摘要
为探讨幽门螺杆菌(HP)感染在胃癌发病中的可能机制,应用银染技术定量观察34例HP阳性及12例HP阴性胃窦粘膜核仁组成区嗜银蛋白(AgNORs)的变化,并对HP阳性者进行抗HP治疗.结果显示HP感染时胃粘膜AgNORs计数显著增高(1.86±0.16与1.54±0.13,P<0.01),且AgNORs计数与胃粘膜炎症程度正相关(r=0.5330,P<0.01),但与HP菌量无相关(r=0.2314,P>0.05);根除HP后,胃粘膜AgNORs计数从1.94±0.01降至1.35±0.14(P<0.01),而HP未根除组AgNORs计数无显著性变化(1.82±0.14与1.73±0.17,P>0.05).提示HP感染增加胃粘膜增殖活性,可能在胃癌发生过程中起重要作用,而根除HP可降低细胞增殖活性,对预防胃癌发生可能具有重要意义.
To explore the role of helicobacter pylori (HP) infection in the development of gastric carcinoma. The argyphilic nucleolar onganizer regions (AgNORs) of gastric antral mucosa were quantitatively observed in 34 HP positive and 12 HP negative patients by silver staining technique, and the patients with HP positive were received anti-HP therapy. The results showed that the number of AgNORs per nuclei in patients with HP positive increased significantly ( 1. 86± 0 . 16 vs 1 . 54± 0 . 13, P< 0 .01 ), furthermore, the number of AgNORs per nuclei positively correlated with the severity of gastric antral inflammation ( r = 0.2314, P>0.05), but didn' t correlate with the quantity of HP ( r= 0.2314, P>0.05). After anti-HP therapy, the number of AgNORs per nuclei in patients with HP eradication decreased significantly from 1.94±0 .11 to 1.35±0 .14 ( P < 0 .01), where as the number of AgNORs per nuclei in patients without HP eradication remained unchanged (1.82±0.14 vs 1. 73 ±0.17, P >0 .05 ). It is suggested that HP infection in gastric mucosa could accelerate the cell proliferating activity and play a significant role in the development of gastric carcinoma, and eradication of HP infection to reduce the cell proliferating activity may be of important in the prevention of genesis of gastric carcinoma.
出处
《临床消化病杂志》
1998年第3期108-110,共3页
Chinese Journal of Clinical Gastroenterology