Hamada H, Haruma K, Mihara M, Kamada T, Yoshihara M, Sumii K, Kajiyama G, Kawanishi M
Gastrointestinal Unit, First Department of Internal Medicine, Hiroshima University School of Medicine, Hiroshima, Japan.
Aliment Pharmacol Ther. 2000 Jun;14(6):729-35. doi: 10.1046/j.1365-2036.2000.00758.x.
Although several recent studies have shown that the eradication of Helicobacter pylori provokes reflux oesophagitis, the results are conflicting.
To investigate the prevalence of reflux oesophagitis in patients after eradication of H. pylori and consider its association with hiatal hernia and corpus gastritis.
A total of 286 patients who underwent H. pylori eradication therapy and 286 age- and disease-matched H. pylori-positive controls who did not undergo eradication therapy were followed prospectively. All patients and controls underwent endoscopy at 1-year intervals or when upper gastrointestinal symptoms recurred. The presence of hiatal hernia and histology of the gastric corpus were evaluated at the time of initial endoscopy.
The estimated prevalence of reflux oesophagitis within 3 years was 18% after eradication therapy and 0.3% without therapy. Patients who developed reflux oesophagitis after therapy had a greater prevalence of hiatal hernia (P=0.0008) and more severe corpus gastritis (P=0.0005) before therapy. Cumulative prevalence of reflux oesophagitis was 26% in patients with hiatal hernia, 7.7% in those without hiatal hernia, 33% in those with corpus atrophic gastritis and 13% in those without corpus atrophic gastritis. When patients had both hiatal hernia and corpus gastritis, the prevalence of reflux oesophagitis was 37%. The newly developed reflux oesophagitis was classified as mild in 35 out of 36 (97%) patients who developed reflux oesophagitis after eradication therapy.
Eradication of H. pylori increased the prevalence of reflux oesophagitis in our patient group. The presence of hiatal hernia and corpus gastritis are closely related to the development of reflux oesophagitis after H. pylori eradication therapy.
尽管最近的几项研究表明根除幽门螺杆菌会引发反流性食管炎，但结果相互矛盾。
调查幽门螺杆菌根除术后患者反流性食管炎的患病率，并探讨其与食管裂孔疝和胃体胃炎的关系。
前瞻性随访286例接受幽门螺杆菌根除治疗的患者以及286例年龄和疾病匹配的未接受根除治疗的幽门螺杆菌阳性对照者。所有患者和对照者每隔1年或出现上消化道症状复发时接受内镜检查。在初次内镜检查时评估食管裂孔疝的存在情况和胃体的组织学情况。
根除治疗后3年内反流性食管炎的估计患病率为18%，未治疗者为0.3%。治疗后发生反流性食管炎的患者在治疗前食管裂孔疝的患病率更高（P=0.0008），胃体胃炎更严重（P=0.0005）。食管裂孔疝患者反流性食管炎的累积患病率为26%，无食管裂孔疝者为7.7%，胃体萎缩性胃炎患者为33%，无胃体萎缩性胃炎者为13%。当患者同时患有食管裂孔疝和胃体胃炎时，反流性食管炎的患病率为37%。在根除治疗后发生反流性食管炎的36例患者中，35例（97%）新发生的反流性食管炎被分类为轻度。
在我们的患者组中，根除幽门螺杆菌增加了反流性食管炎的患病率。食管裂孔疝和胃体胃炎的存在与幽门螺杆菌根除治疗后反流性食管炎的发生密切相关。
