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Low-dose zalcitabine-related toxic neuropathy

Frequency, natural history, and risk factors.

From the Departments of Neurology (Drs. Blum, Dal Pan, Cornblath, and McArthur), Medicine (Dr. Feinberg, Mr. Raines, and Ms. Mayjo), and Epidemiology (Dr. McArthur), Johns Hopkins University, Baltimore, MD.
Supported by the National Institutes of Health grants NS26643, AI76234, AI27668, and RR00722.
Presented in part at the 45th Annual Meeting of the American Academy of Neurology, New York, NY, April 25 to May 1, 1993.
Received September 27, 1994. Accepted in final form August 4, 1995.
Address correspondence and reprint requests to Dr Blum, Department of Neurology, Beth Israel Hospital, 330 Brookline Avenue, GZ-522, Boston, MA 02215.

We studied the features and frequency of sensory neuropathy among 79 HIV-1-infected individuals participating in a multicenter clinical trial of zalcitabine (2 prime 3 prime-dideoxycytidine, or ddC) antiretroviral therapy. The trial compared zalcitabine monotherapy (2.25 mg/day) versus combination therapy (2.25 mg/day ddC) with zidovudine (ZDV, formerly AZT) versus monotherapy with ZDV alone. Neuropathy developed in 34% of ddC recipients but in only 4% of comparable patients treated with ZDV alone--a 7.9-fold increase in the attack rate of neuropathy. Using risk factor analysis, we found that diabetes mellitus was significantly associated with the development of toxic neuropathy (p equals 0.02), and weight loss may contribute to its appearance. Like HIV-associated sensory neuropathy, ddC-related toxic neuropathy is a predominantly sensory, length-dependent, symmetric, painful neuropathy. Dose reduction lessened the severity of symptoms, although objective signs of neuropathy persisted. Patients with subclinical neuropathies or significant neuropathy risks such as diabetes may be poor candidates for ddC therapy.

NEUROLOGY 1996;46: 999-1003.

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