Document 0704
 DOCN  M94A0704
 TI    Transient ischaemic attacks (TIAs) in HIV infection.
 DT    9412
 AU    Brew BJ; Miller J; HIV Medicine Unit, St Vincent's Hospital, Australia.
 SO    Annu Conf Australas Soc HIV Med. 1993 Oct 28-30;5:29 (abstract no. TC7).
       Unique Identifier : AIDSLINE ASHM5/94348951
 AB    OBJECTIVE: TIAs in HIV infection may occur as a result of an underlying
       infection or neoplasm and seemingly as a consequence of HIV itself. The
       frequency, clinical characteristics and results of investigations of
       those TIAs that occur independent of an underlying infection or
       neoplasm, however, have not been defined and so we sought to address
       these issues in a prospective survey. METHODS: Cases were defined by the
       following criteria: i) occurrence within a two year period, ii) a CT
       brain scan that showed no abnormality apart from cerebral atrophy, iii)
       occurrence of a neurological deficit lasting less than 24 hours and iv)
       admission to hospital for evaluation of the deficit. A record of such
       cases was kept by one investigator. To ensure that no cases had been
       missed a retrospective analysis of all admissions to the HIV medicine
       unit for the same two year period was undertaken. Those medical records
       where there was a diagnosis of TIA were selected for further study. To
       estimate the frequency of such TIAs the total number of admissions to
       the HIV medicine unit for the same time period was obtained.
       Additionally, to estimate the comparative frequency of TIAs in HIV
       infection the number of patients with TIAs who did not have HIV
       infection for the same time period and age range was obtained. RESULTS:
       Ten cases were identified for the study period an no additional cases
       were found by the retrospective survey. The mean age of the HIV related
       TIAs was 40 +/- 11 and all were male. The admission frequency of HIV
       relate TIAs per year to the HIV medicine unit was 0.6% as opposed to the
       admission rate for age matched non HIV related TIA's to the Neurology
       unit of 0.25%. All but 2 had CD4 counts less than 50. Half had frequent,
       daily TIAs with 2 having alternate side TIAs but none had
       vertebrobasilar territory events. None developed a permanent deficit.
       Seven patients had platelet counts less than 100. Two of 6 patients had
       low protein S levels while none of the 6 had low protein C levels. Four
       of 7 patients had elevated levels of anticardiolpiin antibodies. One
       patient had an echocardiogram showing changes consistent with a
       cardiomyopathy. Six of the ten had moderately severe AIDS dementia
       complex (ADC) and two had mild ADC. In only one patient was there
       resolution no therapy whereas in 5 of the 5 patients who were able to
       commence or resume either zidovudine or didanosine there was resolution
       of the attacks. In the remaining 4 patients the TIAs persisted till
       death. CONCLUSIONS: TIAs are more frequent in HIV infection especially
       in the advanced phase. The TIAs are not associated clinically with
       cerebral infarction but appear to be related to ADC, anticardiolipin
       antibodies and thrombocytopenia. Treatment with antiretrovirals appear
       to lead to resolution of the TIAs.
 DE    Adult  AIDS Dementia Complex/*DIAGNOSIS/DRUG THERAPY  Cerebral Ischemia,
       Transient/*DIAGNOSIS/DRUG THERAPY/ETIOLOGY  Didanosine/THERAPEUTIC USE
       Human  Leukocyte Count  Male  Middle Age  Platelet Count  Prognosis
       Zidovudine/THERAPEUTIC USE  MEETING ABSTRACT

       SOURCE: National Library of Medicine.  NOTICE: This material may be
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