Open AccessRole of nicotinic acid and nicotinamide in nicorandil‐induced ulcerations: from hypothesis to demonstration
Author(s) -
Trechot Philippe,
Jouzeau JeanYves,
Brouillard Clotilde,
ScalaBertola Julien,
Petitpain Nadine,
Cuny JeanFrançois,
Gauchotte Guillaume,
Schmutz JeanLuc,
Barbaud Annick
Publication year - 2015
Publication title -
international wound journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.867
H-Index - 63
eISSN - 1742-481X
pISSN - 1742-4801
DOI - 10.1111/iwj.12147
Subject(s) - nicorandil , nicotinamide , medicine , nicotinic agonist , pharmacology , nicotinic acids , niacin , anesthesia , biochemistry , enzyme , chemistry , receptor
Nicorandil, a nicotinamide ester, was first reported to be involved in the induction of oral ulcers in 1997. Since then, many reports of single or multiple nicorandil‐induced ulcerations (NIUs) have been reported. We hypothesised that in the case of high‐dosage nicorandil or after an increased dosage of nicorandil, nicotinic acid and nicotinamide (two main metabolites of nicorandil) cannot appropriately merge into the endogenous pool of nicotinamide adenine dinucleotide/phosphate, which leads to abnormal distribution of these metabolites in the body. In recent or maintained trauma, nicotinamide increases blood flow at the edge of the raw area, inducing epithelial proliferation, while nicotinic acid ulcerates this epithelial formation, ultimately flooding the entire scar. We demonstrate, by comparison to a control patient non‐exposed to nicorandil, an abnormal amount of nicotinic acid (×38) and nicotinamide (×11) in the ulcerated area in a patient with NIUs. All practitioners, especially geriatricians, dermatologists and surgeons, must be aware of these serious and insidious side effects of nicorandil. It is critical to rapidly reassess the risk–benefit ratio of this drug for any patient, and not only for those with diverticular diseases.