Abstract

The present study aimed to provide an overview of epidemiology, pathogenicity, clinical diagnosis, and treatment of Candida esophagitis in human immunodeficiency virus (HIV)-infected patients. The review process involved studying all the existing literature published on this Candida infection. Esophageal candidiasis (EC) is the most common manifestation of mucosal candidiasis and patients with HIV are predominantly at the risk of this opportunistic infection. The prevalence of EC indicated diverse ranges among HIV patients in different geographic areas due to antiretroviral therapy (ART). The main factors for EC were gastric ulcers, CD4+cell count 400 cells/mL in the ART era. However, a low CD4+ cell count (<200 cells/mL) was significantly associated with EC in the pre-ART era. The interactions between the Candida virulence factor and host immune defense lead to the host responses against this fungal pathogen. During the Candida albicans invasion, secretion of candidalysin which is encoded by the hyphal gene ECE1 has a potential role in epithelial cell damage and secretion of stimulated cytokine. Early trials of the empirical antifungal therapy are recommended before an endoscopic examination. Esophageal biopsy should be considered in patients with a failure of empiric antifungal treatment as it may allow the possibility of drug-resistant Candida and other opportunistic pathogens. The first-line induction treatment of Candida esophagitis is based on oral fluconazole. The shift from C. albicans to non-albicans Candida (NAC) may be correlated with the development of fluconazole resistance and relapse or therapeutic failure in this infection. An increase in the intrinsic and acquired resistance has raised the significance of the optimal antifungal therapy for the critically ill patient. Candida esophagitis requires a systematic suspicion for early diagnosis and appropriate management of HIV infected patients in order to prevent delayed treatment related to undesirable morbidity or even mortality scores.

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