Alkaline reflux gastritis: a critical reappraisal.

Ritchie, Wallace P.

doi:10.1136/gut.25.9.975

Cited by 79 publications

(41 citation statements)

References 35 publications

(8 reference statements)

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“…After distal gastrectomy, the primary causes of remnant gastritis are H. pylori infection and bile reflux. 34 Distal gastrectomy increases the occurrence of biliary enterogastric reflux and potentially inhibits the growth of H. pylori in the stomach, 35 or even eradicates the organism. 36,37 These observations may explain the high rate of spontaneous H. pylori clearance in this study.…”

Section: Discussionmentioning

confidence: 99%

Randomised clinical trial: the effects ofHelicobacter pylorieradication on glandular atrophy and intestinal metaplasia after subtotal gastrectomy for gastric cancer

Cho

Choi

Kook

et al. 2013

Aliment Pharmacol Ther

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Section: Discussionmentioning

confidence: 99%

Randomised clinical trial: the effects ofHelicobacter pylorieradication on glandular atrophy and intestinal metaplasia after subtotal gastrectomy for gastric cancer

Cho

Choi

Kook

et al. 2013

Aliment Pharmacol Ther

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“…Their data revealed that bile alone was not carcinogenic, and that pancreatic exocrine secretions were necessary. It is known that bile salts are ulcerogenic, however, it may be the addition of lysolecithin and/or other byproducts of pancreatic enzymatic digestion that promotes carcinogenesis (Ritchie, 1984).…”

Section: Yamaguchi Et Almentioning

confidence: 99%

Association of Spasmolytic Polypeptide–Expressing Metaplasia with Carcinogen Administration and Oxyntic Atrophy in Rats

Yamaguchi

Goldenring

Kaminishi

et al. 2002

Laboratory Investigation

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SUMMARY:Spasmolytic polypeptide (TFF2)-expressing metaplasia (SPEM) is a gastric metaplastic lineage associated with the development of intestinal-type gastric adenocarcinoma. To study the etiology of this potential neoplastic precursor metaplasia, we used surgical rat models of remnant gastric adenocarcinoma studied with and without exposure to nitroso carcinogen. Animals with truncal vagotomy without duodenogastric reflux procedures demonstrated normal mucous neck cell spasmolytic polypeptide (SP) immunostaining. In these animals, anti-proliferating cell nuclear antigen (PCNA)-labeled nuclei were found in the normal midgland progenitor zone. Rats that received anatomic alterations that augmented the degree of duodenogastric reflux, however, revealed expansion of basally placed SP immunoreactive cells with early phenotypic changes of SPEM. Seventy percent of animals with antrectomy and carcinogen (with or without vagotomy) developed SPEM at the base of the gastric mucosa. In association with the appearance of this metaplastic lineage, a distinct second zone of PCNA-labeled nuclei developed in the deepest portion of the mucosa. Of interest, three animals demonstrating these changes developed intestinal-type gastric adenocarcinoma. Finally, we studied the immunostaining pattern of intrinsic factor, normally a chief cell marker in rat fundic mucosa. In animals with SPEM, we observed coexpression of SP and intrinsic factor in SPEM cells at the base of the mucosa. These findings support our hypothesis that SPEM develops from a second progenitor cell population, reflecting either the unmasking of a cryptic zone or transdifferentiation of chief cells. (Lab Invest 2002, 82:1045-1052.

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“…However, the results of this surgery are not entirely satisfactory [8,14,20,21], and for this reason there is doubt as to the existence of PARG as a medical entity [22,23]. This has given rise to a period of greater scientific rigor when diagnosing PARG, with duodeno gastric reflux (DGR) being quantified in these subjects before they are operated on [ 12,[24][25][26]. When quantify ing DGR in both asymptomatic and symptomatic pa tients, most authors [27,28] find a higher quantity of DGR in the latter.…”

Section: Introductionmentioning

confidence: 99%

“…This made the concepts of postoperative alkaline reflux gastritis' (PARG) [9] and 'alkaline gastri tis' [10] popular. Some 15-30% of patients undergoing resection or derivation gastric surgery show symptoms which can be attributed to PARG [11][12][13]. In order to improve the medical management of these patients, some authors [8,[14][15][16][17][18][19] have suggested treatment with bile derivation surgery.…”

Section: Introductionmentioning

confidence: 99%

24-Hour Intragastric pH Measurement in the Quantification of Duodenogastric Reflux

R¹,

Parrilla²,

Luján³

et al. 1988

Dig Surg

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Duodenogastric reflux (DGR) was quantified in 40 patients, 10 of them being healthy subjects used as a control group. The remaining 30 underwent gastric surgery and fell into two groups according to their medical history: symptomatic and asymptomatic patients. As a DGR study method, 24-hour gastric pH measurement was used, in association with the determination of bile acids in aspirated gastric juice. Bile acid determination was used in order to differentiate the pH increases due to hyposecretion from those due to DGR. Our results show that, in symptomatic patients, the mean size of the reflux areas (pH > 4) and the mean total bile acid concentration are statistically significantly larger than those of asymptomatic patients (p < < 0.01).

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Alkaline reflux gastritis: a critical reappraisal.

Cited by 79 publications

References 35 publications

Randomised clinical trial: the effects ofHelicobacter pylorieradication on glandular atrophy and intestinal metaplasia after subtotal gastrectomy for gastric cancer

Randomised clinical trial: the effects ofHelicobacter pylorieradication on glandular atrophy and intestinal metaplasia after subtotal gastrectomy for gastric cancer

Association of Spasmolytic Polypeptide–Expressing Metaplasia with Carcinogen Administration and Oxyntic Atrophy in Rats

24-Hour Intragastric pH Measurement in the Quantification of Duodenogastric Reflux

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