Iatrogenic neuropathies

This review discusses the literature on peripheral neuropathy caused by medication-induced toxicity or immunological mechanism with special attention to recent advancements.

The number of reports of immune-mediated neuropathies associated with antitumor necrosis factor alpha (anti-TNFalpha) therapy is increasing. But long-term follow-up suggests that the cessation of anti-TNFalpha therapy is not always necessary. The cases of acute inflammatory demyelinating polyneuropathy induced by polyethylene glycol-interferon alpha-2a and of polyradiculoneuropathy induced by polyethylene glycol-interferon alpha-2b were reported for the first time, and the latter was associated with antiganglioside antibodies. The mechanism of chemotherapy-induced peripheral neuropathy is still in the process of being elucidated with the use of animal models or axonal excitability techniques. In the phase III Assessment of Proteasome Inhibitor for Extending Remissions trial, it proved that dose modification using a specific guideline improved bortezomib-induced peripheral neuropathy management.

Peripheral neuropathy can be associated with anti-TNFalpha therapy or interferon alpha therapy, and to the contrary, anti-TNFalpha therapy or interferon alpha therapy may have potential as a treatment option for a spectrum of immune-mediated neuropathy, similar to a double-edged sword. To take advantage of the effect of chemotherapy and to reduce neurotoxicity, a guideline of dose modification is useful.