ackground : 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 showingendoscopic gastric red spots, sixteen with liver
cirrhosis not showing gastric lesions, and twenty-five normal controls.
Results : In control groups, the results showed higher levels of serum pepsinogen I in
smokers thanin nonsmokers. Serum Pepsinogen I levels were significantly lower in cirrhotic
patients than normal control groups (73.64±4.65 ng/ml vs. 118.85±5.45 ng/ml: p<0.001) and
were significantly lower in cirrhotic patients with gastric red spots than in cirrhotics without
these lesions (57.78±7.02 ng/ml vs. 83.55±4.81 ng/ml: p<0.005). Serum pepsinogen I levels
were not influeced by the etiology of liver cirrhosis, the for m of esophageal varices, and
everity of liver cirrhosis.
Conclusion : 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 dedreased levels of
serum pepsinogen I.
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