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Colchicine-induced vacuolar myopathy.
CMAJ
January 2025
Departments of Neurology and Neurosurgery (Pekeles, Altman), Pediatrics (Pekeles), and Pathology (Karamchandani), McGill University; Department of Neurology (Altman), Jewish General Hospital, Montréal, Que.
Use of Colchicine for Pericardial Inflammation: Risks and Toxicities-A Cautionary Tale.
JACC Case Rep
November 2022
Faculty of Medicine, Hebrew University, Jerusalem, Israel.
Colchicine is commonly used as part of the treatment of acute and recurrent pericarditis. Neuromyopathy is a well-known, but probably underreported, side effect of colchicine. Here we present a unique case of a 56-year-old woman with recurrent episodes of colchicine-induced neuromyopathy over many years.
View Article and Find Full Text PDF[A case report of colchicine-induced myopathy in a patient with chronic kidney disease].
Beijing Da Xue Xue Bao Yi Xue Ban
December 2021
Department of Rheumatology, Beijing Hospital; National Center of Gerontology; Institute of Geriatric Medicine, Chinese Academy of Medical Sciences, Beijing 100730, China.
Colchicine plays an important role in the treatment of gout and some other diseases. Besides gastrointestinal symptoms, myopathy has been reported as a rare side effect of colchicine in some patients. We report a case of myopathy in a patient with chronic kidney disease caused by high-dose colchicine, and then review literature on colchicine-induced myopathy, so as to provide some experience for the clinical diagnosis, treatment and medication safety.
View Article and Find Full Text PDFTeaching NeuroImages: Colchicine-induced vacuolar myopathy.
Neurology
December 2019
From the Department of Neurology, University of Illinois College of Medicine at Peoria.
Activation of the Keap1/Nrf2 stress response pathway in autophagic vacuolar myopathies.
Acta Neuropathol Commun
October 2016
Department of Pathology, University of California, San Francisco, CA, USA.
Nrf2 (nuclear factor [erythroid-derived 2]-like 2; the transcriptional master regulator of the antioxidant stress response) is regulated through interaction with its cytoplasmic inhibitor Keap1 (Kelch-like ECH-associated protein 1), which under basal conditions targets Nrf2 for proteasomal degradation. Sequestosome 1 (SQSTM1)/p62-a multifunctional adapter protein that accumulates following autophagy inhibition and can serve as a diagnostic marker for human autophagic vacuolar myopathies (AVMs)-was recently shown to compete with Nrf2 for Keap1 binding, resulting in activation of the Nrf2 pathway. In this study, we used 55 human muscle biopsies divided into five groups [normal control, hydroxychloroquine- or colchicine-treated non-AVM control, hydroxychloroquine- or colchicine-induced toxic AVM, polymyositis, and inclusion body myositis (IBM)] to evaluate whether Keap1-SQSTM1 interaction led to increased Nrf2 signaling in human AVMs.
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