RISK-FACTORS FOR DIDEOXYNUCLEOSIDE-INDUCED TOXIC NEUROPATHY IN PATIENTS WITH THE HUMAN-IMMUNODEFICIENCY-VIRUS INFECTION

Dideoxynucleosides induce a dose-related toxic neuropathy; however, th ere is a paucity of information on whether other risk factors influenc e the development of neuropathy. We reviewed the records of 103 patien ts at an AIDS Clinical Trials Unit who were taking didanosine and/or z alcitabine to determine the risk factors for dideoxynucleoside-induced toxic neuropathy. Most were homosexual or bisexual (85%) men with a m ean age of 39 years. The median CD4(+) lymphocyte count was 59 cells/m m(3), and 35% had a previous diagnosis of AIDS. Toxic neuropathy was m ore common in patients taking zalcitabine compared with those taking d idanosine (14 of 51 versus seven of 55, p = 0.08). In the patients who took zalcitabine, those who had a low baseline serum cobalamin level, a history of heavy ethanol consumption, or a history of symptoms of p eripheral nerve dysfunction were more likely to develop a toxic neurop athy (10 of 14 versus 12 of 37, p = 0.01). Conversely, there were no f actors associated with the development of didanosine-induced toxic neu ropathy. Dideoxynucleoside-induced toxic neuropathy is a common proble m that can be disabling but is usually reversible. A history of sympto ms of peripheral nervous system disease, heavy ethanol consumption, or a low serum cobalamin level may be useful in distinguishing patients at higher risk of developing zalcitabine-induced toxic neuropathy.