Document 2890
 DOCN  M94A2890
 TI    Electrophysiological evaluation of 2',3',-dideoxycytidine (ddC) caused
       polyneuropathy. A follow-up study.
 DT    9412
 AU    Roick H; von Giesen HJ; Jablonowski H; Arendt G; Department of Neurology
       & Medicine, Heinrich-Heine-University,; Duesseldorf, FRG.
 SO    Int Conf AIDS. 1994 Aug 7-12;10(1):201 (abstract no. PB0232). Unique
       Identifier : AIDSLINE ICA10/94369685
 AB    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.
 DE    Comparative Study  Demyelinating Diseases/CHEMICALLY
       INDUCED/COMPLICATIONS/  PHYSIOPATHOLOGY  Follow-Up Studies  Human  HIV
       Infections/COMPLICATIONS/*DRUG THERAPY  Neural Conduction  Peripheral
       Nervous System Diseases/*CHEMICALLY INDUCED/
       COMPLICATIONS/PHYSIOPATHOLOGY  Sensation Disorders/CHEMICALLY
       INDUCED/COMPLICATIONS/  PHYSIOPATHOLOGY  Treatment Outcome
       Zalcitabine/*ADVERSE EFFECTS/THERAPEUTIC USE  Zidovudine/ADVERSE
       EFFECTS/THERAPEUTIC USE  MEETING ABSTRACT

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