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Cardiopulmonary Toxicity after Liposomal Amphotericin B Infusion

Stewart J. Levine, MD; Thomas J. Walsh, MD; Anthony Martinez, MD; Peter Q. Eichacker, MD; Gabriel Lopez-Berestein, MD; and Charles Natanson, MD
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Requests for Reprints: Stewart J. Levine, MD, Critical Care Medicine Department, National Institutes of Health, Building 10, Room 10D48, 9000 Rockville Pike, Bethesda, MD 20892.

Current Author Addresses: Drs. Levine, Martinez, Eichacker, and Natanson: Critical Care Medicine Department, Warren G. Magnuson Clinical Center, National Institutes of Health, Building 10, Room 10D48, Bethesda, MD 20892.

Dr. Walsh: Infectious Diseases Section, Pediatric Branch, National Cancer Institute, National Institutes of Health, Building 10, Room 13N240, Bethesda, MD 20892.

Dr. Lopez-Berestein: Section of Immunobiology and Drug Carriers, Division of Medicine, The University of Texas M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030.

Ann Intern Med. 1991;114(8):664-666. doi:10.7326/0003-4819-114-8-664
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This excerpt has been provided in the absence of an abstract.

Liposomal and lipid-complex drug delivery systems are being developed to enhance the therapeutic activity, decrease the toxicity, and provide site-specific delivery of high doses of amphotericin B (1-3). Incorporation within liposomes is thought to produce lipid-stabilized, ribbon-like amphotericin B aggregates that may decrease toxicity by allowing selective transfer of the drug directly to ergosterol-containing fungal cell membranes (4). Toxic reactions associated with liposomal amphotericin B (L-AmpB) therapy in humans have included fever, chills, nausea, and electrolyte disturbances (5-7). This report supplements the known toxicities by describing reversible abnormalities in pulmonary gas exchange and cardiopulmonary hemodynamics in a patient receiving high-dose


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