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)

Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) are associated with skeletal muscle complaints, including clinically important myositis and rhabdomyolysis, mild serum creatine kinase (CK) elevations, myalgia with and without elevated CK levels, muscle weakness, muscle cramps, and persistent myalgia and CK elevations after statin withdrawal. We performed a literature review to provide a clinical summary of statin-associated myopathy and discuss possible mediating mechanisms. We also update the US Food and Drug Administration (FDA) reports on statin-associated rhabdomyolysis. Articles on statin myopathy were identified via a PubMed search through November 2002 and articles on statin clinical trials, case series, and review articles were identified via a PubMed search through January 2003. Adverse event reports of statin-associated rhabdomyolysis were also collected from the FDA MEDWATCH database. The literature review found that reports of muscle problems during statin clinical trials are extremely rare. The FDA MEDWATCH Reporting System lists 3339 cases of statin-associated rhabdomyolysis reported between January 1, 1990, and March 31, 2002. Cerivastatin was the most commonly implicated statin. Few data are available regarding the frequency of less-serious events such as muscle pain and weakness, which may affect 1% to 5% of patients. The risk of rhabdomyolysis and other adverse effects with statin use can be exacerbated by several factors, including compromised hepatic and renal function, hypothyroidism, diabetes, and concomitant medications. Medications such as the fibrate gemfibrozil alter statin metabolism and increase statin plasma concentration. How statins injure skeletal muscle is not clear, although recent evidence suggests that statins reduce the production of small regulatory proteins that are important for myocyte maintenance.
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PMID:Statin-associated myopathy. 1292 63

A 55-year-old Caucasian man who had received a second kidney graft in July 1993, was switched from cyclosporine to tacrolimus in June 2000 due to deterioration of renal function. Thereafter, he began to complain of muscle cramps in both quadriceps with an increased CPK and EMG findings of polyneuropathy. A muscle biopsy demonstrated acute myositis. Prednisone was administered with amelioration of the patient's symptoms, but with persistently increased CPK and myoglobin levels. In February 2001, mycophenolate mofetil was introduced and tacrolimus tapered to 3 mg daily to seek a toxic role of this immunosuppressant, since there was no other cause of myositis. A sudden decrease in CPK was observed, but the complete normalization took place only after its withdrawal in September 2002. This case represents a tacrolimus-associated myositis.
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PMID:Tacrolimus-associated myositis: a case report in a renal transplant patient. 1511 Jun 39

Diagnosing mitochondrial disorder remains a challenge. In a 75-year-old women, with short stature, muscle cramps, ptosis, fasciculations and progressive, proximal limb weakness and wasting, hyponatriemia, abnormal lactate-stress-test, and slightly abnormal electromyography, muscle biopsy suggested granulomatous myositis. Corticosteroids and azathioprin were ineffective. After a second work-up amyotrophic-lateral-sclerosis was diagnosed. Riluzole was started, without effect. She developed respiratory insufficiency, requiring mechanical ventilation. Apical ballooning was found. After switching to non-invasive positive pressure ventilation and physiotherapy, she markedly improved. After a third diagnostic work-up, mitochondrial disorder was suspected. Unfortunately, she died suddenly from a cardiac arrhythmia at home. Mitochondrial disorder may mimic motor neuron disease, muscle biopsy may mimic myositis, and may show only little evidence for respiratory chain disorder.
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PMID:Consequences of misdiagnosing mitochondrial disorder. 1686 Nov 55

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

Takotsubo syndrome may be associated with neuromuscular disorders, but has never been described in a patient with mitochondrial disorder. A 75-year-old woman developed muscle cramps, ptosis, fasciculations and slowly progressive weakness and wasting of all four limbs, starting 2.5 years earlier. After exclusion of various differential diagnoses, including non-specific granulomatous myositis, inclusion body myositis, and motor neuron disease, mitochondrial disorder was assumed. Muscle weakness progressed to respiratory insufficiency, requiring mechanical ventilation. Five days after intubation, she developed hypotension, torsades de pointes, ST-segment elevation, and negative T waves. Echocardiography revealed apical ballooning with akinesia of the left ventricular anteroseptal, apical, apicolateral and inferior segments. Coronary angiography was normal, and ventriculography confirmed apical hypokinesia and ballooning. Takotsubo syndrome was diagnosed, resolving completely within 7 weeks under bisoprolol. This case shows that Takotsubo syndrome occurs also in mitochondrial disorder and under mechanical ventilation, and may be triggered by stress from respiratory insufficiency, intubation, pain from tracheostomy, stress from mechanical ventilation, medication, or from the uncertain prognosis.
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PMID:Apical ballooning (Takotsubo syndrome) in mitochondrial disorder during mechanical ventilation. 1788 29

The juvenile idiopathic inflammatory myopathies (JIIM) are systemic autoimmune diseases characterized by skeletal muscle weakness, characteristic rashes, and other systemic features. In follow-up to our study defining the major clinical subgroup phenotypes of JIIM, we compared demographics, clinical features, laboratory measures, and outcomes among myositis-specific autoantibody (MSA) subgroups, as well as with published data on adult idiopathic inflammatory myopathy patients enrolled in a separate natural history study. In the present study, of 430 patients enrolled in a nationwide registry study who had serum tested for myositis autoantibodies, 374 had either a single specific MSA (n = 253) or no identified MSA (n = 121) and were the subject of the present report. Following univariate analysis, we used random forest classification and exact logistic regression modeling to compare autoantibody subgroups. Anti-p155/140 autoantibodies were the most frequent subgroup, present in 32% of patients with juvenile dermatomyositis (JDM) or overlap myositis with JDM, followed by anti-MJ autoantibodies, which were seen in 20% of JIIM patients, primarily in JDM. Other MSAs, including anti-synthetase, anti-signal recognition particle (SRP), and anti-Mi-2, were present in only 10% of JIIM patients. Features that characterized the anti-p155/140 autoantibody subgroup included Gottron papules, malar rash, "shawl-sign" rash, photosensitivity, cuticular overgrowth, lowest creatine kinase (CK) levels, and a predominantly chronic illness course. The features that differed for patients with anti-MJ antibodies included muscle cramps, dysphonia, intermediate CK levels, a high frequency of hospitalization, and a monocyclic disease course. Patients with anti-synthetase antibodies had higher frequencies of interstitial lung disease, arthralgia, and "mechanic's hands," and had an older age at diagnosis. The anti-SRP group, which had exclusively juvenile polymyositis, was characterized by high frequencies of black race, severe onset, distal weakness, falling episodes, Raynaud phenomenon, cardiac involvement, high CK levels, chronic disease course, frequent hospitalization, and wheelchair use. Characteristic features of the anti-Mi-2 subgroup included Hispanic ethnicity, classic dermatomyositis and malar rashes, high CK levels, and very low mortality. Finally, the most common features of patients without any currently defined MSA or myositis-associated autoantibodies included linear extensor erythema, arthralgia, and a monocyclic disease course. Several demographic and clinical features were shared between juvenile and adult idiopathic inflammatory myopathy subgroups, but with several important differences. We conclude that juvenile myositis is a heterogeneous group of illnesses with distinct autoantibody phenotypes defined by varying clinical and demographic characteristics, laboratory features, and outcomes.
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PMID:The myositis autoantibody phenotypes of the juvenile idiopathic inflammatory myopathies. 2387 55