Vistide was approved for the treatment for CMV retinitis in subjects with AIDS.
Vistide is known to have a much longer duration of activity than other antiviral treatments and therefore requires less frequent dosing. Vistide was administered in clinical studies only once every other week after a two-dose induction and does not require a chronic catheter for administration.
This approval was based upon data from two pivotal studies demonstrating that Vistide delays the time to progression of CMV retinitis. These studies were conducted in subjects with CMV retinitis and AIDS. One study enrolled newly diagnosed subjects who had not received prior CMV treatment and the other study enrolled subjects with relapsing disease that had progressed despite extensive treatments with other intravenous therapies for CMV retinitis.
A third clinical study of Vistide is being conducted by an independent NIH-sponsored research group, the Studies of Ocular Complications of AIDS (SOCA). In March 1996, enrollment of new subjects in this study was stopped based upon an interim analysis of safety and efficacy data suggesting Vistide delayed the time to progression of CMV retinitis.
The major toxicity of Vistide is renal impairment. The potential for nephrotoxicity can be minimized with the administration of probenecid tablets and hydration on the day of each Vistide infusion. In addition, laboratory measurements of a subject's urine protein and serum creatinine, a blood marker of kidney function, are monitored before each dose of Vistide. Proper use of these tests can guide physicians to adjust the Vistide dosage and minimize the potential for toxicity.
CMV retinitis is caused by a viral infection that, if untreated progresses rapidly, affects a subject's vision over time, and may ultimately lead to blindness. It is estimated that up to 40% of subjects with AIDS may develop retinitis and that 95% of subjects with AIDS are infected with CMV. As people with AIDS live longer, the incidence of CMV retinitis has been increasing.
When CMV invades the retina, lesions form on the light-sensitive layer of cells at the back of the eye that transmit images to the brain. As these CMV lesions progress, the subject’s vision deteriorates over time.