Gastric ulcers, blood groups, and acid secretion

Johnson, H. Daintree; Love, A. H. G.; Rogers, N; Wyatt, A P

doi:10.1136/gut.5.5.402

Cited by 65 publications

(17 citation statements)

References 25 publications

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“…The excellent effect in gastric ulcers was unexpected, because there are still strong ar guments against acid being a major cause of gastric ulcers [4,11,20,21,28,34], What ever the initiating cause may be, acid must also be the final effector in the development of gastric ulcers. Obviously very little acid is sufficient to cause ulcerations in predisposed stomachs.…”

Section: Discussionmentioning

confidence: 99%

Therapy with Omeprazole in Patients With Peptic Ulcerations Resistant to Extended High-Dose Ranitidine Treatment

et al. 1988

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94 patients with peptic ulcerations of duodenum, stomach, and esophagus, who did not respond to 3 or more months high-dose (450 or 600 mg) treatment with ranitidine, were treated orally with 40 mg omeprazole daily. After healing all patients were offered long-term maintenance therapy with the same dose for 5 years. In 75 patients the peptic ulcerations healed within 4 weeks, in 13 patients within 8 weeks, and in 3 patients only after an increase to 60 mg omeprazole daily. In 3 patients the ulcers did not heal. So far 83 patients have entered long-term maintenance therapy. 59 of these patients are on the drug between 1 and 4 years. During maintenance therapy with 40 mg omeprazole no relapses have occurred up to now as demonstrated by endoscopy and no drug-related adverse effects were observed. Routine laboratory tests remained without significant changes in all patients including 18 patients with concomitant liver cirrhosis. Serum gastrin levels were already elevated during the initial high-dose ranitidine treatment (106 ± 15.4 pg/ml). 4 weeks after the start of omeprazole treatment serum gastrin levels rose to 4 times normal levels (195 ± 28 pg/ml). Thereafter, no further increase in serum gastrin was observed even up to 4 years of continuous observation. It is therefore concluded that omeprazole is highly effective in healing ranitidine-resistant peptic ulcerations and that omeprazole maintenance therapy with 40 mg omeprazole is safe during the time observed and highly effective in the prevention of ulcer recurrence.

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Section: Discussionmentioning

confidence: 99%

Therapy with Omeprazole in Patients With Peptic Ulcerations Resistant to Extended High-Dose Ranitidine Treatment

et al. 1988

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“…Gastric ulcers have been divided into two categories. The first category is the classical lesser curve gastric ulcer to the left of the angulus with no other radiological lesion in the stomach or duodenum, and corresponds to type I of Johnson, Rogers, and Wyatt (1964). The second category, which corresponds to types II and III of Johnson et al (1964), contains all gastric ulcers which areaccompanied by any abnormality of the duodenum, and all gastric ulcers to the right of the angulus.…”

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confidence: 99%

“…The first category is the classical lesser curve gastric ulcer to the left of the angulus with no other radiological lesion in the stomach or duodenum, and corresponds to type I of Johnson, Rogers, and Wyatt (1964). The second category, which corresponds to types II and III of Johnson et al (1964), contains all gastric ulcers which areaccompanied by any abnormality of the duodenum, and all gastric ulcers to the right of the angulus. The two categories have been separated in this way because types II and III of Johnson et al (1964) both seem to possess such features of duodenal ulcer as hypersecretion and association with blood group 0.…”

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confidence: 99%

ABO blood groups in gastric bleeding.

Horwich¹,

Evans²,

McConnell³

et al. 1966

Gut

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EDITORIAL SYNOPSIS This paper confirms previous studies showing the increased risk of bleeding associated with blood group 0. There is an indication that this may also be true for acute perforation and indeed the relationship may be with the severity of the ulcer disease.In a previous paper (Horwich and Evans, 1966) a relationship was shown between the loss of gastric mucosal cells in 160 volunteer subjects and their ABO blood groups and ABH secretor status. Aspirin enhanced the loss from the gastric mucosa, and it was postulated that clinical overt bleeding from the gastric mucosa, whether aspirin-induced or not, may also be related to the ABO blood groups and secretor status. The present investigation concerns this problem, and it was also thought to be of value to extend the investigation to include subjects with duodenal ulcer because of the reported association with blood group 0 (Aird, Bentall, Mehigan, and Roberts, 1954) and with ABH non-secretion (Clarke, Edwards, Haddock, Howel-Evans, McConnell, and Sheppard, 1956). While the work was in progress, Langman and Doll (1965) reported an increased frequency of group 0 in gastric and duodenal ulcer subjects who had bled and an increased incidence of non-secretors in those who had undergone operation. METHODSTwo separate series of patients were ascertained. Case records were examined for a history of salicylate ingestion during the 48 hours before the onset of bleeding and recorded at the time of admission. Details were abstracted of a barium meal examination carried out within two weeks after the bleeding episode. Where the radiologist gave a firm opinion on the presence or absence of a gastric or duodenal lesion, this diagnosis was accepted for the purpose of this investigation. Persistent duodenal deformity was accepted as being due to scarringfrom ulceration. Gastric ulcers have been divided into two categories. The first category is the classical lesser curve gastric ulcer to the left of the angulus with no other radiological lesion in the stomach or duodenum, and corresponds to type I of Johnson, Rogers, and Wyatt (1964). The second category, which corresponds to types II and III of Johnson et al. (1964), contains all gastric ulcers which areaccompanied by any abnormality of the duodenum, and all gastric ulcers to the right of the angulus. The two categories have been separated in this way because types II and III of Johnson et al. (1964) both seem to possess such features of duodenal ulcer as hypersecretion and association with blood group 0.Cases were included in this series if the barium meal was normal or showed a duodenal or gastric ulcer. Cases were excluded if there was any suspicion of bleeding from other sites, such as epistaxis, haemoptysis, oesophageal varices, hiatus hernia, carcinoma, or lesions of the large bowel. In order to be comparable with the experimental gastric-cell-shedding series, cases were excluded if there had been a previous gastric operation, except suture of a simple perforation, and for the same reason subjects of blood g...

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“…3 The researchers at start thought that patients with blood group O might be producing the large amount of Hydrochloric acid than others. 5 Later it was found that in people with blood group O, there was increased binding of Helicobacter pylori to the epithelial cells. 6 It was concluded that denser colonisation of epithelial cells and increased inflammatory reactions as a result of bacterial binding in group O people might be one reason that this population is more prone.…”

Section: Discussionmentioning

confidence: 99%

Observations on Blood Group Distribution in Peptic Ulcer Perforation and Gastric Perforation

Sureshkumar¹,

Rajavelu²,

Udhayasankar³

2016

jemds

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BACKGROUNDAim of this study is to establish and determine the relationship between the A, B, O blood groups' association with complicated peptic ulcer. MATERIALS AND METHODSThis retrospective study was conducted in a tertiary care centre, Government Vellore Medical College Hospital, on patients who underwent emergency laparotomy for complicated peptic ulcer and gastric perforation from January 2011 to January 2016. One hundred and seventy two (172) male patients were enrolled in the study. And data was collected based on Age wise and Blood group wise distribution of duodenal ulcer perforation and gastric perforation. RESULTSIn 172 patients, all patients were male. In patients with duodenal ulcer perforation, the O blood group association was 45.39% followed by A 36.84%. In patients with gastric perforation, the association with A blood group was 70%, followed by O group 20%. The age of the patients ranged from 11 to 90 years. The incidence of duodenal ulcer perforation was highest in the age group of 31-40 years (31.57%), followed by 41-50 years (23.68%). The highest incidence of duodenal ulcer perforation occurs in Positive group, 141 individuals (92.76%). In gastric perforation, highest incidence was seen in positive group individuals 19 patients (95%). CONCLUSIONAfter interpretation of the data in the study, it was concluded that 1. Gastric perforation was more common in the blood group A. 2. Duodenal ulcer perforation was common in blood group O, followed by blood group A. 3. The incidence of perforation was highest in the age group of 31-40 years. 4. Incidence of gastric perforation was highest in the age group of 61-70 years. 5. Highest incidence of duodenal ulcer perforation as well as gastric perforation was seen in Rh positive individuals (92.76%, 95%).

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Gastric ulcers, blood groups, and acid secretion

Cited by 65 publications

References 25 publications

Therapy with Omeprazole in Patients With Peptic Ulcerations Resistant to Extended High-Dose Ranitidine Treatment

Therapy with Omeprazole in Patients With Peptic Ulcerations Resistant to Extended High-Dose Ranitidine Treatment

ABO blood groups in gastric bleeding.

Observations on Blood Group Distribution in Peptic Ulcer Perforation and Gastric Perforation

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