Peraza S, Vivas J, López G, Carrillo E, Oliver W, Andrade O, Castro D, Cano E, Sánchez V
Centro de Control de Cáncer Gastrointestinal Dr. Luis E. Anderson, San Cristóbal, Edo. Táchira, Venezuela.
G E N. 1995 Jan-Mar;49(1):55-63.
Intestinal Metaplasia (IM) and Helicobacter Pylori (HP) infection had been related to gastric carcinogenesis. With the intention to know the relationship among HP infection, IM and inflammatory response of the mucosa in an area of high prevalence of gastric cancer, we studied 800 persons that attended the Gastric Cancer Mass Survey, ongoing in the State Tachira, Venezuela, since 1981. Out of these subjects, 259 had histology diagnosis of IM (32.4%) 52.1% were IM type Y, 19.3% type II and 22.8% type III (sulfomucin secretory). Histology demonstrated with Giemsa stain HP in 94.6% of the cases. Association between HP and inflammation response in gastric mucosa with IM, was statistically significant (p = 0.001). The are heavier bacteria overload in IM type I than in type III although it is not statistically significant. We ponder if gastric mucosa inflammation due to HP, conditions development of IM as a hostile way of the gastric environment to restrain bacterial growth. This phenomenon ally with other oncogeneous factors could induce to premalignant lesions and eventually gastric cancer.
肠化生(IM)和幽门螺杆菌(HP)感染与胃癌发生有关。为了解胃癌高发地区HP感染、IM与黏膜炎症反应之间的关系,我们对自1981年以来在委内瑞拉塔奇拉州进行的胃癌大规模调查中的800人进行了研究。在这些受试者中,259人经组织学诊断为IM(32.4%),其中52.1%为Y型IM,19.3%为II型,22.8%为III型(分泌硫酸黏蛋白)。组织学检查用吉姆萨染色显示94.6%的病例中有HP。HP与IM患者胃黏膜炎症反应之间的关联具有统计学意义(p = 0.001)。I型IM中的细菌负荷比III型更重,尽管差异无统计学意义。我们推测,HP引起的胃黏膜炎症是否是胃环境抑制细菌生长的一种不利方式,从而导致IM的发生。这种现象与其他致癌因素共同作用,可能诱发癌前病变并最终导致胃癌。