Long term therapy of cytomegalovirus retinitis with ganciclovir in a child with acquired immunodeficiency syndrome

Abstract

Cytomegalovirus retinitis is the most severe ophthalmological complication of patients with acquired immune deficiency syndrome (aids). Ganciclovir must be given continuously to control progression of the disease or relapse typically occurs. Data in children are limited; this report describes a nine-year-old boy with transfusion-acquired aids who was treated with ganciclovir for 23 months for control of cytomegalovirus retinitis. The retinal disease was exacerbated when ganciclovir was temporarily withheld because of presumed drug toxicity, and improved with re-institution of therapy. When ganciclovir was finally discontinued because of complete loss of vision, the patient rapidly deteriorated and died; widespread cytomegalovirus infection was found at autopsy. Subcapsular cataracts appearing during therapy were thought to be a toxic effect of ganciclovir. Ganciclovir can be effective in controlling cytomegalovirus retinitis in children; however, similarities in laboratory findings may lead to confusion between systemic drug toxicity and disease progression.

Keywords: Acquired immune deficiency syndrome (AIDS); Cataracts; Cytomegalovirus; Ganciclovir; Retinitis.

Figure 1

Ophthalmological findings of CMV infection treated long term with ganciclovir. a Left fundus showing acute necrotizing CMV retinitis before treatment. b After initial treatment, the lesions have almost disappeared leaving behind thinned area of retina with sclerotic vessels. c Right lens showing early vesicular posterior lenticular changes attributable to the chronic use of ganciclovir

Figure 2

Histological involvement with CMV infection (hematoxylin and eosin stain). Top left Endstage calcification (arrow) of the retina reflects severe damage to the eye caused by CMV (60×). Top centre Periventricular destruction associated with giant astrocytes, often with CMV intranuclear inclusions (arrow) (250×). Top right CMV inclusions (arrow) in myocytes of the heart (250×). Bottom left Diffuse alveolar pulmonary damage with CMV inclusion (arrow) (250×). Bottom centre CMV inclusions (arrow) in bowel, probably in endothelium of submucosal capillary (250×). Bottom right Hepatic inclusions (arrow) associated with extensive fatty change, lobular disarray, and degeneration (250×)