Pyloric reflux and the healing of gastric ulcers

Cocking, J. B.; Grech, Paul

doi:10.1136/gut.14.7.555

Cited by 20 publications

(7 citation statements)

References 11 publications

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“…Although these results may be considered to cast serious doubt on the previous suggestion that the stomach is the primary route of carbenoxolone absorption in man (Downer & others, 1970;Parke, 1972), it is possible that because of the high degree of tissue binding much of the administered carbenoxolone is adsorbed or precipitated onto the gastric mucosal surfaces so that a relatively small portion of the dose is available for subsequent absorption from the duodenum. Sodium taurodeoxycholate has been shown to increase the permeability of rat small intestine (Feldman, Reinhard & Willson, 1973) so that biliary reflux, which is quite common in gastric ulcer patients (Cocking & Grech, 1973) might further promote gastric absorption.…”

Section: Discussionmentioning

confidence: 99%

Gastrointestinal absorption of carbenoxolone in the rat determined in vitro and in situ: deviations from the pH-partition hypothesis

Bridges

Houston

Humphrey

et al. 1976

Journal of Pharmacy and Pharmacology

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The absorption of [14C] carbenoxolone from everted rat ileum in vitro and from rat stomach and ileum in situ has been examined. The rate of its mucosal to serosal transfer in vitro increases as pH increases from 5 to 8 whereas the amount bound to ileum tissue decreases with increased pH; absorption closely parallels the drug's solubility. The uptake of carbenoxolone in situ is bi-exponential and the rate constants for the two processes, have been calculated. Absorption in situ, and biliary excretion, of the drug increases with increasing pH from 5.0 to 7.4. Tissue binding to the ileum in situ is not dependent on pH except below pH 5.0 when extensive tissue accumulation of carbenoxolone occurs because of its low solubility. Tissue binding to the stomach increases markedly with decrease of pH from 7.4 to 6.5 and at pH 6.5 is 80 times greater than binding to the intestine. The rate of absorption from the stomach, at pH 6.5-7.4, was much less than that from the intestine in situ. When allowance is made for the binding of carbenoxolone to the stomach, contrary to the pH-partition hypothesis, correlation is apparent between its absorption and the amount present in the ionized form.

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Section: Discussionmentioning

confidence: 99%

Gastrointestinal absorption of carbenoxolone in the rat determined in vitro and in situ: deviations from the pH-partition hypothesis

Bridges

Houston

Humphrey

et al. 1976

Journal of Pharmacy and Pharmacology

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“…However, gastric ulcers may also be secondary to DGR, posing the "chicken-or-egg question". Cocking et al [16] discussed this in their manuscript and proposed smoking as another presumable primary cause of DGR. Read et al demonstrated that the reflux occurred within 30 s from the time that an individual would start to smoke, as viewed in most cases of 13 normal volunteers [22].…”

Section: Introductionmentioning

confidence: 99%

“…Those classified as Primary are those that did not receive surgical interventions [15]. Primary DGR is considered a rare disease entity [16,17]. In the 1960s, it was reported that bile acid impaired the gastric mucosa and may be related to gastric ulcers; however, this remained unclear [18,19].…”

Section: Introductionmentioning

confidence: 99%

“…In the 1960s, it was reported that bile acid impaired the gastric mucosa and may be related to gastric ulcers; however, this remained unclear [18,19]. In the 1970s, researchers enthusiastically investigated the cause of DGR [16,[20][21][22][23][24], wherein pyloric incompetence was indicated as a possibility [20]. In primary DGR/BRG, gastroduodenal ulcers were proposed as one of the factors for pyloric incompetence [16].…”

Section: Introductionmentioning

confidence: 99%

“…In the 1970s, researchers enthusiastically investigated the cause of DGR [16,[20][21][22][23][24], wherein pyloric incompetence was indicated as a possibility [20]. In primary DGR/BRG, gastroduodenal ulcers were proposed as one of the factors for pyloric incompetence [16]. The mechanism of gastric ulcers diminishing the competence of the pylorus is explained as decreasing antral motility in the presence of gastric ulcers [20,25].…”

Section: Introductionmentioning

confidence: 99%

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Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis

et al. 2022

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Duodenogastric reflux (DGR) causes bile reflux gastritis (BRG) and may develop into gastric cancer. DGR is classified as primary in non-operated stomachs or secondary to surgical intervention. Primary DGR and Helicobacter pylori (H. pylori) infection are reportedly related. However, the mechanism is not fully understood. This study aimed to elucidate the relationship between H. pylori infection and pyloric incompetence in a non-operated stomach. A total of 502 non-operated participants who underwent an upper intestinal endoscopy were prospectively enrolled. Endoscopic findings (EAC, endoscopic atrophy classification; nodular gastritis; xanthoma; fundic gland polyp; and incompetence of pylorus), sex, age, gastrin, pepsinogen (PG) I and PG II levels were evaluated. PG I/PG II ratio, anti-H. pylori-Ab positivity, and atrophic gastritis status were significantly different between the normal and incompetent pylori (p = 0.043, <0.001, and 0.001, respectively). Open-type atrophic gastritis was significantly higher in the incompetent pylori. Incompetence of the pylorus and EAC were moderately correlated (Cramer’s V = 0.25). Multivariate analysis revealed that the presence of anti-H. pylori-Ab was the only independent factor associated with the incompetence of the pylorus, with an adjusted odds ratio of 2.70 (95% CI: 1.47–4.94, p = 0.001). In conclusion, pyloric incompetence was associated with H. pylori infection and moderately correlated to the severity of atrophic gastritis in non-operated stomachs.

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Milk 99Tcm-EHIDA test for enterogastric bile reflux

Mackie

Wisbey

Cuschieri

1982

Journal of British Surgery

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The study and clinical assessment of enterogastric bile reflux has been restricted for want of a simple non-invasive test for its detection and quantification. This paper describes such a test in which biliary excretion scintigraphy has been combined and a mild meal provocation. Two of 10 healthy volunteers studied showed probable reflux of approximately 5 per cent of total initial abdominal field activity. Among 73 patients studied, 37 patients showed definite reflux of up to 47 per cent. Reflux occurred in 19 of 22 post-gastric surgery patients and in 7 of 22 patients with peptic ulcer disease, gastritis or gastro-oesophageal reflux. None of 7 patients with 'non-specific' abdominal pain showed any reflux, but 11 of 22 patients with gallstone disease or previous cholecystectomy showed reflux of up to 35 per cent, including 9 of 11 patients with loss of gallbladder reservoir function.

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Pyloric reflux and the healing of gastric ulcers

Cited by 20 publications

References 11 publications

Gastrointestinal absorption of carbenoxolone in the rat determined in vitro and in situ: deviations from the pH-partition hypothesis

Gastrointestinal absorption of carbenoxolone in the rat determined in vitro and in situ: deviations from the pH-partition hypothesis

Pyloric Incompetence Associated with Helicobactor pylori Infection and Correlated to the Severity of Atrophic Gastritis

Milk 99Tcm-EHIDA test for enterogastric bile reflux

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