Early studies have shown serum copper depletion in patients undergoing acute plasma exchange, a feature that led to use of plasmapheresis as a bridging therapy to liver transplantation in Wilson’s disease patients with fulminant hepatic failure. Though serum copper level has been observed to stabilize after the initial acute depletion, intense and protracted plasmapheresis may result in depletion of total body copper stores. Neurologic manifestations of copper deficiency include peripheral neuropathy, myeloneuropathy, and AIDP/CIPD-like presentation. Patients can thus present with gait difficulties, sensory ataxia, spasticity, and paresthesia that mimic the very same conditions for which the plasmapheresis is treating.

Copper levels decrease during periods of maintenance plasmapheresis with recovery on cessation of plasmapheresis sessions. Physicians may consider obtaining baseline copper levels prior to initiation of plasmapheresis and monitoring of levels during maintenance plasmapheresis.