Peek Richard M.
Division of Gastroenterology, Vanderbilt University School of Medicine, C-2104 Medical Center North, Nashville, TN 37232-2279, USA.
Curr Treat Options Gastroenterol. 2004 Feb;7(1):59-70. doi: 10.1007/s11938-004-0026-0.
Since the rediscovery of Helicobacter pylori two decades ago, it has become increasingly clear that the true relationships between this organism and diseases of the upper gastrointestinal tract are highly complex. H. pylori colonization is a strong risk factor for peptic ulceration and distal gastric cancer; however, gastritis has no adverse consequences for most hosts, and the prevalence of H. pylori is inversely related to gastroesophageal reflux disease (GERD) and its sequelae, which include Barrett's esophagus and esophageal adenocarcinoma. One clinical implication stemming from these data is that H. pylori eradication may not be appropriate in certain human populations due to potential beneficial effects conferred by persistent gastric inflammation. However, the majority of published intervention trials indicate that H. pylori treatment neither leads to the development of clinically significant de novo esophagitis nor exacerbates existing reflux disease. Superimposed upon these observations are reports that long-term acid suppression induced by proton-pump inhibitors (PPIs) in conjunction with H. pylori colonization may enhance the development of atrophic gastritis, a well-recognized histologic step in the progression to intestinal-type gastric cancer. Therefore, current evidence-based recommendations regarding management of H. pylori-positive individuals with GERD include the following. H. pylori should not be treated with the intent to either improve reflux symptoms or prevent the development of reflux complications. However, if patients are to receive long-term acid suppressive therapy, they should be tested for H. pylori and treated if positive, due to the potential for PPIs to accelerate atrophy within H. pylori-infected mucosa. Optimal first-line regimens in this country consist of a PPI in combination with clarithromycin and either amoxicillin or metronidazole (triple therapy) for at least 7, but preferably 10, days. Because the most effective second-line regimens contain metronidazole, it is advisable to use amoxicillin instead of metronidazole as first-line therapy in order to optimize results should subsequent therapy be required. If first-line regimens fail to eliminate H. pylori, patients should receive quadruple therapy consisting of a PPI, bismuth subsalicylate, metronidazole, and tetracycline for 14 days. Due to the availability and accuracy of noninvasive diagnostic tests for H. pylori, it is recommended that successful cure be confirmed after intervention.
自二十年前幽门螺杆菌被重新发现以来，这种微生物与上消化道疾病之间的真实关系愈发复杂。幽门螺杆菌定植是消化性溃疡和远端胃癌的一个重要危险因素；然而，胃炎对大多数宿主并无不良后果，而且幽门螺杆菌的流行率与胃食管反流病（GERD）及其后遗症（包括巴雷特食管和食管腺癌）呈负相关。这些数据带来的一个临床启示是，由于持续性胃炎可能带来潜在益处，在某些人群中根除幽门螺杆菌可能并不合适。然而，大多数已发表的干预试验表明，治疗幽门螺杆菌既不会导致临床上显著的新发食管炎，也不会加重现有的反流病。除了这些观察结果之外，还有报告称质子泵抑制剂（PPI）联合幽门螺杆菌定植长期抑制胃酸可能会加速萎缩性胃炎的发展，而萎缩性胃炎是公认的进展为肠型胃癌的组织学阶段。因此，目前关于GERD幽门螺杆菌阳性个体管理的循证建议如下。不应为改善反流症状或预防反流并发症而治疗幽门螺杆菌。然而，如果患者要接受长期抑酸治疗，应检测幽门螺杆菌，若为阳性则应进行治疗，因为PPI有可能加速幽门螺杆菌感染黏膜内的萎缩。该国最佳的一线治疗方案是PPI联合克拉霉素以及阿莫西林或甲硝唑（三联疗法），持续至少7天，但最好为10天。由于最有效的二线治疗方案含有甲硝唑，因此建议在一线治疗时使用阿莫西林而非甲硝唑，以便在后续需要治疗时优化治疗效果。如果一线治疗方案未能根除幽门螺杆菌，患者应接受由PPI、次水杨酸铋、甲硝唑和四环素组成的四联疗法，持续14天。鉴于针对幽门螺杆菌的非侵入性诊断检测的可用性和准确性，建议在干预后确认成功治愈。
