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Editor,—Cytomegalovirus (CMV) retinitis predominantly occurs in severely immunocompromised patients with CD4+ counts below 50 cells ×106/l. Before the use of combinations of protease inhibitors and other antiretroviral agents, CMV retinitis invariably progressed in the absence of specific anti-CMV therapy. This highly active antiretroviral therapy (HAART) can decrease human immunodeficiency virus (HIV) load and increase CD4 T cell counts in patients with AIDS.1 2 In this study we describe two patients receiving HAART, who present with probable inactive CMV retinitis although they never received anti-CMV therapy. In one of these patients, CMV retinitis recurred shortly after his CD4+ cell counts fell below 50 cells ×106/l despite continued combination antiretroviral therapy.
Patient No 1
A 28 year old man with AIDS and a history of one positive blood culture for CMV and a CD4+ cell count of 13 cells ×106/l was placed on ritonavir, zidovudine, and lamivudine in April 1996. Within 2 months the CD4+ cell count increased to 65 cells ×106/l and the patient developed blurred vision and floaters in his left eye. Examination of the left eye revealed mild vitritis and a large area of retinal atrophy with several small haemorrhages at the border, consistent with inactive CMV retinitis (Fig1). The right eye was normal. He was placed on no anti-CMV therapy. The haemorrhages resolved and no new progression of the retinitis was observed.
In January 1997 the patient’s CD4+ cell count fell to 21 cells ×106/l despite continued combination antiretroviral therapy. Eye examination revealed active CMV retinitis in the right eye; the retinal scar in the left eye remained unchanged. The patient was treated with intravenous ganciclovir and the CMV retinitis became inactive.
Patient No 2
A 44 year old white man with AIDS had a CD4+ cell count of 25 cells ×106/l and no evidence of CMV retinitis on serial eye examinations. Combination antiretroviral therapy with saquinavir, zidovudine, and lamivudine was begun in March 1996 and 1 month later the patient developed a temporal scotoma in his left eye. Examination of the left eye showed mild anterior uveitis, vitritis, and a large area of retinal atrophy in the nasal midperiphery consistent with inactive CMV retinitis (Fig 2). The area of inactive retinitis has remained stable over the past 12 months despite the fact that he has received no anti-CMV therapy. A CD4+ T cell count in October 1996 was 111 cells ×106/l.
We describe two patients who presented with mild uveitis and an area of retinal atrophy consistent with inactive CMV retinitis despite never having received specific anti-CMV therapy. Both patients had prior CD4+ cell counts below 50 cells ×106/l , and each experienced an elevation to above 50 cells ×106/l in response to combination antiretroviral therapy concurrent with the onset of their symptoms. We hypothesise that these patients developed subclinical CMV retinitis in the setting of severely suppressed CD4+ T cell counts, but became symptomatic when HAART induced elevations of their CD4+ cell counts enhanced the immune response to CMV. This led to the development of a significant and symptomatic uveitis, a finding uncommon in patients with CMV retinitis before the use of HAART. These observations support the notion that HAART induced restoration in immune function can lead to spontaneous and sustained resolution of CMV retinitis. The fact that patient no 1 developed reactivation of CMV retinitis soon after his CD4+ T lymphocyte count fell below 50 cells ×106/l supports the initial diagnosis of CMV retinitis. Additionally, CD4+ cell counts may continue to provide valuable information regarding the risk of reactivation of opportunistic infections in patients receiving HAART. These findings are in accordance with recent publications addressing the relation between protease inhibitors and sustained inactivity of CMV retinitis.3 4 Additional studies are required to further delineate the role of HAART and CD4+ cell counts in the natural history of CMV retinitis.