Accumulation of microtubule-based motor protein in a patient with colchicine myopathy

Colchicine has been used therapeutically for gout for more than 200 years. Recently, the drug has also been used for autoimmune diseases such as Behçet disease. However, long-term use of colchicine can cause vacuolar myopathy.1,2⇓ Concomitant use of cyclosporin or renal insufficiency exaggerates the toxic effect of colchicine.1,2⇓ Colchicine myopathy sometimes occurs in organ transplant recipients, although it may be unrecognized.3 Colchicine inhibits polymerization of microtubules by interacting with tubulin, a monomeric component of microtubules. As particles and membranous organelles including lysosomes and autophagic vacuoles are conveyed along the microtubule-dependent cytoskeletal network,4 disruption of this cytoskeletal network by colchicine may result in the intracellular accumulation of autophagic vacuoles.2

We report a patient with Behçet disease who had been treated with colchicine and cyclosporin. The patient showed subacute proximal myopathy, and his muscle biopsy findings were compatible with colchicine myopathy. To confirm the pathogenesis of colchicine myopathy, we immunolocalized dynein, a driving force of organelles along microtubules.5,6⇓