PATHOPHYSIOLOGY OF HELICOBACTER-PYLORI INFECTION
PATHOPHYSIOLOGY OF HELICOBACTER-PYLORI INFECTION
复制标题
DOI：
10.3109/00365529409105353
复制
发表时间：
1994-01-01
影响因子：
1.9
通讯作者：
DIXON, MF
中科院分区：
文献类型：
--
作者：
DIXON, MF
幽门螺杆菌是引起慢性胃炎的主要原因。对感染的最初反应是急性嗜酸性胃炎，在大多数人中发展为活动性慢性胃炎。目的：明确H.幽门螺杆菌，无论是慢性胃炎的个体组织学特征和它的地形图模式必须表明是由感染引起的。表面上皮变性可能是细菌产物直接损伤组织的结果。候选物是氨或铵产物、细胞毒素、磷脂酶和促炎产物如脂多糖和血小板活化因子。中性粒细胞多形性和慢性炎性细胞浸润是粘膜对细菌抗原的免疫应答的结果。补体产物和白细胞介素（IL）-8是多晶型趋化因子，单核细胞处理抗原，随后是T辅助细胞和B淋巴细胞反应，解释了这些细胞在粘膜中的存在。萎缩可能是中性粒细胞和单核细胞活化的自身破坏性产物，如活性氧代谢产物和蛋白酶的结果。肠上皮化生很可能是一种适应性反应，可能是对H。幽门螺杆菌感染，加重了其他有害因素，如胆汁反流和饮食刺激。Pangaiti是H之后的通常结果。幽门感染其次是多灶性萎缩和肠上皮化生。后一种变化进一步削弱粘膜防御，可能导致消化性溃疡。感染H.幽门将表现出胃炎的胃窦限制，因为高酸输出保护粘膜体免受细菌粘附和炎性后果。这类患者在近端十二指肠也有酸诱导的胃化生。然后细菌可以在十二指肠的胃型上皮上定植，并形成活动性慢性胃炎。该部位的慢性炎症会削弱粘膜，使其易受酸/消化性攻击，导致明显的溃疡。
Helicobacter pylori is now accepted as the major cause of chronic gastritis. The initial response to infection is acute neutrophilic gastritis, which progresses to active chronic gastritis in most people. To confirm the pathogenic role of H. pylori, both the individual histological features of chronic gastritis and its topographical patterns must be shown to be caused by the infection. Surface epithelial degeneration is a probable result of direct tissue injury by bacterial products. Candidates are ammonia or ammonium products, cytotoxins, phospholipases and pro-inflammatory products such as lipopolysaccharide and platelet-activating factor. Neutrophil polymorph and chronic inflammatory cell infiltration are consequences of the mucosal immune response to bacterial antigens. Complement products and interleukin (IL)-8 are polymorph chemotaxins, and monocyte processing of antigens, followed by T helper cell and B lymphocyte responses, explain the presence of these cells in the mucosa. Atrophy may be a consequence of autodestructive products of neutrophil and monocyte activation, such as reactive oxygen metabolites and proteases. Intestinal metaplasia is most probably an adaptive response, possibly to H. pylori infection, exacerbated by other injurious agents such as bile reflux and dietary irritants. Pangastritis is the usual outcome after H. pylori infection. This is followed by multifocal atrophy and intestinal metaplasia. The latter changes weaken mucosal defences further and peptic ulceration may ensue. Patients with an increased parietal cell mass who become infected with H. pylori will exhibit antral restriction of the gastritis because the high acid output protects the corpus mucosa from bacterial adhesion and the inflammatory consequences. Such patients also have acid-induced gastric metaplasia in the proximal duodenum. Bacteria can then colonize the gastric-type epithelium in the duodenum and set up an active chronic duodenitis. Chronic inflammation at this site weakens the mucosa and renders it susceptible to acid/peptic attack, leading to frank ulceration.