Bojarski C, Epple H J, Kirstein F W, Fromm M, Bisson S, Riecken E O, Schulzke J D
Department of Gastroenterology, Universitätsklinikum Benjamin Franklin, Freie Universität Berlin, Germany.
Z Gastroenterol. 2000 Mar;38(3):211-9. doi: 10.1055/s-2000-14860.
In order to investigate the potential of Helicobacter pylori (HP) to induce dyspepsia, we performed a randomized prospective study on the long-term effect of HP-eradication on symptoms of HP-positive dyspeptic patients in whom other organic causes for dyspepsia were carefully ruled out.
201 patients referred to our endoscopy unit with dyspeptic symptoms for at least six months entered the study. Patients with previous peptic ulcer were excluded.
After endoscopy of the upper alimentary tract and 13C-urea breath test, patients with active peptic ulcer, hiatal hernia, macroscopic evidence for esophagitis and negative HP-status were excluded. The remaining patients underwent abdominal sonography, H2-exhalation test with lactose, and 24-h pH monitoring in order to exclude other organic causes for dyspepsia. In 20 patients, dyspepsia was assumed to be due to HP-gastritis. Patients received eradication therapy and were controlled as assessed by the 13C-urea breath test six weeks and six months after completion of the therapy. Dyspeptic symptoms were monitored by means of a validated symptom score.
Out of 20 patients with HP-gastritis the first eradication treatment was successful in 13, while seven patients remained HP-positive after antibiotic treatment. Six months after completion of therapy the symptoms of HP-eradicated patients improved considerably (score values 17.4 +/- 1.5 and 10.2 +/- 0.8, respectively, p < 0.01) whereas symptoms of patients with persistent infection remained unchanged (21.1 +/- 1.7 and 20.4 +/- 1.5, n.s.) and only improved after successful retherapy (20.4 +/- 1.5 and 11.7 +/- 2.1, p < 0.05). In total, 17 of 20 patients (85%) improved after successful eradication. Also, neutrophil infiltration in the gastric mucosa correlated to both dyspeptic symptoms before therapy (r = 0.85) and the decrease in symptom score after HP-eradication (r = 0.61). In contrast, the symptoms of eight patients with gastroesophageal reflux disease were not improved after eradication (20.0 +/- 1.1 and 18.2 +/- 1.0, n.s.)
HP-infection per se contributes to dyspepsia. 17 of 20 (85%) HP-positive dyspeptic patients improved after HP-eradication, when other potential organic causes for dyspepsia had been ruled out. However, many patients did not completely recover but the symptoms only partly decreased which parallels the persistence of part of the inflammatory infiltration in the gastric mucosa. This emphasizes the importance of HP-gastritis as an organic disease causing dyspeptic symptoms.
为了研究幽门螺杆菌（HP）诱发消化不良的可能性，我们针对根除HP对HP阳性消化不良患者症状的长期影响进行了一项随机前瞻性研究，这些患者已被仔细排除其他导致消化不良的器质性病因。
201名因消化不良症状至少持续6个月而转诊至我们内镜科的患者进入了研究。既往有消化性溃疡的患者被排除。
在上消化道内镜检查和13C尿素呼气试验后，排除患有活动性消化性溃疡、食管裂孔疝、食管炎的宏观证据以及HP检测阴性的患者。其余患者接受腹部超声检查、乳糖氢呼气试验以及24小时pH监测，以排除其他导致消化不良的器质性病因。20名患者被认为消化不良是由HP胃炎引起的。患者接受根除治疗，并在治疗完成后6周和6个月通过13C尿素呼气试验进行评估。消化不良症状通过有效的症状评分进行监测。
在20名HP胃炎患者中，首次根除治疗13例成功，7例患者在抗生素治疗后仍为HP阳性。治疗完成6个月后，HP根除患者的症状有显著改善（评分分别为17.4±1.5和10.2±0.8，p<0.01），而持续感染患者的症状保持不变（21.1±1.7和20.4±1.5，无统计学意义），仅在再次成功治疗后有所改善（20.4±1.5和11.7±2.1，p<0.05）。总共20名患者中有17名（85%）在成功根除后症状改善。此外，胃黏膜中的中性粒细胞浸润与治疗前的消化不良症状（r=0.85）以及HP根除后的症状评分降低（r=0.61）均相关。相比之下，8名胃食管反流病患者在根除后症状未改善（20.0±1.1和18.2±1.0，无统计学意义）
HP感染本身会导致消化不良。在排除其他潜在的导致消化不良的器质性病因后，20名HP阳性消化不良患者中有17名（85%）在根除HP后症状改善。然而，许多患者并未完全康复，症状仅部分减轻，这与胃黏膜中部分炎症浸润的持续存在情况相符。这强调了HP胃炎作为一种导致消化不良症状的器质性疾病的重要性。
