Cases reported "Rhabdomyolysis"

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1/335. Judicious evaluation of adverse drug reactions: inaccurate assessment of 3-hydroxy-3-methylglutaryl coenzyme a reductase inhibitor-induced muscle injury.

    Adverse reactions in two patients who received HMG CoA reductase inhibitor therapy were reinvestigated because of their rarity. A case of permanent forearm myalgia was thought to be caused by atorvastatin. Closer evaluation and work-up revealed underlying lateral epicondylitis, and atorvastatin was not considered the cause of the disability. In another patient, rhabdomyolysis was suspected to be secondary to simvastatin. However, after an extensive review, the reaction was believed to be compartment syndrome of the anterior tibial area. An adverse drug reaction report requires careful and judicious assessment to assign the correct probability for the event.
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2/335. rhabdomyolysis associated with naltrexone.

    OBJECTIVE: To report a possible association between naltrexone therapy and the development of rhabdomyolysis in one patient. CASE SUMMARY: A 28-year-old white man in good physical health was started on naltrexone 50 mg/d for inpatient treatment of alcohol dependence and depression. A routine serum chemistry panel obtained on day 9 of naltrexone therapy showed marked new elevations in creatine kinase and aspartate aminotransferase. The patient remained asymptomatic and did not develop renal insufficiency. The serum enzyme concentrations returned to normal within eight days of naltrexone discontinuation. DISCUSSION: rhabdomyolysis has not been previously reported to occur in patients during treatment with naltrexone. alcoholism may result in a reversible acute muscle syndrome, but our patient did not fit the appropriate clinical profile for such a syndrome. Additionally, the other prescribed medications could not be implicated as possible causative agents. CONCLUSIONS: This case report illustrates a possible association between naltrexone therapy and rhabdomyolysis.
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3/335. Respiratory chain deficiency presenting as recurrent myoglobinuria in childhood.

    myoglobinuria is an abnormal urinary excretion of myoglobin due to an acute destruction of skeletal muscle fibres. Several metabolic diseases are known to account for myoglobinuria including defects of glycolysis and fatty acid oxidation. Here, we report on respiratory chain enzyme deficiency in three unrelated children with recurrent episodes of myoglobinuria and muscle weakness (complex I: one patient, complex IV: two patients). All three patients had generalized hyporeflexia during attacks, a feature which is not commonly reported in other causes of rhabdomyolysis. Studying respiratory chain enzyme activities in cultured skin fibroblasts might help diagnosing this condition, especially when acute rhabdomyolysis precludes skeletal muscle biopsy during and immediately after episodes of myoglobinuria.
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4/335. Non-traumatic acute rhabdomyolysis.

    A boy developed sudden severe generalized muscle stiffness, bulbar weakness and passed dark coloured urine. Laboratory tests revealed marked elevation of creatinine kinase(CK) levels and myoglobinuria. Histopathology of quadriceps muscle showed features of acute rhabdomyolysis. Patient made complete clinical recovery over a period of three weeks and CK returned to normal level. The possible aetiologies of non-traumatic rhabdomyolysis are discussed and the relevant literature reviewed.
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5/335. Muscle phosphofructokinase deficiency (Tarui's disease): report of a case.

    A 14-year-old girl had an acute episode of rhabdomyolysis after vigorous exercise and seizures. Laboratory studies revealed elevated creatine phosphokinase (CPK) activity and myoglobinuria without acute renal failure, as well as mild indirect hyperbilirubinemia, and hyperuricemia. The elevated CPK activity, mild indirect hyperbilirubinemia, and hyperuricemia persisted during a 10-month follow-up period, during which chronic hemolysis without overt anemia was also noted. A muscle biopsy specimen from the left biceps muscle revealed occasional muscle fiber necrosis and mild excess of glycogen accumulation on periodic acid-Schiff staining. Histochemical reactions were negative with phosphofructokinase (PFK) stain when fructose-6-phosphate was used as the substrate, but positive when fructose 1,6-bisphosphate was used as the substrate. These findings confirmed the diagnosis of muscle PFK deficiency (Tarui's disease), which is a defect of glycolysis in muscles and erythrocytes. Less than 40 such patients have been reported to date. When a specific metabolic myopathy is suspected in children with rhabdomyolysis, symptoms of hemolysis should also be sought to identify Tarui's disease. To the best of our knowledge, this is the first case of Tarui's disease identified in taiwan.
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6/335. rhabdomyolysis in association with Duchenne's muscular dystrophy.

    PURPOSE: To present a case of rhabdomyolysis which developed in a child with a known history of Duchenne's muscular dystrophy, following an anesthetic which included sevoflurane. CLINICAL FEATURES: An 11 yr old boy with a known history of Duchenne's muscular dystrophy underwent anesthesia for strabismus repair. The anesthetic consisted of sevoflurane and nitrous oxide without the use of a muscle relaxant. His postoperative course was complicated by a complaint of heel pain and the development of myoglobinuria. He was treated with dantrolene sodium and discharged home after two days, without further complication. CONCLUSION: Sevoflurane anesthesia has not been shown previously to be associated with the development of acute rhabdomyolysis in a child with a history of Duchenne's muscular dystrophy. As with halothane and isoflurane, the continued use of sevoflurane in the presence of Duchenne's muscular dystrophy should be questioned.
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7/335. hyponatremia-associated rhabdomyolysis.

    BACKGROUND: hyponatremia is the most frequent electrolyte disorder. However, hyponatremia rarely results from excessive water intake, unless the kidney is unable to excrete free water, such as in patients on thiazide diuretics; in addition, hyponatremia is an uncommon cause of rhabdomyolysis. methods: We present a 51-year-old hypertensive woman on chronic hydrochlorothiazide therapy who developed acute water intoxication and severe myalgias. RESULTS: The patient developed acute hypotonic hyponatremia and subsequent rhabdomyolysis. We discuss the mechanisms responsible for the development of hyponatremia and its association with rhabdomyolysis. CONCLUSION: Muscle enzymes should be monitored in patients with acute hyponatremia who develop muscle pain, and hyponatremia-induced rhabdomyolysis must be considered in patients with myalgias receiving thiazide diuretics.
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8/335. Case of the month: February 1999--54 year old man with severe muscle weakness.

    A 54 year old man developed rhabdomyolysis one year after beginning treatment with a combination of lovastatin (an HMGCoA reductase inhibitor) and niacin. Muscle biopsy showed a severe necrotizing myopathy affecting both fibre types. Recovery occured gradually with cessation of medication. The spectrum of cholesterol lowering agent myopathy may include delayed cases of unusual severity.
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9/335. rhabdomyolysis in DOMS.

    A 26-year-old man with a previous history of external twin bursitis was remitted to our Department for a bone scintigraphy. Before the study, the patient performed an elevated number of intense sprints. Bone scintigraphy showed a bilaterally increased activity in both anterior rectum muscles suggesting rhabdomyolysis. Biochemical studies and MRT confirmed the diagnosis.
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10/335. rhabdomyolysis and acute renal failure associated with influenza virus type A.

    Two patients with rhabdomyolysis-induced acute renal failure due to influenza a virus infection are presented. Both had influenza symptoms, with high fever and severe muscular pain leading to walking problems. In addition, they were dehydrated due to vomiting and diarrhoea. Both had evidence of an ongoing influenza infection according to serological tests. Muscle injury due to the viral infection gave rise to rhabdomyolysis with efflux of myoglobin from the muscles, causing renal failure. In conclusion, influenza a virus infection can cause rhabdomyolysis accompanied by reversible acute renal failure.
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