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Nicorandil: a new case of corneal ulceration
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AbstractPurpose To describe a case of corneal ulceration induced by nicorandil.Methods A 78‐year old woman presented a persistant corneal ulceration (RE), resistant to local treatment. She complained of pain and photophobia and visual acuity was 20/125. Slit‐lamp examination revealed epithelial erosion, stroma thinning and folds of Descemet’s membrane. Anterior chamber and fundus examination were normal. Neither mechanical nor infectious local causes explained the lesions. The trigger was most likely a cataract surgery, two months earlier. In her past medical history she reported angor treated by nicorandil for 2 years, treatment that has been suspected to impede corneal healing. With the appointment of her cardiologist we decided to stop nicorandil and observed complete resolution of the symptoms and ulceration after a few weeks.Results Pathogenesis of nicorandil‐induced ulcerations is not yet elucidated. Recently it has been hypothesized that during prolonged high‐dose treatment with nicorandil, or after increased dosage, nicotinic acid (a metabolite) may accumulate outside the endogenous pool of nicotinamide adenine dinucleotide/phosphate and become abnormally distributed. In case of a rather recent or sustained trauma (surgery in our case), nicotinic acid, thanks to nicotinamide, a potassium channel openers with vasodilatator effects, may ulcerate the epithelial proliferation of the edge of the raw area, ultimately flooding the whole scar. The sequence of events of this case strongly suggests a nicorandil‐induced ocular side effect.Conclusion Attention should be paid to the possible ocular iatrogenic role of nicorandil in cases of unexplained corneal ulceration.
Title: Nicorandil: a new case of corneal ulceration
Description:
AbstractPurpose To describe a case of corneal ulceration induced by nicorandil.
Methods A 78‐year old woman presented a persistant corneal ulceration (RE), resistant to local treatment.
She complained of pain and photophobia and visual acuity was 20/125.
Slit‐lamp examination revealed epithelial erosion, stroma thinning and folds of Descemet’s membrane.
Anterior chamber and fundus examination were normal.
Neither mechanical nor infectious local causes explained the lesions.
The trigger was most likely a cataract surgery, two months earlier.
In her past medical history she reported angor treated by nicorandil for 2 years, treatment that has been suspected to impede corneal healing.
With the appointment of her cardiologist we decided to stop nicorandil and observed complete resolution of the symptoms and ulceration after a few weeks.
Results Pathogenesis of nicorandil‐induced ulcerations is not yet elucidated.
Recently it has been hypothesized that during prolonged high‐dose treatment with nicorandil, or after increased dosage, nicotinic acid (a metabolite) may accumulate outside the endogenous pool of nicotinamide adenine dinucleotide/phosphate and become abnormally distributed.
In case of a rather recent or sustained trauma (surgery in our case), nicotinic acid, thanks to nicotinamide, a potassium channel openers with vasodilatator effects, may ulcerate the epithelial proliferation of the edge of the raw area, ultimately flooding the whole scar.
The sequence of events of this case strongly suggests a nicorandil‐induced ocular side effect.
Conclusion Attention should be paid to the possible ocular iatrogenic role of nicorandil in cases of unexplained corneal ulceration.
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