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GE-Portuguese Journal of Gastroenterology

versão impressa ISSN 2341-4545versão On-line ISSN 2387-1954

Resumo

SIMAS, Diogo et al. Olmesartan-Induced Gastropathy: An Important Cause to Think about in Refractory Peptic Ulcer Disease. GE Port J Gastroenterol [online]. 2025, vol.32, n.4, pp.62-66.  Epub 19-Dez-2024. ISSN 2341-4545.  https://doi.org/10.1159/000543202.

Background:

Angiotensin receptor blockers are a pharmacological class widely used as antihypertensive therapy. Recently, a relationship between these agents and gastrointestinal disease has been described, namely, enteropathy, gastropathy, and microscopic colitis. The mechanism is unknown, but it is thought that a cell-mediated immune reaction is involved and does not appear to be a class effect. Treatment consists of stopping the drug and rechallenge can confirm the diagnosis.

Case Presentation:

An 85-year-old man with a history of hypertension treated with olmesartan/hydrochlorothiazide for 12 years presented to the emergency department with months of epigastric pain, without vomiting, blood loss, diarrhea, or weight loss. A recent upper gastrointestinal endoscopy (UGE) showed congested mucosa, irregular erosions, and friability in the distal body, notch, and antrum. Histology revealed moderate chronic gastritis, severe inflammatory activity, abundant eosinophils, intestinal metaplasia with low-grade dysplasia, and marked atrophy, with no signs of malignancy or Helicobacter pylori (Hp). The patient had previously been treated by his family doctor with lansoprazole and sucralfate, without improvement, and was subsequently discharged on esomeprazole with a referral for a gastroenterology consultation. Three months later, a follow-up UGE showed persistent erosions despite good adherence to esomeprazole. Hp serology was positive, and the patient was started on bismuth-based quadruple therapy. A post-treatment urea breath test confirmed Hp eradication. Six months later, UGE still showed multiple ulcers in the distal body and antrum. Olmesartan was switched to lisinopril, and after another 6 months, a follow-up UGE showed no ulcers or erosions. Biopsies revealed reduced inflammation and no dysplasia, indicating histological improvement. Olmesartan-induced gastropathy was diagnosed.

Conclusions:

This case report illustrates olmesartan-induced gastropathy, an important diagnosis to consider in cases of non-Hp gastritis and refractory peptic ulcer disease.

Palavras-chave : Angiotensin receptor blockers; Refractory peptic ulcer disease; Drug-induced gastropathy.

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