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Electrophysiological evaluation of 2',3',-dideoxycytidine (ddC) caused polyneuropathy. A follow-up study.

Roick H, von Giesen HJ, Jablonowski H, Arendt G; International Conference on AIDS.

Int Conf AIDS. 1994 Aug 7-12; 10: 201 (abstract no. PB0232).

Department of Neurology & Medicine, Heinrich-Heine-University, Duesseldorf, FRG.

18 HIV-seropositive individuals (5 CDC II, 2 CDC III, 11 CDC IV; age 41.97 +/- 10.41 years) were followed-up by nerve conduction velocity studies and clinical examination before and during an antiretroviral therapy with 2',3',-dideoxycytidine (ddC) (3 * 0.01 mg/kg body weight/day;). The mean follow-up time was 174 days, ranging from 28 to 529 days of ddC therapy. Nerve conduction velocity studies were performed on the ulnar nerve (motor/sensory), the deep peroneal nerve (motor) and the sural nerve (sensory) to find out electrophysiologically detectable deficits of the peripheral nervous system. Results were compared to those of 45 HIV-seropositives without antiretroviral treatment and to those of 46 HIV-seropositives treated with azidothymidine (AZT). The course of HIV-infection was progressive during follow-up time. 2 CDC II and the 2 CDC III individuals entered CDC IV, 1 CDC II entered CDC III. The T4/T8 ratio started with 0.13 +/- 0.08 (0.01-0.26) and decreased to 0.07 +/- 0.06 (0.00-0.16). Before ddC treatment there was electrophysiological evidence of demyelinating sensorimotor polyneuropathy in 1 patient and for axonal sensory polyneuropathy in another one (= 11%). During follow-up 10 patients developed electrophysiologically detectable peripheral nerve deficits: 6 (= 33%) a pure demyelinating sensorimotor polyneuropathy, 3 (= 17%) a mixed axonal-demyelinating sensorimotor polyneuropathy and 1 (= 6%) a pure axonal sensory polyneuropathy. 8 patients (= 44%) became clinically symptomatic of peripheral nerve damage. HIV-seropositives without antiretroviral therapy developed pure demyelinating sensorimotor polyneuropathy in 33% and pure axonal sensorimotor polyneuropathy in 4%. The group treated with AZT showed pure demyelinating polyneuropathy in 23.9%, mixed axonal-demyelinating polyneuropathy in 2.2% and pure axonal polyneuropathy in 2.2%. In summary, ddC-treated patients showed a higher percentage of electrophysiologically detectable axonal nerve damage than AZT or non-treated patients to be accompanied in 44% by clinical symptoms. Further follow-up studies must clarify whether electrophysiologically detectable peripheral nerve deficits are followed sooner or later in every case by clinical symptoms thus would be reason enough to stop antiretroviral treatment with ddC.

Publication Types:
  • Meeting Abstracts
Keywords:
  • Centers for Disease Control and Prevention (U.S.)
  • Demyelinating Diseases
  • Follow-Up Studies
  • HIV Infections
  • HIV Seropositivity
  • Humans
  • Peripheral Nerves
  • Peripheral Nervous System Diseases
  • Peroneal Nerve
  • Polyneuropathies
  • Sural Nerve
  • Zalcitabine
  • Zidovudine
  • etiology
  • methods
  • therapy
Other ID:
  • 94369685
UI: 102208511

From Meeting Abstracts




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