Colchicine induced neuromyopathy in a patient with normal renal function.

Area of Science:

• Neurology
• Toxicology

Background:

• Colchicine is a medication commonly used for gout and other inflammatory conditions.
• Neuromyopathy is a known, albeit uncommon, adverse effect of colchicine therapy.
• Impaired renal function is a recognized risk factor for developing colchicine-induced neuromyopathy.

Purpose of the Study:

• To report a case of colchicine-induced neuromyopathy in a patient with normal renal function.
• To highlight the clinical presentation, diagnostic findings, and outcome of this adverse effect.
• To emphasize the importance of monitoring for neuromyopathy even in patients with preserved kidney function.

Main Methods:

• A case report of a 69-year-old male patient experiencing subacute muscle weakness.
• Clinical assessment including neurological examination, nerve conduction studies, and electromyography.
• Monitoring of creatine phosphokinase (CPK) levels and muscle strength following colchicine withdrawal.

Main Results:

• The patient presented with painless proximal muscle weakness and elevated CPK levels.
• Nerve conduction studies showed a mild axonal neuropathy; electromyography was unremarkable.
• Following discontinuation of colchicine, muscle strength and CPK levels normalized within 4 months.

Conclusions:

• Colchicine neuromyopathy can occur in patients with normal renal function.
• Neuromyopathy associated with colchicine is generally reversible upon drug withdrawal.
• Caution and monitoring of muscle strength and CPK levels are advised, particularly in patients with renal impairment, but also in those with normal kidney function if myopathy is suspected.