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)

We report a fatal case of toxic myopathy in a patient with a transplanted heart for severe ischemic coronary artery disease. He was on long-term cyclosporine, prednisone, and mycofenolate. Four months before the development of proximal muscle weakness, his simvastatin dose was doubled, and he was also started on colchicine for acute exacerbation of gout. He developed progressive muscle weakness leading to shortness of breath and hospitalization for respiratory failure. Colchicine and simvastatin were stopped on admission. He received high-dose methylprednisolone for continued muscle weakness while he was sedated with propofol. These changes led to a marked elevation of creatine kinase, peaking at 33,580 U/ml. The muscle biopsy revealed toxic vacuolization, mitochondrial damage, and no evidence of inflammation. Based on the timing of events, the combination of propofol, high-dose methylprednisolone, and cyclosporine have triggered rhabdomyolysis, which may have been facilitated by prior administration of colchicine and simvastatin.
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PMID:Fatal toxic myopathy attributed to propofol, methylprednisolone, and cyclosporine after prior exposure to colchicine and simvastatin. 1762 39

A 60-year-old African American man with end stage renal disease on hemodialysis (HD) for the past 2.5 years developed severe hyperparathyroidism. Other past medical history included atrial fibrillation, type II diabetes mellitus, hypertension, gout, pericardial effusion needing pericardial window, deep vein thrombosis, mitral insufficiency, and cardiomyopathy with implantable cardioversion device placement. His parathyroid hormone (PTH) level peaked at 4,191 pg/mL despite being on cinacalcet, sevelamer, and paricalcitol. He underwent a subtotal parathyroidectomy in January 2015, after which his PTH levels dropped to 184 pg/mL. Approximately 4 weeks later he developed extensive, painful necrotic skin lesions in both his lower extremities and buttocks, suggestive of calciphylaxis which was confirmed by tissue biopsy. The patient was treated with elaborate wound care, wound debridements, increased dialysis dose, and IV sodium thiosulfate (STS) during hemodialysis. Besides STS, he was treated with narcotics, gabapentin, topical lidocaine on intact skin, and oral steroids for pain control. Even though his lesions improved initially, he deteriorated due to recurrent sepsis, respiratory failure, and prolonged hospitalization which culminated in stopping dialysis before he passed away. Calciphylaxis, or calcific uremic arteriolopathy, is a life-threatening complication of end stage renal disease. Treatment of this condition is multidisciplinary which includes elaborate wound care, increasing dialysis dose, and discontinuing vitamin D supplements and calcium containing phosphate binders. Even though STS has been recommended off-label, several studies have shown promising results with resolution of lesions. Thus, sodium thiosulfate has become the mainstay of treatment. Parathyroidectomy is a recommended modality of treatment in those with high PTH levels. Our case was unique in that calciphylaxis developed after subtotal parathyroidectomy. We believe that this is due to a decreased PTH level and decreasing bone turnover which resulted in more circulating calcium facilitating vascular and soft tissue calcification. The exact mechanism of developing calciphylaxis after parathyroidectomy is unknown. Even though parathyroidectomy is an effective treatment for calciphylaxis, clinicians should be aware that it can rarely present after parathyroidectomy.
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PMID:Calciphylaxis after parathyroidectomy. 2906 76