Dr. Bhattacharyya further said that the real reason amphotericin B is controversial is because there’s a lot more to be learned about the pathophysiology and the mechanism of action of amphotericin B. Also, the underlying evidence for fungi as the cause-complete for CRS is actually weak. If you look at detailed studies, you can find people who have evidence of an allergic sensitivity to the fungus, but no symptoms.
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March 2008
Another component, he said, is that there is evidence that amphotericin B as a chemical agent alone is an anti-inflammatory, meaning that it may be working on the inflammation in chronic rhinosinusitis but not killing fungus.
On the plus side, Dr. Bhattacharyya said amphotericin B is a relatively low-toxicity agent when applied topically. I see little downside in trying this as one modality of therapy for patients who are medically refractory, he said, adding that it might be a good choice for patients who have already had surgery (surgery that allows the drug to reach the surface of the sinus cavities more directly). I do have a subset of patients who have benefited from it. But, I’ve also had patients who have not.
About Amphotericin B
An antifungal treatment-specifically, amphotericin B-was chosen by the Mayo Clinic and later tested by others for efficacy in treating CRS. Originally extracted from the filamentous bacterium Streptomyces nodosus, amphotericin B is used to kill fungus that can cause serious or life-threatening infections, but it is not effective against bacterial infections or viruses. Although administration of the drug can cause side effects-some potentially severe-the small amount used as a lavage to kill noninvasive fungus in the nose and sinus cavities is considered much safer. It has low systemic absorption, with less than 5% systemic absorption across mucous membranes. As its mechanism of action, amphotericin B binds to sterols-preferentially to the primary fungal cell membrane sterol, ergosterol-disrupting osmotic integrity of the fungal membrane. The result is leakage of intracellular potassium, magnesium, sugars, and metabolites, followed by cellular death.
©2008 The Triological Society
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