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)

A 54-year-old man with dermatomyositis initially responsive to corticosteroids and methotrexate developed severe myalgias, increasing weakness, and fevers. Laboratory studies were suggestive of disseminated histoplasmosis, and muscle biopsy revealed myositis, fasciitis, and yeast in the perimysial connective tissue. Histoplasma capsulatum was cultured from skeletal muscle. Despite antifungal therapy, necrotizing fasciitis progressed to gluteal abscess formation. Disseminated histoplasmosis may present atypically in immunocompromised hosts as fasciitis and myositis. Patients with dermatomyositis could be particularly vulnerable to soft tissue invasion by fungi due to their underlying microangiopathy.
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PMID:Disseminated histoplasmosis presenting as myositis and fasciitis in a patient with dermatomyositis. 773 41

Demonstration of myositis in juvenile dermatomyositis (JDM) has traditionally required the presence of two out of three objective findings including muscle enzyme studies, electromyography, and muscle biopsy. Magnetic resonance imaging (MRI) is considered another objective criterion and has been recommended for follow-up studies as well. We report on a 6-year-old girl with JDM, presenting with facial rash and proximal muscle weakness, in whom MRI, in conjunction with elevated creatinine kinase (CK) levels, was diagnostic, with an increased T2 signal of proximal muscles. MRI reflected exacerbation of myositis in spite of steroid therapy 2 weeks later, but failed to mirror normalization of muscle strength and CK values 10 weeks later. In fact, improvement of MRI followed clinical and laboratory normalization with a delay of 2 months. This possible delay should be considered when MRI is used to monitor the response to therapy.
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PMID:Serial magnetic resonance imaging in juvenile dermatomyositis--delayed normalization. 783 73

The management of the muscular and extramuscular manifestations of the inflammatory myopathies remains a challenge for the practicing rheumatologist. Although corticosteroids remain the first line of therapy, their side effects often limit their usefulness. Paradoxically, one of the side effects of steroids, muscle weakness, is the very symptom at which therapy is aimed. Other immunosuppressive agents are of proven benefit alone or in combination with corticosteroids. The identification of characteristic autoantibodies that identify poor prognostic outcomes and the availability of newer immunosuppressive regimens should contribute to a more aggressive but perhaps safer therapeutic approach to the patient with myositis.
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PMID:Therapy of inflammatory myopathy. 785 28

We describe 2 patients with refractory inflammatory myositis who had an initial favorable response to intravenous immunoglobulin (IVIG) therapy. In contrast to all other reported cases, our patients reached a nadir in creatine phosphokinase (CPK) levels at 6 and 14 weeks after initiation of therapy, respectively, then experienced a relentless rise in CPK levels as well as a return of muscle weakness while still receiving IVIG. While IVIG may benefit some patients with refractory myositis, future studies must address the sustained efficacy of this agent.
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PMID:Tachyphylaxis of intravenous immunoglobulin in refractory inflammatory myopathy. 793 46

We reported a family case of HAM and HTLV-I carrier including two sisters presenting with myositis. Both the 65-year-old elder sister and her 53-year-old younger sister initially noted lumbago and developed difficulty in walking several years later. Neurologic examination revealed muscle weakness of the proximal parts of the upper and lower limbs (especially the latter). Mild hyperreflexia in all extremities, urinary disturbance and constipation were detected in the elder sister, while only urinary disturbance and constipation were seen in the younger. Anti-HTLV-I antibody in both serum and CSF was positive in both sisters. Muscle biopsy specimens showed features of myositis with perivascular, perimysial and endomysial lymphocyte infiltration. Although an association between HTLV-I and polymyositis had not yet been established, we think that our cases support such an association.
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PMID:[A family case of HAM and HTLV-I carrier including two sisters presenting with myositis]. 795 14

A patient with longstanding scleroderma with myositis was treated with interleukin 2 (IL-2) and lymphokine activated killer (LAK) cells for locally metastatic renal cell carcinoma. A rapid progression of truncal skin thickening and muscle weakness occurred within weeks of the initial infusion. Studies using supernatants from peripheral T lymphocytes of patients with scleroderma have shown increased levels of IL-2, IL-2 receptor, IL-4 and B cell growth factors, indications of activation of immune mechanisms. The rapid progression of our patient's illness during immunotherapy suggests a primary role for IL-2 and LAK cells in this disorder. Patients with scleroderma who receive IL-2 and LAK cells should be monitored prospectively for exacerbation of their illness.
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PMID:Rapid exacerbation of scleroderma in a patient treated with interleukin 2 and lymphokine activated killer cells for renal cell carcinoma. 859 71

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

Six Indonesian buffaloes (Bubalus bubalis) were inoculated intravenously with 10(5) Trypanosoma evansi, examined clinically, haematologically and serologically, and then killed 1, 2, 3, 4, 8 or 12 weeks after infection for detailed pathological study. Relapsing fever was related to the waves of parasitaemia and fluctuations of pulse and respiration rates. Anaemic mucous membranes, depression, weakness, refusal to walk, loss of appetite and emaciation were seen. Body weight, packed cell volume, total platelet and red cell counts, and haemoglobin values were below those of two uninfected control buffaloes, as well as below the normal range; on the other hand antibody titres against T. evansi in infected animals were all above those in controls. Emaciation, serous atrophy of fat, hydropericardium, petechial to larger haemorrhages in the pericardium, pneumonia, congested liver and spleen, oedematous enlargement of the superficial lymph nodes and hyperplastic bone marrow were the major gross pathological changes. Histologically, the severity of the disease increased from 1 to 7 weeks after infection and became less obvious at 12 weeks. The most consistent lesions were interstitial pneumonia, interstitial myocarditis, splenic multifocal necrosis, interstitial myositis and hyperplastic bone marrow. The last three lesions appear not to have been reported previously in T. evansi infection in buffaloes or other animals. The clinicopathological findings in this study show that T. evansi is both an intravascular and extravascular parasite.
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PMID:The pathology of experimental Trypanosoma evansi infection in the Indonesian buffalo (Bubalus bubalis). 804 Mar 89

Myositis due to the etiologic agent of Lyme disease, Borrelia burgdorferi, has been reported nine times in the English-language literature; there has been but a single report of exacerbation of dermatomyositis due to B. burgdorferi in a patient with known dermatomyositis. Multiple infectious agents, but not B. burgdorferi, have been hypothesized to trigger dermatomyositis. We report the first case of dermatomyositis that appears to have been triggered by B. burgdorferi. This case involved an individual from Westchester County, NY, who presented with skin lesions suggestive of erythema migrans and who was seropositive for Lyme disease. He soon developed a clinical syndrome suggestive of dermatomyositis: periorbital edema, dysphagia, proximal muscle weakness, and a markedly elevated level of creatine phosphokinase. We also review the clinical presentation and response to treatment of patients with Lyme myositis.
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PMID:Dermatomyositis associated with Lyme disease: case report and review of Lyme myositis. 816 22

Some patients of dermatomyositis (DM) with interstitial pneumonia (IP) have common clinical features. Clinical features of these patients are acute onset, very poor prognosis and that patients have fever, arthritis, typical skin rash, mild myositis and show low ratio of CPK/LDH, low incidence of antinuclear antibody (ANA) appearance, low inflammatory signs. We experienced two cases of this category of DM with IP and examined immunological aspects. Case 1. A 52-year-old woman was admitted in June 1, 1990 with a one-month history of arthralgia and a ten-days history of fever, skin rash, myalgia and dyspnea on exertion. On examination she had Gottron's papules on her fingers, erythema on back, bilateral elbows and legs, proximal muscle weakness and arthritis. Fine crackles were audible in the lower lung fields. Laboratory data included CPK 200 IU/l, ALD 3.2 IU/l, LDH 805 IU/l. Analysis of bronchoalveolar lavage fluid (BALF) revealed increased cellularity with lymphocytosis. She was treated with oral corticosteroid (CS), pulse CS, cyclosporin A. Inspite of these therapies, she died of progressive respiratory insufficiency in July 10, 1990. Case 2. A 23-year-old woman was admitted in April 1, 1991, with a two-month history of arthralgia and a one-month history of fever, skin rash, stomatitis, alopecia. On examination she had Gottron's papules on her fingers, erythema on malar, bilateral elbows and legs, arthritis and stomatitis. Laboratory data included CPK 97 IU/l, ALD 8.5 IU/l, LDH 779 IU/l. She began experiencing dry cough and dyspnea on exertion in May 1991. Analysis of BALF revealed increased cellularity with lymphocytosis. She was treated with oral corticosteroid(CS), pulse CS, pulse cyclophosphamide.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Two cases of acute progressive interstitial pneumonia associated with dermatomyositis--clinical features and immunological disorders]. 823 10


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