Lipsosomal amphotericin B: a review of its properties, function, and use for treatment of cutaneous leishmaniasis

The genus Leishmania includes a number of protozoan parasites that cause a wide range of infections named leishmaniasis. Leishmaniasis may be appear in three clinical forms — cutaneous (CL), visceral, and mucocutaneous (MCL) — with variation in their presentation and severity: diffuse CL and post–kala-azar dermal leishmaniasis). The prevalent signs of CL are nonhealing ulcers on exposed skin, but infected patients may have other dermatologic symptoms. In the 1960s, amphotericin B deoxycholate was introduced as a second-line therapy for CL and MCL. However, widespread administration of the agent was prevented, due to its renal and systemic toxicity, high price, and obstacles to intravenous use in leishmaniasis-endemic regions. Amphotericin B binds to ergosterol in the photogenic cell membranes and causes changes in membrane permeability, leakage of ions, and finally cell death. Compared to amphotericin B deoxycholate, a higher dose of liposomal amphotericin B should be administered to show the treatment effect. A high percentage of liposomal amphotericin B is “fastened” in the liposome and not biologically effective. Amphotericin B deoxycholate has some toxic effects, and liposomal amphotericin B is meaningfully less toxic compared to it. Treatment options for CL are limited, due to variation in species causing CL and pharmacokinetic issues. Amphotericin B is effective against some particular forms of CL.