长期饮酒胃黏膜病理改变与PGE2和EGF的关系

摘要

目的 探讨长期饮酒患者胃黏膜病理改变与PGE2和EGF的关系.方法 选择因长期饮酒于2007年1月～2010年12月在我院进行胃镜检查并进行胃黏膜活检及血液和胃液前列腺素E2( PGE2)和表皮生长因子(EGF)检测的120例患者作为研究对象.按组织病理学分组进行对照研究.结果 与长期饮酒轻度胃黏膜慢性炎症组患者比较,长期饮酒胃黏膜中重度慢性炎症组患者血清和胃液EGF明显升高(P =0.000;P =0.028),而血清和胃液PGE2升高不明显(P =0.089;P =0.760).与长期饮酒胃黏膜轻度萎缩组患者比较,长期饮酒胃黏膜中重度萎缩组患者血清EGF明显升高(P=0.000),而胃液EGF和血清PGE2降低(P =0.846;P=0.362),胃液PGE2略升高(P=0.936).与长期饮酒胃黏膜轻度肠化组患者比较,长期饮酒胃黏膜中重度肠化组患者血清EGF明显升高(P=0.000),而胃液EGF、血清和胃液PGE2升高,但差异无统计学意义(P =0.123;P=0.621;P =0.154).与长期饮酒胃黏膜无不典型增生组患者比较,长期饮酒胃黏膜不典型增生组患者血清和胃液EGF明显升高(P=0.000；P=0.003),而血清和胃液PGE2虽升高,但差异无统计学意义(P=0.329；P=0.618).结论 长期饮酒引起EGF分泌升高与胃黏膜慢性炎症、胃黏膜癌前状态和癌前病变的发生和发展有一定的关系,但PGE2在上述病变中变化并不一致,有待于进一步研究.%Objective To explore the relationship of pathological changes of gastric mucosa with Prostaglandin E2 and Epidermal growth factors of serum and gastric juice in patients with chronic ethanol ingestion. Methods A study of gastric mucosa acquired by gastroscope and measurement of ECF and PGE2 in serum and gastric juice were conducted in 120 consecutive patients of chronic ethanol ingestion from January 2007 to December 2010. Histopathological contrast research was done. Results Compared with patients with mild chronic inflammation of gastric mucosa in chronic ethanol ingestion, ECF in the serum and gastric juice in the moderate and severe chronic inflammation of gastric mucosa significantly increased (P =0. 000;P =0. 028) , but the PGE2 in serum and gastric juice were not obviously raised (P = 0.089; P =0.760). Compared with paients with mild gastric mucosa atrophy in chronic ethanol ingestion, ECF in the serum ECF in the moderate and severe chronic inflammation of gastric mucosa significantly increased (P =0.000) , but no statistical significance was seen in the reduction of EGF in gastric juice and PGE2 in serum ( P = 0. 846; P = 0. 362) and the slightly increase of PGE2 in gastric juice {P = 0.936). Compared with patients with mild intestinal metaplasia in chronic ethanol ingestion, EGF in serum in the moderate and severe intestinal metaplasia of gastric mucosa significantly increased (P =0.000) , but EGF in the gastric juice and PGE2 in the serum and gastric juice were higher and no significant difference (P =0. 123; P =0. 621; P =0. 154). Compared with patients with mild gastric mucosal dysplasia in chronic ethanol ingestion, EGF in the serum and gastric juice in the moderate and severe gastric mucosal dysplasia significantly increased (P =0. 000; P =0.003), PCE2 in the serum and gastric juice were higher but no significant difference (P =0.329; P= 0.618). Conclusion The chronic gastric mucosa inflammation, gastric precancerous state and precancerous lesions were caused by increase of EGF secretion in chronic ethanol in-gestion, due to no consistent with the changes of PGE2, it needs further investigation.