Prevention and Management of Drug-Induced Peripheral Neuropathy

Abstract

When symptoms of peripheral neuropathy appear, the possibility that they have been induced by drugs should be considered. A large number of drugs of all kinds, several of which are considered indispensable, have been implicated in peripheral neuropathy. A list of some of these drugs is provided. Neuropathy is a universal and dose-limiting factor during treatment with vinca alkaloids, but is otherwise a rare complication of drug therapy. Drug-induced peripheral neuropathy is almost always due to a dose-dependent primary axonal degeneration caused either by toxic reactions or by metabolic changes in neurons or their surroundings. The use of drugs should be restricted, especially in patients with a risk for development of neuropathy or with already existing neuropathy, e.g. patients with hepatic or renal failure, diabetes mellitus, or malnutrition. Patients should be given vitamins, prophylactically or therapeutically, which will sometimes allow a treatment to be continued. In other cases of drug-induced neuropathy the drug should be stopped. Reversal depends on the severity of the neuropathy, intensity and duration of the treatment and existence of causative cofactors, but generally the prognosis is good. While waiting for recovery physiotherapy is of importance, and when paraesthesia and pain are troublesome the patient should be treated with carbamazepine, imipramine or lidocaine (lignocaine).

Peripheral Neuropathy Associated with Fluoroquinolones

“…Clarification of these issues is beyond the scope of this survey. For now, it appears that immediate discontinuation is required for patients presenting with fluoroquinolone-related peripheral neuropathies (or CNS or musculoskeletal symptoms), 34 and further antibiotic therapy should be provided from a different antibiotic group. Physicians should be aware that fluoroquinolone-associated events can occur after a single dose.…”

Peripheral neuropathy in patients treated with leflunomide*1

“…Peripheral neuropathy is a well-recognized adverse effect of a variety of medications including chemotherapeutic, antiretroviral, and immunosuppressive agents used to prevent organ transplant rejection. [1][2][3] Neuropathy has also been reported with a number of diseasemodifying antirheumatic drugs, including gold, sulfasalazine, penicillamine, chloroquine, and hydrochloroquine. 1,4 Leflunomide, a disease-modifying drug for the treatment of rheumatoid arthritis (RA), was approved in the United States in September 1998.…”

“…[1][2][3] Neuropathy has also been reported with a number of diseasemodifying antirheumatic drugs, including gold, sulfasalazine, penicillamine, chloroquine, and hydrochloroquine. 1,4 Leflunomide, a disease-modifying drug for the treatment of rheumatoid arthritis (RA), was approved in the United States in September 1998. It is nearly completely metabolized to its active metabolite, which is highly bound (Ͼ99%) to albumin.…”

Effect of leflunomide on the peripheral nerves in rheumatoid arthritis

“…Mononeuritis multiplex and severe distal sensorimotor neuropathies are usually confined to patients with an aggressive form of RA, 16 or with signs of vasculitis. In the past, drug‐induced neuropathies caused by gold, sulfasalazine, penicillamine, chloroquine and hydrochloroquine therapy have also been observed 17–19 …”

“…In the past, drug-induced neuropathies caused by gold, sulfasalazine, penicillamine, chloroquine and hydrochloroquine therapy have also been observed. [17][18][19] The aim of this study was to investigate whether neurophysiological abnormalities in peripheral nerves occur in patients who have commenced leflunomide, the relationship of any changes to symptoms and, if so, whether these changes persist or revert.…”