ABSTRACT
Thirty patients with endoscopically proven peptic ulcer and thirty healthy adult volunteers with no history of dyspepsia, were admitted to this study. Basal gastric juice were obtained in the fasting state for measurement of basal acid output, analysis of gastric mucin fractions and pH studies in these two groups. The mean basal acid output was 3.04mmol/hr for patients with peptic ulcer disease and 1.32mmol/hr of healthy controls. The results obtained showed a significant difference (P<0.001) between the control group and patients with peptic ulcer. These figures are much lower than values obtained from western countries, but similar to those reported from studies in noncaucasians. The mean values obtained for pH levels in healthy controls and patients with peptic ulcer were 2.22 and 1.8 respectively. The pH of the gastric juice was significantly lower (P<0.025) in peptic ulcer patients when compared to controls. The mean level of acidic mucoprotein-pepsin complex in healthy controls and peptic ulcer patients were 165.3ug/ml and 253.4ug/ml respectively. Meanwhile, the mean values obtained for neutral glycoprotein-mucoproteose complex were 211.3ug/ml (healthy controls) and 110.5ng/ml (patients with peptic ulcer). The concentration of acidic mucoprotein-pepsin complex was significantly increased (P<0.001) whereas neutral glycoproteinmucoproteose complex was significantly decreased (P<0.001) in patients with peptic ulcer disease as compared to healthy controls. The ucoprotective index was significantly decreased (P<0.025) in patients with peptic ulcer disease. The mean values were 56.1% and 30.4% for healthy controls and patients with peptic ulcer respectively. The significant increase in acid mucoprotein-pepsin complex and a marked reduction in the concentration of neutral glycoprotein-mucoproteose complex may be considered as a reduction in mucosal protective mechanism against potential ulcerogenic agents such as acid and pepsin. Taken overall, the association between dietary intake, alcohol ingestion, smoking and ulcer is weak and these factors can best play a minor causal role in ulcer development. The data presented above give support to the hypothesis that peptic ulceration is an heterogenous disease but it is likely that a high acid output and low mucoprotect ive index may be indicative of peptic ulceration. It is concluded that a reduction in the neutral glycoprotein-mucoproteose complex is indicative of a reduction in mucosal protective mechanism against endogenous ulcerogenic agents such as acid and pepsin, because this fraction of the gastric mucin may contain the inhibitor found by other investigators in human gastric juice.