Publication Details
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 When this hormonal support is withdrawn, H. pylori eradication removes the bacterium but leaves the mucosa biologically vulnerable to recurrence and delayed healing.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.