Cases reported "Rhabdomyolysis"

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1/15. Serious adverse events attributed to nevirapine regimens for postexposure prophylaxis after hiv exposures--worldwide, 1997-2000.

    In September 2000, two instances of life-threatening hepatotoxicity were reported in health-care workers taking nevirapine (NVP) for postexposure prophylaxis (PEP) after occupational human immunodeficiency virus (hiv) exposure. In one case, a 43-year-old female health-care worker required liver transplantation after developing fulminant hepatitis and end-stage hepatic failure while taking NVP, zidovudine, and lamivudine as PEP following a needlestick injury (1). In the second case, a 38-year-old male physician was hospitalized with life-threatening fulminant hepatitis while taking NVP, zidovudine, and lamivudine as PEP following a mucous membrane exposure. To characterize NVP-associated PEP toxicity, CDC and the food and Drug Administration (FDA) reviewed MedWatch reports of serious adverse events in persons taking NVP for PEP received by FDA (Figure 1). This report summarizes the results of that analysis and indicates that healthy persons taking abbreviated 4-week NVP regimens for PEP are at risk for serious adverse events. Clinicians should use recommended PEP guidelines and dosing instructions to reduce the risk for serious adverse events.
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2/15. Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis?

    The use of anabolic steroids among competitive athletes, particularly bodybuilders, is widespread. Numerous reports have noted "hepatic" dysfunction secondary to anabolic steroid use based on elevated serum aminotransferase levels. The authors' objective was to assess whether primary care physicians accurately distinguish between anabolic steroid-induced hepatotoxicity and serum aminotransferase elevations that are secondary to acute rhabdomyolysis resulting from intense resistance training. Surveys were sent to physicians listed as practicing family medicine or sports medicine in the yellow pages of seven metropolitan areas. physicians were asked to provide a differential diagnosis for a 28-year-old, anabolic steroid-using male bodybuilder with an abnormal serum chemistry profile. The blood chemistries showed elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) levels, and normal gamma-glutamyltransferase (GGT) levels. In the physician survey (n = 84 responses), 56% failed to mention muscle damage or muscle disease as a potential diagnosis, despite the markedly elevated CK level of the patient. Sixty-three percent indicated liver disease as their primary diagnosis despite normal GGT levels. Prior reports of anabolic steroid-induced hepatotoxicity that were based on aminotransferase elevations may have overstated the role of anabolic steroids. Correspondingly, the medical community may have been led to emphasize anabolic steroid-induced hepatotoxicity and disregard muscle damage when interpreting elevated aminotransferase levels. Therefore, when evaluating enzyme elevations in patients who use anabolic steroids, physicians should consider the CK and GGT levels as essential elements in distinguishing muscle damage from liver damage.
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3/15. rhabdomyolysis after concomitant use of cyclosporine, simvastatin, gemfibrozil, and itraconazole.

    OBJECTIVE: To report a case of rhabdomyolysis in a patient receiving cyclosporine, simvastatin, gemfibrozil, and itraconazole. CASE REPORT: rhabdomyolysis occurring in transplant patients receiving both cyclosporine and the hydroxymethylglutaryl coenzyme a (HMG-CoA) reductase inhibitor lovastatin has been well documented. The exact mechanism by which this interaction leads to rhabdomyolysis is unknown. Experience with newer agents of the statin drug class in transplant patients is limited. Since the interaction between cyclosporine and HMG-CoA reductase inhibitors involves the CYP3A4 enzyme system, the possibility of amplifying this interaction exists when other drugs affecting the same enzyme system are coprescribed. We describe a case in which a heart transplant recipient stable on a drug regimen that included cyclosporine, simvastatin, and gemfibrozil developed rhabdomyolysis after initiation of the antifungal agent itraconazole. DISCUSSION: Drug-drug interactions due to shared metabolism via the CYP3A4 pathway can result in significant adverse outcomes. This article discusses concurrent use of an HMG-CoA reductase inhibitor with other drugs that inhibit the CYP3A4 isoenzyme, leading to a case of possible fatal rhabdomyolysis. CONCLUSIONS: Clinicians must be aware of drugs metabolized via cytochrome P450 isoenzymes and identify those requiring risk-versus-benefit analysis before prescribing. patients need to be educated as to signs and symptoms requiring immediate physician intervention.
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4/15. Venlafaxine poisoning complicated by a late rise in creatine kinase: two case reports.

    Newer anti-depressants are often considered to be safer than more established anti-depressants. However, clinical experience of the effects of these agents in overdose is limited. Here, we present two cases of venlafaxine overdose that were complicated by a delayed rise in plasma creatine kinase. Although the clinical consequences were not serious, physicians should be alerted to the possibility of delayed rhabdomyolysis or serotonin syndrome in patients who have taken venlafaxine in overdose.
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5/15. Fluvastatin-induced rhabdomyolysis.

    OBJECTIVE: To demonstrate a case of rhabdomyolysis with acute renal failure in a patient receiving fluvastatin and to present evidence that this was an adverse drug reaction to fluvastatin. CASE SUMMARY: A 51-year-old white man with a past medical history significant for hyperlipidemia treated with fluvastatin presented with malaise, myalgias, nausea, and lumbar back pain. The patient had azotemia with elevated creatine kinase (CK), lactate dehydrogenase, and transaminases. He developed hematuria and proteinuria. Laboratory results demonstrated a normal antinuclear antibody, rheumatoid factor, angiotensin-converting enzyme, antineutrophil cytoplasmic antibody, and thyroid-stimulating hormone. cytomegalovirus and Epstein-Barr virus titers were negative for recent infection. There were no signs of systemic infection; the white blood cell count was normal and blood and urine cultures were negative. Renal ultrasound showed hyperechoic renal cortices with no obstruction. The discontinuation of fluvastatin and hemodialysis led to a rapid decrease in CK and improvement in symptoms. DISCUSSION: Hydroxymethylglutaryl coenzyme a (HMG-CoA) reductase inhibitors have the potential to cause rhabdomyolysis. However, fluvastatin is rarely associated with rhabdomyolysis when compared to other statins. Differences in biochemical and pharmacokinetic properties between fluvastatin and other HMG-CoA reductase inhibitors may be important in the development of rhabdomyolysis. CONCLUSIONS: Fluvastatin was the precipitating factor causing rhabdomyolysis in this case report. This patient had no other findings to suggest infection or other disorder inducing rhabdomyolysis. An objective causality assessment revealed that the adverse drug reaction was probable as determined by the Naranjo probability scale. Fluvastatin has the potential to cause serious adverse effects. Therefore, a heightened awareness by the patient and physician for potential signs of myopathy is recommended.
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6/15. Cerivastatin monotherapy-induced muscle weakness, rhabdomyolysis and acute renal failure.

    Statins are now widely prescribed and without doubt save many lives. However there are rare potentially serious side-effects, including acute renal failure. Patient education and physician vigilence are vital.
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7/15. Two cases of exertional rhabdomyolysis precipitated by personal trainers.

    INTRODUCTION: Numerous cases of exertional rhabdomyolysis have been reported in the literature, and these cases mostly involve individuals who were inexperienced exercisers, uneducated in fitness and health principles, dehydrated or heat stressed, taking drugs, or military recruits in basic training. PURPOSE: The purpose of this article is to review two cases of exertional rhabdomyolysis in healthy, experienced exercisers. methods/RESULTS: The cases reviewed are for a 22-yr-old female college student and a 37-yr-old male physician who presented with rhabdomyolysis secondary to exercise in a local health club that was part of a national chain. DISCUSSION: In these two cases individuals, both well educated and experienced in fitness, were encouraged by fitness instructors in a local health club to overexertion during their exercise routine leading to rhabdomyolysis.
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8/15. Severe hypokalaemic paralysis and rhabdomyolysis due to ingestion of liquorice.

    Chronic ingestion of liquorice induces a syndrome with findings similar to those in primary hyperaldosteronism. We describe a patient who, with a plasma K of 1.8 mmol/l, showed a paralysis and severe rhabdomyolysis after the habitual consumption of natural liquorice. Liquorice has become widely available as a flavouring agent in foods and drugs. It is important for physicians to keep liquorice consumption in mind as a cause for hypokalaemic paralysis and rhabdomyolysis.
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9/15. Recurrent rhabdomyolysis in a collegiate athlete: a case report.

    PURPOSE: Hereditary metabolic disorders can cause rhabdomyolysis in athletes. Team physicians should be aware of the presentation, workup, and management of the most common of these disorders, carnitine palmitoyltransferase (CPT) II deficiency and muscle phosphorylase deficiency. methods: The case of a collegiate athlete with recurrent bouts of rhabdomyolysis is presented, and the diagnostic workup is discussed. RESULTS: The patient described in this case has CPT II deficiency. The diagnosis and management of CPT II deficiency and muscle phosphorylase deficiency (McArdle's disease) are discussed. CONCLUSION: athletes with rhabdomyolysis, in the absence of an obvious cause such as drug toxicity, severe trauma, or excessive exercise, should be evaluated for the presence of a metabolic myopathy.
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10/15. Rare case of rhabdomyolysis with therapeutic doses of phendimetrazine tartrate.

    Phendimetrazine tartrate is a newer drug that acts as a central stimulant and indirectly acting sympathomimetic with a host of uses similar to the class amphetamines. Its main use is as an anorectic in the short-term treatment of obesity, although stimulants are no longer indicated for this purpose. This drug appeals to the younger American population for immediate weight loss through decreased appetite and early satiety. The european union markets have already withdrawn this medication as well as other countries, but phendimetrazine is still used within the united states. rhabdomyolysis is a potentially life-threatening complication reported with higher doses of amphetamines. We present a case of rhabdomyolysis and myoglobinuria developing in a 23-year-old patient after oral administration of phendimetrazine tartrate for 3 days in suggested therapeutic doses. The medication was taken for short-term treatment of obesity, and patient did not have any predisposing factors to precipitate rhabdomyolysis. rhabdomyolysis resolved within 5 days. To our knowledge, this is the first reported case of rhabdomyolysis from administration of therapeutic amounts of phendimetrazine tartrate. The purpose of this case report is to create an awareness among physicians about the potentially life-threatening complications associated with phendimetrazine use as an anorectic even in suggested therapeutic doses as was the case in our patient. Additional awareness is needed to educate their patients about the side effects associated with these drugs and to strongly discourage their unsupervised use.
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