A histologic study of the liver in patients affected with peptic ulcer

Schnitker, Maurice A.; Hass, George M.

doi:10.1007/bf02998920

Cited by 32 publications

(4 citation statements)

References 26 publications

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“…In the present study, 2 out of 20 (10%) patients with cirrhosis had a duodenal ulcer and both had appreciably high gastric acid levels. Other workers have also ob served increased acid secretion in cirrhotics with peptic ulcer compared to those without an ulcer [3,4]. In this respect, a cirrhotic is not different from a normal person with a duodenal ulcer, however, it remains unclear as to why these patients are more prone to the defect.…”

Section: Discussionmentioning

confidence: 93%

“…Moreover, the gastric hyposection was as marked in the patients with NCPF as in those with cirrhosis, although the former did not suffer from any hepatic decompensation. It is concluded that gastric hyposccrction is not due to a derangement of hepatocyte function but may be secondary to portal hypertension and collateral circulation.It is well established that peptic ulcer oc curs more frequently in patients with cirrho sis compared to the general population [1][2][3]. By contrast, most studies report reduced gastric acid levels in cirrhotics except for those with an ulcer who have raised acid lev els [4][5][6][7], The mechanism of this discrepancy has not been explained and, moreover, the pathogenesis of reduced gastric secretion is not clear.…”

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confidence: 99%

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Gastric Secretion in Cirrhosis and Non-Cirrhotic Portal Fibrosis

Gaur

Vij²,

Sarin³

et al. 1988

Digestion

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Studies on basal and pentagastrin-stimulated gastric secretion were carried out in 20 patients with cirrhosis, 20 with non-cirrhotic portal fibrosis (NCPF) and 20 control subjects. There was no significant difference in the basal volume and acid output between the three groups. However, maximal volume and acid output were significantly lower in patients with cirrhosis and NCPF compared with the control group. There was no correlation between the acid secretion and the degree of hepatocellular dysfunction in patients with cirrhosis. Moreover, the gastric hyposection was as marked in the patients with NCPF as in those with cirrhosis, although the former did not suffer from any hepatic decompensation. It is concluded that gastric hyposecretion is not due to a derangement of hepatocyte function but may be secondary to portal hypertension and collateral circulation.

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Section: Discussionmentioning

confidence: 93%

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confidence: 99%

Gastric Secretion in Cirrhosis and Non-Cirrhotic Portal Fibrosis

Gaur

Vij²,

Sarin³

et al. 1988

Digestion

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“…The concurrent occurrence rate of peptic ulcer in several diseases was investigated to compare with insulinoma. A variety of diseases which have been reported to be associated with a high percentage of peptic ulcers are as follows ; 14.6 to 34.0% (Schnitker and Hass 1934 ;Palmer and Brick 1953;Christensen et al 1981) in chronic liver diseases, 6.8 to 34.0% (Elliot et al 1964;Dreiling and Nagvi 1969 ;Sato et al 1981;Vantini et al 1982) in chronic pancreatitis, 4.6 to 10.0% (Gifford et al 1970 ;Dimitrios et al 1978) in hyperparathyroidism and 12.7 to 21.1% (Barabas et al 1971;Goonetilleke 1979) in arterio-coronary diseases. In our series of insulinoma, the rate to associate peptic ulcer is 20%, which is almost the same high percentage as other disorders listed above.…”

Section: Discussionmentioning

confidence: 99%

Peptic ulcer and gastric acid secretion in patients with insulinoma.

Naitö

Sasaki

Funayama

et al. 1988

Tohoku J. Exp. Med.

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We evaluated the incidence of associated peptic ulcers and the gastric acid secretion in our 20 series of insulinoma, and obtained the following results : 1) Four out of 20 patients (20%) with insulinoma were associated with peptic ulcers. 2) Except for the maximum acid concentration, the preoperative gastric secretion tests, such as the basal acid output and maximum acid output, failed to indicate hyperacidity in those patients. And patients with a short duration of illness by insulinoma neither showed hyperacidity nor were associated with peptic ulcers. 3) A tendency of reduced gastric acid secretion and the amelioration of peptic ulcers was observed in those who underwent the extirpation of insulinoma. 4) In the most recent case received gastric analysis with continuous monitoring of blood glucose level, an increase of basal acid output was observed during the hypoglycemic period in which the blood glucose levels reduced to around 30 mg/100 ml. These results indicate that the low blood glucose level and the high gastric acid secretion produced under the condition on an empty stomach, may be important factors related to the high association rates of the peptic ulcers in patients with insulinoma. -insulinoma : gastric acid secretion ; peptic ulcerIn patients with insulinoma, hypoglycemic attacks, caused by the exess amount of insulin from the pancreatic islet cell tumor, are frequently observed at hunger state. On the other hand, the intravenous injection of insulin is well known to be one of gastric secretion tests, in which stimulation of the vagus nerve induced by hypoglycemia results in the promotion of gastric secretion. Thereby, it is speculated that patients with insulinoma may have an high association rate of peptic ulcer due to the repeated gastric hypersecretions caused by hypoglycemic conditions. However, since the time that the conception of insulinoma was established (Whipple and Frantz 1935), there have been no reports referring the gastric secretion and the occurence of peptic ulcer in patients with insulinoma. From these viewpoints we studied patients with insulinoma who were operated on in our facility.

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“…It seems that the ability of the stomach to secrete PLASMA Pg/mi * 0 incidence of duodenal ulceration with liver disease 20 (Schnitker and Hass, 1934;Ask-Upmark, 1940;co Fainer and Halsted, 1955;Tabaqchali and Dawson, 1964), though disputed (Ratnoff and Patek, 1942; 10 0 Doll, 1952;Sullivan et al, 1954), is therefore difficult to explain in terms of hypersecretion of acid .. so or gastrin. OBSERVED VOLUME (ml/15ml)…”

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confidence: 99%