Yin G Y, He X F, Yin Y F
Wuxi No. 3 Hospital.
Zhongguo Zhong Xi Yi Jie He Za Zhi. 1995 Dec;15(12):719-23.
Eighty-eight gastropathic patients with Spleen deficiency syndrome by using transmission electron microscope (TEM), X-ray energy disperse analysis system (EDAX), histochemical staining and radioimmuno methods were examined. The authors found that the gastric mucosa cAMP, SOD level, the quantity of mitochondria and its crista, the ratio of diameter between ventricle and cavity of mitochondria and the content of Zn, Cu of mitochondria were reduced in the trend of healthy control group, Spleen Qi deficiency group, Spleen deficiency with Qi stagnation group; chronic superficial gastritis group, chronic atrophic gastritis group, gastric cancer group: complete small intestinal metaplasia group, incomplete small intestinal metaplasia group, complete colonic intestinal metaplasia group, incomplete colonic intestinal metaplasia group (P < 0.05-0.001). While the degeneration rate of mitochondria, the Cu/Zn ratio of mitochondria, the metaplasia rate of gastric, the rate of incomplete colonic intestinal metaplasia and the content of serum LPO were increased in the above turn. It is suggested that the comprehensive effect of the degeneration of mitochondria and the quantitative changes of its correlative factors is the physiopathologic base for inducing Spleen deficiency disease, gastric mucosa metaplasia and canceration. Much attention must be paid in clinic to the cancerization trend of gastric disease with Spleen deficiency syndrome.
采用透射电镜（TEM）、X射线能谱分析系统（EDAX）、组织化学染色及放射免疫法对88例脾虚证胃病患者进行检测。作者发现，胃黏膜cAMP、SOD水平、线粒体及其嵴的数量、线粒体的直径与内腔直径之比以及线粒体的锌、铜含量在健康对照组、脾气虚组、脾虚气滞组；慢性浅表性胃炎组、慢性萎缩性胃炎组、胃癌组：完全性小肠化生组、不完全性小肠化生组、完全性大肠化生组、不完全性大肠化生组中呈降低趋势（P<0.05 - 0.001）。而线粒体的退变率、线粒体的铜/锌比值、胃化生率、不完全性大肠化生率及血清LPO含量则依次升高。提示线粒体退变及其相关因素的量的变化的综合作用是导致脾虚证、胃黏膜化生及癌变的病理生理基础。临床应高度重视脾虚证胃病的癌变倾向。
