Frequency of oropharyngeal candidiasis in HIV-infected patients on protease inhibitor therapy.

OBJECTIVE: The purpose of this study was to investigate the effect of HIV-1 protease inhibitors on the frequency of oropharyngeal candidiasis in HIV-infected patients. STUDY
DESIGN: A clinical and analytic follow-up was carried out to determine the number of episodes of oropharyngeal candidiasis during HIV-1 protease inhibitor therapy and the relation of this incidence to the CD4 lymphocyte count and circulating neutrophils level. Seventy-five HIV-positive patients were selected, and HIV-1 protease inhibitor therapy was administered to each patient over a minimum of 6 months. These patients did not receive long-term preventive antifungal therapy for oral candidiasis, even as secondary prophylaxis against cryptococcosis. Results were compared with those obtained during the previous 6 months, during which patients had been treated only with reverse transcriptase inhibitors.
RESULTS: At least one episode of oropharyngeal candidiasis was seen in 56% (42/75) of patients during reverse transcriptase inhibitor therapy and in only 9.3% (7/75) of patients after the initiation of protease inhibitor therapy. The number of relapses decreased significantly when the 2 follow-up periods were compared (P<.0001). The CD4 and CD8 lymphocyte counts increased significantly with protease inhibitor therapy (P<.001 and P<.05, respectively). During reverse transcriptase inhibitor treatment, the probability of the presentation of oropharyngeal candidiasis correlated with falling CD4 counts (P<.0001). The HIV-1 protease inhibitor therapy was associated with a significant increase in the neutrophil count (P<.01). The probability of the occurrence of some episode of candidiasis correlated inversely with the circulating neutrophil level (P<.05).
CONCLUSIONS: Protease inhibitor therapy decreases the frequency of HIV-related oropharyngeal candidiasis. The mechanism involved is unknown, but it can be speculated that a reduction of the viral load increases the number of intact T helper cells, which in turn enhances the number of circulating polymorphonuclear neutrophils and regulates their function by means of colony-stimulating factors.