Acute Porphyria Drug Database

A10BB07 - Glipizide
Propably not porphyrinogenic
PNP

Rationale
Glipizide is metabolized by CYP2C9. There are no clinical studies indicating that glipizide is an inhibitor or inducer of CYP enzymes. Risk for gastrointestinal adverse events in the form of nausea, vomiting and diarrhoea motivates vigilance against insufficient intake of food, especially of carbohydrate.
Chemical description
sulfonylurea antidiabetic.
Therapeutic characteristics
Glipizide is indicated for the treatment of type 2 diabetes. 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 nausea, vomiting, diarrhoea, obstipation and abdominal pain. A less common side effect is hypoglycaemia, which also may be potentially porphyrinogenic.
Metabolism and pharmakokinetics
Glipizide is metabolized by CYP2C9 (Rogers 2002) and the elimination half-life is 2-4 hours. There are no clinical studies indicating that glipizide is an inhibitor or inducer of CYP enzymes.
Personal communication
C.Andersson; patient reports: tolerated (n=1)
Published experience
Glipizide is listed to have been associated with acute porphyria attacks in humans (Moore 1997).

References

  1. Scientific articles
  2. 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
  3. Rogers JF, Nafziger AN, et al. Pharmacogenetics affects dosing, efficacy, and toxicity of cytochrome P450-metabolized drugs. Am J Med. 2002 Dec 15;113(9):746-50. PMID 12517365. #4357
  4. Summary of Product Characteristics
  5. Norwegian medicines agency. Summary of Product Characteristics (SPC). glipizid. #1111

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