Ulceration as a Possible Link between Duodenogastric Reflux and Neoplasms in the Stomach of Rats

Øvrebø, Kjell; Aase, Steinar; Grong, Ketil; Viste, Asgaut; Svanes, Knut; Sørbye, Halfdan

doi:10.1006/jsre.2002.6501

Cited by 6 publications

(1 citation statement)

References 45 publications

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“…A study from the Arab Emirates showed that 24 of 29 patients with ulcer perforation were HP-positive ( 13 C urea breath test) 8 days after operation, but population data were not available [39]. In an ongoing study in Bergen, Norway, 67% of ulcer perforation patients were HP-positive (serology) at the time of perforation and 37% were HP-positive ( 13 C urea breath test) 8 weeks after ulcer perforation surgery [40]. Thus ulcer perforation seem to differ from uncomplicated ulcer with regard to the importance of H. pylorii infection.…”

Section: Etiology Of Ulcer Perforationmentioning

confidence: 99%

Trends in Perforated Peptic Ulcer: Incidence, Etiology, Treatment, and Prognosis

2000

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After increasing steeply at the beginning of the twentieth century, ulcer perforation incidence during the last decades has declined in the young and in men, and it has risen among the elderly and in women. These changes can be attributed to a cohort phenomenon: Ulcer perforation risk is particularly common in the cohorts born after the turn of the twentieth century and is less common in previous and succeeding birth cohorts. A decline in total incidence is expected with the death of the high risk cohorts. Most ulcer perforations among subjects < 75 years of age can be attributed to smoking. Subjects with a history of ulcer perforation therefore have poorer long-term survival than the general population, most pronounced for younger generations. About one of four ulcer perforations can be attributed to the use of nonsteroidal antiinflammatory drugs, a risk factor of particular importance in the elderly. Ulcer perforation was frequently treated by gastric resection in former days, whereas suture, being the first method introduced in 1887, is the method of choice today. The introduction of antibiotics improved the prognosis of ulcer perforation surgery greatly. Postoperative lethality decreased until 1950 but has remained stable since then. Lethality is higher in the elderly and is higher after gastric than after duodenal perforation. The delay before surgical treatment is a strong determinant for lethality, complication rates, and hospital costs. Treatment delay seems to have increased during the last

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Section: Etiology Of Ulcer Perforationmentioning

confidence: 99%

Trends in Perforated Peptic Ulcer: Incidence, Etiology, Treatment, and Prognosis

2000

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Effects of duodenogastric reflux on gastrin cells, somatostatin cells and serotonin cells in human antral gastric mucosa

Tzaneva

2004

Pathology - Research and Practice

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Farnesoid X receptor protects human and murine gastric epithelial cells against inflammation-induced damage

Fan

Xing

Yuan

et al. 2011

Biochemical Journal

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Bile acids from duodenogastric reflux promote inflammation and increase the risk for gastro-oesophageal cancers. FXR (farnesoid X receptor/NR1H4) is a transcription factor regulated by bile acids such as CDCA (chenodeoxycholic acid). FXR protects the liver and the intestinal tract against bile acid overload; however, a functional role for FXR in the stomach has not been described. We detected FXR expression in the normal human stomach and in GC (gastric cancer). FXR mRNA and protein were also present in the human GC cell lines MKN45 and SNU5, but not in the AGS cell line. Transfection of FXR into AGS cells protected against TNFα (tumour necrosis factor α)-induced cell damage. We identified K13 (keratin 13), an anti-apoptotic protein of desmosomes, as a novel CDCA-regulated FXR-target gene. FXR bound to a conserved regulatory element in the proximal human K13 promoter. Gastric expression of K13 mRNA was increased in an FXR-dependent manner by a chow diet enriched with 1% (w/w) CDCA and by indomethacin (35 mg/kg of body weight intraperitoneal) in C57BL/6 mice. FXR-deficient mice were more susceptible to indomethacin-induced gastric ulceration than their WT (wild-type) littermates. These results suggest that FXR increases the resistance of human and murine gastric epithelial cells to inflammation-mediated damage and may thus participate in the development of GC.

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Ulceration as a Possible Link between Duodenogastric Reflux and Neoplasms in the Stomach of Rats

Cited by 6 publications

References 45 publications

Trends in Perforated Peptic Ulcer: Incidence, Etiology, Treatment, and Prognosis

Trends in Perforated Peptic Ulcer: Incidence, Etiology, Treatment, and Prognosis

Effects of duodenogastric reflux on gastrin cells, somatostatin cells and serotonin cells in human antral gastric mucosa

Farnesoid X receptor protects human and murine gastric epithelial cells against inflammation-induced damage

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