improve detection. Management of osteoporosis in sarcoidosis patients requires special attention because these patients often have an underlying disorder in calcium metabolism that results in hypercalcuria and hypercalcemia. Joint manifestations, such as the classic Lofgren syndrome with accompanying erythema nodosum, may be self-limited or may become chronic, presenting an ongoing therapeutic challenge. Sarcoidosis vasculitis can be devastating, affecting virtually any vessel in any organ and causing significant morbidity. Muscle involvement, like the bony involvement, is underdiagnosed. Symptoms of muscle weakness, aches, tenderness, and fatigue should prompt consideration of occult sarcoid myositis, often with accompanying neurogenic atrophy. Sarcoidosis treatment usually starts with a period of observation before pharmacologic intervention. Corticosteroids remain the first-line therapy. Alternatives to corticosteroids are often introduced either because of steroid intolerance or in an attempt to reduce steroid dose and side effects. The advantages and disadvantages of these second line therapies are reviewed. Medical vigilance, with attention to new patient symptoms, is important in the management of sarcoidosis, because of the tendency of this disease to present in so many and diverse patterns.
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PMID:Sarcoidosis: immunology, rheumatic involvement, and therapeutics. 1114 21


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