Risk of HIV dementia and opportunistic brain disease in AIDS and zidovudine therapy
a Division of
Neuroscience and Psychological Medicine, Imperial College School of
Medicine, London W6 8RP, UK, b Department of HIV Medicine, Chelsea and
Westminster Hospital, London SW10 9NH, UK
Correspondence to: Dr Torsten Baldeweg, Imperial College School of Medicine, Division of Neuroscience and Psychological Medicine, St Dunstan's Road, London W6 8RP, UK. Telephone 0044 181 846 7343; fax 044 181 846 1670.
Received 22 July 1997 and in revised form 1 December 1997;
Accepted 9 January 1998
OBJECTIVE
To
determine the incidence of HIV dementia and opportunistic brain disease
in AIDS relative to the use of licensed antiretoviral medication
(zidovudine, zalcitabine, didanosine, and stavudine).
METHODMedical records
were evaluated retrospectively in a longitudinal cohort of 1109 patients with AIDS during the period 1991-4. Treatment groups were
defined by start and duration of zidovudine treatment, the drugs used
most often during this period were: (a) no
zidovudine, (b) zidovudine before AIDS,
(c) zidovudine before and after AIDS, and
(d) zidovudine used in AIDS. Main outcome measures were cumulative incidence and survival from AIDS to onset of
HIV dementia, progressive multifocal leukoencephalopathy (PML), cerebral toxoplasmosis, and primary CNS lymphoma.
RESULTSRisk of brain
disease including HIV dementia and opportunistic brain disease was
reduced in patients who started zidovudine before AIDS and continued in
AIDS (relative risk (RR) 0.55, 95% confidence interval (95% CI)
0.36-0.84) as well as zidovudine initiated in AIDS (RR 0.27, 95% CI
0.17-0.45) compared with untreated subjects. Treatment effects were
not constant over time, decreasing by 14%-32% for each six months of
follow up. This was supported by unadjusted incidences across groups
stratified by duration of zidovudine use, indicating reduced risk with
treatment for up to 18 months but not with longer duration of use of
zidovudine. Other antiretroviral drugs had no significant effect,
although these were used by only 14% of patients in this cohort.
CONCLUSIONThe time
limited but effective neuroprotection offered by zidovudine monotherapy
for <18 months suggests that non-specific mechanisms of cerebral
immunological defence may benefit from antiretroviral treatment. Due to
the limitations of a retrospective study these findings require
confirmation and further investigation in the context of current
combination drug treatments.
© 1998 by Journal of Neurology, Neurosurgery, and Psychiatry
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