Pantoprazole is an inducer of CYP3A4, but only a weak one. It is not a mechanism based inhibitor of CYP2C9 or CYP3A4, and CYP-related drug interactions have not been observed in clinical use. Should perhaps be used with caution in high dose therapy, e.g. in the treatment of Zollinger Ellison syndrome.

Pantoprazole sodium is a substituted benzimidazole structurally related to esomeprazole, lansoprazole, omeprazole, and rabeprazole. It is a weak base that concentrates under acidic conditions and is then activated by rearrangement to a cationic cyclic sulfenamide.

Pantoprazole is a proton pump inhibitor used in the treatment of gastro-oesophageal reflux disease, peptic ulcer disease, NSAID-associated ulceration, for eradication of Helicobacter pylori or for pathological hypersecretory states such as the Zollinger-Ellison syndrome. It is administered orally or intravenously. Adverse reactions of pantoprazole that can be confused with an acute porphyric attack are diarrhoea, nausea, constipation and abdominal pain.

Pantoprazole is extensively metabolized, mainly via CYP2C19; CYP3A4, CYP2D6, and CYP2C9 isoenzymes metabolize the drug to a much lesser extent. However, no clinically important drug interactions between pantoprazole and other drugs metabolized by the same isoenzymes were identified in clinical studies, and it may have lower potential for drug interactions than lansoprazole and omeprazole (Masubuchi, 1998). Pantoprazole is a competitive inhibitor of both CYP2C9 and CYP3A4 (Li, 2004). Pantoprazole is a weak inducer of CYP1A1, 1A2, and 3A4 (Zhou, 2007; Rendic, 2002; Masubuchi, 1998).

One report of an attack requiring hospitalisation in AIP patient who had been exposed to pantoprazole, but the case report lacks details on the timing of the attack in relation to drug use, and also on other precipitating factors (Kumar, 2010).

Uneventful use reported in 9 patients with acute porphyria.