Amphotericin-induced stridor: a review of stridor, amphotericin preparations, and their immunoregulatory effects

Various adverse effects have been reported with the use of amphotericin B. The respiratory adverse effects include dyspnea, tachypnea, bronchospasm, hemoptysis, and hypoxemia. Stridor has not been previously reported with the use of amphotericin B. To review the mechanism of action and reports of respiratory adverse effects for amphotericin B, the liposomal preparations of amphotericin B, and the differential diagnosis of stridor. A MEDLINE search from 1966 to 2002 was performed to review the current literature for possible mechanisms and immunoregulatory effects related to the infusion of amphotericin B. Amphotericin B has been shown to increase tumor necrosis factor α (TNF-α) concentrations in macrophages. In addition, it induces prostaglandin E 2 synthesis and increases the production of interleukin 1β (IL-1β) in mononuclear cells. The immunoregulatory effects of amphotericin B include increases in apoptosis, production of monocyte chemoattractant protein 1, superoxide anion, nitric oxide, and intercellular adhesion molecule 1 expression. Amphotericin B induces the production of TNF-α, interferon-γ, and IL-1β, which may potentiate its toxic effects. Some liposomal preparations induced lower levels of TNF-α and nitric oxide and may be useful in patients unable to tolerate amphotericin B deoxycholate.