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 second generation fibric acid derivative, bezafibrate (Bezalip, Norlip) is widely used as a hypolipemic agent throughout Europe and Israel. Its side-effects are well documented, and include myositis, which is considered very rare. We report a 55-year-old diabetic woman with hypertension who had mild renal dysfunction (creatinine 2.0 mg/dl) who received 400 mg/d bezafibrate because of combined (Type IIb) hyperlipoproteinemia. She developed acute myositis, with extreme muscle weakness, pain and CPK levels of up to 3500 units. On discontinuation of the drug all clinical and biochemical features ceased and complete cure followed. No other symptoms have appeared during 2 years of followup. The few reports of such cases in the German literature point to a greater prevalence of myositis in those with renal dysfunction. Early diagnosis of bezafibrate-induced myositis is crucial, a discontinuation of the drug results in cure.
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PMID:[Acute severe myositis due to bezafibrate treatment]. 272 79

Myositis was proven histopathologically in 4 patients (age range 36-66 years) who suffered from early or late stages of Borrelia burgdorferi infection. Muscle weakness was present in 3 patients, 1 complaining of additional myalgias. One man came to medical attention because of skin discoloration and swelling of one leg. Deep biopsy from skin, fascia and muscle revealed acrodermatitis chronica atrophicans, panniculitis, fasciitis, and myositis, respectively. Creatine kinase was slightly elevated in 3 cases and normal in one. Infiltrates were found in the perimysium and within the muscle bundles, mainly around small vessels. The infiltrates consisted of many B cells and T4 lymphocytes with fewer cytotoxic T cells, suggesting that Borrelia myositis might be due to a local immune response to unknown Borrelia antigens. Cultivation of Borrelia from muscle was not successful. Antibiotic therapy cured the myositis.
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PMID:Myositis caused by Borrelia burgdorferi: report of four cases. 274 90

A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin was reported. The patient was a 67-year-old man. His birth and development was normal. There was no family history of neuromuscular disease. On 26th March 1987 he was admitted to a hospital because of dysarthria and dysphagia after fever and diagnosed as having viral myositis. His conditions improved spontaneously with bed rest and he left hospital on 14th April. On 23rd April he had chill and sore throat with fever. On 27th he was admitted to the same hospital because of dysarthria and muscle weakness of the proximal portion of the upper limbs. These symptoms also improved with bed rest. He had repeated these symptoms several times and then he was admitted to our hospital on 12th June. On examination he showed the skin pigmentation under the right eye and the eruption in the back of hands and the buttocks. Muscle weakness was observed in the proximal portion of the upper limbs and the neck flexor. Laboratory tests in admission were as follows: sGOT 49 mU/ml, sGPT 104 mU/ml, LDH 1064 mU/ml, CPK 565 mM/ml, aldolase 25.2 IU/1/37 degrees C. Electromyography showed the typical myogenic changes and biopsy of left biceps brachii revealed inflammatory cells in the muscle fiber which are specific to polymyositis. Immuno-histochemical study is performed to analyse the subpopulation of mononuclear cells in biopsied muscle and skin. Mononuclear cells infiltrated into perimysium, endomysium and epidermis were positive for T11 and T8, but less positive for T4, B1 and Leu11. On the basis of these findings he was diagnosed as having "polymyositis syndrome".
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PMID:[A case of polymyositis with repeated dysphagia and muscle weakness associated with peculiar findings of skin]. 280 15

Murine polymyositis (PM) induced by coxsackievirus B1 (CVB1) has been used as a model of human PM. Our study was undertaken to investigate the role of T cells in CVB1 induced PM by examining disease development in neonatally thymectomized mice. Clinical weakness and histological inflammatory myositis occurred in 42.7% of sham operated animals but only 7.7% of thymectomized mice. These experiments demonstrate the importance of T cells in the pathogenesis of this virus induced autoimmune disorder.
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PMID:T cells are required for coxsackievirus B1 induced murine polymyositis. 283 72

Thirty patients with SLE were studied retrospectively and subjected to clinical neurological examination. The accumulated neurological manifestations from the beginning of the disease until the time of examination were thus collected. Twenty-five patients (83%) had experienced neuropsychiatric manifestations while 11 patients (37%) had neuromuscular manifestations. The most frequent single symptom was migraine which had occurred in 40% of the patients. This was followed by severe protracted headache in 20%, vertigo in 20%, and psychiatric problems in 17%. Carpal tunnel syndrome and muscular weakness both occurring in 23% of the patients were the most prevalent neuromuscular manifestations, followed by myositis in 10%.
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PMID:Clinical neuropsychiatric and neuromuscular manifestations in systemic lupus erythematosus. 283 97

A 38-year-old male developed a new muscle weakness in his left thigh 35 years after having acute paralytic poliomyelitis with residual right distal leg weakness and atrophy. EMG studies showed widespread denervation in proximal and distal muscles regardless the clinical involvement. Muscle biopsy from an affected muscle showed the findings of inclusion-body myositis consisting of perivascular and interstitial mononuclear infiltration, sarcoplasmic granular inclusions with membranous whorls and typical filamentous inclusions in several myonuclei. This raises the possibility of inclusion body myositis in other cases of progressive post-poliomyelitis muscular atrophy, especially those with perivascular infiltration of mononuclear cells in the muscle biopsy.
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PMID:Inclusion body myositis in post-poliomyelitis muscular atrophy. 284 1

Recent research findings implicate picornaviruses in the etiology of human polymyositis/dermatomyositis and suggest that genetic factors play a role in susceptibility to these diseases. We compared 2 variants of encephalomyocarditis (EMC) virus for their ability to induce polymyositis in adult mice, and evaluated what role the genetic background of the host plays in the degree of myositis induced. While BALB/c mice developed minimal myositis when infected with a diabetogenic variant (EMC-D), the same strain inoculated with a newly isolated myopathic variant (EMC-221A) developed viral dose-dependent elevations in muscle-associated enzymes, bilateral limb muscle weakness, and the histopathologic changes of severe polymyositis. Mice with different genetic backgrounds showed significantly different susceptibilities to EMC-221A. These data suggest that the severity of polymyositis induced by EMC virus is influenced by both the viral and host genomes.
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PMID:Viral and host genetic factors influence encephalomyocarditis virus-induced polymyositis in adult mice. 303 71

Chronic inflammatory myositis similar to human polymyositis occurs in mice after infection with a strain of Coxsackievirus B 1 (CVB 1). To investigate the role of T cells in the pathogenesis of this disorder, we compared disease expression in T cell-deficient athymic nude (nu/nu) mice and heterozygotes (nu/+) with normal T cell function. Acute infectious myositis occurred in nu/nu and nu/+ mice. Chronic (greater than 21 d postinfection) weakness and myositis, however, developed only in nu/+. Resistance to disease in nu/nu mice was not explained by insusceptibility to infection; the amount of virus lethal for 50% of mice and virus replication were comparable in both groups. Additionally, anti-CVB 1 antibody production was similar in both groups. Reconstitution of infected nu/nu mice with spleen cells from normal mice resulted in disease. These results demonstrate that chronic weakness after infection with this virus is not simply a sequela of acute myonecrosis and suggest that T cells play a pivotal role in the pathogenesis of chronic myositis.
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PMID:Coxsackievirus B 1-induced polymyositis. Lack of disease expression in nu/nu mice. 303 60

BMT has become an important therapy for many hematologic disorders. Following BMT, the recipient may develop GVHD when it appears that immunocompetent donor lymphocytes react to host antigens. Acute and chronic GVHD represent two distinct syndromes. Acute GVHD has not been associated with primary neurologic involvement. Polymyositis has been reported in 12 patients with chronic GVHD, with the most common underlying illness being aplastic anemia. The clinical, serologic, and muscle biopsy features of the myositis in GVHD have been similar to those observed in idiopathic polymyositis. Weakness was moderate to severe and responded to prednisone, sometimes with the addition of azathioprine. Prognosis depended upon the underlying disease and not on the severity of the myositis. MG occurs rarely in chronic GVHD. Most patients with MG and GVHD have had aplastic anemia; those with aplastic anemia are more likely to have anti-AchR prior to BMT. The clinical manifestations of GVHD MG have not differed from classic autoimmune MG; each patient had elevated antiacetylcholine receptor antibodies titers. All patients have responded well to cholinesterase inhibitors but have received other immunosuppressants. These observations suggest that aplastic anemia is an important host factor in the development of the autoimmune disorders seen with chronic GVHD, certainly of myositis and MG. Herpes zoster peripheral nerve infections have occurred in patients with chronic GVHD. One patient had mononeuritis multiplex. In both acute and chronic GVHD, CNS impairment is usually caused by metabolic encephalopathy or infection. Primary CNS involvement has not been recognized.
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PMID:Neurologic complications of graft-versus-host disease. 304 48

Few guidelines exist for the use of corticosteroid therapy in polymyositis-dermatomyositis (PM-DM). We retrospectively examined the relationship between serum creatine kinase (CK), muscle strength and the dosage and method of administration of prednisone in 30 patients with PM-DM observed monthly for a minimum of one year. Forty-two corticosteroid treated episodes of proximal muscle weakness associated with CK elevations formed the final study group. Each patient course was designated as having a good or poor biochemical and clinical outcome based on predetermined criteria. Adherence to 3 principles predicted a favorable biochemical and clinical outcome in the treatment of myositis: (1) administration of an adequate initial (loading) corticosteroid dose; (2) continuation of the initial dose until or after the time that the serum CK had become normal; and (3) a slow corticosteroid taper rate. Achievement of a CK within the low normal range predicted a prolonged biochemical remission, and a rise of CK within the normal range signalled a subsequent biochemical and clinical relapse. Tapering the corticosteroid dose when the CK was elevated frequently resulted in a further increase in CK. These observations allowed us to develop practical guidelines for the management of PM-DM.
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PMID:Relationship between serum creatine kinase level and corticosteroid therapy in polymyositis-dermatomyositis. 317 94


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