Helicobacter pylori infection, chronic active gastritis, and intestinal metaplasia share similar epidemiologic patterns, and are significantly associated with each other, Dr. Amnon Sonnenberg and colleagues reported in an article appearing in the December issue of Gastroenterology.

Moreover, all three diagnoses are inversely associated with the presence of Barrett’s metaplasia, the researchers found.

Dr. Sonnenberg of the Portland (Oregon) VA Medical Center and Oregon Health and Science University, Portland, and colleagues looked at histology reports from 78,985 patients who had gastric and esophageal biopsies between April 2007 and March 2008. Patients were treated by approximately 1,500 gastroenterologists distributed throughout the United States (Gastroenterology 2010 December [doi:10.1053/j.gastro.2010.08.018]).

All samples were processed by Caris Life Sciences Inc., a gastrointestinal laboratory that works with private outpatient endoscopy centers, at facilities in Phoenix, Boston, and Irving, Texas.

The researchers found that patients who were positive for H. pylori infection had a startlingly high odds ratio for chronic active gastritis: 456 (95% confidence interval, 415-502). They were also twice as likely to have intestinal metaplasia (OR, 2.00; 95% CI, 1.87-2.14).

However, having H. pylori was apparently protective against a diagnosis of Barrett’s metaplasia, in the esophagus: The OR for having the latter among H. pylori-positive patients was 0.42 (95% CI, 0.36-0.50).

Similarly, patients who were histologically positive for chronic active gastritis were extremely likely to have H. pylori (OR, 457; 95% CI, 415-502), more than twice as likely to have intestinal metaplasia (OR, 2.10; 95% CI, 1.97-2.24), and roughly half as likely to have Barrett’s metaplasia (OR, 0.48; 95% CI, 0.41-0.56).

Finally, analyses linking intestinal metaplasia to these conditions revealed an OR of 2.07 for H. pylori (95% CI, 1.93-2.21), 2.15 for chronic active gastritis (95% CI, 2.02-2.29), and 0.61 for Barrett’s esophagus (95% CI, 0.51-0.72).

Dr. Sonnenberg and colleagues also found that all three diagnoses were more common among men than women, and that “compared with other insurance types, Medicaid (U. S. government-funded health insurance) was more common in patients with all three diagnoses.”

Additionally, the researchers found that there was a higher concentration of all three diagnoses in Puerto Rico, New York, South Carolina, and New Mexico, compared with the rest of the country, possibly because of “an underlying variation in the socio-economic well-being among populations from different states,” Dr. Sonnenberg noted.

According to the authors, although an inverse relationship between H. pylori–induced gastritis and Barrett’s esophagus has already been suggested in multiple studies, many of those analyses “were based on small population samples, clinical observations, or indirect evidence of opposing epidemiologic trends among H. pylori or peptic ulcer versus gastroesophageal reflux disease.”

In contrast, the current study offers a “direct and inverse relationship between the histologic findings of Barrett’s mucosa and H. pylori–induced gastritis,” they wrote.

“Using histological findings to assess the underlying epidemiology represents a new way to study epidemiologic patterns,” they added.

However, the researchers conceded that the study was not without limitations. For one, it “lacks any data to assess the influence of H. pylori–induced gastritis on hyposecretion of acid,” they wrote.

Moreover, “recent publications have indicated substantial misclassification of Barrett’s esophagus if only pathology reports are used,” meaning that the prevalence of this condition could have been underestimated in this study.

Lead author Dr. Sonnenberg disclosed being supported by a grant from Takeda Pharmaceutical Co. Two other investigators are employees of Caris Life Sciences.

Copyright (c) 2010 Elsevier Global Medical News. All rights reserved. This material may not be published, broadcast, rewritten, or redistributed.

《胃肠病学》(Gastroenterology)12月刊上发表的一项研究显示，幽门螺旋杆菌感染、慢性活动性胃炎和肠化生具有相似的流行病学模式，并且彼此之间显著相关。此外，这3种疾病均与Barrett化生的发生呈负相关。

 

研究者对2007年4月~2008年3月间进行胃和食管活检的78,985例患者的组织学报告进行了分析。这些患者由全美约1,500位胃肠病学专家诊治。所有样本由Caris生命科学公司进行处理。(Gastroenterology 2010 December [doi:10.1053/j.gastro.2010.08.018])

 

研究者发现，幽门螺旋杆菌感染阳性患者发生慢性活动性胃炎的比值比(OR)高达456 (95% CI 415~502)，发生肠化生的OR为2.00 (95% CI 1.87~2.14)。然而，幽门螺旋杆菌感染似乎可预防Barrett食管化生的发生。幽门螺旋杆菌感染阳性患者发生Barrett食管化生的OR为0.42 (95% CI 0.36~0.50)。同样，慢性活动性胃炎阳性患者发生幽门螺旋杆菌感染的OR也高达457(95% CI 415~502)，发生肠化生的OR为2.10(95% CI 1.97~2.24)，发生Barrett化生的OR为0.48 (95% CI 0.41~0.56)。肠化生患者发生幽门螺旋杆菌感染、慢性活动性胃炎和Barrett食管化生的OR分别为2.07 (95% CI 1.93~2.21)、2.15 (95% CI 2.02~2.29)和0.61 (95% CI 0.51~0.72)。

 

这3种疾病均在男性中较在女性中多见，并且这3种疾病的患者更多地是参与医疗补助计划(Medicaid)。此外，波多黎各、纽约州、南卡罗来纳州和新墨西哥州罹患这3种疾病的患者人数高于其他州。

 

本研究表明，Barrett黏膜与幽门螺旋杆菌胃炎的组织学结果之间存在直接负相关。研究者表示，应用组织学结果来评估潜在流行病学代表了一种新的研究流行病学模式的方式。但本研究存在不少局限性。一是缺乏数据来评估幽门螺旋杆菌胃炎对胃酸分泌过少的影响。另外，近期文献表明如仅根据病理报告进行诊断，会造成大量的Barrett食管患者误诊，这意味着本研究可能低估了该病的患病率。

 

本研究的第一作者声明获得武田制药公司的资助。其他2位研究者为Caris生命科学公司的员工。

 

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