Bahare Salehi
Given the high mortality rate of invasive fungal infections (IFIs), it appears essential for therapeutic efficacy and safety to receive the proper antifungal exposure. Materials and procedures: In this study, the pharmacokinetic data on systemically administered antifungals with an emphasis on target-site penetration, comorbidities, and combination antifungal therapy are summarised. Discussion and conclusions: Through the urine and faeces, amphotericin B is removed unaltered. Both flucytosine and fluconazole have a low affinity for proteins and are excreted by the kidney. The liver is where itraconazole, voriconazole, posaconazole, and isavuconazole are metabolised. Azoles are implicated in a variety of drug-drug interactions because they are substrates and inhibitors of the cytochrome P450 (CYP) isoenzymes. In the plasma, anidulafungin degrades on its own. CYP is not involved in the enzymatic metabolism of capsofungin or micafungin in the liver. Despite the fact that various drug-drug interactions take place Echinocandins exhibit a lesser likelihood for drug-drug interactions when used in the caspofungin and micafungin treatments. The majority of pertinent tissues can be reached by flucytosine and azoles. Amphotericin B builds up in the spleen and liver. Its concentrations in the brain and myocardium are moderate, whereas those in the kidney and lung are low. Echinocandins have a comparable tissue distribution as amphotericin. For other IFIs such invasive aspergillosis and mucormycosis, such as cryptococcosis, combination antifungal therapy is debatable but has been proven effective for cryptococcosis
KeywordsPolyenes, Amphotericin B lipid formulations, Liposomal amphotericin B, Itraconazole, Voriconazole, Echinocandins, Caspofungin, Critically ill, Renal replacement therapy, Extracorporeal membrane oxygenation.
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