Citalopram × Fluconazole

Fluconazole prolongs QT by directly blocking the Ikr potassium current, in the words of its SmPC, which also contraindicates QT-prolonging drugs metabolised through CYP3A4. The citalopram SmPC lists ongoing treatment with any drug capable of prolonging the QT interval among its contraindications, with no exceptions. Kinetics adds a second layer: fluconazole inhibits CYP2C19, the main path for citalopram. The citalopram SmPC caps the dose at 20 mg a day in poor CYP2C19 metabolisers, and an enzyme inhibitor turns any patient into one.

QTc prolongation on ECG, palpitations, dizziness, syncope. The end point is polymorphic ventricular tachycardia of the torsade type progressing to ventricular fibrillation. The risk is higher with hypokalaemia, hypomagnesaemia, bradycardia, decompensated heart failure and in women.

The pair sits in the citalopram SmPC contraindications, so the question is which drug stays, not how far to cut the dose. In superficial mycoses topical forms give almost no systemic absorption and the question disappears. In systemic mycosis an echinocandin is chosen: caspofungin, micafungin or anidulafungin. Swapping fluconazole for another azole does not solve the problem, because the voriconazole and posaconazole SmPCs also describe QTc prolongation. If the pair continues anyway, potassium, magnesium and QTc stay under watch.