Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018099 (gout)
 5,192 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Renal transplant recipients are prone to develop drug toxicities because of polypharmacy and drug-drug interactions. Colchicine is often used for the treatment of gout in these patients as nonsteroidal medications are contraindicated. In addition, patients are often on corticosteroids and frequent, periodic, dose escalation for gouty flare may lead to side effects. Colchicine-induced myopathy has been very well described in the literature. Several cases of colchicine toxicity have been reported in cyclosporine-treated patients due to a drug-drug interaction. We report a 62-year-old African American renal transplant recipient who had been doing well on tacrolimus-based immunosuppression and was started on colchicine (0.6 mg twice daily) for gouty flare. A few days later, he was found to have a 4-fold increase in aspartate aminotransferase and an elevated creatine phosphokinase. Although this interaction is very well known with cyclosporine, it has not yet been reported in patients on tacrolimus.
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PMID:Colchicine-Induced Myopathy in a Tacrolimus-Treated Renal Transplant Recipient: Case Report and Literature Review. 2473 5

Colchicine is an approved agent in the management and prophylaxis of gout and familial Mediterranean fever but its therapeutic value is limited by its narrow therapeutic index. Multisystem toxicity is uncommonly reported; and is often associated with renal impairment and/or specific drug interactions. We report two cases of colchicine toxicity marked by severe neuromyopathy in a diabetic with stage 4 chronic kidney disease (CKD) and a renal transplant recipient. Both patients presented with diarrhea, acute on chronic kidney injury and progressive muscle weakness while on colchicine for several weeks or longer. In addition to kidney disease, risk factors for colchicine toxicity included maintenance therapy with simvastatin in the first patient and cyclosporine in the second. Creatine phosphokinase (CPK) was elevated in both cases at presentation and neurophysiologic studies showed a pattern of severe myopathy with axonal sensorimotor neuropathy. The first patient recovered from neurological weakness in a few weeks, but the second patient suffered an extraordinarily protracted and severe neuromuscular disability for a year. The two cases reinforce the need for extra vigilance in prescribing and monitoring colchicine therapy in renal patients with specific attention to drug interactions known to increase the risk of toxicity, thus avoiding such combinations in patients with renal impairment.
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PMID:Colchicine toxicity in renal patients - Are we paying attention? 2624 46

An 83-year-old man with multiple medical problems, including gout, pseudogout, and renal insufficiency, presented with more than a year of proximal weakness. He had an extensive previous medical workup, including a normal creatinine kinase. His weakness persisted despite endurance and strength training. Electrodiagnostic findings were consistent with a myopathy, although without abnormal spontaneous activity and a length-dependent neuropathy. On the basis of these findings, colchicine was discontinued. The patient experienced marked symptomatic improvement within a week. Myopathies with neuropathies may be found with the use of colchicine. This case was unusual because of the absence of abnormal spontaneous activity and increased creatinine kinase, as typically reported with colchicine myopathy.
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PMID:Unusual Electromyographic Findings Associated With Colchicine Neuromyopathy: A Case Report. 2697 60

Colchicine is derived from Colchicum autumnale and Gloriosa superba and is used to treat acute gout and familial Mediterranean fever (FMF). Musculoskeletal adverse effects range from myopathy to rhabdomyolysis. An 18-year-old woman, with a 2-year history of FMF treated with colchicine, took 9 colchicine pills (4.5 mg) to relieve severe abdominal pain. On the sixth day of hospitalization, the patient's condition worsened, and she died. As this was a case of fatal poisoning, a forensic autopsy was performed, and the cause of death was determined to be complications of muscle destruction due to colchicine intoxication with the findings of myocytolysis, positive antimyoglobin antibody staining kidney tubules. Colchicine toxicity begins with gastrointestinal symptoms. Multiorgan effects follow the gastrointestinal effects. Serious outcomes of colchicine toxicity are rhabdomyolysis, bone marrow suppression, and disseminated intravascular coagulation. In chronic diseases that require lifelong treatment with medications, adverse effects can arise with long periods of use. Our patient had been treated for FMF with colchicine for 2 years but took too many colchicine pills to relieve her severe abdominal pain. Warning patients about the effects of high doses of drugs and providing information about their toxic effects and what to do "in case" of overuse could be lifesaving.
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PMID:Colchicine-Induced Rhabdomyolysis: An Autopsy Case. 2704 58

Colchicine is a medication most commonly used in the treatment of gout and familial mediterannean fever. A rare complication of therapy is toxicity causing proximal myopathy and polyneuropathy. Colchicine myopathy has been associated with the coadministration of other medications with colchicine, such as statins or tacrolimus, and is more common in patients with renal impairment. Otherwise, it is unclear which patients are at greatest risk of developing this adverse drug reaction. ABCB1 is important to the metabolism of colchicine, so we speculated that it was possible that colchicine myopathy patients may have a particular genotype that is associated with this side effect. We describe two cases of colchicine myopathy which occurred with co-administration of rosuvastatin. From one case, we present the first published data on muscle MRI in this condition. We additionally present an analysis of four genetic polymorphisms in ABCB1 and transcript levels in muscle tissue, and demonstrate the descriptive finding of reduced ABCB1 transcript levels in the colchicine myopathy patients.
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PMID:Colchicine Myopathy: A Case Series Including Muscle MRI and ABCB1 Polymorphism Data. 3117 24


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