J C Canzano1, J B Reed, L S Morse. 1. Department of Ophthalmology, University of California, Davis, Sacramento 95816-7051, USA.
Abstract
PURPOSE: To report the development of vitreomacular traction syndrome (VMT) following highly active antiretroviral therapy (HAART) in AIDS patients with cytomegalovirus retinitis (CMV-R). METHODS: We identified two AIDS patients with evidence of CMV-R who later developed VMT following HAART-associated immune recovery vitritis. RESULTS: The CD4+ T-lymphocyte count increased from 5 to 190 cells/microL in Patient 1 and from 26 to 713 cells/microL in Patient 2. HIV-RNA copies/mL decreased from 341,000 to less than 400 in Patient 1 and from 43,900 to less than 400 in Patient 2. Increased vitreous inflammation occurred during this period of immune recovery. After resolution of vitritis, VMT developed in both patients and was confirmed by B-scan ultrasound and fluorescein angiography. In both patients, CMV-R was clinically inactive at the time of VMT development. Both patients underwent pars plana vitrectomy with peeling of the posterior hyaloid, which confirmed VMT intraoperatively. CONCLUSIONS: VMT appears to be a sequelae of HAART-associated immune recovery vitritis in AIDS-related CMV-R. Changes in immune status may permit an inflammatory response that can lead to VMT. As advances in pharmacologic intervention continue, clinical manifestations and ocular sequelae in CMV-R will change, as will the approach and management of this disease.
PURPOSE: To report the development of vitreomacular traction syndrome (VMT) following highly active antiretroviral therapy (HAART) in AIDSpatients with cytomegalovirus retinitis (CMV-R). METHODS: We identified two AIDSpatients with evidence of CMV-R who later developed VMT following HAART-associated immune recovery vitritis. RESULTS: The CD4+ T-lymphocyte count increased from 5 to 190 cells/microL in Patient 1 and from 26 to 713 cells/microL in Patient 2. HIV-RNA copies/mL decreased from 341,000 to less than 400 in Patient 1 and from 43,900 to less than 400 in Patient 2. Increased vitreous inflammation occurred during this period of immune recovery. After resolution of vitritis, VMT developed in both patients and was confirmed by B-scan ultrasound and fluorescein angiography. In both patients, CMV-R was clinically inactive at the time of VMT development. Both patients underwent pars plana vitrectomy with peeling of the posterior hyaloid, which confirmed VMT intraoperatively. CONCLUSIONS: VMT appears to be a sequelae of HAART-associated immune recovery vitritis in AIDS-related CMV-R. Changes in immune status may permit an inflammatory response that can lead to VMT. As advances in pharmacologic intervention continue, clinical manifestations and ocular sequelae in CMV-R will change, as will the approach and management of this disease.