Does the declining prevalence of Helicobacter pylori unmask patients with idiopathic peptic ulcer disease? Trends over an 8 year period

Abstract

The prevalence of patients with H. pylori negative ulcer disease significantly decreased in our study population due to an increase in the number of patients with NSAID associated peptic ulcer disease. IPUD was rare and its prevalence did not increase over a period of 8 years.

Etiological factors of duodenal and gastric ulcers

“…Table 3. Histology findings of the biopsy samples: according to the updated Sydney system (12) While incidence of PUD associated with Hp infection is decreasing, especially in western countries (5,7,8), in our country, the most common cause is Hp (76%). It may be associated with the fact that Hp prevalence remains an important health problem in our country, and prevalence in the community is very high.…”

“…The rate of patients classified as idiopathic (Hpnegative, NSAID-negative) was reported as 4%-20% (5,8,17). Among 140 patients, 19 (13%) were Hp-and NSAID-negative.…”

Helicobacter pylori—Associated Dyspepsia in Paediatrics

“…Population-based studies in patients with organic dyspepsia suggest that peptic ulcer disease related to H. pylori infection is decreasing in prevalence in Western countries, along with a decrease in the prevalence of infection [94]. The former should be a direct consequence of the second; with improved living standards, cohorts of children became progressively less likely to acquire the organism and thus suffer from H. pylori-associated diseases.…”

Telomere shortening is associated with reduced duodenal HCO3−secretory but normal gastric acid secretory capacity in aging mice

“…However, the ratios of cystic fibrosis transmembrane conductance regulator (CFTR) and solute-linked carrier 26 gene family (Slc26a6) mRNA expression in relation to cytokeratin-18 were not altered in duodenal mucosa. The further knockout of p21, which is a downstream effector of telomere shortening-induced senescence, rescued villus atrophy of duodenal mucosa, and basal and forskolinstimulated duodenal HCO 3 Ϫ secretion and Isc in mTERC Ϫ/Ϫ p21 Ϫ/Ϫ double-knockout mice were not different from wild-type controls. In conclusion, genetic ablation of telomerase resulted in p21-dependent duodenal mucosal atrophy and reduced duodenal HCO 3 Ϫ secretory capacity, whereas gastric morphology and acid secretory function were preserved.…”

“…This suggests that telomere shortening during aging may result in an imbalance between aggressive and protective secretions against duodenal mucosa and thus predispose to ulcer formation. telomere shortening; gastric acid secretion; duodenal HCO 3 Ϫ secretion; duodenal ulcer; aging PEPTIC ULCER, ESPECIALLY DUODENAL ulcer, is a common disease. The majority of duodenal ulcer is widely considered as related to Helicobacter pylori infection (3,4,8,10,20,26).…”