Antifungal Prophylaxis in Pancreas Transplant Recipients?

Robert J. Stratta, MD

Disclosures

August 05, 2002

Question

What are your recommendations for antifungal prophylaxis in pancreas transplant recipients?

Professor Alfonso Navarro

Response from Robert J. Stratta, MD

Pancreas transplant recipients have an intermediate risk of fungal infections when compared with kidney and liver transplant recipients. Because all pancreas transplant recipients are by definition diabetic, receive anti-T-cell therapy, and undergo an intraperitoneal procedure usually with enteric drainage, the inherent risk of fungal infection after pancreas transplantation is higher than in kidney transplantation, but lower than in liver transplantation. There are no specific recommendations for antifungal prophylaxis after pancreas transplantation, but most centers follow some basic guidelines.

If one could adequately prep the bowel prior to transplant, the risk of fungal infection would be lower because most fungal infections are due to Candida spp. that reside as normal commensals in the gastrointestinal (GI) tract. However, in practice, this is logistically difficult and diabetic patients with enteropathy are not infrequently either intolerant of or unresponsive to vigorous bowel preps. Even in pancreas transplants with bladder drainage, reducing Candida colony counts in the GI tract would be helpful. Most of these patients are managed with nasogastric tubes, which further permits candidal colonization and contamination. In addition, prolonged antibiotic therapy and prolonged use of indwelling lines or catheters places patients at higher risk. Consequently, I recommend using only a first-generation cephalosporin for 24 hours for surgical antibiotic prophylaxis and routine administration of oral fluconazole 200 mg/day for a total of 2 months. A side effect of fluconazole is increased tacrolimus and cyclosporine levels, which can be difficult to maintain in the early postoperative period in the diabetic patient with gastroparesis and enteropathy. It is important to monitor drug levels closely when stopping fluconazole, and we typically double the dose of the calcineurin inhibitor when we discontinue fluconazole.

Most fungal infections occur in the first month after transplantation, hence the rationale for stopping prophylaxis at 2 months. If the patient undergoes a reoperation, is treated for rejection, or is treated for a bacterial or viral infection, then we continue fluconazole prophylaxis for an additional 2 months. If the patient is receiving an anticonvulsant drug or some other strong hepatic microsomal enzyme inducer, then we continue the fluconazole indefinitely in order to maintain calcineurin inhibitor levels, or switch to some other strong hepatic enzyme inhibitor (ie, erythromycin, diltiazem).

I have little experience with (or confidence in) nystatin and clotrimazole as effective agents in pancreas transplant recipients, although we use these agents routinely after kidney transplantation. The newer antifungal agents (itraconazole, caspofungin) and amphotericin preparations are not indicated unless Aspergillus is identified. Probably one of the most important points is to avoid prolonged use of broad-spectrum antibiotics and to remove indwelling devices in a timely fashion. With fluconazole prophylaxis, our incidence of fungal infection after pancreas transplantation has been extremely low.

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