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207 - Antifungal therapy
- from Part XXV - Antimicrobial therapy: general considerations
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- By Nathan P. Wiederhold, University of Texas Health Science Center, Thomas F. Patterson, University of Texas Health Science Center
- Edited by David Schlossberg, Temple University, Philadelphia
-
- Book:
- Clinical Infectious Disease
- Published online:
- 05 April 2015
- Print publication:
- 23 April 2015, pp 1344-1352
-
- Chapter
- Export citation
-
Summary
This chapter focuses on the use of drugs that treat systemic mycoses (Table 207.1). Treatment of cutaneous fungal infections is discussed in Chapter 26, Superficial fungal diseases of the hair, skin, and nails.
AMPHOTERICIN B
Amphotericin B is a polyene antifungal synthesized by Streptomyces nodosus. Its chemical structure confers it with amphoteric properties that are essential for the drug’s ability to form channels through the cytoplasmatic membrane. The pores formed from preferential binding of amphotericin B to ergosterol, the primary fungal cell sterol, result in an increase in membrane permeability, leading to a loss of essential elements such as potassium and other molecules that impairs fungal viability. Amphotericin B binds with less affinity to cholesterol, the primary cell sterol of mammalian cells, which are therefore less affected by amphotericin B than is the fungal target.
Amphotericin B is commercially available as a complex with sodium deoxycholate: commercial vials contain amphotericin B, 50 mg, sodium deoxycholate, 41 mg, and a sodium phosphate buffer, 25.2 mg. The clinical pharmacology of amphotericin B is characterized by extensive binding to plasma proteins (>95%) and wide distribution to the peripheral compartment with preferential accumulation in liver and spleen, with lesser amounts in kidney and lung. Intravenous administration of therapeutic doses results in peak plasma levels of 1.0 to 1.5 μg/mL falling to 0.5 to 1.0 μg/mL 24 hours later. At therapeutic doses, less than 5% of the drug is excreted in the urine. The elimination of amphotericin B is not altered in patients with renal or liver dysfunction and does not require dose adjustment in patients who are anephric or undergoing hemodialysis.
204 - Antifungal Therapy
- from Part XXV - Antimicrobial Therapy – General Considerations
-
- By Nathan P. Wiederhold, The University of Texas at Austin, Thomas F. Patterson, University of Texas Health Science Center at San Antonio
- Edited by David Schlossberg
-
- Book:
- Clinical Infectious Disease
- Published online:
- 05 March 2013
- Print publication:
- 12 May 2008, pp 1423-1432
-
- Chapter
- Export citation
-
Summary
This chapter focuses on the use of drugs that treat systemic mycoses (Table 204.1). Treatment of cutaneous fungal infections is discussed in Chapter 25, Superficial Fungal Infection of the Hair, Skin, and Nails.
AMPHOTERICIN B
Amphotericin B is a polyene antifungal synthesized by Streptomyces nodosus. Its chemical structure confers it with amphoteric properties that are essential for the drug's ability to form channels through the cytoplasmatic membrane. The pores formed from preferential binding of amphotericin B to ergosterol, the primary fungal cell sterol, result in an increase in membrane permeability, leading to a loss of essential elements such as potassium and other molecules that impairs fungal viability. Amphotericin B binds with less affinity to cholesterol, the primary cell sterol of mammalian cells, which are therefore less affected by amphotericin B than is the fungal target.
Amphotericin B is commercially available as a complex with sodium deoxycholate: commercial vials contain amphotericin B, 50 mg, sodium deoxycholate, 41 mg, and a sodium phosphate buffer, 25.2 mg. The clinical pharmacology of amphotericin B is characterized by extensive binding to plasma proteins (>90%) and wide distribution to the peripheral compartment with preferential accumulation in liver and spleen, with lesser amounts in kidney and lung. Intravenous administration of therapeutic doses results in peak plasma levels of 1.0 to 1.5 μg mL falling to 0.5 to 1.0 μg mL 24 hours later. At therapeutic doses, less than 5% of the drug each dose is excreted in the urine.