Ljubicić N, Banić M, Kujundzić M, Antić Z, Vrkljan M, Kovacević I, Hrabar D, Doko M, Zovak M, Mihatov S
Division of Gastroenterology, Sestre Milosrdnice University Hospital, Zareb, Croatia.
Eur J Gastroenterol Hepatol. 1999 Jul;11(7):727-30. doi: 10.1097/00042737-199907000-00008.
Histopathological and clinical data strongly suggest that Helicobacter pylori is the cause of chronic gastritis and peptic ulceration. However, little has been written about the potential causal relation of H. pylori infection to hyperplastic and adenomatous gastric polyps. We therefore carried out a prospective study to determine the effect of eradicating H. pylori infection on the course of hyperplastic and adenomatous gastric polyps.
From November 1996 to December 1997, 6700 patients who had undergone upper gastrointestinal endoscopy at the two centres in Zagreb, Croatia, were candidates for participation in the study. Hyperplastic and adenomatous polyps were diagnosed on a basis of at least three histological samples taken from the polyp. In seven patients endoscopy had to be repeated because forceps biopsy sampling either provided inadequate tissue for correct histological diagnosis, or accurate characterization of gastric polyp histology was not possible. Upon completion of all endoscopic examinations before and after treatment, biopsy samples were taken from the antrum (two) and the body of the stomach (two) so that gastritis could be graded and classified, and the presence of H. pylori sought by histology. Two other samples were taken from the antrum for a rapid urease test. Follow-up examinations were performed by using endoscopy. Control endoscopy was performed at least 4 weeks after the treatment of H. pylori infection had been completed, and then every 3-4 months. The follow-up ranged from 4 to 17 months, with a median of 14 months. The treatment of H. pylori infection consisted of a 1-week course of either omeprazole (20 mg twice daily) or pantoprazole 40 mg twice daily), and a 1-week course of amoxicillin 2g twice daily) and metronidazole (400 mg three times daily), and clarithromycin (500 mg twice daily). Eradication of H. pylori infection was assessed by repeated histology and rapid urease test.
Twenty-one patients (nine women, 12 men; median age 52 years) with histologically proven hyperplastic gastric polyps, and seven patients (two women, five men; median age, 67 years) with adenomatous gastric polyps were included in the study. Among 21 patients with hyperplastic gastric polyps, 16 patients (76%) were positive for H. pylori infection. Only two patients (29%) with adenomatous gastric polyps were positive for the infection. Complete eradication of H. pylori was initially achieved in all patients positive for H. pylori. Total regression of the gastric polyps was observed only among the patients with hyperplastic gastric polyps in whom H. pylori had been eradicated. Complete regression of the hyperplastic gastric polyps was observed in seven of the 16 evaluable patients (44%; 95% CI, 19-68%) after H. pylori eradication. The endoscopic snare polypectomy was carried out in nine patients with hyperplastic polyps and two patients with adenomatous gastric polyps in whom regression of the polyps was not observed after H. pylori eradication, as well as in five patients with hyperplastic and four with adenomatous gastric polyps who were negative for H. pylori. Exploratory laparotomy and gastrotomy with polyps excision were carried out in one patient with multiple adenomatous gastric polyps. In only one patient who was not positive for H. pylori recurrence of hyperplastic gastric polyp was recorded during follow-up, and no re-infection with H. pylori has been detected.
Our results suggest that the development of hyperplastic gastric polyps may be directly related to chronic active gastritis and concomitant H. pylori infection. Cure of H. pylori infection associated with hyperplastic gastric polyps resulted in complete polyp regression in more than 40% of patients. Therefore, for patients with hyperplastic gastric polyps and concurrent H. pylori infection an antibiotic treatment designed to eradicate H. pylori appears to be recommended before further therapeutic options are consi
组织病理学和临床数据有力地表明，幽门螺杆菌是慢性胃炎和消化性溃疡的病因。然而，关于幽门螺杆菌感染与增生性和腺瘤性胃息肉之间潜在因果关系的报道甚少。因此，我们进行了一项前瞻性研究，以确定根除幽门螺杆菌感染对增生性和腺瘤性胃息肉病程的影响。
1996年11月至1997年12月，在克罗地亚萨格勒布的两个中心接受上消化道内镜检查的6700例患者参与了本研究。增生性和腺瘤性息肉根据从息肉获取的至少三个组织学样本进行诊断。7例患者因钳取活检样本提供的组织不足以进行正确的组织学诊断，或无法准确鉴定胃息肉组织学特征而需重复内镜检查。在完成治疗前后的所有内镜检查后，从胃窦（两处）和胃体（两处）取活检样本，以便对胃炎进行分级和分类，并通过组织学检查寻找幽门螺杆菌。另外从胃窦取两个样本进行快速尿素酶试验。通过内镜检查进行随访。在完成幽门螺杆菌感染治疗后至少4周进行对照内镜检查，然后每3 - 4个月检查一次。随访时间为4至17个月，中位数为14个月。幽门螺杆菌感染的治疗包括为期1周的奥美拉唑（20mg，每日两次）或泮托拉唑（40mg，每日两次）疗程，以及为期1周的阿莫西林（2g，每日两次）、甲硝唑（400mg，每日三次）和克拉霉素（500mg，每日两次）疗程。通过重复组织学检查和快速尿素酶试验评估幽门螺杆菌感染的根除情况。
21例经组织学证实为增生性胃息肉的患者（9例女性，12例男性；中位年龄52岁）和7例腺瘤性胃息肉患者（2例女性，5例男性；中位年龄67岁）纳入本研究。在21例增生性胃息肉患者中，16例（76%）幽门螺杆菌感染阳性。腺瘤性胃息肉患者中仅2例（29%）感染阳性。所有幽门螺杆菌感染阳性的患者最初均实现了幽门螺杆菌的完全根除。仅在根除幽门螺杆菌的增生性胃息肉患者中观察到胃息肉完全消退。根除幽门螺杆菌后，16例可评估患者中的7例（44%；95%CI，19 - 68%）增生性胃息肉完全消退。9例增生性息肉患者、2例根除幽门螺杆菌后息肉未消退的腺瘤性胃息肉患者以及5例幽门螺杆菌阴性的增生性胃息肉患者和4例幽门螺杆菌阴性的腺瘤性胃息肉患者接受了内镜圈套息肉切除术。1例患有多发性腺瘤性胃息肉的患者接受了剖腹探查和胃切开息肉切除术。在随访期间，仅1例幽门螺杆菌阴性患者记录到增生性胃息肉复发，且未检测到再次感染幽门螺杆菌。
我们的结果表明，增生性胃息肉的发生可能与慢性活动性胃炎及同时存在的幽门螺杆菌感染直接相关。根除与增生性胃息肉相关的幽门螺杆菌感染使超过40%的患者息肉完全消退。因此，对于增生性胃息肉并同时感染幽门螺杆菌的患者，在考虑进一步治疗方案之前，似乎建议进行旨在根除幽门螺杆菌的抗生素治疗。
