Statins and Peripheral Neuropathy: Causation or Coincidence?
Statins and Peripheral Neuropathy: Causation or Coincidence?
A 50-year-old man presented with clinical features of peripheral neuropathy with numbness in both feet. He had been prescribed statin therapy for a mixed hyperlipidaemia following a myocardial infarction at 40 years of age. After four years of continuous statin therapy the development of neuropathic symptoms prompted the patient to request further evaluation. Clinical examination at this time revealed bilateral sensory loss in all modalities tested but was otherwise unremarkable. Nerve conduction studies were performed and indicated an axonal sensory neuropathy. He consumed between 20 and 30 units of ethanol per week which he reduced. Extensive investigation revealed no secondary cause, including normal fasting glucose, renal and thyroid function, serum B12 level, autoantibody screen, syphilis serology and lumbosacral MRI. At the time it was suggested that statins could be responsible for his symptoms, but as these were not progressive and his cardiovascular risk high, statin therapy was continued. He had previously used simvastatin and atorvastatin but was switched to rosuvastatin 10 mg o.d. with the view that this might ameliorate his neuropathic symptoms. No improvement was noted with this change; however, the patient noticed a significant reduction in symptoms approximately two weeks after deliberately discontinuing his statin at a later date, which then returned within one week of restarting.
Case Report
A 50-year-old man presented with clinical features of peripheral neuropathy with numbness in both feet. He had been prescribed statin therapy for a mixed hyperlipidaemia following a myocardial infarction at 40 years of age. After four years of continuous statin therapy the development of neuropathic symptoms prompted the patient to request further evaluation. Clinical examination at this time revealed bilateral sensory loss in all modalities tested but was otherwise unremarkable. Nerve conduction studies were performed and indicated an axonal sensory neuropathy. He consumed between 20 and 30 units of ethanol per week which he reduced. Extensive investigation revealed no secondary cause, including normal fasting glucose, renal and thyroid function, serum B12 level, autoantibody screen, syphilis serology and lumbosacral MRI. At the time it was suggested that statins could be responsible for his symptoms, but as these were not progressive and his cardiovascular risk high, statin therapy was continued. He had previously used simvastatin and atorvastatin but was switched to rosuvastatin 10 mg o.d. with the view that this might ameliorate his neuropathic symptoms. No improvement was noted with this change; however, the patient noticed a significant reduction in symptoms approximately two weeks after deliberately discontinuing his statin at a later date, which then returned within one week of restarting.
