Communicating information about drug interactions

Abstract

Drug interactions are bread and butter to journals of clinical pharmacology, and their ramifications are varied. In this issue, for example, we publish evidence that clarithromycin increases plasma glibenclamide concentrations, probably by inhibition of P glycoprotein [1]; this presumably explains previous reports of hypoglycaemia in patients taking this combination. In another report, a suspected interaction of fluvoxamine and tizanidine, via inhibition of CYP1A2, caused fatigue, loss of energy, drowsiness, and dizziness; when milnacipran was used instead of fluvoxamine, piloerection occurred and was attributed to α1-adrenoceptor stimulation by endogenous noradrenaline, after re-uptake inhibition by milnacipran [2]. Elsewhere, we learn that artemisinin can induce its own metabolism [3], in what might be regarded as a narcissistic drug interaction; the semiphysiological model that was used to analyse this phenomenon was also of interest.