Colchicine, a microtubule polymerization inhibitor, can very occasionally induce
myopathy. We report two cases of
colchicine myopathy. Both patients presented with
myalgia and proximal
muscle weakness. The first patient, an 80-year-old woman, had
chronic renal failure related to renal
amyloidosis. She had been treated by
colchicine for 4 months. The second, a 75-year-old man with normal renal function, suffering from
gout, was treated by
colchicine for 3 weeks. Muscle biopsies displayed the same alterations, but the degree of severity was different. Conventional histology revealed vacuolar changes characterized by
acid phosphatase-positive vacuoles and myofibrillar disarray foci. The lesions were selective for type I fibers. Ultrastructural study demonstrated autophagic vacuoles. Most of the vacuoles expressed
dystrophin but not
merosin. Several fibers reacted with anti-MHC class I antibody and granular deposits of
membrane attack complex were observed on the surface of numerous myofibers. Anti-alphaB-
crystallin antibody strongly reacted with vacuolar content. Physiopathologically, microtubules are primordial for vesicle movements and
colchicine induces autophagic vacuole accumulation by preventing their fusion with lysosomes. The selective type I involvement is probably due to the higher
tubulin amount in type I fibers. AlphaB-
crystallin overexpression is related to its microtubule protection properties. Moreover, we suggest that vacuoles randomly floating in sarcoplasm might occasionally meet the plasma membrane and open in the extracellular space, leading to complement activation. Accurate diagnosis of
colchicine myopathy is relevant because the treatment is based on
colchicine interruption.