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Objectives: Patients with cirrhosis often have gastric mucosal lesions associated with portal hypertension. Microvascular changes due to portal hypertension may cause mucosal ischaemia. The decrease in intramucosal pH is used as an index of this condition. In this study we compared the gastric intramucosal pH in patients with cirrhosis and portal hypertension and in control group.
Methods: Estimates of pH were calculated using the Henderson-Hasselbalch equation, assuming that measured concentrations of CO2 in the gastric lumen (pCO2) and of HCO3- in arterial blood represented intramucosal CO2 and intramucosal HCO3- concentrations, respectively. Tonometer measurements of intragastric CO2, validated in vitro, were made in patients treated by famotidine (10 mg.h-1 continuous infusion) to suppress gastric acid secretion and minimize CO2 production from luminal gastric bicarbonate. Intramucosal pH was determined in 19 control patients (mean age: 50.2 years) and in 25 patients with cirrhosis and portal hypertensive gastropathy (mean age: 54.2 years). In the patients with cirrhosis the severity of mucosal and parietal abnormalities induced by portal hypertension were graded according to endoscopic score from 0 to 9 and endoscopic ultrasonography score from 0 to 3.
Results: The mean endoscopic and ultrasonographic scores were 5.0 and 1.8 respectively. The median gastric intramucosal pH of patients with cirrhosis (7.42; range: 7.36 to 7.53) was similar to that of the controls (7.42; range: 7.33-7.51). A positive correlation was found between intramucosal pH and severity of portal hypertensive gastropathy, in the antrum, but not in the fundus.
Conclusion: These findings do not support the hypothesis that gastric mucosal lesions are the consequence of ischaemia in patients with cirrhosis.
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