Sipponen P, Kekki M, Seppälä K, Siurala M
Department of Pathology, Jarvi Hospital, Espoo, Finland.
Aliment Pharmacol Ther. 1996 Apr;10 Suppl 1:103-18. doi: 10.1046/j.1365-2036.1996.22164011.x.
Helicobacter pylori is the main cause of chronic gastritis in humans. Autoimmune mechanisms and Helicobacter heilmannii infection are other causes, both of which are of minor significance in a worldwide perspective. Atrophic gastritis is a quite common late consequence of H. pylori gastritis and will develop on a multifactorial basis, but not in all infected persons. The evolution of atrophic gastritis is a slow and gradually worsening process leading to subtypes, in which the antrum and corpus are affected to dissimilar extent and degree. The distal part of the stomach is the site where the atrophic sequelae (atrophic gastritis and intestinal metaplasia) of H. pylori infection occur most often. A minority of cases develop corpus-limited, or corpus-predominant atrophic gastritis. Along with the worsening of atrophic gastritis, inflammation and density of colonization of the mucosa by H. pylori tend to decrease in grade. In general, the degree of gastric mucosal inflammation, acute and chronic, is positively related to the degree of colonization of the mucosa by H. pylori. Acid secretion and local acidity are factors which modulate the ecology and density of colonization of H. pylori in the stomach, and may thus also modulate the evolution of chronic gastritis into topographically dissimilar subtypes. Acid secretion varies among individuals, this variation being perhaps caused by hereditary differences in parietal cell mass, or by differences in the sensitivity of parietal cells to hormonal or neural stimuli. It is hypothesized that in genuine hypersecretors, H. pylori colonization and subsequent gastritis with atrophic and metaplastic sequelae may be limited to the antrum, while in hyposecretors gastritis predominates in the corpus. In the latter, atrophic gastritis in the corpus then leads to further impairment of acid output. In these cases, H. pylori infection and gastritis may, finally, heal in the antrum, resulting in hypochlorhydria and atrophic gastritis that is limited to, or predominant in the corpus.
幽门螺杆菌是人类慢性胃炎的主要病因。自身免疫机制和海氏螺杆菌感染是其他病因，从全球范围来看，这两种病因的重要性相对较小。萎缩性胃炎是幽门螺杆菌胃炎相当常见的晚期后果，其发展是多因素的，但并非所有感染者都会出现。萎缩性胃炎的演变是一个缓慢且逐渐恶化的过程，会导致不同亚型，其中胃窦和胃体受影响的程度和范围不同。胃的远端是幽门螺杆菌感染萎缩性后遗症（萎缩性胃炎和肠化生）最常发生的部位。少数病例会发展为局限于胃体或胃体为主的萎缩性胃炎。随着萎缩性胃炎的加重，幽门螺杆菌在黏膜的炎症和定植密度往往会降低。一般来说，胃黏膜急慢性炎症的程度与幽门螺杆菌在黏膜的定植程度呈正相关。胃酸分泌和局部酸度是调节幽门螺杆菌在胃内生态和定植密度的因素，因此也可能调节慢性胃炎演变为不同部位亚型的过程。个体之间胃酸分泌存在差异，这种差异可能是由壁细胞数量的遗传差异，或壁细胞对激素或神经刺激的敏感性差异引起的。据推测，在真正的胃酸分泌过多者中，幽门螺杆菌定植及随后伴有萎缩和化生后遗症的胃炎可能局限于胃窦，而在胃酸分泌过少者中，胃炎以胃体为主。在后者中，胃体部的萎缩性胃炎会进一步导致胃酸分泌受损。在这些情况下，幽门螺杆菌感染和胃炎最终可能在胃窦愈合，导致胃酸过少和局限于胃体或胃体为主的萎缩性胃炎。
