Adverse Effects Contraindications and Drug Interactions

The most clinically significant adverse effect of foscarnet is renal impairment. Nephrotoxicity is most likely to occur during the second week of induction therapy but may occur at any time during induction or maintenance therapy. Serum creatinine levels may be elevated in up to 33 to 50% of patients; this effect is usually reversible upon drug discontinuation. Dehydration, previous renal impairment, and concurrent administration of other nephrotoxic drugs increase the risk of renal toxicity. Infusion of fluids along with foscarnet decreases the likelihood of renal impairment to about 12%. Dosage adjustment is required for patients with renal insufficiency.

Foscarnet is also associated with adverse effects on a variety of other organ systems. It may induce changes in serum electrolytes, including hypocalcemia, hy-pophosphatemia, hyperphosphatemia, hypomagne-semia, and hypokalemia. Neurological and cardiovascular signs such as paresthesia, tetany, arrhythmias, and seizures may result from these mineral imbalances. Anemia and granulocytopenia occur fairly commonly but seldom require discontinuation of therapy. Headache, vomiting, and diarrhea also occur with regularity. Genital ulceration has been reported and is likely due to high levels of ionized drug in the urine. While studies in rats indicate a lack of carcinogenicity, cell culture studies suggest a mutagenic effect. The safety of foscarnet during childhood, pregnancy, and lactation has not been established.

Foscarnet should not be used in combination with drugs that cause renal toxicity (e.g., acyclovir, aminoglycosides, amphotericin B, NSAIDs). Abnormal renal function has been noted when foscarnet is used with ri-tonavir or ritonavir and saquinavir. Pentamidine may increase the risk of nephrotoxicity, hypocalcemia, and hypomagnesemia. Caution should be used when foscarnet is given in combination with agents that can cause mineral imbalances.

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