Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042384 (vasculitis)
 20,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There have been recent reports of rhabdomyolysis associated with cocaine abuse. The pathologic findings from these cases have not been described. Pathologic abnormalities in two fatalities with cocaine-associated rhabdomyolysis, including one with hyperpyrexia, acute renal failure, and disseminated intravascular coagulation, are discussed in detail. Skeletal muscle in both cases showed necrosis without evidence of vasculitis, polarizable foreign crystals, or other specific lesions. The individual with renal failure showed acute tubular necrosis with granular myoglobin casts in tubules. The mechanism of cocaine-associated rhabdomyolysis is unclear, but potentially includes ischemia due to vasoconstriction, direct toxicity, hyperpyrexia, and increased muscle activity from agitation or seizure. Adulterants may also play a role. In unexplained cases of rhabdomyolysis, toxicologic evidence of cocaine should be sought. In those cases of rhabdomyolysis associated with acute renal failure, the presence of cocaine in blood may be prolonged because of impaired renal clearance.
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PMID:Rhabdomyolysis associated with cocaine abuse. 174 98

Acute rhabdomyolysis is a rare complication in patients with status asthmaticus receiving mechanical ventilation. Individual reports implicate several factors, whereby the simultaneous use of high-dose glucocorticoids and non-depolarizing muscle blocking agents appears to be the major patho-physiological mechanism. A 48 year-old female patient with a 3-year history of granulomatous vasculitis Churg-Strauss was admitted to the intensive care unit (ICU) due to severe status asthmaticus, which necessitated endotracheal intubation and mechanical ventilation. Antiobstructive therapy consisted of beta 2-sympathomimetics, theophylline and high-dose intravenous prednisolone (5440 mg in 10 days). Additionally, the patient was treated with non-depolarizing muscle blocking agents (atracurium 2070 mg over 7 days). Six days after admission to the ICU the patient developed severe rhabdomyolysis, with an increased creatine kinase (CK) level and myoglobinuria. The maximum CK value occurred 12 days after ICU admission (3810 U/l), accompanied by a serum myoglobin level of 13,900 ng/ml. 5 days after cessation of muscle relaxant therapy and reduction of intravenous glucocorticoids, the serum CK level decreased, reaching normal values 9 days later.
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PMID:[Acute rhabdomyolysis in status asthmaticus]. 896 96

A 66-year-old female was admitted to our hospital in January, 1998, complaining of low grade fever and muscle weakness of her legs. Physical examination revealed muscle weakness of her neck (4/5) and proximal skeletal muscles of her bilateral legs (3/5-4/5). She showed proteinuria and microhematuria. Her serum levels of ureanitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, creatinekinase, aldolase and myoglobin were all within the normal ranges. Antinuclear antibodies were negative, but her serum levels of pANCA (743 EU) and C reactive protein (18.0 mg/dl) were elevated. Neuroconduction velocity of her left common peroneal nerve was decreased to 40.8 m/sec and electric myograph showed neurogenic changes. Magnetic resonance images (MRI) of her bilateral thigh depicted high signal intensity in quadriceps by T 2 weighed images, but the signals were not enhanced by gadolinium injection. Muscle and renal biopsies revealed necrotizing vasculitis of the small arteries. Crescentic glomerulonephritis was also observed by renal biopsy. These findings supported the diagnosis of microscopic PN. On 16 th admission day, she developed acute cardiac and respiratory failures due to cardiac and respiratory muscle involvements with PN, and was assisted by mechanical ventilation. She was treated with methylprednisolone pulse therapy (500 mg/day, three consecutive days) on 18 th admission day, followed by 40 mg of oral prednisolone daily. However, her symptoms deteriorated, and herserum creatinine levels increased to 2.4 mg/dl. On 24 th admission day, intravenous cyclophosphamide pulse therapy (500 mg/day) was instituted. Her cardiac wall motion on echocardiography and serum creatinine levels gradually improved, but her skeletal and respiratory muscle weakness did not improve. On 38 th admission day, she was complicated with respiratory infection by methicillin resistant Staphylococcus aures. On 62 th admission day, she died of endotoxic shock. This is the first report describing respiratory muscle involvement with PN, and the second report describing MRI findings of muscle involvement by PN. Therefore, our case provides important clinical information for the diagnosis and treatment of the disease.
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PMID:[A case of microscopic polyangiitis with severe cardiac and respiratory muscle involvement]. 1061 70

Inflammatory myopathies are a heterogeneous group of conditions characterized by proximal muscle weakness, nonsuppurative inflammation of skeletal muscle, with elevated muscle enzyme levels and characteristic electromyography and muscle biopsy findings. The authors describe a clinical case of a young woman, admitted with a four day history of bilateral thigh myalgia. She was afebrile and without skin, mucosal or joint involvement. Thigh muscle palpation was painful. Complete blood count revealed leukopenia and thrombocytopenia. High levels of creatine kinase, serum aminotransferases and myoglobin were detected. Metabolic, toxic and drug-related causes were excluded as well as infectious diseases, malignant tumours and endocrine myopathies. Auto-antibodies for connective diseases were negative. Magnetic resonance imaging and electromyography of lower limbs were suggestive of inflammatory myopathy. Generalized muscle weakness and dysphagia were reported subsequently. Clinical and laboratorial improvement was seen after corticotherapy. Muscle biopsy revealed myopathy signs without inflammatory changes or vasculitis. After prednisolone reduction, presently without treatment, she remains asymptomatic with normal laboratorial findings. The authors emphasize in this case of inflammatory myopathy the unusual clinical and laboratory evolution and the importance of a cautious differential diagnosis.
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PMID:[Inflammatory myopathy with an unusual evolution]. 2071 Oct 99

Rhabdomyolysis is a syndrome characterized by the breakdown of skeletal muscle and leakage of intracellular myocyte contents, such as creatine phosphokinase (CPK) and myoglobin, into the interstitial space and plasma resulting in acute kidney injury (AKI). Elevated CPK of at least 5 times the upper limit of normal is an important diagnostic marker of Rhabdomyolysis. We present a case of rhabdomyolysis with severe AKI with a normal CPK at presentation. A 32-year-old man presented with acute respiratory failure and AKI after an overdose of recreational drugs. Urinalysis at presentation showed trace amounts of blood, identified as rare red blood cells under microscopy. CPK was 156 U/L at presentation. Workup for glomerulonephritis and vasculitis was negative. He was initiated on renal replacement therapy, and a kidney biopsy showed severe acute tubular injury with positive myoglobin casts. Supportive management and renal replacement therapy was provided, and renal function spontaneously improved after a few weeks. This is an uncommon clinical presentation of severe rhabdomyolysis complicated by AKI. This suggests that CPK alone may not be a sensitive marker for rhabdomyolysis-induced AKI in some cases.
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PMID:Rhabdomyolysis-Associated Acute Kidney Injury With Normal Creatine Phosphokinase. 2928 68