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-i nfected patients. Study design. A clinical and analytic follow-up was carried out to determin e 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 patient s were selected, and HIV-I protease inhibitor therapy was administered to e ach 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, dur ing which patients had been treated only with reverse transcriptase inhibit ors. 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-u p periods were compared (P < .0001). The CD4 and CD8 lymphocyte counts incr eased significantly with protease inhibitor therapy (P < .001 and P < .05, respectively). During reverse transcriptase inhibitor treatment, the probab ility of the presentation of oropharyngeal candidiasis correlated with fall ing CD4 counts (P < .0001). The HIV-1 protease inhibitor therapy was associ ated with a significant increase in the neutrophil count (P < .01). The pro bability of the occurrence of some episode of candidiasis correlated invers ely with the circulating neutrophil level (P < .05). Conclusions. Protease inhibitor therapy decreases the frequency of HIV-rela ted oropharyngeal candidiasis. The mechanism involved is unknown, but it ca n 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 pol ymorphonuclear neutrophils and regulates their function by means of colony- stimulating factors.