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British Journal of Ophthalmology 2001;85:837-841; doi:10.1136/bjo.85.7.837
Copyright © 2001 by the BMJ Publishing Group Ltd.
Br J Ophthalmol 2001;85:837-841 ( July )

CMVR diagnoses and progression of CD4 cell counts and HIV viral load measurements in HIV patients on HAART

Hadi J Zambarakjia, Roger B Newsonb, Suzanne M Mitchella

a Department of Ophthalmology, Chelsea and Westminster Hospital, London, UK, b Department of Epidemiology and Public Health, Division of Primary Care and Population Sciences, Imperial College School of Medicine, London, UK

Correspondence to: Miss Suzanne M Mitchell, Ophthalmology Department, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK s.mitchell{at}doctors.org.uk

Accepted for publication 22 November 2000

AIM---To assess the impact of highly active antiretroviral therapy (HAART) on the prevalence and progression of CMV retinitis (CMVR) among AIDS patients with baseline CD4 cell counts <100 cells × 106/l.
METHODS---A longitudinal cohort study of 1292 patients. CD4 cell counts and HIV viral load measurements were obtained before commencing therapy, at 3 months, 1 year, 2 years, and at last follow up. The CMVR prevalence rate was measured for the subgroup with baseline CD4 cell counts <100 cells × 106/l. CMVR adverse event (AE) rates per 100 person days at risk were calculated for the subgroup with CMVR and baseline CD4 cell counts <100 cells × 106/l.
RESULTS---1292 patients were started on HAART. 8% of patients had CD4 counts <50 cells × 106/l and 40% had detectable HIV viral load at last follow up. The prevalence of CMVR for the subgroup with baseline CD4 <100 cells × 106/l was 10%. For those with baseline CD4 <100 cells × 106/l, the mean CMVR AE rate was greatest during the first 6 months of follow up after HAART commencement (p <0.003). The mean AE rate per 100 person days at risk was 0.36 (95% CI 0.167 to 0.551) before starting HAART, and 0.14 (95% CI 0.085 to 0.199) after starting HAART (p = 0.03).
CONCLUSIONS---HAART significantly prolongs the disease-free intervals in patients with pre-existing disease but recurrences persist within the first 6 months of starting therapy. AE were absent beyond 18 months of follow up in all patients including those with persistently low CD4 counts and detectable HIV viral load indicating clinical immunorestoration. New methods for monitoring the response to therapy are needed to identify those at risk.


© 2001 by British Journal of Ophthalmology

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