Mecanismo de ação e toxicidade da anfotericina B no tratamento de micoses

Abstract

The main commercially available antifungal agents have similar mechanisms of action and the main target of these compounds is represented by the fungal cell membrane sterols. Although numerous studies focusing on the development of antifungal drugs are being carried out in recent decades, few agents were available for clinical use in systemic mycoses: amphotericin B, 5-flucytosine, miconazole, ketoconazole, fluconazole, itraconazole, voriconazole, posaconazole and caspofungin. Amphotericin B, the first commercially available systemic antifungal drug, remains the drug of choice in most cases of such infections. Despite the recent introduction of imidazole derivatives of low toxicity and systemic antifungal, amphotericin B is particularly important against invasive fungi in severe disseminated mycosis, especially in immunocompromised patients. Amphotericin B is an antifungal administered intravenously slowly because it is poorly absorbed from the gastrointestinal tract. Amphotericin B interacts mainly with ergosterol, which is the main sterol of fungal plasma membrane, altering the selective permeability by a permeable pores leading to the loss of water and small molecules essential to the survival of the organism, especially potassium ions, ammonium and phosphate. With the progression of injury, also occurs the exit of sugars, esters, nucleotides and proteins. As a result of the disintegration of membrane permeability and metabolic deterioration occurs cell death. This paper presents the mechanism of action of Amphotericin B and its toxicity to the patient's body.