Welin Martin, Holmgren Noél M A, Nilsson Patric, Enroth Helena
Department of Natural Science, University of Skövde, Sweden.
Helicobacter. 2003 Feb;8(1):72-8. doi: 10.1046/j.1523-5378.2003.00110.x.
The bacterium Helicobacter pylori is associated with a number of gastrointestinal diseases, such as gastric ulcer, duodenal ulcer and gastric cancer. Several histological changes may be observed during the course of infection; some may influence the progression towards cancer. The aim of this study was to build a statistical model to discover direct interactions between H. pylori and different precancerous changes of the gastric mucosa, and in what order and to what degree those may influence the development of the intestinal type of gastric cancer.
To find direct and indirect interactions between H. pylori and different histological variables, log-linear analyses were used on a case-control study. To generate mathematically and biologically relevant statistical models, a designed algorithm and observed frequency tables were used.
The results show that patients with H. pylori infection need to present with proliferation and intestinal metaplasia to develop gastric cancer of the intestinal type. Proliferation and intestinal metaplasia interacted with the variables atrophy and foveolar hyperplasia. Intestinal metaplasia was the only variable with direct interaction with gastric cancer. Gender had no effect on the variables examined.
The direct interactions observed in the final statistical model between H. pylori, changes of the mucosa and gastric cancer strengthens and supports previous theories about the progression towards gastric cancer. The results suggest that gastric cancer of the intestinal type may develop from H. pylori infection, proliferation and intestinal metaplasia, while atrophy and foveolar hyperplasia interplay with the other histological variables in the disease process.
幽门螺杆菌与多种胃肠道疾病相关,如胃溃疡、十二指肠溃疡和胃癌。在感染过程中可观察到几种组织学变化;其中一些可能影响癌症的进展。本研究的目的是建立一个统计模型,以发现幽门螺杆菌与胃黏膜不同癌前变化之间的直接相互作用,以及这些变化可能以何种顺序、在何种程度上影响肠型胃癌的发生发展。
为了找出幽门螺杆菌与不同组织学变量之间的直接和间接相互作用,在一项病例对照研究中采用了对数线性分析。为了生成数学和生物学上相关的统计模型,使用了一种设计算法和观察频率表。
结果表明,幽门螺杆菌感染患者需要出现增殖和肠化生才能发展为肠型胃癌。增殖和肠化生与萎缩和小凹上皮增生变量相互作用。肠化生是与胃癌有直接相互作用的唯一变量。性别对所检查的变量没有影响。
在最终统计模型中观察到的幽门螺杆菌、黏膜变化与胃癌之间的直接相互作用,强化并支持了先前关于胃癌进展的理论。结果表明,肠型胃癌可能由幽门螺杆菌感染、增殖和肠化生发展而来,而萎缩和小凹上皮增生在疾病过程中与其他组织学变量相互作用。