THE UVEOVASCULAR BARRIER IN HIV-ASSOCIATE D RETINAL MICROANGIOPATHY

Citation
M. Kiener et al., THE UVEOVASCULAR BARRIER IN HIV-ASSOCIATE D RETINAL MICROANGIOPATHY, Klinische Monatsblatter fur Augenheilkunde, 212(5), 1998, pp. 345-349
Citations number
23
Categorie Soggetti
Ophthalmology
Journal title
Klinische Monatsblatter fur Augenheilkunde
ISSN journal
00232165 → ACNP
Volume
212
Issue
5
Year of publication
1998
Pages
345 - 349
Database
ISI
SICI code
0023-2165(1998)212:5<345:TUBIHD>2.0.ZU;2-9
Abstract
Background HIV-associated retinal microangiopathy is understood as a s ign of uveovascular barrier breakdown and associated with an increasin g risk to develop opportunistic infections. Hence no controled studies have been available, the underlying study was undertaken to validate this clinical impression. Patients and Methods HIV-positive patients w ith or without clinical signs of retinal angiopathy were included into this study and followed up longitudinally with fotodocumentation, las er-flare and, sporadically, fluorescein angiography to quantify the di sturbance of their uveovascular barrier. The data were correlated to t he CD4 cell counts and the development of opportunistic infections. Re sults 104 patients have been included into-one of four groups: patient s without signs of ocular vascular disease (group 1, n = 46), with new ly diagnosed HIV-associated microangiopathy (group 2, n = 37), with an giopathy for more than six months (group 3, n = 16), and with viral re tinitis (group 4, n = 5). We found no difference in the flare between patients with and without angiopathy (p = 0.3), but a significant incr ease after the development of retinitis (p < 0.001). In contrast, the presence and duration of angiopathy were associated with a reduction i n CD4 cell counts (p = 0.03). Using fluorescein angiography, we found vascular occlusions on the capillary level without leakages correspond ing to a not relevant disruption of the retinovascular barrier. Conclu sions In HIV-associated retinal microangiopathy, there exists no relev ant disturbance of the uveovascular barrier. The association of angiop athy with a reduction of CD4 cells is more likely a sign of immuncompl ex-associated rather than infectious etiology. The analysis of drug ef fects on the course of angiopathy during a recovery of the cellular im munity will provide further etiological information in the progress of this study.