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)

It is well recognized that statins affect muscular tissue adversely and that their use is associated with clinically important myositis, rhabdomyolysis, mild elevation of serum creatine kinase (CK) levels, myalgias, muscle weakness, muscle cramps, and persistent myalgias or serum CK level elevations after statin treatment is discontinued. The association between statins and the disclosure of presymptomatic metabolic myopathy is another underrated phenomenon related to statin therapy that was recently recognized in rare cases. The purpose of this report is to provide additional support for this association and to report other neuromuscular disorders that have also been seen following statin intake. The present case series illustrates that statins may act as unmasking agents in asymptomatic patients with a latent neuromuscular disorder. Thus, it may be postulated that statin intake may be a sufficient insult to precipitate neuromuscular symptoms and substantially increase muscle enzymes in presymptomatic patients with an abnormal neuromuscular substrate. In conclusion, muscular symptoms or increased serum CK levels persisting after statin treatment discontinuation should alert the clinician to pursue further diagnostic evaluations for the detection of potential underlying neuromuscular diseases.
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PMID:Presymptomatic neuromuscular disorders disclosed following statin treatment. 1686 63

Benign acute myositis associated with influenza is reported from all over the world. The characteristics of this disorder is calf pain and difficulty walking during a viral illness (3-8 days) and creatine kinase levels are mildly or moderately elevated. Recovery occurred within 1 week. Midchildhood (mean age: 6-8 years) is most commonly affected and boys are more commonly than girls and its ratio is 2.4 : 1 by Shimizu in Japan (1993). Elderly patients are also reported. Viral studies show that influenza B is more commonly than influenza A and the ratio is 6 : 1 by Hu in Taiwan (2004), 2.4 : 1 by Shimizu in Japan (1993). Muscle histology revealed isolated segmental muscle degeneration and necrosis without frank myositis. A direct role of influenza virus in its genesis is not clear. An age-related response and occurrence primarily on boys may reflect a genetic predisposition.
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PMID:[Acute myositis associated with influenza]. 1703 68

Ataxia and peripheral neuropathy are the most common neurological manifestations of gluten sensitivity. Myopathy is a less common and poorly characterized additional neurological manifestation of gluten sensitivity. We present our experience with 13 patients who presented with symptoms and signs suggestive of a myopathy and in whom investigation led to the diagnosis of gluten sensitivity. Three of these patients had a neuropathy with or without ataxia in addition to the myopathy. The mean age at onset of the myopathic symptoms was 54 years. Ten patients had neurophysiological evidence of myopathy. Inflammatory myopathy was the most common finding on neuropathological examination. One patient had basophilic rimmed vacuoles suggestive of inclusion-body myositis. Six patients received immunosuppressive treatment in addition to starting on a gluten-free diet; five improved and one remained unchanged. Among seven patients not on immunosuppressive treatment, four showed clinical improvement of the myopathy with a gluten-free diet. The improvement was also associated with reduction or normalization of serum creatine kinase level. The myopathy progressed in one patient who refused the gluten-free diet. Myopathy may be another manifestation of gluten sensitivity and is likely to have an immune-mediated pathogenesis. A gluten-free diet may be a useful therapeutic intervention.
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PMID:Myopathy associated with gluten sensitivity. 1714 94

Statin use is associated with a variety of overtly related muscle symptoms including muscle pain, myalgia, creatine kinase elevations without pain with myolysis and myositis (rhabdomyolysis), a potentially fatal side effect that led to the withdrawal of cerivastatin in 2001. Unintended drug response phenotypes have an impact on patient compliance and sometimes patient health and the assessment of risk on an individual basis could enhance therapeutic benefit. We therefore investigated whether common single nucleotide polymorphisms were associated with the expression of broadly grouped atorvastatin-induced muscle events in a case-control study (n=263 samples, n=388 SNPs). Of a number of associations identified in a discovery sample (51 atorvastatin-induced muscle and 55 normal) only those corresponding to the CYP2D6*4 allele were significantly associated in the sample (24 atorvastatin-induced muscle and 133 normal) (Discovery P=0.004, odds ratio=3.6; Validation P=0.036, odds ratio=2.7; total P=0.001, odds ratio=2.5). The frequency of the CYP2D6*4 allele was about 50% in atorvastatin-induced muscle patients but only 28% in controls, similar to that of other patient types (28.5%). The association was independent of various demographic variables and not explained by gross demographic, clinical or population-structure differences among cases and controls. Surprisingly, the CYP2D6*4 allele appeared similarly distributed among controls and patients expressing simvastatin-induced muscle events (n=169, frequency in case participants=49.2%, P=0.067, odds ratio=1.7). Our results suggest that the CYP2D6*4 allele is associated with broadly related muscle events caused by at least two structurally dissimilar HMG-CoA reductase inhibitors, and as such, may have implications for a better understanding of this statin-wide phenomena.
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PMID:CYP2D6*4 polymorphism is associated with statin-induced muscle effects. 1770 Mar 59

We presented a 43-year-old Japanese woman who acutely developed weakness of all extremities and difficulty in swallowing and drooping of eyelids, characterized by easy fatigability at the end of December, 2005. On general physical examination, she had moderate goiter. No cervical lymphadenopathy, cardiac murmur, or skin rash was noted. Neurologically, she had blepharoptosis, more on the right, only in the upright position with easy fatigability and marked weakness in the neck flexor, trunk, and all limb muscles much more proximally than distally. She had neither muscular atrophy nor upper motor neuron sign. Laboratory data showed slight leukocytosis with eosinophilia (up to 31%), and serum creatine kinase was markedly increased to over 2,000 IU/l. TSH receptor antibody (11.9%) and anti-acetylcholine receptor antibody (46.6 nmol/L) were also increased. Edrophonium test was positive. Electrophysiologically, muscle evoked potentials by repetitive motor nerve stimulation showed 13% and 50% waning in abductor pollicis brevis and deltoid muscle, respectively, at low frequency and no waxing at high frequency. Needle EMG showed fibrillation potentials and positive sharp waves in proximal muscles. Polymyositis was diagnosed by muscle biopsy which showed infiltration of lymphocytes in the endomysium and around non-necrotic muscle fibers. Upper arm muscle MRI showed multifocal high signal intensity lesions on T2-weighted images which were likely related to myositis. This finding is atypical for polymyositis. X-ray and CT of chest showed a mass lesion in the left pulmonary hilum, which was histologically diagnosed as type B1 thymoma. Thus, the present case had myasthenia gravis, polymyositis, thyroidititis and eosinophilia associated with type B1 thymoma. After the thymectomy, corticosteroid administration and immunoadsorption therapy, clinical symptoms and all laboratory abnormalities markedly improved.
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PMID:[Concurrence of myasthenia gravis, polymyositis, thyroiditis and eosinophilia in a patient with type B1 thymoma]. 1771 Aug 86

The association between idiopathic inflammatory myositis and cancer is well recognized. Most descriptions have been of dermatomyositis-associated cancer, however, a few have been of polymyositis-associated adrenal cancer. Here, we report a 69-year-old man in whom polymyositis-associated adrenal cancer was diagnosed. The patient complained of difficulty with walking and with standing unassisted. Physical examination and electrophysiological studies revealed an abnormality of the proximal muscles. Serum levels of creatine kinase and lactic dehydrogenase were increased. Imaging studies showed a solid tumor measuring 14 x 9 cm in the retroperitoneum. After surgical excision of the tumor, including the left kidney, the serum levels of creatine kinase and lactic dehydrogenase normalized, and symptoms of myositis disappeared.
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PMID:A case of polymyositis associated with adrenal carcinoma. 1788 Feb 99

Compartment syndrome has rarely been reported associated with acute rhabdomyolysis. In the case described, the rhabdomyolysis was severe enough to cause compartment syndrome and acute renal failure after moderate exercise and alcohol intake and had the appearance of a myositis. The case emphasizes the importance of early recognition of compartment syndrome, as loss of pulses is a very late sign, and the examination of the urine to detect myoglobinuria in rhabdomyolysis. Measurement of creatine kinase is predictive of the extent of muscle damage and the development of renal failure.
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PMID:Rhabdomyolysis associated with compartment syndrome resulting in acute renal failure. 1796 8

A 24-year-old Japanese woman had been suffering from a periodic fever since 10 months of age. She developed deformities in her fingers, with severe atrophy of subcutaneous adipose tissue, myositis, and frostbitten hands. She showed elevated C-reactive protein, creatine kinase, and gamma-globulin. She was also positive for antinuclear, anti-DNA, anti-SS-B, and anti-U1RNP antibodies. Her myositis was similar to amyopathic dermatomyositis rather than juvenile dermatomyositis. Although consanguineous marriage of her parents and early onset of disease suggested her disease as a hereditary disorder with periodic fever, her clinical feature and laboratory tests were unlike any known periodic fever syndromes. Her disease was regarded as a unique type of periodic-fever-syndrome-like disorder with autoimmune abnormalities.
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PMID:A case of periodic-fever-syndrome-like disorder with lipodystrophy, myositis, and autoimmune abnormalities. 1834 May 5

We report a 72-year-old man with eosinophilic myositis (EM). At age 71 he noticed a painful nodule in his left calf. A biopsy (first biopsy) showed marked infiltration of mononucleated cells and necrotic muscle fibers. Several phagocytosed fibers were also seen. He was diagnosed as having myositis. The painful nodule disappeared spontaneously. At age 72, he again had a painful nodule, but this time in his right calf; again, this disappeared spontaneously on the first admission. Just after discharge, he noted painful nodules in the left thigh and right anterior tibial muscles and was again admitted (second admission). Neurological examination revealed mild proximal-dominant weakness in all four extremities but no other abnormalities. Laboratory studies showed elevated creatine kinase (CK) level (38,803 U/l; normal 62-287) and positive Jo-1 antibody, but no eosinophilia. Needle electromyography of the limb muscles showed myogenic patterns. Magnetic resonance imaging of the lower limbs demonstrated several T2-high and gadolinium (Gd)-enhanced lesions. Muscle biopsy (second biopsy) from the left quadriceps femoris showed marked infiltration of eosinophils; he was diagnosed as having EM. Administration of prednisolone was initiated at 60 mg/day and then gradually tapered. After starting treatment with steroids, his muscle weakness gradually ameliorated, CK level dramatically decreased, and the nodules disappeared. Clinically, the patient had developed localized nodular myositis (LNM), but pathologically it was EM without peripheral blood eosinophilia and positive Jo-1 antibody that is occasionally found in polymyositis (PM). Thus, this patient demonstrated overlapping characteristics of EM, LNM, and possibly PM, suggesting that a common mechanism underlay these conditions. As discussed, the involvement of eosinophils in three inflammatory myopathies was indicated.
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PMID:[Case of eosinophilic myositis in continuum from localized nodular myositis]. 1838 30

Skeletal muscle disorder, inclusion-body myositis (IBM) has been known for accumulation of amyloid characteristic proteins in muscle. To understand the biophysical basis of IBM, the interaction of amyloid fibrils with skeletal myoblast cells (SMC) has been studied in vitro. Synthetic insulin fibrils and Abeta(25-35) fibrils were used for this investigation. From the saturation binding analysis, the calculated dissociation constant (K(d)) for insulin fibril and Abeta(25-35) fibrils were 69.37+/-11.17nM and 115.60+/-12.17nM, respectively. The fibrillar insulin comparatively has higher affinity binding to SMC than Abeta fibrils. The competitive binding studies with native insulin showed that the amount of bound insulin fibril was significantly decreased due to displacement of native insulin. However, the presence of native insulin is not altered the binding of beta-amyloid fibril. The cytotoxicity of insulin amyloid intermediates was measured. The pre-fibrillar intermediates of insulin showed significant toxicity (35%) as compared to matured fibrils. Myoblast treated with beta-amyloid fibrils showed more oxidative damage than the insulin fibril. Cell differentiating action of amyloidic insulin was assayed by creatine kinase activity. The insulin fibril treated cells differentiated more slowly compared to native insulin. However, beta-amyloid fibrils do not show cell differentiation property. These findings reinforce the hypothesis that accumulation of amyloid related proteins is significant for the pathological events that could lead to muscle degeneration and weakness in IBM.
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PMID:Amyloid toxicity in skeletal myoblasts: Implications for inclusion-body myositis. 1839 59


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