Lansoprazole is metabolized by CYP2C19 and CYP3A4. It is not listed as a mechanism-based inhibitor of CYP enzymes and is not an inducer of CYP1A2 or CYP3A4. Risk for gastrointestinal adverse events in the form of nausea, vomiting and diarrhoea motivates vigilance against insufficient intake of food, especially of carbohydrate.

Pyridylsulphinyl benzamidazole derivative with secondary as well as tertiary amine functions.

Lansoprazole is indicated for the treatment of duodenal and gastric ulcer, gastroesophageal reflux disease, esophagitis, Helicobacter pylori eradication, ventricular hyper secretion and NSAID-associated gastric ulcer. Common side effects of lansoprazole that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack are diarrhoea, nausea and vomiting. Other common side effects are obstipation and abdominal pain.

Lansoprazole is metabolized primarily by CYP2C19 with minor contribution by CYP3A4 (Naritomi 2003 and SPC). In vitro studies have shown that lansoprazole is a weak inhibitor of CYP3A4, 2B6, 2D6, 2C9, 2C8 and 1A2 (Zyvaga 2012). The elimination half-life is 1-2 hours. Co-administration of lansoprazole with tacrolimus, a CYP3A4 substrate and P-gp substrate, increased the AUC of tacrolimus up to 81 % (Itagaki 2004 and SPC). These data may indicate that lansoprazole is an inhibitor of CYP3A4. In vitro data indicates that lansoprazole does not have the potential to be a mechanism-based inhibitor (Zyvaga 2012). Other studies state that it is a competitive inhibitor of CYP2C19 and CYP2C9, a non-competitive inhibitor of CYP3A4 and a mixed inhibitor of CYP2D6 (Ishizaki 1999, Ko 1997 and Li 2004). Lansoprazole is listed as an inducer of CYP3A4 in vitro (Rendic 2002) and in vitro studies have also shown that it can induce CYP1A1 and CYP1A2 (Curi-Pedrosa 1994, Rendic 2002 and Krusekopf 2003). Data from clinical studies indicates that lansoprazole does not induce CYP1A2 activity (Andersson 1998 and Dilger 1999). When lansoprazole was co-administrated with ivabradine, a CYP3A4 substrate, no statistically significant effect was seen on the AUC of ivabradine (Portolés 2006). This may indicate that lansoprazole does not inhibit or induce CYP3A4.

Uneventful use reported in 9 patients with acute porphyria.