Among patients with peptic ulcer disease, early eradication of Helicobacter pylori protects against the development of gastric cancer, Dr. Chun-Ying Wu and colleagues wrote in an article appearing in the November issue of Gastroenterology.
In a retrospective cohort study of more than 80,000 patients throughout China who were hospitalized for peptic ulcer disease, those who received therapy to eradicate H. pylori soon after recovery showed a risk of gastric cancer similar to that in the general population. In contrast, patients who did not receive such therapy until years later had a higher risk of developing gastric cancer.
Dr. Wu and associates studied this issue because even though a causal link between H. pylori infection and gastric cancer seems apparent, it has never been definitively established in humans. In animal models, this link has been proved, with studies showing that H. pylori induces gastric cancer by first causing atrophic gastritis, intestinal metaplasia, and dysplasia.
However, the findings in human studies have been conflicting. In one randomized, controlled trial in China, therapy to eradicate H. pylori did not significantly reduce the rate of subsequent gastric cancer.
In four small studies, the eradication of H. pylori prevented the progression of precancerous lesions such as atrophic gastritis and intestinal metaplasia. However, when the results of these studies were pooled, the eradication of H. pylori did not significantly affect the incidence of gastric cancer.
A prospective, randomized controlled study would definitively determine a causal link, but it would be unethical to create a control group by withholding treatment to eradicate H. pylori from half of the subjects in such a study. So Dr. Wu of China Medical University in Taichung, Taiwan, and colleagues instead conducted a retrospective study comparing 54,576 patients who received timely treatment with 25,679 who, for unknown reasons, did not receive treatment to eradicate H. pylori until 1 or more years after an index hospitalization for peptic ulcer disease.
All the study subjects were initially hospitalized between 1997 and 2005 with a primary diagnosis of peptic ulcer, including gastric, duodenal, and nonspecific ulcer. Treatment to eradicate H. pylori included a proton pump inhibitor or H2 receptor blocker, plus clarithromycin or metronidazole, plus amoxicillin or tetracycline, with or without the addition of bismuth.
All the subjects were followed for 2-10 years, with an average of 7.5 years of follow-up.
In the “early-eradication group,” the median interval between hospitalization for peptic ulcer disease and receipt of eradication therapy was 14 days. In contrast, in the “late-eradication group,” the median interval was 1,053 days.
Patients in the early-eradication group received their treatment to eradicate H. pylori an average of 2.8 years earlier than did those in the late-eradication group.
The cumulative incidence of gastric cancer in the early-intervention group was similar to that in the general Chinese population, but such incidence was significantly higher in the late-eradication group.
Moreover, gastric cancer risk was higher still in late-eradication patients who were at high risk because of older age, male sex, or ulcer complications. “The result [indicates that there is a] stronger protective role of H. pylori eradication in high-risk populations,” the investigators said.
In addition, “the consistently decreasing trend of relative risk in our study may predict that the protective effect of H. pylori eradication is even higher with longer follow-up,” they said.
H. pylori eradication conveyed protection in all age groups, not just in young patients. “The highest protective effect was actually found in the 60-69 age group, with the second-highest protective effect in the 50-59 age group,” the researchers said.
The study was limited in that Dr. Wu and colleagues could not determine whether treatment to eradicate H. pylori was successful or not, and therefore could not compare patients in whom H. pylori was eradicated in those for whom it persisted.
This study was supported in part by China’s National Health Research Institutes. No financial conflicts of interest were reported.
Copyright (c) 2009 Elsevier Global Medical News. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.
消化性溃疡患者早期根治幽门螺杆菌可以预防胃癌的发生，11月出版的《胃肠病学》(Gastroenterology)发表的Wu Chun-Ying博士及其同事的一篇文章报道。
在一项回顾性队列研究中，纳入了80,000余名因消化性溃疡住院的中国患者，痊愈后立即采用幽门螺杆菌根治疗法的患者，其发生胃癌的风险与普通人群相似。相反，多年后才接受这种治疗的患者发展为胃癌的风险更高。
虽然幽门螺杆菌感染和胃癌很可能有因果关系，但在人类还没有得到证实，因此Wu博士及其同事进行了这项研究。在动物模型，这种因果关系已经得到证实，研究显示幽门螺杆菌首先引起萎缩性胃炎、肠上皮化生和发育异常，之后导致胃癌。
然而，对人类进行的研究结果不太一致。在一项中国的随机对照研究中，根治幽门螺杆菌并没有显著降低胃癌的发生率。
在4项小型研究中，根治幽门螺杆菌可以预防癌前期病变的进展，例如萎缩性胃炎和肠上皮化生。然而，把这些研究的结果综合分析，根治幽门螺杆菌并没有显著影响胃癌的发生率。
一项前瞻性随机对照研究能确定其中的因果关系，但在这样的研究中，一半受试者位于对照组，如果不采用幽门螺杆菌根治治疗不符合伦理。因此，台湾台中市中国医药大学的Wu博士和他的同事们采用了回顾性研究，对及时根治幽门螺杆菌的54,576名患者和因不明原因在消化性溃疡住院后1年或多年后才接受该治疗的25,679名患者进行了比较。
所有的受试者最初在1997年~2005年住院，主要诊断是消化性溃疡，包括胃溃疡、十二指肠溃疡和非特异性溃疡。根治消化性溃疡的疗法包括质子泵抑制剂或H2受体阻滞剂，联合克拉霉素或甲硝唑、阿莫西林或四环素治疗，采用或不采用铋剂治疗。
所有的受试者随访2~10年，平均随访7.5年。
在“早期根治组”，因消化性溃疡住院和接受根治治疗的间隔时间平均为14天。而在“晚期根治组”，平均间隔为1,053天。
早期根治组的患者接受幽门螺杆菌根治治疗的时间比晚期根治组的患者早2.8年。
在早期干预组，胃癌的累积发病率与普通中国人群类似，但是在晚期根治组，该发病率显著增高。
而且，具有年老、男性或溃疡并发症高风险的晚期根治组的患者，患胃癌的风险更高。“该结果提示在高风险人群，幽门螺杆菌根治疗法能很好预防胃癌。”研究者说道。
此外，他们说道：“在我们的研究中，相对风险一致降低的趋势可以预测幽门螺杆菌根治疗法的保护作用，在更长期的随访中，保护作用更好。”
幽门螺杆菌根治疗法在任何年龄段均有保护作用，不只是在年轻的患者。“最大的保护作用出现在60~69岁年龄组，50~59岁年龄组次之。”研究者说道。
该研究的不足之处在于，Wu博士及其同事不能确定根治幽门螺杆菌的治疗是否有效，因此不能比较已经根治幽门螺杆菌的患者和幽门螺杆菌仍旧存在的患者。
该研究的部分资金来源于台湾的卫生研究院，本研究没有利益冲突。
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