The pathogenesis of gastric mucosal lesions in liver cirrhosis

In order to clarify the pathogenesis of peptic ulcers and erosions in patients with liver cirrhosis (LC), I studied concentrations of antral mucosal gastrin (Ant-Ga) and somatostatin (Ant-St), and gastric mucosal blood flow (MBF) in patients with LC. Furthermore, using rats with chronic liver damage induced by carbon tetrachloride, I studied gastric acidity, pepsin activity, serum gastrin (Se-Ga), Ant-Ga and Ant-St concentrations, and MBF. Of 155 patients with LC, peptic ulcers or erosions were observed in 121 patients (78.1%). Ant-Ga was significantly raised in the LC patients without mucosal lesions compared to the LC patients with mucosal lesions and in control patients without liver cirrhosis. MBF was significantly lower in the LC patients compared to the control patients. In the rats with carbon tetrachloride injured livers, gastric acidity, pepsin activity, Ant-St and MBF were significantly lower than in control rats with intact livers. In contrast, Se-Ga and Ant-Ga in the rats with the injured livers were significantly higher than those in the control rats. These results suggest that impairment of the defensive factor represented by MBF rather than the aggressive factor represented by the gastrin level, gastric acidity and pepsin activity play an important role in the pathogenesis of the gastric mucosal lesions in LC.