Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication
Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication
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DOI：
10.1056/nejm199604183341603
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发表时间：
1996-04-18
影响因子：
158.5
通讯作者：
Meuwissen, SGM
中科院分区：
文献类型：
--
作者：
Kuipers, EJ;Lundell, L;Meuwissen, SGM
背景。幽门螺杆菌感染在萎缩性胃炎和肠化生的发展中起着重要作用，这些疾病使患者容易患上胃癌。胃酸的深度抑制与幽门螺杆菌引起的胃炎的严重程度增加有关，但尚不清楚胃酸抑制是否会增加萎缩性胃炎的风险。方法。我们研究了来自两个不同队列的正在接受反流性食管炎治疗的患者：瑞典的 72 名患者接受胃底折叠术治疗，荷兰的 105 名患者接受奥美拉唑（20 至 40 毫克，每天一次）治疗。在这两个队列中，患者平均随访五年（范围为三到八年）。胃底折叠术后，患者未接受抑酸治疗。首次就诊时，胃底折叠术组通过组织学评估以及奥美拉唑组通过组织学和血清学评估评估幽门螺杆菌的存在。患者未接受幽门螺杆菌感染治疗。治疗前和随访期间，患者重复接受胃镜检查，并活检取样进行组织学评估。结果。在接受胃底折叠术治疗的患者中，基线时感染幽门螺杆菌的 31 名患者和未感染的 41 名患者均未发展为萎缩性胃炎； 1例感染幽门螺杆菌的患者治疗前患有萎缩性胃炎，治疗后持续存在。在接受奥美拉唑治疗的患者中，基线时没有患有萎缩性胃炎的患者中，59 名幽门螺杆菌感染者中，有 18 名患者发展为萎缩性胃炎（P
Background. Helicobacter pylori infection plays an important part in the development of atrophic gastritis and intestinal metaplasia, conditions that predispose patients to gastric cancer. Profound suppression of gastric acid is associated with increased severity of gastritis caused by H. pylori, but it is not known whether acid suppression increases the risk of atrophic gastritis.Methods. We studied patients from two separate cohorts who were being treated for reflux esophagitis: 72 patients treated with fundoplication in Sweden and 105 treated with omeprazole (20 to 40 mg once daily) in the Netherlands. In both cohorts, the patients were followed for an average of five years (range, three to eight). After fundoplication, the patients did not receive acid-suppressive therapy. The presence of H. pylori was assessed at the first visit by histologic evaluation in the fundoplication group and by histologic and serologic evaluation in the omeprazole group. The patients were not treated for H. pylori infection. Before treatment and during follow-up, the patients underwent repeated gastroscopy, with biopsy sampling for histologic evaluation.Results. Among the patients treated with fundoplication, atrophic gastritis did not develop in any of the 31 who were infected with H. pylori at base line or the 41 who were not infected; 1 patient infected with H. pylori had atrophic gastritis before treatment that persisted after treatment. Among the patients treated with omeprazole, none of whom had atrophic gastritis at base line, atrophic gastritis developed in 18 of the 59 infected with H. pylori (P