Gastric Secretion in Cirrhosis and Non-Cirrhotic Portal Fibrosis

Abstract

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.

Does portal hypertension contribute to the pathogenesis of gastric ulcer associated with liver cirrhosis?

“…The mechanisms of decreased acid secretion in liver cirrhosis are not well understood. Gaur et al 18 did not find a correlation between acid secretion and the degree of hepatocellular dysfunction in patients with cirrhosis. Moreover, pentagastrin-stimulated gastric acid secretion was significantly lower in their portal hypertensive patients with liver cirrhosis as well as in their patients with non-cirrhotic portal fibrosis when compared with controls, suggesting that portal hypertension is responsible for decreased acid secretion in cirrhosis patients.…”

Portal Hypertensive Gastropathy

“…Second, portal-systemic shunt surgery appears to be effective in the management of diffuse gastric mucosal bleed ing secondary to severe PHG [54], Finally, PHTN may be responsible at least in part for the stasis and congestion observed in such patients. PHG in both humans and experi mental animals is associated with hypochlorhydria or achlorhydria [8,47,[55][56][57], hypergastrinemia [8,47], low serum pepsinogen I level [8], reduced gastric transmural potential difference and greater permeability to acid back-diffusion [58][59][60]. In addition, there are alterations of the gastric microcirculation [2.…”

“…The morphologic and hemodynamic changes of the gastric microcirculation have been extensively investigated in rats, using the staged portal vein ligation model [3,54,56,75]. Early experimental studies were per formed 2 and 5 days following partial or com plete portal vein constriction [2,3,77], Five days after the first stage of portal vein occlu sion, the gastric mucosa becomes swollen and hyperemic, and the lumen of the microvessels at the level of the muscularis mucosa is re duced, due to a prominent increase of vascu lar endothelium [2], Thus, it has been postu lated that diminution of the vascular lumen and the arteriovenous shunting cause a de crease in effective mucosal blood flow, ren dering the gastric mucosa more susceptible to injury [3].…”

Effects of ammonia solution on the gastric mucosa in cirrhotic rats and therapeutic effects of geranylgeranylacetone

“…Gastric mucosal lesions are frequently observed in cirrhotic patients 1 , 2 . The aetiology of the lesions has been considered to be mainly related to portal hypertension 3–6 . Other factors, such as Helicobacter pylori infection, superimposed to cirrhosis should be investigated if those are related to the aetiology of the lesions.…”

“…1,2 The aetiology of the lesions has been considered to be mainly related to portal hypertension. [3][4][5][6] Other factors, such as Helicobacter pylori infection, superimposed to cirrhosis should be investigated if those are related to the aetiology of the lesions. However, the few data available concerning the prevalence of H. pylori infection and its epidemiology in cirrhosis are contradictory.…”