Publication Details
Issue: Vol 21, No (2026)
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Abstract

Postpartum Peptic ulcer disease (PUD) affects 5–15% of the global population, with H. pylori implicated in 80–95% of duodenal and 70–90% of gastric ulcers. While eradication therapy effectively eliminates the bacterial aetiology in both sexes, clinical outcomes in postmenopausal women frequently remain suboptimal. The underlying cause is a profound, persistent estrogen deficiency — serum estradiol drops from approximately 197 pg/mL in reproductive-age women to below 33 pg/mL in postmenopause — that compromises multiple mucosal defence mechanisms simultaneously: prostaglandin E2 synthesis, bicarbonate secretion, microvascular regulation, and fibroblast-mediated mucosal repair. Estrogens also exert anti-inflammatory effects by suppressing α-TNF synthesis in immune cells. When this hormonal support is withdrawn, H. pylori eradication removes the bacterium but leaves the mucosa biologically vulnerable to recurrence and delayed healing. A combined pharmacological strategy — targeting both the infectious aetiology and the hormonal deficiency — represents a scientifically grounded advancement in PUD management for this growing patient population. 

Keywords
peptic ulcer disease postmenopause H. pylori eradication hormone replacement therapy estradiol estriol mucosal healing quality of life personalized medicine