Rantidine is re-classified as PNP. Ranitidine appears to only minimally inhibit hepatic metabolism of some drugs. No observations pointing to clinical CYP induction. The drug maufacturing companies and some national formularies warn against the use of Ranitidine in acute porphyria based on a few case reports. The references indicate that an attack has been associated with Ranitidine, but the clinical data question the causality of this observation. There are uneventfull clinical experiences (n=10), which points to non-porphyrinogenicity.

Aminoalkylfurane. Unlike cimetidine, ranitidine contains an aminoalkyl-substituted furan ring rather than an imidazole ring.

Histamine-receptor antagonist used in peptic ulcer and gastro-oesophageal reflux. Oral and intravenous administration.

Significant.

Substrate of CYP1A2, 2C19 and 2D6. Weak CYP 1A2 inhibitor. Inhibitor of augmented CYP-mediated metabolism. Following oral administration, the drug undergoes extensive first-pass metabolism. About 10% of the given dose is excreted as inactive metabolites and the remaining is excreted as unmetabolized ranitidine. The metabolites are N-oxide, S-oxide, and desmethylranitidine; the N-oxide is the major metabolite but accounts for only about 4 to 6% of a dose. About 30% of an oral dose and 70% of an intravenous dose is excreted unchanged in the urine in 24 hours, primarily by active tubular secretion; there is some excretion in the faeces too. Since ranitidine interacts with the hepatic cytochrome P-450 (microsomal) enzyme system differently than does cimetidine, ranitidine appears to only minimally inhibit hepatic metabolism of some drugs (e.g., coumarin anticoagulants, theophylline, diazepam, propranolol). Ranitidine forms a ligand complex with the cytochrome P-450 enzyme system; however, ranitidine appears to interact with different forms of cytochrome P-450 than does cimetidine. The affinity of ranitidine for cytochrome P-450 is about 10% that of cimetidine and the extent of inhibition of the enzyme system is about 2.4 times less than that with cimetidine. Inhibition of hepatic microsomal enzyme activity appears to be structurally determined rather than associated with H2-receptor blockade, since ranitidine and cimetidine differ substantially in their effects on this enzyme system.

Used in Swedish Porphyria wards. Patient reports : tolerated (n=2). Used by 1 AIP patient with unknown susceptibility , Norway.

Uneventful use reported in 24 patients with acute porphyria.