Pathogenesis of duodenal ulcer disease: the rest of the story

Dore, Maria Pina; Graham, David Y.

doi:10.1053/bega.1999.0061

Cited by 24 publications

(18 citation statements)

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“…Study of patients with or without H pylori infection and of patients before and after infection eradication allowed investigators to identify abnormalities directly attributable to the infection. Although the details of these dysregulations in gastric secretory physiology are still being elucidated at the molecular level, all of the previously described physiologic alterations, except for the abnormally increased parietal cell mass in duodenal ulcer, are reversible epiphenomena related to H pylori infection [19,20].…”

Section: Effect Of H Pylori Infection On Gastroduodenal Physiology Anmentioning

confidence: 99%

“…Reducing acid secretion by any method eliminates this restriction and promotes corpus gastritis [10,23]. The lack of significant inflammation in the gastric corpus coupled with the H pylori-associated dysregulations of acid secretion (eg, impaired down-regulation of acid secretion when the antral pH falls to 3 or less) results in a markedly increased duodenal acid load [19,26,27]. Both the inflammation induced by H pylori and the injury caused by the duodenal acid load impair bicarbonate secretion by duodenal mucosa; this impairment further augments the functional duodenal acid load.…”

Section: Effect Of H Pylori Infection On Gastroduodenal Physiology Anmentioning

confidence: 99%

“…Both the inflammation induced by H pylori and the injury caused by the duodenal acid load impair bicarbonate secretion by duodenal mucosa; this impairment further augments the functional duodenal acid load. H pylori growth is inhibited by glycine-conjugated bile acids; this renders the normal duodenal bulb a hostile environment for H pylori [19,26]. The high duodenal acid load decreases the mean duodenal pH, which precipitates the glycineconjugated bile acids and allows H pylori colonization within, but rarely beyond, the duodenal bulb.…”

Section: Effect Of H Pylori Infection On Gastroduodenal Physiology Anmentioning

confidence: 99%

“…Subtle changes in behavior, such as starting or stopping smoking, could affect the balance between acidity, infection, and injury versus alkalinity, infection eradication, and repair to tip the scale one way or the other. Similarly, administration of an H 2 -receptor antagonist reduces the duodenal acid load, thereby permitting the glycine-conjugated bile acids to remain in solution to inhibit H pylori growth [19,26]. Various effects may tip the balance and result in ulcer exacerbation or remission and could explain how and why agents and actions might have influenced duodenal ulcer disease in the past.…”

Section: Effect Of H Pylori Infection On Gastroduodenal Physiology Anmentioning

confidence: 99%

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Pathogenesis and therapy of gastric and duodenal ulcer disease

Shiotani

Graham

2002

Medical Clinics of North America

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Section: Effect Of H Pylori Infection On Gastroduodenal Physiology Anmentioning

confidence: 99%

Section: Effect Of H Pylori Infection On Gastroduodenal Physiology Anmentioning

confidence: 99%

Section: Effect Of H Pylori Infection On Gastroduodenal Physiology Anmentioning

confidence: 99%

Section: Effect Of H Pylori Infection On Gastroduodenal Physiology Anmentioning

confidence: 99%

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Pathogenesis and therapy of gastric and duodenal ulcer disease

Shiotani

Graham

2002

Medical Clinics of North America

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“…In both cases, imbalance between protective and damaging factors can lead to ulcer (12)(13)(14). Physiological prostaglandins (PGE) are extremely critical in protecting gastric mucosa.…”

Section: Discussionmentioning

confidence: 99%

Atherosclerosis and acetylsalicylic acid are independent risk factors for hemorrhage in patients with gastric or duodenal ulcer

Özdil¹,

Coşar²,

Akkız³

et al. 2011

Anadolu Kardiyol Derg

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ÖZETAmaç: Üst gastrointestinal (Gİ) endoskopide gastrik ve/veya duodenal ülser saptanan vakalarda ülser kanaması için risk faktörleri araştırıldı. Yöntemler: Üst Gİ endoskopisinde duodenum ve gastrik ülser saptanan 350 vakanın (226 Erkek, 124 Kadın) dosyalarından retrospektif analiz yapıldı. İncelenen 92 vakada endoskopi sırasında Gİ kanama saptanmıştı. Kanaması olan ve olmayan hastaların tümünde nonsteroidal antienflamatuvar ilaç (NSAID) ve asetil salisilik asit (ASA) kullanımı ile koroner arter hastalığı (KAH) varlığı araştırıldı. Sonuçlar Ki-kare testi ve lojistik regresyon analizi ile değerlendirildi. Bulgular: Vakaların yaş ortalaması 50.4±15.7 (25-82) yıl idi. Doksan iki vakada (%26) gastrik veya duodenal ülsere bağlı kanama görüldü. Kanamalı hastalarda yaş ortalaması 64.6±11.4/ yıl, kanama olmayanlarda 45.7±13.9/yıl idi. Ülser kanaması olan vakalarda ASA kullanımı daha fazlaydı (NSAID, n=35 (%40); ASA, n=51 (%60); p=0.035). Ülseri olan kadınların %20'sinde kanama görülürken, erkeklerin %28'inde kanama görül-dü (p=0.055). Kanama riski KAH'lı vakalarda (OR:24.75, %95 güven aralığı (GA)=1.6-96.7, p=0.001), ASA (OR:9.76, %95 GA=2.1-37.5, p=0.021), NSAID (OR:4.72, %95 GA=1.1-16.5 p=0.032), yaş (OR:11.59, %95 GA=2.7-12.1, p=0.001), erkek cinsiyet için (OR:2.56, %95 GA=0.8, 9.6, p=0.052) olarak belirlendi. Sonuç: İleri yaş, ateroskleroz, erkek cinsiyet ve NSAİD (özellikle aspirin) kullanımı gastrik ve/veya duodenal ülserli hastalarda üst Gİ kanaması bakımından majör risk faktörleridir. (Anadolu Kardiyol Derg 2011 1: 53-6) Anahtar kelimeler: Aspirin, koroner arter hastalığı, üst gastrointestinal kanama, nonsteroidal anti-inflamatuvar ilaç, lojistik regresyon analizi ABSTRACT Objective: Risk factors for hemorrhage due to gastric and/or duodenal ulcer in patients diagnosed by upper gastrointestinal (GI) endoscopy were investigated in the present study. Methods: Medical records of 350 patients (226 males, 124 females) diagnosed as duodenal or gastric ulcers by GI endoscopy in the gastroenterology clinic were scanned retrospectively. Upper GI hemorrhage was detected in 92 patients by upper endoscopic examination. The medical history of non-steroidal anti-inflammatory drugs (NSAIDs) or acetylsalicylic acid (ASA) usage and the presence of coronary artery disease (CAD) were investigated in all patients with or without hemorrhage. Results were evaluated by Chi-square test and logistic regression analysis. Results: The mean age of the patients was 50.4±15.7 years (range: 25 to 82 years). Hemorrhage due to gastric or duodenal ulcer was identified in 92 patients (26%). Mean age was 64.6±11.4 years in patients with hemorrhage and 45.7±13.9 years in patients without hemorrhage. ASA usage was more common than NSAID in patients with ulcer hemorrhage (NSAID usage n=35 (40%); ASA usage n=51 (60%); p=0.035). Hemorrhage was reported in 20% of the females and in 28% of the males who have ulcer (p=0.055). Risk factors for hemorrhage were CAD (OR:24.75, 95% CI=1.6-96.7, p=0.001), ASA usage (OR:9.76, 95% CI=2.1-37.5, p=0.021), NSAID us...

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