Prokinetic agents such as metoclopramide accelerate gastric emptying, shorten time (tmax) to<unk>  peak blood plasma concentration (Cmax), and increase Cmax. Medications slowing gastric emptying such as propantheline and morphine lengthen tmax and decrease Cmax. The interaction with morphine may result in patients failing to achieve the therapeutic concentration of<unk> ; the clinical significance of interactions with metoclopramide and propantheline is unclear. There have been suspicions that cytochrome inducers may enhance the toxic pathway of<unk>  metabolism to NAPQI (see<unk> #Pharmacokinetics). By and large, these suspicions have not been confirmed. Out of the inducers studied, the evidence of potentially increased liver toxicity in<unk>  overdose exists for phenobarbital, primidone, isoniazid, and possibly St John's wort. On the other hand, the anti-tuberculosis drug isoniazid cuts the formation of NAPQI by 70%. Ranitidine increased<unk>  area under the curve (AUC) 1.6-fold. AUC increases are also observed with nizatidine and cisapride. The effect is explained by these drugs inhibiting glucuronidation of<unk> .<unk>  raises plasma concentrations of ethinylestradiol by 22% by inhibiting its sulfation.<unk>  increases INR during warfarin therapy and should be limited to no more than 2 g per week.
Paracetamol
Ketoprofen
Ibuprofen
Ketorolac
Meloxicam
Lornoxicam
Etodolac
Loxoprofen