Acute Porphyria Drug Database

M01CB03 - Auranofin
Propably not porphyrinogenic
PNP

Rationale
Auranofin is most probably not an inhibitor or inducer of CYP enzymes. Risk for gastrointestinal adverse events in the form of abdominal pain and diarrhoea motivates vigilance against insufficient intake of food, especially of carbohydrate.
Therapeutic characteristics
Auranofin is indicated for the treatment of rheumatoid arthritis. Common side effects that can be potentially porphyrinogenic through reduction in carbohydrate intake and that also can be confused with an acute porphyria attack are abdominal pain and diarrhoea.
Metabolism and pharmakokinetics
About 25% of a given dose of auranofin is absorbed (Gottlieb 1986 and SPC). 40% of the absorbed dose is excreted in faeces and 60% is excreted in urine. Half-life elimination is 15-30 days with big individual differences. No drug-drug interactions with auranofin as a perpetrator are observed (Interaksjoner and Interaktionsdatabasen), which may indicate that auranofin is not an inhibitor or inducer of CYP enzymes.
Published experience
Auranofin is listed to have been associated with acute attacks of porphyria (Moore 1997).

References

  1. Scientific articles
  2. Gottlieb NL. Pharmacology of auranofin: overview and update. Scand J Rheumatol Suppl. 1986;63:19-28. PMID 3110942. #2390
  3. Moore MR, Hift RJ. Drugs in the acute porphyrias--toxicogenetic diseases. Cell Mol Biol (Noisy-le-grand). 1997 Feb;43(1):89-94. PMID 9074793. #1110
  4. Drug interaction databases
  5. Interaksjoner. Auranofin #2391
  6. Interaktionsdatabasen. Auranofin #2392
  7. Summary of Product Characteristics
  8. Swedish National Formulary. FASS. Summary of Product Characteristics (SPC). Auranofin. www.fass.se #2393

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