fusidic acid

Increased risk of statin-induced myopathy, rhabdomyolysis, and acute kidney injury.

Concomitant use is generally contraindicated. If co-administration is unavoidable, fusidic acid should be discontinued, and statin therapy should be temporarily suspended during the course of fusidic acid treatment and for 7 days after the last dose. If statin therapy is essential, consider alternative antibiotics or statins not metabolized by CYP3A4/OATP1B1, or use a significantly reduced statin dose with close monitoring for muscle symptoms and creatine kinase levels.

Increased cyclosporine levels, leading to increased risk of nephrotoxicity, neurotoxicity, and other adverse effects.

Concomitant use should be avoided. If unavoidable, cyclosporine levels must be closely monitored (e.g., daily or every other day) and the dose significantly reduced (e.g., by 50-75%) to maintain therapeutic levels. Monitor renal function and other signs of toxicity.

Increased risk of statin-induced myopathy, rhabdomyolysis, and acute kidney injury.

Concomitant use is generally contraindicated. If co-administration is unavoidable, fusidic acid should be discontinued, and statin therapy should be temporarily suspended during the course of fusidic acid treatment and for 7 days after the last dose. If statin therapy is essential, consider alternative antibiotics or statins not metabolized by CYP3A4/OATP1B1, or use a significantly reduced statin dose with close monitoring for muscle symptoms and creatine kinase levels.

Increased tacrolimus levels, leading to increased risk of nephrotoxicity, neurotoxicity, and other adverse effects.

Concomitant use should be avoided. If unavoidable, tacrolimus levels must be closely monitored (e.g., daily or every other day) and the dose significantly reduced (e.g., by 50-75%) to maintain therapeutic levels. Monitor renal function and other signs of toxicity.

Increased corticosteroid levels, leading to increased risk of Cushing's syndrome, adrenal suppression, and other corticosteroid-related adverse effects.

Monitor for signs of corticosteroid toxicity. Consider reducing the corticosteroid dose during fusidic acid treatment, especially with prolonged co-administration. Taper corticosteroid dose carefully upon discontinuation of fusidic acid.

Increased midazolam levels, leading to enhanced and prolonged sedative effects, respiratory depression.

Avoid concomitant use if possible. If co-administration is necessary, significantly reduce midazolam dose and monitor closely for sedation and respiratory depression. Consider alternative benzodiazepines not metabolized by CYP3A4.

Potential for increased phenytoin levels, leading to increased risk of phenytoin toxicity (e.g., nystagmus, ataxia, lethargy).

Monitor phenytoin levels closely when co-administering with fusidic acid. Adjust phenytoin dose as necessary. Monitor for signs of phenytoin toxicity.

Potential for increased fusidic acid levels (though less clinically significant as fusidic acid has a wide therapeutic index). More importantly, additive CYP3A4 inhibition could lead to increased levels of other co-administered CYP3A4 substrates.

Monitor for increased adverse effects of fusidic acid (e.g., gastrointestinal upset, jaundice) and other co-administered CYP3A4 substrates. Dose adjustments for other CYP3A4 substrates may be necessary.

Increased risk of rosuvastatin-induced myopathy, rhabdomyolysis.

Concomitant use should be avoided if possible. If co-administration is necessary, rosuvastatin dose should be significantly reduced (e.g., 50% reduction) and the patient should be closely monitored for muscle symptoms and creatine kinase levels. Consider temporarily suspending rosuvastatin during fusidic acid treatment.

Increased saquinavir levels, potentially leading to increased adverse effects (e.g., gastrointestinal disturbances, QT prolongation).

Monitor for increased saquinavir adverse effects. Consider saquinavir dose reduction if toxicity occurs. ECG monitoring may be warranted due to potential for QT prolongation.

Increased INR and risk of bleeding. The mechanism is not fully elucidated but clinical cases suggest an interaction.

Monitor INR closely (e.g., daily or every other day) when initiating or discontinuing fusidic acid in patients on warfarin. Adjust warfarin dose as necessary to maintain therapeutic INR. Educate patients on signs of bleeding.

Theoretical risk of reduced efficacy of oral contraceptives, leading to breakthrough bleeding or unintended pregnancy. This interaction is less well-documented for fusidic acid compared to broad-spectrum antibiotics.

Advise patients to use an additional non-hormonal method of contraception during fusidic acid treatment and for 7 days after the last dose, especially if the fusidic acid course is prolonged or if breakthrough bleeding occurs.