Background: Gastric mucosal lesions in chronic liver diseases are uncommon. However, the pathogenesis and mechanism of gastric mucosal lesions are unclear. To investigate the cause of gastric red spots (Mucosal vascular ectasia), we measured fasting s...
Background: Gastric mucosal lesions in chronic liver diseases are uncommon. However, the pathogenesis and mechanism of gastric mucosal lesions are unclear. To investigate the cause of gastric red spots (Mucosal vascular ectasia), we measured fasting serum pepsinogen I level. Method: To investgate the secretory function of gastric mucosa in liver cirrhosis and the causes of gastric red spots, we measured fasting serum pepsinogen. I. Forty-one subjects were studied: ten with liver cirrhosis showing endoscopic gastric red spots, sixteen with liver cirrhosis not showing gastric lesions, and twenty-five normal controls. Result: In control groups, the results showed higher levels of serum pepsinogen I in smokers than in nonsmokers. Serum Pepsinogen I levels were significantly lower in cirrhotic patients than normal control groups (73.64±4.65ng/ml vs, 118.85±5.45ng/ml: p<0.001) and were significantly lower in cirrhotic patients with gastric red spots than in cirrhotics without these lesions (57.78±7.02ng/ml vs. 83.55±4.81ng/ml: p<0.005). Serum pepsinogen I levels were not influenced by the etiology of liver cirrhosis, the form of esophageal varices, and severity of liver cirrhosis. Conclustion: Serum pepsinogen I levels were significantly lower in cirrhotics and especially much lower in cirrhotics with gastric red spots than without these lesion, and these results suggest that the pathogenesis of gastric red spots may be related to the decreased levels of serum pepsinogen I.