Helicobacter pylori increases gastric antral juxtamucosal pH

Kelly, Steven M.; Crampton, J. R.; Hunter, JO

doi:10.1007/bf01296784

Cited by 25 publications

(14 citation statements)

References 15 publications

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“…Talley et al [20] failed to demonstrate a reduced gastric juxtamucosal pH in HP+ subjects, but pH measurements were obtained from five specific sites and not always below acid luminal fluid [20], Quigley and Turnberg [2], on the contrary, demonstrated the inability to maintain a lumen to mucosa pH gradient in patients with duodenal ulcer (and therefore much prob-ably infected by HP), but only following gastric acid per fusion. Our data, in accordance with another study [20], do not confirm the rise of antral and body pH in the HPinfected stomach observed by others [6,7] and considered partially responsible of HP-associated postprandial hypergastrinemia. A different technique used in in vitro study and a different patient selection for in vivo study may explain our different results.…”

Section: Discussionsupporting

confidence: 70%

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Gastric and Duodenal Juxtamucosal pH and Helicobacter pylori

Frieri

Petris²,

Aggio³

et al. 1995

Digestion

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One of the results of gastric cytoprotection is the generation of a juxtamucosal stable pH, maintained close to neutrality by several factors among which bicarbonate secretion and mucus layer. Since Helicobacter pylori (HP) induces structural and functional changes in the gastric mucus, this study was carried out to investigate the relationship between juxtamucosal pH and HP colonization. Thirty-one dyspeptic subjects who denied a past history of gastric or duodenal ulcer and free of endoscopic lesions were studied. Juxtamucosal pH of the gastric body, antrum and duodenum and gastric luminal fluid pH were measured during upper gastrointestinal endoscopy by a flexible glass electrode passed through the biopsy channel of a gastroscope. Multiple biopsies were subsequently taken for histological investigation, HP culture and a urea quick test. Twelve subjects (39%) were infected by HP (HP+). Juxtamucosal pH (mean ± SE) was significantly lower (p = 0.0014) in the gastric body (5.67 ± 0.16) in HP+ than in HP-negative (HP- 6.41 ± 0.13 subjects, but not in the antrum (6.50 ± 0.20 in HP+ vs. 6.52 ± 0.09 in HP-) and in the duodenum (6.80 ± 0.14 in HP+ vs. 6.94 ± 0.08 in HP- subjects). No difference was found in gastric luminal fluid pH (1.71 ± 0.23 in HP+ vs. 1.80 ± 0.22 in HP-subjects). In conclusion, this study shows that dyspeptic HP+ patients have a reduced juxtamucosal pH in the gastric body but a pH in the antrum and duodenum similar to HP-subjects.

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Section: Discussionsupporting

confidence: 70%

“…An increase in juxtamucosal pH has in fact been dem onstrated in the infected stomach [6,7] and has been thought responsible for the postprandial hypergastrinemia in patients with duodenal ulcer [8] even if this patho genetic mechanism has recently been challenged [9,10].…”

Section: Introductionmentioning

confidence: 99%

Gastric and Duodenal Juxtamucosal pH and Helicobacter pylori

Frieri

Petris²,

Aggio³

et al. 1995

Digestion

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“…These experiments were run in parallel at pH 7.4 and 5.8, because most H. pylori colonize the mucous layer and gastric pits of the antrum, where it is assumed that the pH is about 5.5 (62). However, the urease of H. pylori generates ammonia in its immediate surroundings, which thus increases the pH to about neutrality (63,64). Bactericidal activity was defined in accordance with convention as a reduction in plate counts of Ն1,000 cfu͞ml.…”

Section: Resultsmentioning

confidence: 99%

Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains ofHelicobacter pyloriand prevents benzo[a]pyrene-induced stomach tumors

Fahey

Haristoy

Dolan

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

724

495

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Gastric infection with Helicobacter pylori is a cosmopolitan problem, and is especially common in developing regions where there is also a high prevalence of gastric cancer. These infections are known to cause gastritis and peptic ulcers, and dramatically enhance the risk of gastric cancer. Eradication of this organism is an important medical goal that is complicated by the development of resistance to conventional antimicrobial agents and by the persistence of a low level reservoir of H. pylori within gastric epithelial cells. Moreover, economic and practical problems preclude widespread and intensive use of antibiotics in most developing regions. We have found that sulforaphane [(؊)-1-isothiocyanato-(4R)-(methylsulfinyl)butane], an isothiocyanate abundant as its glucosinolate precursor in certain varieties of broccoli and broccoli sprouts, is a potent bacteriostatic agent against 3 reference strains and 45 clinical isolates of H. pylori [minimal inhibitory concentration (MIC) for 90% of the strains is

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“…The enzyme urease by breaking down urea in the gastric juice appears to generate enough bicarbonate and ammonium ions around the organism to allow its safe passage through the gastric acid barrier to reach the protective mucous layer. Ammonia elevates the pH of the gastric mucous layer from about 6 to 7 [3]. It is known to deplete aerobic cells of alpha keto-glutarate, an essential substrate for the tricarboxylic acid cycle.…”

Section: It Is the Primary Cause Of Ulceration (N Ananthakrishnanmentioning

confidence: 99%

IsHelicobacter pyloriInfection the Primary Cause of Duodenal Ulceration or a Secondary Factor? A Review of the Evidence

Kate

Ananthakrishnan

Tovey

2013

Gastroenterology Research and Practice

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Helicobacter pylori (H. pylori) has a role in the multifactorial etiology of peptic ulcer disease. A link between H. pylori infection and duodenal ulcer disease is now established. Other contributing factors and their interaction with the organism may initiate the ulcerative process. The fact that eradication of H. pylori infection leads to a long-term cure in the majority of duodenal ulcer patients and the fact that the prevalence of infection is higher in ulcer patients than in the normal population are cogent arguments in favor of it being the primary cause of the ulceration. Against this concept there are issues that need explanation such as the reason why only a minority of infected persons develop duodenal ulceration when infection with H. pylori is widespread. There is evidence that H. pylori infection has been prevalent for several centuries, yet duodenal ulceration became common at the beginning of the twentieth century. The prevalence of duodenal ulceration is not higher in countries with a high prevalence of H. pylori infection. This paper debate puts forth the point of view of two groups of workers in this field whether H. pylori infection is the primary cause of duodenal ulcer disease or a secondary factor.

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Helicobacter pylori increases gastric antral juxtamucosal pH

Cited by 25 publications

References 15 publications

Gastric and Duodenal Juxtamucosal pH and <i>Helicobacter pylor</i><i>i</i>

Gastric and Duodenal Juxtamucosal pH and <i>Helicobacter pylor</i><i>i</i>

Sulforaphane inhibits extracellular, intracellular, and antibiotic-resistant strains ofHelicobacter pyloriand prevents benzo[a]pyrene-induced stomach tumors

IsHelicobacter pyloriInfection the Primary Cause of Duodenal Ulceration or a Secondary Factor? A Review of the Evidence

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