Foscarnet is a structural mimic of the anionpyrophosphate that selectively inhibits the pyrophosphate binding site on viralDNA polymerases atconcentrations that do not affect human DNA polymerases.[11]
In individuals treated with the DNA polymerase inhibitorsacyclovir organciclovir, HSV or CMV particles can develop mutant protein kinases (thymidine kinase or UL97 protein kinase, respectively) that make them resistant to these antiviral drugs.[12][13] However, unlike acyclovir and ganciclovir, foscarnet is not activated by viral protein kinases, making it useful in acyclovir- or ganciclovir-resistant HSV and CMV infections.[5]
However, acyclovir- or ganciclovir-resistant mutants with alterations in viral DNA polymerase may also be resistant to foscarnet.[14][15]
Nephrotoxicity — increase in serum creatinine levels and renal injury can occur in patients receiving foscarnet.[5][16] Other nephrotoxic drugs should be avoided. Nephrotoxicity is usually reversible and can be reduced by dosage adjustment and adequate hydration.[17]
Genitalulceration — a less common reported side effect which occurs more in men and usually during induction use of foscarnet.[5] It is most likely a contact dermatitis due to high concentrations of foscarnet in urine. It usually resolves rapidly following discontinuation of the drug.[20]
^Wagstaff AJ, Bryson HM (August 1994). "Foscarnet. A reappraisal of its antiviral activity, pharmacokinetic properties and therapeutic use in immunocompromised patients with viral infections".Drugs.48 (2):199–226.doi:10.2165/00003495-199448020-00007.PMID7527325.S2CID260483894.
^Ota R, Hirata A, Noto K, Yokoyama S, Hosomi K, Takada M, Matsuoka H (May 2020). "Relationship between serum calcium and creatinine in hematopoietic stem cell transplantation patients treated with foscarnet".International Journal of Clinical Pharmacology and Therapeutics.58 (5):274–281.doi:10.5414/CP203650.PMID32101522.S2CID211537187.
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