Konturek S J, Konturek P C, Pieniazek P, Bielański W
Department of Physiology, Jagiellonian University School of Medicine, Cracow, Poland.
J Physiol Pharmacol. 1999 Dec;50(5):683-94.
Numerous studies initiated by Warren and Marshall in 1982 confirmed the crucial role of H. pylori infection in the pathogenesis of gastritis, peptic ulcer and possibly also gastric cancer leading to reappraisal of fundamental concept of gastric pathophysiology. These topics were covered, in part, by our previous H. pylori-related symposium I (1995), II (1997) and III (1999) organized in Cracow. H. pylori is one of the most frequent causes of gastroduodenal infection worldwide, resulting in the release of various bacterial and host dependent cytotoxic substances including ammonia, platelet activating factor (PAF), cytotoxins and lipopolysaccharides (LPS) as well as cytokines such as interleukins (IL)-1-12, tumor necrosis factor alpha (TNF(alpha), interferon gamma (INFgamma) and reactive oxygen species (ROS). Recently, several extradigestive pathologies have been linked to H. pylori infection including cardiovascular, cutaneous, autoimmune, esophageal and other diseases such as sideropenic anemia, growth retardation, extragastric MALT-lymphoma etc. The potential role of H. pylori infection in the pathogenesis of these extradigestive disorders has been based on facts that 1) local gastric inflammation may exert systemic effects, 2) chronic infection of gastric mucosa induces immune responses that are able to cause the lesions remote to primary site of infection and 3) H. pylori eradication improves the extradigestive disorders. The aim of present III International Symposium is to provide critical reviews based on personal experience and the available literature about extragastric manifestations of H. pylori infection. The ultimate goal of this symposium is to foster interdisciplinary research and exchange of opinion about the possible involvement of H. pylori in extradigestive pathologies.
1982年沃伦和马歇尔发起的众多研究证实了幽门螺杆菌感染在胃炎、消化性溃疡乃至胃癌发病机制中的关键作用,这导致了对胃病理生理学基本概念的重新评估。我们之前于1995年、1997年和1999年在克拉科夫举办的与幽门螺杆菌相关的研讨会I、II和III部分涵盖了这些主题。幽门螺杆菌是全球范围内胃十二指肠感染最常见的病因之一,会释放各种细菌和宿主依赖性细胞毒性物质,包括氨、血小板活化因子(PAF)、细胞毒素和脂多糖(LPS),以及细胞因子,如白细胞介素(IL)-1至12、肿瘤坏死因子α(TNFα)、干扰素γ(INFγ)和活性氧(ROS)。最近,几种消化系统外的病症已与幽门螺杆菌感染相关联,包括心血管疾病、皮肤疾病、自身免疫性疾病、食管疾病以及其他疾病,如缺铁性贫血、生长发育迟缓、胃外黏膜相关淋巴组织淋巴瘤等。幽门螺杆菌感染在这些消化系统外疾病发病机制中的潜在作用基于以下事实:1)局部胃部炎症可能产生全身影响;2)胃黏膜的慢性感染诱导免疫反应,能够导致远离感染原发部位的病变;3)根除幽门螺杆菌可改善消化系统外疾病。本次第三届国际研讨会的目的是基于个人经验和现有文献,对幽门螺杆菌感染的胃外表现进行批判性综述。本次研讨会的最终目标是促进跨学科研究,并就幽门螺杆菌可能参与消化系统外疾病的问题交流意见。