Endogenes Plasma-Histamin und »hepatogenes« gastroduodenales Ulkus bei Leberzirrhose

Stopik, D; Hampel, K. E.; Kleist, D. von

doi:10.1055/s-0028-1104991

Dtsch med Wochenschr

1977

DOI: 10.1055/s-0028-1104991

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Endogenes Plasma-Histamin und »hepatogenes« gastroduodenales Ulkus bei Leberzirrhose

D Stopik¹,

K. E. Hampel²,

D. von Kleist³

Abstract: Because of its anatomical relationship to the gastrointestinal tract, the normal liver is able to act as a controlling "filter" against the influx of plasma histamine chiefly by uptake and breakdown. This prevents unwanted effects on the systemic circulation. The ability to eliminate histamine from plasma is decreased in cirrhosis. Plasma histamine levels in peripheral venous blood of ten patients with liver cirrhosis and gastric ulcer, proven radiologically and by endoscopy, indicated a significantly higher c… Show more

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1995

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Cited by 3 publications

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“…1,[5][6][7][8][9] Most of the former studies have been performed in alcoholic-related etiologies, mainly liver cirrhosis.…”

mentioning

confidence: 99%

“…1 Suggested pathogenesis of peptic ulcers in patients with cirrhosis includes increased levels of gastrin and histamine, the presence of Helicobacter pylori, increased duodenogastric reflux, impaired gastric emptying, reduced prostaglandin level in gastric mucosa and reduced mucosal oxygen saturation. 1,[5][6][7][8][9] Most of the former studies have been performed in alcoholic-related etiologies, mainly liver cirrhosis. 10 Therefore, we conducted our study to find out the frequency of peptic ulcer disease in patients with portal hypertension of different etiologies, mainly nonalcoholic.…”

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confidence: 99%

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Frequency of Peptic Ulcers in Patients with Portal Hypertension

Amri

1995

Annals of Saudi Medicine

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To find the frequency of peptic ulceration in portal hypertension, 137 patients with portal hypertension were studied retrospectively. Patients with hepatocellular carcinoma, other malignancies or underlying severe systemic disease were excluded and the remaining 114 patients were included in the study. There were 81 males (mean age 49.1 ± 13.7 years) and 33 females (mean age 52.9 ± 10 years). Portal hypertension was secondary to viral liver disease in 75%. Fifty-seven patients had no evidence of peptic ulcers (group I) and another 57 patients (group II) had peptic ulcers diagnosed during upper gastrointestinal endoscopy. There was no significant difference between the two groups regarding age, sex, Child-Pugh score or variceal size. Duodenal ulcers were found in 24% while gastric ulcers were found in 4.4%; other endoscopic findings included erosive gastritis and duodenitis in 21% and 18.4% respectively. Twelve percent of the patients from group II developed bleeding from the ulcers and the majority of bleeding ulcers responded to conservative treatment. The study concludes that the frequency of peptic ulcers in patients with portal hypertension is high. Bleeding peptic ulcers respond to conservative treatment. Ann Saudi Med 1995;15 (5) The incidence of peptic ulcer disease in cirrhotic patients has been reported to range from 8% to 20%.1-4 The complication rate and mortality are also increased in such patients.1 Suggested pathogenesis of peptic ulcers in patients with cirrhosis includes increased levels of gastrin and histamine, the presence of Helicobacter pylori, increased duodenogastric reflux, impaired gastric emptying, reduced prostaglandin level in gastric mucosa and reduced mucosal oxygen saturation. 1,[5][6][7][8][9] Most of the former studies have been performed in alcoholic-related etiologies, mainly liver cirrhosis. 10Therefore, we conducted our study to find out the frequency of peptic ulcer disease in patients with portal hypertension of different etiologies, mainly nonalcoholic. Patients and MethodsOne hundred and thirty-seven consecutive patients with portal hypertension diagnosed at the Gastroenterology Unit of King Khalid University Hospital between AH 1413 to AH 1414 were included. Twenty-three patients subsequently were excluded because of the presence of hepatocellular carcinoma, gastric carcinoma or severe systemic disease such as end stage renal failure or end stage respiratory and cardiac disease.The remaining 114 patients entered the study. There were 81 males (mean age 49.1 ± 13.7 years) and 33 females (mean age 52.9 ± 10 years). The diagnosis of portal hypertension was based on the presence of prominent submucosal veins that protrude into the esophageal lumen. Esophageal varices were graded on a scale from 1 to 4 according to size. The diagnosis of portal hypertension was substantiated with upper abdominal ultrasonography. An ulcer was defined as the presence of an ulcer crater.The patient's history was reviewed regarding the presence of abdominal pain, hematemesis or melena, smoking h...

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“…1,[5][6][7][8][9] Most of the former studies have been performed in alcoholic-related etiologies, mainly liver cirrhosis.…”

mentioning

confidence: 99%

mentioning

confidence: 99%

Frequency of Peptic Ulcers in Patients with Portal Hypertension

Amri

1995

Annals of Saudi Medicine

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Peptic Ulcer Surgery in Patients with Liver Cirrhosis

Lehnert

Herfarth

1993

Annals of Surgery

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Frequent non-response to histamine H2-receptor antagonists in cirrhotics.

Walker

Krishna

Klotz

et al. 1989

Gut

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SUMMARY The effect of ranitidine 300 mg po given at 18 00 h (famotidine 40 mg/cimetidine 800 mg) on the night time gastric pH was tested using longterm intragastric pH monitoring in 27 patients with and 32 patients without liver cirrhosis. A rise in the gastric pH above 4.0 for more than six hours between 1800 h and 0600 h was considered as sufficient effect (response) of the H2-receptor antagonists on gastric acidity. Among the patients with cirrhosis, there were significantly (p<0005) more non-responders to ranitidine (16 of 27 patients) than in the control group (six of32). When 13 of the 22 non-responders to ranitidine were subsequently treated with famotidine, only two showed a sufficient rise in their gastric pH. Of the 11 patients not responding to both H2-receptor antagonists, 10 were finally treated with cimetidine and eight did not respond. Plasma levels of all three drugs measured two and four hours after oral administration were not significantly different between cirrhotic and noncirrhotic patients as well as between responders and non-responders. In addition, in all patients plasma levels were far above the corresponding IC50 values. Therefore, differences in the absorption and plasma levels of these drugs cannot account for the frequent non-response in cirrhotics.Some peptic ulcers are resistant to adequate treatment with a histamine H2-receptor antagonist.' Few of these ulcers heal after changing the H2-antagonist. The efficacy of H2-receptor antagonists is mainly judged by the criterion of ulcer healing -that is, only after four to eight weeks of treatment. It is generally accepted that the nocturnal suppression of gastric acid secretion is most important2 for the therapeutic effect of the H2-receptor antagonists. In patients with ulcers resistant to H2-receptor antagonists, failure of acid suppression was observed.L5 Therefore, socalled non-responders to these agents may be identified by monitoring the gastric acidity at the beginning of the therapy. It has recently been shown that longterm intragastric pH registration is equivalent to pH measurements of gastric aspirates.6 In contrast with the aspiration method, longterm intragastric pH

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Endogenes Plasma-Histamin und »hepatogenes« gastroduodenales Ulkus bei Leberzirrhose

Cited by 3 publications

References 1 publication

Frequency of Peptic Ulcers in Patients with Portal Hypertension

Frequency of Peptic Ulcers in Patients with Portal Hypertension

Peptic Ulcer Surgery in Patients with Liver Cirrhosis

Frequent non-response to histamine H2-receptor antagonists in cirrhotics.

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