Colchicine-induced Rhabdomyolysis Research Articles

Rhabdomyolysis and acute neuromyopathy associated with the combined use of statin and colchicine: A case report and a review of the literature

To report a case of colchicine-induced rhabdomyolysis and neuromyopathy in a patient treated with atorvastatin and colchicine and to review the literature about this topic. A 69-year-old man affected by diabetes mellitus and chronic renal insufficiency was prescribed atorvastatin, after that an ischemic stroke occurred, with no side effect. After 2 months colchicine (0.5 mg three times a day) was added to treat pericarditis and six weeks later, the patient began to experience increasing symmetrical proximal muscle weakness which was worse in the legs. Laboratory results suggested rhabdomyolysis, while physical examination and electromyography findings were consistent with neuromyopathy. One month after the discontinuation of colchicine and atorvastatin, the patient weakness improved and muscle enzymes levels returned to normal levels. Eleven patients with clinical and laboratory characteristics similar to our patient’s caused by the combined use of colchicine and statins have been previously described in literature. Both colchicine and statin therapy may be associated with myopathy. Co-administration may exacerbate the myotoxicity because both drugs metabolism depend on hepatic demethylation through CYP450 3A4. Combination therapy with colchicine and statin should be avoided because of the risk of developing myopathy and rhabdomyolysis even after a long uneventful statin or colchicine medication.

Colchicine-induced rhabdomyolysis following a concomitant use of clarithromycin in a haemodialysis patient with familial Mediterranean fever.

Sir, Renal amyloidosis secondary to familial Mediterranean fever (FMF) is one of the common causes of nephrotic syndrome and chronic kidney disease in Turkey [1]. Colchicine is a microtubule-depolymerizing drug widely used for the treatment of gout which may prevent the development of secondary amyloidosis. In end-stage renal disease (ESRD), although the dose of colchicine is suggested to be reduced, there is limited information on efficacy and safety [2]. Inappropriately high doses or co-prescription of CYP3A4 or P-glycoprotein inhibitors have been reported to cause serious adverse effects, including death [3–7]. Herein, we present a case of colchicine-induced rhabdomyolysis after using clarithromycin, a macrolide antibiotic and a potent inhibitor of CYP3A4 and P-glycoprotein ABCB1. A 40-year old male patient on maintenance haemodialysis was admitted with recently developed fatigue, anorexia, headache, dizziness, diffuse myalgia and gastrointestinal symptoms including epigastric pain, diarrhoea and bloating. He presented with FMF in childhood (with frequent attacks of fever and abdominal pain with arthritis) and had developed secondary amyloidosis 10 years previously and ESRD 6 months previously. His long-term medication was colchicine 0.5 mg twice daily, doxazosin 4 mg once daily and 40 mg furosemide on non-dialysis days and sevelamer 1600 mg three times a day. A further history revealed that the patient had recently been diagnosed with acute sinusitis and was prescribed clarithromycin 500 mg twice daily in another hospital a week beofore. On his initial examination the patient's blood pressure was 100/60 mmHg, he was in a euvolaemic state and had no significant finding except diffuse tenderness, but there was no rebound on abdominal palpation. In his biochemistry, his creatine kinase (CK)(5732 U/L- 9035 U/L) and transaminase levels (ALT:110 U/L, AST:309 U/L) were elevated and raised upon follow-up. Due to high CK and transaminases, colchicine-induced rhabdomyolysis was diagnosed and colchicine discontinued. The patient's pain subsided 3 days after discontinuation of colchicine. An EMG was performed because of high levels of CK to exclude the diseases causing myopathie. During outpatient follow-up, the patient's transaminases and CK returned to normal levels and his EMG was normal. After complete recovery, the patient started colchicine 0.5 mg/day again without recurrence of symptoms.

Statin-Induced Lung Injury; Colchicine-Induced Rhabdomyolysis Caused by Interaction with Clarithromycin; Disulfiram Ethanol Reaction Mimicking Anaphylactic, Cardiogenic, and Septic Shock; Weight Gain with Abdominal Enlargement in a Patient Receiving Tocilizumab; Nilotinib-Associated Acute Pancreatitis

The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), discuss methods of prevention, and promote reporting of ADRs to the US Food and Drug Administration's (FDA's) MedWatch program (800-FDA-1088). If you have reported an interesting, preventable ADR to MedWatch, please consider sharing the account with our readers.

Colchicine-Induced Rhabdomyolysis Caused by Interaction With Clarithromycin in a Patient With Behcet Disease

Colchicine-Induced Rhabdomyolysis Caused by Interaction With Clarithromycin in a Patient With Behcet Disease

Colchicine-Induced Rhabdomyolysis Caused by Interaction With Clarithromycin in a Patient With Behçet Disease

Kim, Ji-Beom MD; Kim, Sujeong MD; Yoon, Sun-young MD; Lee, Taehoon MD; Lee, Yoon Su MD; Kwon, Hyouk-Soo MD, PhD; Cho, You Sook MD, PhD; Moon, Hee-Bom MD, PhD; Kim, Yong-Gil MD, PhD; Kim, Tae-Bum MD, PhD Author Information

Colchicine-Induced Rhabdomyolysis in a Heart/Lung Transplant Patient With Concurrent Use of Cyclosporin, Pravastatin, and Azithromycin

We report a case of colchicine-induced rhabdomyolysis in a heart/lung-transplanted man treated with cyclosporin. A treatment was to resolve an acute gouty arthritis and was started with 3 mg of colchicine the first day, then 2 mg the second and the third day, and finally 1 mg/d during 6 days. Eight days later, the patient developed multiple organ failure and rhabdomyolysis. The concentration of colchicine analyzed was greater than the standard 153 hours after his last intake. Pharmacokinetic interactions are responsible of this toxicity. Cyclosporin, pravastatin, and azithromycin are known to inhibit P-glycoprotein, which will enhance the intracellular colchicine level by acting in its bioavailability and moderating hepatic and renal excretion. Moreover, long-term treatment by cyclosporin generates chronic renal failure that will, in the same time, decrease colchicine elimination. Even short-term administration of therapeutic colchicine dose may cause colchicine-related toxicity, especially in the setting of a renal failure and/or polymedicinal treatment.

Colchicine-Induced Rhabdomyolysis and Possible Amiodarone Interaction ——Colchicine-Induced Rhabdomyolysis

Objective: To report a case of drug interaction leading to rhabdomyolysis. Case Summary: A 65-year old woman suf-fering from chronic atrial fibrillation was treated with amiodarone and acenocoumarol. Two weeks after administration of conventional dosage of colchicine for pericarditis, the patient developed rhabdomyolysis. colchicine-induced rhabdomyolysis was suspected. Colchicine was stopped and the patient underwent supportive therapy. Clinical symptoms improved rapidly. Discussion: Colchicine-induced neuromuscular toxicity and rhabdomyolysis have been reported with chronic treatment in therapeutic doses. Concomitant use of several drugs with colchicine may potentiate the development of myopathy. In our case, a co-administration of colchicine, a well known substrate of cytochrome P450 3A4 and P-glycoprotein, and amiodarone had possibly precipitated rhabdomyolysis. Amiodarone may increase colchicine toxicity by a dual mechanism. Amiodarone inhibits P-glycoprotein which may theoretically result in increased intrace- llular colchicine concentrations and decreased hepatic and renal excretion of the drug. Conclusion: Amiodarone may potentiate the development of colchicine-induced rhabdomyolysis.

Short Term Treatment With Clarithromycin Resulting in Colchicine-Induced Rhabdomyolysis

A case of colchicine-induced rhabdomyolysis is reported. A 48 year old African-American male with history of hypertension and chronic gout on colchicine 0.6 mg daily presented with symptoms of a community acquired pneumonia. The patient was started on 500 mg of clarithromycin orally twice daily and represented to the emergency room after 3 days complaining of severe muscle pain. His liver panel showed elevations in the serum aminotransferases; AST 513 mU/ml (nl 15-41) and ALT 182 mU/ml (nl 17-63). His complete blood count showed an elevated white blood cell count of 18,800/ml (nl 4,000-10,000/ml). Urine analysis was positive for myoglobin with no red cells present. Serum creatine kinase (CK) was 22,996 mU/ml (nl 31-221) with a normal troponin I 0.18 (nl <0.4).Investigations confirmed the presence of rhabdomyolysis and discontinuation of colchicine and clarithromycin resulted in resolution of clinical and biochemical features of rhabdomyolysis. By hospital day four, his muscle soreness had improved markedly. His serum CK improved to 3,389 mU/ml (nl 31-221 mU/ml) and serum creatinine improved to 1.5 mg/dl (nl 0.8-1.2). On hospital day five, the patient was discharged on oral anti-hypertensive medication and a ten-day course of doxycycline. Metabolism of colchicine by the cytochrome P450 3A4 system has been previously described, but this is the first published report of colchicine associated rhabdomyolysis secondary to drug metabolism interactions with an antibiotic. A review of medications that are metabolized via the cytochrome 3A4 and A-SLAVED-LIVER (Amiodarone, Simvastatin, Lovastatin, Atorvastatin, Verapamil, Erythromycin, Diltiazem, cLarithromycin, Itraconazole, Voriconazole, colchicinE, Ritonavir) pneumonic was established.

Colchicine-induced rhabdomyolysis

A case of colchicine-induced rhabdomyolysis is reported. A 79-year-old man with ischemic heart disease, chronic atrial fibrillation, chronic renal failure, hypothyroidism, and gout arthritis was hospitalized because of fatigue, myalgia, and leg weakness, shortly after starting treatment with colchicine. Investigation confirmed the diagnosis of rhabdomyolysis, and discontinuation of colchicine resulted in resolution of clinical and biochemical features of rhabdomylysis. Colchicine-induced rhabdomyolysis is a rare complication, and the postulated mechanisms and risk factors for this severe complication are discussed.

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The purpose of this feature is to heighten awareness of specific adverse drug reactions (ADRs), to discuss methods of prevention, and to promote reporting of ADRs to the FDA's medWatch program (800-FDA-1088). If you have reported an interesting preventable ADR to medWatch, please consider sharing the account with our readers.

Colchicine-Induced Rhabdomyolysis

AbstractOBJECTIVE:To report a case of rhabdomyolysis occurring during treatment with colchicine.CASE SUMMARY:A 44-year-old African American man was admitted to the hospital due to persistent diarrhea, vomiting, and diffuse weakness. Past medical history was significant for renal failure requiring peritoneal dialysis, gout, and a new skin lesion. Approximately 2 months prior to admission, he had been started on colchicine and allopurinol. Creatine kinase concentration on admission was >14 000 U/L. Liver function tests were elevated 5 × the upper limit of normal. Colchicine was discontinued on admission. Creatine kinase concentrations decreased significantly, and strength and ambulation improved throughout hospitalization.DISCUSSION:Colchicine was thought to be the causative factor for rhabdomyolysis in conjunction with chronic renal failure and elevated liver function tests. After discontinuation of colchicine, creatinine kinase concentrations declined and the patient's ability to walk improved. Limited case reports of colchicine-induced rhabdomyolysis have been published.CONCLUSIONS:Chronic renal failure in conjunction with elevated liver function tests appear to increase the possibility of colchicine-induced toxicity, specifically, rhabdomyolysis. ResumenOBJETIVO:Informar sobre un caso de rabdomiolisis que ocurrió durante un tratamiento con colchicina.RESUMEN DEL CASO:Un hombre afroamericano de 44 años fue admitido al hospital por diarrea persistente, vómitos, y debilidad general. El historial médico pasado incluía fallo renal recibiendo dialisis peritoneal, gota, y una lesión cutanea nueva. Aproximadamente 2 meses antes de la admisión, el paciente comenzó a recibir colchicina y alopurinol. La concentración de kinasa de creatinina en el momento de la admisión era mayor de 14 000 U/L. Las pruebas de función hepatica estaban elevadas a 5 veces el límite superior normal. Al admitirse el paciente, se descontinuó la colchicina. La concentración de kinasa de creatinina disminuyó significativamente, y la fuerzas y capacidad para ambular mejoraron a través de la hospitalización.DISCUSIÓN:Se pensó que colchicina fue el agente causante de la rabdomiolisis en combinación con el fallo renal crónico y el aumento en pruebas hepaticas. Luego de descontinuar la colchicina, las concentraciones de kinasa de creatinina disminuyeron y la capacidad para ambular mejoró. Se han reportado un número limitado de casos de rabdomiolisis inducidos por colchicina.CONCLUSIONES:El fallo renal crónico en combinación con una elevación en la concentración de enzimas hepaticas parecen aumentar la probabilidad de toxicidad inducida por colchicina, especialmente el desarrollo de rabdomiolisis. RésuméOBJECTIF:Signaler un cas de rhabdomyolyse survenue durant un traitement à la colchicine.PRÉSENTATION SOMMAIRE DU CAS:Un Africain de 44 ans vivant aux États-Unis est admis à l'hôpital à la suite d'une diarrhée persistante, de vomissement, et d'une fatigue généralisée. Comme antécédents médicaux, on note une insuffisance rénale nécessitant une dialyse péritonéale, de la goutte et une lésion cutanée récente. Approximativement 2 mois avant son admission, le patient a débuté un traitement à base de colchicine et d'allopurinol. Le taux de créatine kinase à l'admission est supérieur à 14 000 U/L. Les tests de la fonction hépatique sont 5 fois plus élevés que la limite supérieure de la normale. La colchicine est retirée dès l'admission. Les taux de créatine kinase diminuent de façon significative, la force et la mobilité du patient s'améliorent au cours de l'hospitalisation.DISCUSSION:On pense que la colchicine a causé la rhabdomyolyse dû à la présence concomitante d'une insuffisance rénale chronique et d'une altération des tests de la fonction hépatique. Après le retrait de la colchicine, les taux de créatine kinase ont chuté et l'habilité du patient à déambuler s'est amélioré. Peu de cas de rhabdomyolyse causée par la colchicine ont été signalés dans la documentation scientifique.CONCLUSIONS:L'insuffisance rénale chronique associée à l'altération des tests de la fonction hépatique semblent augmenter la possibilité de toxicité causée par la colchicine, spécifiquement la rhadomyolyse.