CHRONIC COLCHICINE-INDUCED MYOPATHY AND NEUROPATHY

The presented case concerns a 77-year old man who had been chronically taking colchicine for treatment of gout. He was admitted because of a transient ischemic cerebrovascular attack with motor aphasia and comp lained of preexisting paraesthesias in the lower extremities. Neurolog ical examination revealed a global muscular weakness, absent myotatic reflexes adn a diminished sensation. Serum creatine kinase (CK) levels were increased and electromyography showed spontaneous fibrillations in deltoid muscles, positive spikewaves in deltoids and anterior tibia l muscles. Motor and sensory conduction velocities were mildly reduced . Nerve biopsy findings were compatible with a chronic axonal neuropat hy having produced a significant loss of myelinated axons and also den ervation features of unmyelinated axons. In muscle, combined neurogeni c and myogenic features were found. The former result from the axonal neuropathy. The latter were mainly characterized by focal myofibrillar disorganisation and accumulation of autophagic vacuoles in muscle fib res. The presented neuromuscular symptoms and signs, the increased CK values, the electromyographic and nerve conduction velocity findings a s well as nerve and muscle biopsy observations, are consistent with th e diagnosis of colchicine-induced myopathy and neuropathy. Furthermore , the disappearance of paraesthesias, normalisation of CK values, and disappearance of fibrillations and positive spike waves in deltoid and anterior tibial muscles on electromyography, after stopping of the co lchicine therapy, supported the diagnosis.