Amphotericin B deoxycholate belongs to the polyene class of antifungals. It is also known by the name conventional amphotericin B and has been used for the treatment of invasive fungal infections for more than 50 years. It was first isolated as a natural product of a soil actinomycete.
Newer lipid formulations which are less nephrotoxic as compared with conventional amphotericin B are available. These include:
With the advancement of newer antifungals, such as azoles (voriconazole) and Echinocandins, amphotericin B is typically only reserved for selected invasive fungal infections.
Common indications in yeast and invasive mold infections are listed below:
Dose: The recommended daily dose depends upon the type of infection, the organ involved, the host (immunocompetent versus immunocompromised) and ranges from 0.7 to 1 mg/kg per day over 2 to 4 hours, as tolerated.
When prescribing amphotericin B, one should take into consideration the indication, immune status of the host, and side effect profile. Also, the resistance to amphotericin B remains low for Candida species except for Candida lusitaniae. Aspergillus and opportunistic molds have a more variable susceptibility pattern. Secondary resistance is uncommon and is not usually a clinical problem. Clinicians should consider in vitro susceptibility testing in cases of clinical failure, and when treating pathogens such as Candida lusitaniae, Trichosporon species, Fusarium species, or Psudoallescheria boydii.
Clinicians should recall that amphotericin B exerts a concentration-dependent fungicidal activity against susceptible fungi such as Candida, Cryptococcus, and Aspergillus. It also has a prolonged post-antifungal effect of up to 12 hours.
Amphotericin B acts by binding to ergosterol in the cell membrane of most fungi. After binding with ergosterol, it causes the formation of ion channels leading to loss of protons and monovalent cations. This results in depolarization and concentration-dependent cell killing.
In addition, amphotericin B also produces oxidative damage to the cells with the formation of free radicals and subsequent increased membrane permeability. Additionally, amphotericin B has a stimulatory effect on phagocytic cells which assists in fungal infection clearance.
The half-life of amphotericin is from 24 hours to 15 days.
Amphotericin B is amphoteric (can react as both an acid and a base) and virtually water insoluble. It is not absorbable via oral or intramuscular administration. 
Amphotericin B intravenous (IV) infusion is administered over 2 to 6 hours. If the patient experiences any of the following; fever, hypertension, chills, or nausea, premedication 30 to 60 minutes prior to administration with a combination of acetaminophen/ibuprofen plus diphenhydramine and/or hydrocortisone should be considered. The risk of nephrotoxicity is increased at doses greater than 1 mg/kg, and there is no evidence supporting doses greater than 1.5 mg/kg per day.
Topical use of amphotericin B for peritoneal or bladder wash has been reported in the literature but not recommended. Topical amphotericin B is irritating to the skin; therefore, the decision to use topical amphotericin B should be made based on expert consultation.
Amphotericin B achieves high concentrations in tissue such as liver, spleen, bone marrow, kidney, and lungs. Although concentrations in cerebrospinal fluid (CSF) are low (5% of serum) it is effective in the treatment of fungal infections of the central nervous system (CNS).
A high interindividual variability characterizes the reported pharmacokinetic data in children. Children seem to clear the drug from plasma more rapidly than adults.
About 80% of the patients will develop either infusion-related or renal toxicity. Amphotericin B also interacts with cholesterol in human cell membranes which is responsible for its toxicity. The most common side effects of amphotericin B include:
Absolute contraindications include a history of anaphylactic reaction to amphotericin B.
Before potential administration, drug-drug interactions should be reviewed. Concomitant steroid use should be reconsidered to reduce the risk of hypokalemia. Hypokalemia can also potentiate digoxin toxicity and can cause rhabdomyolysis. Simultaneous infusion of amphotericin B and granulocytes has been associated with acute pulmonary reactions and should be avoided.
The monitoring of amphotericin B levels in the serum or CSF is of little value because the relationships between plasma and tissue concentrations and clinical efficacy or toxicity have not been adequately characterized.
Monitoring is recommended to evaluate for the presence of side effects. Initially, daily electrolyte panel including potassium and magnesium levels until the dose is increased and after that weekly electrolyte levels should be obtained. Potassium levels should be obtained immediately if any signs of hypokalemia such as muscle weakness, cramps, drowsiness, or ECG changes of hypokalemia are seen.
Amphotericin exhibits infusion-related toxicity, which accounts for its extended administration times.
Due to the similarity of mammalian and fungal membranes, which both contain sterols (the therapeutic target for amphotericin), amphotericin can exhibit cellular toxicity.
Healthcare workers including nurse practitioners who prescribe amphotericin should be very familiar on its administration and side effects. Close to 80% of the patients will develop either infusion-related or renal toxicity. All patients must be pretreated with a steroid, an antihistamine and a proton pump inhibitor prior to the infusion. Following infusion, the renal function must be monitored