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急性胃炎・慢性胃炎

著者: 小早川雅男 福島県立医科大学 医療研究推進センター

監修: 上村直実 国立国際医療研究センター 国府台病院

著者校正/監修レビュー済:2021/02/10
参考ガイドライン:
  1. 日本消化器病学会:機能性消化管疾患診療ガイドライン2014―機能性ディスペプシア(FD)
  1. 日本ヘリコバクター学会H.pylori感染の診断と治療のガイドライン 2016改訂版
  1. EHMSGManagement of Helicobacter pylori infection—the Maastricht V/Florence Consensus Report
患者向け説明資料

概要・推奨   

  1. 胃粘膜組織中に好中球と単核球を認めた場合には、ピロリ菌感染が原因である活動性慢性胃炎である可能性が高く急性胃炎であるAGMLの一因もピロリ菌の初感染の可能性があり、ピロリ菌の感染診断を考慮することが勧められる(推奨度1)
  1. ピロリ菌感染による慢性胃炎のある患者、特に胃粘膜萎縮の進行した症例には定期的な胃癌のスクリーニングが勧められる(推奨度1)
  1. ピロリ菌による慢性胃炎の患者について、早期胃癌を内視鏡治療によって治療した後はピロリ菌の除菌を行うことが強く勧められる(推奨度1)
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薬剤監修について:
オーダー内の薬剤用量は日本医科大学付属病院 薬剤部 部長 伊勢雄也 以下、林太祐、渡邉裕次、井ノ口岳洋、梅田将光による疑義照会のプロセスを実施、疑義照会の対象については著者の方による再確認を実施しております。
※薬剤中分類、用法、同効薬、診療報酬は、エルゼビアが独自に作成した薬剤情報であり、
著者により作成された情報ではありません。
尚、用法は添付文書より、同効薬は、薬剤師監修のもとで作成しております。
※薬剤情報の(適外/適内/⽤量内/⽤量外/㊜)等の表記は、エルゼビアジャパン編集部によって記載日時にレセプトチェックソフトなどで確認し作成しております。ただし、これらの記載は、実際の保険適用の査定において保険適用及び保険適用外と判断されることを保証するものではありません。また、検査薬、輸液、血液製剤、全身麻酔薬、抗癌剤等の薬剤は保険適用の記載の一部を割愛させていただいています。
(詳細はこちらを参照)
著者のCOI(Conflicts of Interest)開示:
小早川雅男 : 特に申告事項無し[2021年]
監修:上村直実 : 未申告[2021年]

改訂のポイント:
  1. 定期レビューを行い、ピロリ菌以外の原因による慢性胃炎について最近のtopicsを追加した。

病態・疫学・診察

疾患情報(疫学・病態)  
  1. 病理組織学に基づいた急性胃炎・慢性胃炎と、機能性ディスペプシア(functional dyspepsia、FD)としての「症候性胃炎」 機能性ディスペプシア や内視鏡的に観察される「形態学的胃炎」との違いに注意が必要である。
 
わが国で用いられるさまざまな胃炎

わが国では、本来の病理学的な診断名である「組織学的胃炎」、内視鏡所見上確認される「形態学的胃炎」、症状がある場合を示す「症候性胃炎」が混在している。「症候性胃炎」は最近では機能性ディスペプシア(FD:functional dyspepsia)と呼ばれ、ピロリ菌感染が主な原因である「組織学的胃炎」とは区別されるようになっている。

出典

img1:  著者提供
 
 
 
  1. 急性胃炎とは、ピロリ菌の初感染、アルコール多飲、非ステロイド抗炎症薬(NSAIDs)内服などさまざまな原因で引き起こされ、内視鏡的には急性胃粘膜病変(AGML)などとして観察される一過性の病態である。
  1. 急性胃炎の一因である『胃アニサキス症』は他項にあり:胃アニサキス症
  1. 慢性胃炎の多くが、ピロリ菌の持続感染が原因の無症候性感染症である。最近は、ピロリ菌感染率の低下や除菌治療の普及もあり、自己免疫性胃炎や非ピロリ菌ヘリコバクター(Non-Helicobacter pylori-Helicobacter:NHPH)胃炎が注目されつつある。
  1. 慢性胃炎に分類される『自己免疫性胃炎』は他項にあり:自己免疫性胃炎
  1. ピロリ感染胃炎とは異なるピロリ感染症はヘリコバクター・ピロリ感染症を参照
  1. ピロリ菌は5歳以下の幼少期に感染し、高齢になるに従い、表層性胃炎から胃粘膜の萎縮を伴った萎縮性胃炎、および腸上皮化生へと進展する。
 
ピロリ菌感染による慢性胃炎と関連疾患

ピロリ菌は幼少期に感染し、若年期には胃酸分泌を亢進させ、十二指腸潰瘍を引き起こす。年齢とともに胃炎の分布が前庭部から胃体部へと移行し、胃粘膜が萎縮することなどで胃酸分泌が減少し、胃粘膜の脆弱化から胃潰瘍を引き起こす。さらに胃粘膜萎縮が進行すると腸上皮化生が進行して胃癌のハイリスクとなる。

出典

img1:  著者提供
 
 
 
  1. 慢性胃炎を背景に胃・十二指腸潰瘍、胃癌、胃MALTリンパ腫、特発性血小板減少性紫斑病(ITP)などさまざまな疾患が発生する。
 
  1. 一般に、臓器に細菌感染が生じると、好中球が組織中に浸潤する。また持続する慢性炎症ではリンパ球を中心とした単核球の浸潤も認められる。胃粘膜組織中に好中球と単核球を認めた場合には、ピロリ菌感染が原因である活動性慢性胃炎である可能性が高く、急性胃炎であるAGMLの一因もピロリ菌の初感染の可能性があり、ピロリ菌の感染診断を考慮することが勧められる(推奨度1、O)。
  1. まとめ:ピロリ菌が発見される以前には、酸性の胃に細菌は生息できないものと信じられてきた。また細菌のいない胃に慢性胃炎があることは胃特有の不思議な現象とされていた。現在では、好中球浸潤を伴う活動性慢性胃炎の原因のほとんどはピロリ菌感染が原因とされている。
  1. 代表事例:オーストラリアの医師WarrenとMarshallは慢性活動性胃炎の患者にグラム陰性桿菌がいることを発見した[1]。Marshallはピロリ菌の培養液を自ら飲むことでKochの4原則を証明した(①ある一定の病気には一定の微生物が見いだされること、②その微生物を分離できること、③分離した微生物を感受性のある動物に感染させて同じ病気を起こせること、④そしてその病巣部から同じ微生物が分離されること)[2]。このことはMorrisによって追試され、ピロリ菌の感染は胃炎を引き起こすのみならず、胃内のpHも変動させることが証明された[3]。また、MarshallとMorrisによりAGMLの一因がピロリ菌の初感染であることも示されたといえる。
  1. 結論:ピロリ菌は胃粘膜に感染して活動性慢性胃炎を引き起こしており、ピロリ菌のない胃のほとんどは組織学的胃炎を認めない。
  1. 追記:WarrenとMarshallは「ピロリ菌と、その胃炎と消化性潰瘍における役割」の発見によりノーベル賞を受賞した。
  1. コメント:病理学的に「活動性」とは好中球の浸潤を意味し、慢性とは「単核球」の浸潤を意味している。
問診・診察のポイント  
  1. 急性胃炎は激しい上腹部痛を訴えることが多いが、まずは、胆石・胆嚢炎、膵炎、虫垂炎、心筋梗塞などほかの上腹部痛を来す急性疾患を除外することが重要である。内視鏡検査にてAGMLがあれば急性胃炎と診断できる。

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文献 

著者:
雑誌名: Lancet. 1983 Jun 4;1(8336):1273-5.
Abstract/Text
PMID 6134060  Lancet. 1983 Jun 4;1(8336):1273-5.
著者: B J Marshall, J A Armstrong, D B McGechie, R J Glancy
雑誌名: Med J Aust. 1985 Apr 15;142(8):436-9.
Abstract/Text A volunteer with histologically normal gastric mucosa received pyloric campylobacter by mouth. A mild illness developed, which lasted 14 days. Histologically proven gastritis was present on the tenth day after the ingestion of bacteria, but this had largely resolved by the fourteenth day. The syndrome of acute pyloric campylobacter gastritis is described. It is proposed that this disorder may progress to a chronic infection which predisposes to peptic ulceration.

PMID 3982345  Med J Aust. 1985 Apr 15;142(8):436-9.
著者: A Morris, G Nicholson
雑誌名: Am J Gastroenterol. 1987 Mar;82(3):192-9.
Abstract/Text Campylobacter pyloridis was ingested by a volunteer who had a histologically normal gastric mucosa and fasting gastric pH recordings of less than 2. Three days later he developed moderate to severe attacks of epigastric pain. On the 5th day after ingestion C. pyloridis was cultured from antral biopsies which showed histological acute gastritis. However, fundal histology and fasting gastric pH were normal. On the 8th day fasting gastric pH rose to 7.6. On day 11 C. pyloridis was cultured from both antral and fundal biopsies which showed histological gastritis. Doxycycline was taken for 28 days but infection and gastritis persisted. Bismuth subsalicylate was taken for 28 days and final biopsies, taken 1 wk after stopping therapy, were culture negative. Histology showed a minimal residual chronic gastritis. C. pyloridis can cause an acute upper gastrointestinal illness associated with histological gastritis and an increase in fasting gastric pH.

PMID 3826027  Am J Gastroenterol. 1987 Mar;82(3):192-9.
著者: David Y Graham, Antone R Opekun, Fadi Hammoud, Yoshio Yamaoka, Rita Reddy, Michael S Osato, Hala M T El-Zimaity
雑誌名: Am J Gastroenterol. 2003 May;98(5):1005-9. doi: 10.1111/j.1572-0241.2003.07426.x.
Abstract/Text OBJECTIVE: The mechanism of false negative urea breath tests (UBTs) results among proton pump inhibitor (PPI) users is unknown. We studied the time course of PPI-associated negative UBT, the relation to Helicobacter pylori density, and whether gastric acidification would prevent false negative UBT results.
METHOD: In the UBT experiment, H. pylori-infected volunteers received omeprazole 20 mg b.i.d. for 13.5 days. UBTs with citric acid were done before, after 6.5 days of PPI, and 1, 2, 4, 7, and 14 days after therapy. In the culture and histology experiment, after a wash-out of >5 months, nine of the original subjects were rechallenged with omeprazole for 6.5 days. Antral and corpus biopsies for histology and culture were done before and 1 day after PPI administration.
RESULTS: Thirty subjects (mean age 42 yr) were enrolled. UBTs were significantly reduced on day 6.5 (p = 0.031); 10 subjects (33%) developed transient negative UBTs. The UBT recovered in all but one subject by the fourth day post-PPI and in all subjects by day 14. In the culture and histology experiment, upon PPI rechallenge, three of nine subjects (33%) had negative UBTs. H. pylori density, whether measured by culture or histology, decreased with PPI therapy; antral biopsies became histologically negative in five subjects and corpus biopsies in three subjects.
CONCLUSION: PPI-induced negative UBT results were related to the anti-H. pylori effect of the PPI. Acidification of the stomach did not prevent false negative UBT results. Three days is likely the minimum delay from stopping PPI until one should perform a test for active infection. A delay of 14 days is preferred.

PMID 12809820  Am J Gastroenterol. 2003 May;98(5):1005-9. doi: 10.1111・・・
著者: Mayu Takimoto, Toshihiko Tomita, Takahisa Yamasaki, Shota Fukui, Masato Taki, Takuya Okugawa, Takashi Kondo, Tomoaki Kono, Katsuyuki Tozawa, Eitatsu Arai, Yoshio Ohda, Tadayuki Oshima, Hirokazu Fukui, Jiro Watari, Hiroto Miwa
雑誌名: Dig Dis Sci. 2017 Mar;62(3):739-745. doi: 10.1007/s10620-016-4439-0. Epub 2017 Jan 12.
Abstract/Text BACKGROUND AND AIM: Vonoprazan (VPZ) is a new oral potassium-competitive acid blocker that has recently become available. The aim of this study was to investigate the effects of VPZ on the urease activity of H. pylori as measured by the 13C-urea breath test (13C-UBT).
PATIENTS AND METHODS: A total of 60 patients (26 men, 34 women; mean age 53.2 ± 13.6 years) who were diagnosed as H. pylori-positive were recruited. The patients were randomly allocated to three treatment groups: lansoprazole (LPZ) 30 mg (n = 20), VPZ 20 mg (n = 20) once daily for 3 weeks, or the control group (n = 20). The 13C-UBT was carried out at baseline and after 3 weeks of treatment, and the baseline and after treatment results then compared. Δ13C‰ ≥ 2.5‰ was considered H. pylori-positive.
RESULTS: Four patients failed to complete the medication and were omitted from the analysis; data from the LPZ group (n = 18), VPZ group (n = 18), and control group (n = 20) were analyzed. The control group showed no significant change in 13C-UBT data between baseline and the completion of 3-week treatment (baseline: 26.6 ± 23.0‰, completion: 21.1 ± 13.1‰). The 13C-UBT data at week 3 were significantly decreased in both the VPZ group (baseline: 32.8 ± 22.7‰, completion: 7.6 ± 9.2‰, p = 0.0002) and the LPZ group (baseline: 41.8 ± 33.4‰; completion: 9.6 ± 8.8‰, p = 0.0006) compared to baseline.
CONCLUSIONS: VPZ treatment reduced the value of UBT, warning that UBT for patients with VPZ treatment should be evaluated carefully.

PMID 28083842  Dig Dis Sci. 2017 Mar;62(3):739-745. doi: 10.1007/s1062・・・
著者: H Watabe, T Mitsushima, Y Yamaji, M Okamoto, R Wada, T Kokubo, H Doi, H Yoshida, T Kawabe, M Omata
雑誌名: Gut. 2005 Jun;54(6):764-8. doi: 10.1136/gut.2004.055400.
Abstract/Text BACKGROUND AND AIMS: Helicobacter pylori infection and gastric atrophy are both risk factors for gastric cancer. We aimed to elucidate the natural history of gastric cancer development according to H pylori infection and gastric atrophy status. Subjects and
METHODS: A total of 9293 participants in a mass health appraisal programme were candidates for inclusion in the present prospective cohort study: 6983 subjects revisited the follow up programme. Subjects were classified into four groups according to serological status at initial endoscopy. Group A (n = 3324) had "normal" pepsinogen and were negative for H pylori antibody; group B (n = 2134) had "normal" pepsinogen and were positive for H pylori antibody; group C (n = 1082) had "atrophic" pepsinogen and were positive for H pylori antibody; and group D (n = 443) had "atrophic" pepsinogen and were negative for H pylori antibody. Incidence of gastric cancer was determined by annual endoscopic examination.
RESULTS: Mean duration of follow up was 4.7 years and the average number of endoscopic examinations was 5.1. The annual incidence of gastric cancer was 0.04% (95% confidence interval (CI) 0.02-0.09), 0.06% (0.03-0.13), 0.35% (0.23-0.57), and 0.60% (0.34-1.05) in groups A, B, C, and D, respectively. Hazard ratios compared with group A were 1.1 (95% CI 0.4-3.4), 6.0 (2.4-14.5), and 8.2 (3.2-21.5) in groups B, C, and D, respectively. Age, sex, and "group" significantly served as independent valuables by multivariate analysis.
CONCLUSIONS: The combination of serum pepsinogen and anti-H pylori antibody provides a good predictive marker for the development of gastric cancer.

PMID 15888780  Gut. 2005 Jun;54(6):764-8. doi: 10.1136/gut.2004.055400・・・
著者: Shizuka Sasazuki, Manami Inoue, Motoki Iwasaki, Tetsuya Otani, Seiichiro Yamamoto, Shinobu Ikeda, Tomoyuki Hanaoka, Shoichiro Tsugane, Japan Public Health Center Study Group
雑誌名: Cancer Epidemiol Biomarkers Prev. 2006 Jul;15(7):1341-7. doi: 10.1158/1055-9965.EPI-05-0901.
Abstract/Text BACKGROUND: Although accumulating evidence suggests that Helicobacter pylori plays a role in gastric carcinogenesis, the magnitude of the risk remains uncertain. Aim: We aimed to estimate the magnitude of the risk of gastric cancer associated with H. pylori infection by a large case-control study nested within a prospective cohort. Possible effect modification by CagA status, and serum pepsinogen status, as a marker of atrophic gastritis, was also considered to see its effect on developing gastric cancer. Subjects and
METHODS: Subjects (n = 123,576) were followed up from 1990 to 2004; 511 gastric cancer cases matched to 511 controls were used in the analysis. Plasma immunoglobulin G antibody to H. pylori, CagA, and pepsinogen I and II were measured.
RESULTS: The adjusted odds ratio (95% confidence interval) of gastric cancer associated with H. pylori infection was 5.1 (3.2-8.0). Assuming all CagA-positive subjects are true H. pylori positives doubled this risk. Atrophic gastritis was also associated with an elevated risk of gastric cancer and the risk increased further with pepsinogen levels.
CONCLUSIONS: Subjects with pepsinogen levels indicative of severe atrophic gastritis may need careful examination regularly regardless of H. pylori infection. Those who have other pepsinogen levels but who are H. pylori seropositive are likely to benefit from H. pylori eradication therapy. Considering both the cost and the potential for misclassification that may occur using multiple serologic tests, caution is needed in interpreting or extrapolating these findings into a screening strategy.

PMID 16835334  Cancer Epidemiol Biomarkers Prev. 2006 Jul;15(7):1341-7・・・
著者: P Correa
雑誌名: Cancer Res. 1992 Dec 15;52(24):6735-40.
Abstract/Text Evidence from pathology and epidemiology studies has been provided for a human model of gastric carcinogenesis with the following sequential stages: chronic gastritis; atrophy; intestinal metaplasia; and dysplasia. The initial stages of gastritis and atrophy have been linked to excessive salt intake and infection with Helicobacter pylori. The intermediate stages have been associated with the ingestion of ascorbic acid and nitrate, determinants of intragastric nitrosation. The final stages have been linked with the supply of beta-carotene and with excessive salt intake. Nitrosating agents are candidate carcinogens and could originate in the gastric cavity or in the inflammatory infiltrate.

PMID 1458460  Cancer Res. 1992 Dec 15;52(24):6735-40.
著者: N Uemura, S Okamoto, S Yamamoto, N Matsumura, S Yamaguchi, M Yamakido, K Taniyama, N Sasaki, R J Schlemper
雑誌名: N Engl J Med. 2001 Sep 13;345(11):784-9. doi: 10.1056/NEJMoa001999.
Abstract/Text BACKGROUND: Although many studies have found an association between Helicobacter pylori infection and the development of gastric cancer, many aspects of this relation remain uncertain.
METHODS: We prospectively studied 1526 Japanese patients who had duodenal ulcers, gastric ulcers, gastric hyperplasia, or nonulcer dyspepsia at the time of enrollment; 1246 had H. pylori infection and 280 did not. The mean follow-up was 7.8 years (range, 1.0 to 10.6). Patients underwent endoscopy with biopsy at enrollment and then between one and three years after enrollment. H. pylori infection was assessed by histologic examination, serologic testing, and rapid urease tests and was defined by a positive result on any of these tests.
RESULTS: Gastric cancers developed in 36 (2.9 percent) of the infected and none of the uninfected patients. There were 23 intestinal-type and 13 diffuse-type cancers. Among the patients with H. pylori infection, those with severe gastric atrophy, corpus-predominant gastritis, and intestinal metaplasia were at significantly higher risk for gastric cancer. We detected gastric cancers in 21 (4.7 percent) of the 445 patients with nonulcer dyspepsia, 10 (3.4 percent) of the 297 with gastric ulcers, 5 (2.2 percent) of the 229 with gastric hyperplastic polyps, and none of the 275 with duodenal ulcers.
CONCLUSIONS: Gastric cancer develops in persons infected with H. pylori but not in uninfected persons. Those with histologic findings of severe gastric atrophy, corpus-predominant gastritis, or intestinal metaplasia are at increased risk. Persons with H. pylori infection and nonulcer dyspepsia, gastric ulcers, or gastric hyperplastic polyps are also at risk, but those with duodenal ulcers are not.

PMID 11556297  N Engl J Med. 2001 Sep 13;345(11):784-9. doi: 10.1056/N・・・
著者: Theodoros Rokkas, Dimitios Pistiolas, Panos Sechopoulos, Ioannis Robotis, Georgios Margantinis
雑誌名: Helicobacter. 2007 Nov;12 Suppl 2:32-8. doi: 10.1111/j.1523-5378.2007.00563.x.
Abstract/Text BACKGROUND: Helicobacter pylori infection is a crucial factor in the multistep carcinogenic process of gastric cancer. In this process the gastric mucosa evolves through the stages of acute gastritis, chronic gastritis, gastric atrophy (GA), and intestinal metaplasia (IM) before developing gastric adenocarcinoma.
AIMS: The main aim of this study was to systematically review the long-term effects of H. pylori eradication on gastric histology (i.e. effects on GA and IM for both antrum and corpus) by meta-analyzing all relevant studies.
METHODS: Extensive English-language medical literature searches for human studies were performed through October 2006, using suitable key words. Pooled estimates [odds ratio (OR) with 95% confidence intervals (CI)] were obtained using random-effects model.
RESULTS: For antrum GA the pooled OR with 95% CI was 0.554 (0.372-0.825), p=0.004. For corpus GA the pooled OR was 0.209 (0.081-0.538), p<0.001. For antrum IM the pooled OR was 0.795 (0.587-1.078), p=0.14. For corpus IM the pooled OR was 0.891 (0.663-1.253), p=0.506.
CONCLUSION: The results showed significant improvement of GA, whereas improvement was not shown for IM.

PMID 17991174  Helicobacter. 2007 Nov;12 Suppl 2:32-8. doi: 10.1111/j.・・・
著者: Jin Wang, Lijuan Xu, Ruihua Shi, Xiayue Huang, Simon Wing Heng Li, Zuhu Huang, Guoxin Zhang
雑誌名: Digestion. 2011;83(4):253-60. doi: 10.1159/000280318. Epub 2011 Feb 1.
Abstract/Text OBJECTIVE: Whether gastric atrophy (GA) and intestinal metaplasia (IM) are reversible after the eradication of Helicobacter pylori remains controversial. The purpose of this meta-analysis was to systematically review histological alterations in GA and IM by comparing histological scores before and after H. pylori eradication.
METHODS: English-language articles in the medical literature containing information about the association between infection with H. pylori and gastric premalignant lesions (i.e. GA and IM) were identified by searching the Medline, PubMed, and EMBASE databases with suitable key words up to December 2009. Review Manager 4.2.8 was used for the meta-analysis.
RESULTS: Twelve studies containing a total of 2,658 patients were included in the first meta-analysis. Before treatment, 2,648 patients had antrum GA, 2,401 patients had corpus GA, 2,582 patients had antrum IM, and 2,460 patients had corpus IM. Comparing the histological alterations before and after H. pylori eradication, the pooled weighted mean difference (WMD) with 95% CI for antral GA was 0.12 (0.00-0.23), p = 0.06. For corpus GA, the pooled WMD was 0.32 (0.09-0.54), p = 0.006. For antral IM, the pooled WMD was 0.02 (-0.12-0.16), p = 0.76, and for corpus IM, the pooled WMD was -0.02 (-0.05-0.02), p = 0.42.
CONCLUSION: Our study shows that eradication of H. pylori results in significant improvement in GA in the corpus but not in the antrum; it also does not improve gastric mucous IM. Consequently, all patients with GA in the corpus should be tested for H. pylori infection, and eradication therapy should be prescribed for H. pylori-positive patients in those with GA in corpus.

Copyright © 2011 S. Karger AG, Basel.
PMID 21282951  Digestion. 2011;83(4):253-60. doi: 10.1159/000280318. E・・・
著者: Masaaki Kodama, Kazunari Murakami, Tadayoshi Okimoto, Takashi Abe, Yoshifumi Nakagawa, Kazuhiro Mizukami, Masahiro Uchida, Kunimitsu Inoue, Toshio Fujioka
雑誌名: Digestion. 2012;85(2):126-30. doi: 10.1159/000334684. Epub 2012 Jan 19.
Abstract/Text BACKGROUND AND AIM: Helicobacter pylori has been shown to cause atrophic gastritis and intestinal metaplasia (IM), both of which are precancerous lesions. To clarify the mechanism by which H. pylori eradication prevents gastric cancer, we monitored atrophy and IM improvement in gastric mucosa over a long period after H. pylori eradication.
METHODS: We monitored 118 patients (72 males, 46 females; mean age 61.3 ± 5.1 years) for a mean of 8.6 years (range 5-13) after successful H. pylori eradication. Biopsy specimens were taken from the greater curvatures of the antrum (A2) and the corpus (B2).
RESULTS: Atrophy was significantly decreased in patients with successful H. pylori eradication, both at A2 (from 1.60 ± 0.09 to 1.02 ± 0.08; p < 0.001) and B2 (from 0.71 ± 0.10 to 0.02 ± 0.02; p < 0.001), and IM score was significantly decreased at B2 (from 0.17 ± 0.12 to 0.00 ± 0.00; p < 0.05), but not at A2 (from 0.60 ± 0.11 to 0.43 ± 0.09; p = NS). In patients without successful eradication, however, there were no differences in scores over time. Before eradication, IM score was significantly higher in males than in females, both at A2 (0.81 ± 0.12 vs. 0.25 ± 0.10; p < 0.05) and B2 (0.32 ± 0.08 vs. 0.07 ± 0.04; p < 0.05).
CONCLUSION: We were able to monitor the gastric mucosa for a mean of 8.6 years after H. pylori eradication, the longest period reported to date. Significant improvements in gastric atrophy and IM after H. pylori eradication may decrease the risk of gastric cancer.

Copyright © 2012 S. Karger AG, Basel.
PMID 22269293  Digestion. 2012;85(2):126-30. doi: 10.1159/000334684. E・・・
著者: N Uemura, T Mukai, S Okamoto, S Yamaguchi, H Mashiba, K Taniyama, N Sasaki, K Haruma, K Sumii, G Kajiyama
雑誌名: Cancer Epidemiol Biomarkers Prev. 1997 Aug;6(8):639-42.
Abstract/Text Although epidemiological studies strongly suggest an association between gastric cancer and Helicobacter pylori infection, there has been no clinical report indicating that cure of the infection prevents cancer. We conducted a nonrandomized H. pylori eradication trial in patients whose gastric cancer was removed by endoscopic resection (ER). We investigated the effect of treatment on the histopathology of the gastric mucosa, as well as on the incidence of metachronous gastric cancer during the long-term clinical and endoscopic follow-up. One hundred and thirty-two patients with early gastric cancer underwent ER and had H. pylori infection. Sixty-five (group A) were treated with omeprazole and antibiotics to eradicate the infection, and 67 (group B) were not. All patients were followed for 2 years post ER. After eradication treatment in group A, the disappearance of neutrophil infiltration in the antrum and body of the stomach was observed as was a decrease of the severity of intestinal metaplasia. Endoscopy after ER detected no new gastric cancers in these patients. After 3 years of follow-up, 6 (9%) of the 67 patients in group B had a new early-stage, intestinal-type gastric cancer endoscopically diagnosed. The above results suggest that H. pylori eradication may improve neutrophil infiltration and intestinal metaplasia in the gastric mucosa and inhibit the development of new carcinomas. This finding should be confirmed in a randomized, controlled trial.

PMID 9264278  Cancer Epidemiol Biomarkers Prev. 1997 Aug;6(8):639-42.・・・
著者: Kazutoshi Fukase, Mototsugu Kato, Shogo Kikuchi, Kazuhiko Inoue, Naomi Uemura, Shiro Okamoto, Shuichi Terao, Kenji Amagai, Shunji Hayashi, Masahiro Asaka, Japan Gast Study Group
雑誌名: Lancet. 2008 Aug 2;372(9636):392-7. doi: 10.1016/S0140-6736(08)61159-9.
Abstract/Text BACKGROUND: The relation between Helicobacter pylori infection and gastric cancer has been proven in epidemiological studies and animal experiments. Our aim was to investigate the prophylactic effect of H pylori eradication on the development of metachronous gastric carcinoma after endoscopic resection for early gastric cancer.
METHODS: In this multi-centre, open-label, randomised controlled trial, 544 patients with early gastric cancer, either newly diagnosed and planning to have endoscopic treatment or in post-resection follow-up after endoscopic treatment, were randomly assigned to receive an H pylori eradication regimen (n=272) or control (n=272). Randomisation was done by a computer-generated randomisation list and was stratified by whether the patient was newly diagnosed or post-resection. Patients in the eradication group received lansoprazole 30 mg twice daily, amoxicillin 750 mg twice daily, and clarithromycin 200 mg twice daily for a week; those in the control group received standard care, but no treatment for H pylori. Patients were examined endoscopically at 6, 12, 24, and 36 months after allocation. The primary endpoint was diagnosis of new carcinoma at another site in the stomach. Analyses were by intention to treat. This trial is registered with the UMIN Clinical Trials Registry, number UMIN000001169.
FINDINGS: At 3-year follow-up, metachronous gastric carcinoma had developed in nine patients in the eradication group and 24 in the control group. In the full intention-to-treat population, including all patients irrespective of length of follow-up (272 patients in each group), the odds ratio for metachronous gastric carcinoma was 0.353 (95% CI 0.161-0.775; p=0.009); in the modified intention-to-treat population, including patients with at least one post-randomisation assessment of tumour status and adjusting for loss to follow-up (255 patients in the eradication group, 250 in the control group), the hazard ratio for metachronous gastric carcinoma was 0.339 (95% CI 0.157-0.729; p=0.003). In the eradication group, 19 (7%) patients had diarrhoea and 32 (12%) had soft stools.
INTERPRETATION: Prophylactic eradication of H pylori after endoscopic resection of early gastric cancer should be used to prevent the development of metachronous gastric carcinoma.
FUNDING: Hiroshima Cancer Seminar Foundation.

PMID 18675689  Lancet. 2008 Aug 2;372(9636):392-7. doi: 10.1016/S0140-・・・
著者: Seung Bae Yoon, Jae Myung Park, Chul-Hyun Lim, Yu Kyung Cho, Myung-Gyu Choi
雑誌名: Helicobacter. 2014 Aug;19(4):243-8. doi: 10.1111/hel.12146.
Abstract/Text BACKGROUND: Although endoscopic resection is widely accepted as the curative treatment modality for early gastric cancer, secondary metachronous cancer may subsequently develop in the residual gastric mucosa. The preventive effect of Helicobacter pylori eradication on the development of metachronous gastric cancer in such cases remains controversial. The aim of this study was to determine the effect of H. pylori eradication on the development of metachronous gastric cancer after endoscopic resection of gastric neoplasm by a meta-analysis of all relevant studies.
MATERIALS AND METHODS: We performed a systematic literature search of PubMed, EMBASE, Google Scholar, and the Cochrane Library without language restrictions through March 31, 2014. We included all relevant articles, including prospective, observational, and retrospective studies. Pooled estimates (odds ratios with 95% confidence intervals) were obtained using a random effects model.
RESULTS: Thirteen studies were considered to be appropriate for this meta-analysis. Compared with the control group, the pooled odds ratio in the eradication group was 0.42 (95% confidence interval, 0.32-0.56), and there was no heterogeneity across the studies (p = .853, I(2) = 0%). Subgroup analysis of three prospective trials also showed a lower incidence of metachronous cancer in the eradication group (odds ratio, 0.39; 95% confidence interval, 0.20-0.75). There was no evidence of publication bias in this meta-analysis.
CONCLUSION: Helicobacter pylori eradication reduces the occurrence of metachronous gastric cancer in patients who have undergone endoscopic resection.

© 2014 John Wiley & Sons Ltd.
PMID 25056262  Helicobacter. 2014 Aug;19(4):243-8. doi: 10.1111/hel.12・・・
著者: Yi-Chia Lee, Tsung-Hsien Chiang, Chu-Kuang Chou, Yu-Kang Tu, Wei-Chih Liao, Ming-Shiang Wu, David Y Graham
雑誌名: Gastroenterology. 2016 May;150(5):1113-1124.e5. doi: 10.1053/j.gastro.2016.01.028. Epub 2016 Feb 2.
Abstract/Text BACKGROUND & AIMS: Eradication of Helicobacter pylori infection has been reported to reduce the risk of gastric cancer among asymptomatic individuals in high-risk areas. The magnitude of benefit of H pylori eradication in populations with different levels of gastric cancer risk and in different clinical scenarios is unclear. We performed a systematic review and meta-analysis of randomized controlled trials and observational studies to investigate the effects of H pylori eradication on the incidence of gastric cancer.
METHODS: We searched PubMed, Cochrane Library, and ClinicalTrials.gov, reviewing titles and abstracts of studies of the effects of eradication of H pylori infection on risk of gastric cancer, through May 2015. We also searched bibliographies of included studies, related reviews, and abstracts presented at Digestive Disease Week. Twenty-four eligible studies (22 research manuscripts and 2 abstracts) were included in our meta-analysis (715 incident gastric cancers among a total of 48,064 individuals/340,255 person-years). We assessed the effects, as well as their modification by baseline gastric cancer incidence, study design (randomized trial vs observational study), clinical scenario (asymptomatic infected individuals vs individuals after endoscopic resection of early gastric cancer), demographic characteristics of patients (age and sex), and duration of follow-up.
RESULTS: After adjustment for baseline gastric cancer incidence, individuals with eradication of H pylori infection had a lower incidence of gastric cancer than those who did not receive eradication therapy (pooled incidence rate ratio = 0.53; 95% confidence interval: 0.44-0.64). There was little heterogeneity among studies. Baseline gastric cancer incidence modified the benefit of H pylori eradication (P = .037 for interaction); the incidence rate ratio of gastric cancer decreased in a nonlinear fashion with increasing baseline incidence of gastric cancer (P = .018, in comparison with the linear model). The benefit also modestly increased with age (P = .023 for interaction), but this might be due to correlation between age and baseline gastric cancer incidence. Eradication provided significant benefit for asymptomatic infected individuals (pooled incidence rate ratio, 0.62; 95% CI: 0.49-0.79) and individuals after endoscopic resection of gastric cancers (pooled incidence rate ratio, 0.46; 95% CI: 0.35-0.60). The benefits of H pylori eradication did not differ with study design, sex, or follow-up period.
CONCLUSIONS: In a systematic review and meta-analysis, we associated eradication of H pylori infection with a reduced incidence of gastric cancer. The benefits of eradication vary with baseline gastric cancer incidence, but apply to all levels of baseline risk.

Copyright © 2016 AGA Institute. Published by Elsevier Inc. All rights reserved.
PMID 26836587  Gastroenterology. 2016 May;150(5):1113-1124.e5. doi: 10・・・
著者: K McColl, L Murray, E El-Omar, A Dickson, A El-Nujumi, A Wirz, A Kelman, C Penny, R Knill-Jones, T Hilditch
雑誌名: N Engl J Med. 1998 Dec 24;339(26):1869-74. doi: 10.1056/NEJM199812243392601.
Abstract/Text BACKGROUND: The eradication of Helicobacter pylori infection is beneficial in patients with gastric or duodenal ulcers. The value of eradicating the infection in patients with dyspepsia and no evidence of ulcer disease is not known.
METHODS: We performed a randomized, placebo-controlled trial comparing the efficacy of treatment for two weeks with 20 mg of omeprazole orally twice daily, 500 mg of amoxicillin three times daily (with 500 mg of tetracycline three times daily substituted for amoxicillin in patients allergic to penicillin), and 400 mg of metronidazole three times daily (160 patients) with that of omeprazole alone (158 patients) for resolving symptoms of dyspepsia in patients with H. pylori infection but no evidence of ulcer disease on upper gastrointestinal endoscopy. Symptoms were assessed with the Glasgow Dyspepsia Severity Score, with resolution of symptoms defined as a score of 0 or 1 in the preceding six months (maximal score, 20). One year later the patients were assessed to determine the frequency of the resolution of symptoms.
RESULTS: One month after the completion of treatment, 132 of 150 patients (88 percent) in the group assigned to received omeprazole and antibiotics had a negative test for H. pylori, as compared with 7 of 152 (5 percent) in the group assigned to receive omeprazole alone. One year later, dyspepsia had resolved in 33 of 154 patients (21 percent) in the group given omeprazole and antibiotics, as compared with 11 of 154 (7 percent) in the group given omeprazole alone (95 percent confidence interval for the difference, 7 to 22 percent; P<0.001). Among the patients in the group given omeprazole and antibiotics, the symptoms resolved in 26 of the 98 patients (27 percent) who had had symptoms for five years or less, as compared with 7 of the 56 patients (12 percent) who had had symptoms for more than five years (P=0.03).
CONCLUSIONS: In patients with H. pylori infection and nonulcer, or functional, dyspepsia, treatment with omeprazole and antibiotics to eradicate the infection is more likely to resolve symptoms than treatment with omeprazole alone.

PMID 9862941  N Engl J Med. 1998 Dec 24;339(26):1869-74. doi: 10.1056・・・
著者: A L Blum, N J Talley, C O'Moráin, S V van Zanten, J Labenz, M Stolte, J A Louw, A Stubberöd, A Theodórs, M Sundin, E Bolling-Sternevald, O Junghard
雑誌名: N Engl J Med. 1998 Dec 24;339(26):1875-81. doi: 10.1056/NEJM199812243392602.
Abstract/Text BACKGROUND: It is uncertain whether treatment of Helicobacter pylori infection relieves symptoms in patients with nonulcer, or functional, dyspepsia.
METHODS: We conducted a double-blind, multicenter trial of patients with H. pylori infection and dyspeptic symptoms (moderate-to-very-severe pain and discomfort centered in the upper abdomen). Patients were excluded if they had a history of peptic ulcer disease or gastroesophageal reflux disease and had abnormal findings on upper endoscopy. Patients were randomly assigned to seven days of treatment with 20 mg of omeprazole twice daily, 1000 mg of amoxicillin twice daily, and 500 mg of clarithromycin twice daily or with omeprazole alone and then followed up for one year. Treatment success was defined as the absence of dyspeptic symptoms or the presence of minimal symptoms on any of the 7 days preceding the 12-month visit.
RESULTS: Twenty of the 348 patients were excluded after randomization because they were not infected with H. pylori, were not treated, or had no data available. For the remaining 328 patients (164 in each group), treatment was successful for 27.4 percent of those assigned to receive omeprazole and antibiotics and 20.7 percent of those assigned to receive omeprazole alone (P=0.17; absolute difference between groups, 6.7 percent; 95 percent confidence interval, -2.6 to 16.0). After 12 months, gastritis had healed in 75.0 percent of the patients in the group given omeprazole and antibiotics and in 3.0 percent of the patients in the omeprazole group (P<0.001); the respective rates of H. pylori eradication were 79 percent and 2 percent. In the group given omeprazole and antibiotics, the rate of treatment success among patients with persistent H. pylori infection was similar to that among patients in whom the infection was eradicated (26 percent vs. 31 percent). There were no significant differences between the groups in the quality of life after treatment.
CONCLUSIONS: In patients with nonulcer dyspepsia, the eradication of H. pylori infection is not likely to relieve symptoms.

PMID 9862942  N Engl J Med. 1998 Dec 24;339(26):1875-81. doi: 10.1056・・・
著者: N J Talley, N Vakil, E D Ballard, M B Fennerty
雑誌名: N Engl J Med. 1999 Oct 7;341(15):1106-11. doi: 10.1056/NEJM199910073411502.
Abstract/Text BACKGROUND: The relation between Helicobacter pylori infection and nonulcer dyspepsia is uncertain. We tested the hypothesis that curing the infection will relieve symptoms of dyspepsia.
METHODS: We randomly assigned 170 H. pylori-infected patients with nonulcer dyspepsia to receive twice-daily treatment with 20 mg of omeprazole, 1000 mg of amoxicillin, and 500 mg of clarithromycin for 14 days and 167 such patients to receive identical-appearing placebos; all patients were then followed through regular visits for 12 months. Symptoms were scored on diary cards for seven days before each visit. A carbon-13 urea breath test was performed at base line and repeated at 1 and 12 months, and endoscopic biopsy was performed at 12 months to determine H. pylori status. Treatment was considered successful if the patient had only mild pain or discomfort or none at all.
RESULTS: The rate of eradication of H. pylori infection was 90 percent in the active-treatment group and 2 percent in the placebo group at four to six weeks (P<0.001). At 12 months, there was no significant difference between groups in the rate of successful treatment (46 percent in the active-treatment group and 50 percent in the placebo group; relative likelihood of success with active treatment, 0.93; 95 percent confidence interval, 0.73 to 1.18; P=0.56). There was also no significant difference in the rate of successful treatment at 12 months between patients who were H. pylori-negative and those who were H. pylori-positive (48 percent vs. 49 percent). The rates of successful treatment were also similar when patients were analyzed according to the type of dyspepsia (ulcer-like, reflux-like, or dysmotility-like) and changes in the quality of life. There was no significant association between treatment success and histologic improvement in chronic gastritis at 12 months (P=0.68).
CONCLUSIONS: We found no evidence that curing H. pylori infection in patients with nonulcer dyspepsia leads to relief of symptoms.

PMID 10511608  N Engl J Med. 1999 Oct 7;341(15):1106-11. doi: 10.1056/・・・
著者: P Moayyedi, S Soo, J Deeks, B Delaney, A Harris, M Innes, R Oakes, S Wilson, A Roalfe, C Bennett, D Forman
雑誌名: Cochrane Database Syst Rev. 2006 Apr 19;(2):CD002096. doi: 10.1002/14651858.CD002096.pub4. Epub 2006 Apr 19.
Abstract/Text BACKGROUND: Helicobacter pylori (H pylori) is the main cause of peptic ulcer disease. The role of H pylori in non-ulcer dyspepsia is less clear.
OBJECTIVES: To determine the effect of H pylori eradication on dyspepsia symptoms in patients with non-ulcer dyspepsia.
SEARCH STRATEGY: Trials were identified through electronic searches of the Cochrane Controlled Trials Register (CCTR), MEDLINE, EMBASE, CINAHL and SIGLE, using appropriate subject headings and keywords, searching bibliographies of retrieved articles, and through contacts with experts in the fields of dyspepsia and with pharmaceutical companies.
SELECTION CRITERIA: All parallel group randomised controlled trials (RCTs) comparing drugs to eradicate H pylori with placebo or other drugs known not to eradicate H pylori for patients with non-ulcer dyspepsia.
DATA COLLECTION AND ANALYSIS: Data were collected on individual and global dyspeptic symptom scores, quality of life measures and adverse effects. Dyspepsia outcomes were dichotomised into minimal/resolved versus same/worse symptoms.
MAIN RESULTS: Twenty one randomised controlled trials were included in the systematic review. Eighteen trials compared antisecretory dual or triple therapy with placebo antibiotics +/- antisecretory therapy, and evaluated dyspepsia at 3-12 months. Seventeen of these trials gave results as dichotomous outcomes evaluating 3566 patients and there was no significant heterogeneity between the studies. There was a 10% relative risk reduction in the H pylori eradication group (95% CI = 6% to 14%) compared to placebo. The number needed to treat to cure one case of dyspepsia = 14 (95% CI = 10 to 25). A further three trials compared Bismuth based H pylori eradication with an alternative pharmacological agent. These trials were smaller and had a shorter follow-up but suggested H pylori eradication was more effective than either H2 receptor antagonists or sucralfate in treating non-ulcer dyspepsia.
AUTHORS' CONCLUSIONS: H pylori eradication therapy has a small but statistically significant effect in H pylori positive non-ulcer dyspepsia. An economic model suggests this modest benefit may still be cost-effective but more research is needed.

PMID 16625554  Cochrane Database Syst Rev. 2006 Apr 19;(2):CD002096. d・・・
著者: Luiz Edmundo Mazzoleni, Guilherme Becker Sander, Carlos Fernando de Magalhães Francesconi, Felipe Mazzoleni, Diego Mendonça Uchoa, Laura Renata De Bona, Tobias Cancian Milbradt, Pâmela Schitz Von Reisswitz, Otavio Berwanger, Mathias Bressel, Maria Isabel Edelweiss, Stela Scaglioni Marini, Cynthia Goulart Molina, Luciano Folador, Roberta Perin Lunkes, Renata Heck, Oscar Augusto Birkhan, Bianca Michel Spindler, Natan Katz, Bruno da Silveira Colombo, Pedro Proença Guerrieri, Luiza Brusius Renck, Elisa Grando, Bianca Hocevar de Moura, Franciele Darsie Dahmer, Juliano Rauber, João Carlos Prolla
雑誌名: Arch Intern Med. 2011 Nov 28;171(21):1929-36. doi: 10.1001/archinternmed.2011.533.
Abstract/Text BACKGROUND: Eradication of Helicobacter pylori in patients with functional dyspepsia continues to be a matter of debate. We studied eradication effects on symptoms and quality of life of primary care patients.
METHODS: Helicobacter pylori -positive adult patients with functional dyspepsia meeting the Rome III International Consensus criteria were randomly assigned to receive omeprazole, amoxicillin trihydrate, and clarithromycin, or omeprazole plus placebo for 10 days. Endoscopy and H pylori tests were performed at screening and at 12 months. Outcome measures were at least 50% symptomatic improvement at 12 months using a validated disease-specific questionnaire (primary end point), patient global assessment of symptoms, and quality of life.
RESULTS: We randomly assigned 404 patients (78.7% were women; mean age, 46.1 years); 201 were assigned to be treated with antibiotics (antibiotics group) and 203 to a control group. A total of 389 patients (96.3%) completed the study. The proportion of patients who achieved the primary outcome was 49.0% (94 of 192) in the antibiotics group and 36.5% (72 of 197) in the control group (P = .01; number needed to treat, 8). In the patient global assessment of symptoms, 78.1% in the antibiotics group (157 of 201) answered that they were better symptomatically, and 67.5% in the control group (137 of 203) said that they were better (P = .02). The antibiotics group had a significantly larger increase in their mean (SD) Medical Outcomes Study 36-Item Short Form Health Survey physical component summary scores than the control group did (4.15 [8.5] vs 2.2 [8.1]; P = .02).
CONCLUSION: Helicobacter pylori eradication provided significant benefits to primary care patients with functional dyspepsia.
TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00404534.

PMID 22123802  Arch Intern Med. 2011 Nov 28;171(21):1929-36. doi: 10.1・・・
著者: M Asaka, T Sugiyama, M Kato, K Satoh, H Kuwayama, Y Fukuda, T Fujioka, T Takemoto, K Kimura, T Shimoyama, K Shimizu, S Kobayashi
雑誌名: Helicobacter. 2001 Sep;6(3):254-61.
Abstract/Text BACKGROUND: Two triple therapies with lansoprazole (LPZ)/amoxicillin (AMPC)/clarithromycin (CAM) for eradication of Helicobacter pylori were studied in multicenter, double-blind fashion to evaluate the eradication rate of H. pylori and safety of eradiation treatment in Japanese patients with H. pylori-positive active gastric ulcers or duodenal ulcers.
METHODS: Patients were randomly chosen for the control treatment of LPZ 30 mg twice a day (b.i.d.; Group A-LPZ-only) or the test treatments of LPZ 30 mg plus AMPC 750 mg and CAM 200 mg b.i.d. (Group B-LAC200) and LPZ 30 mg, AMPC 750 mg and CAM 400 mg b.i.d. (Group C-LAC400). All eradication treatments lasted for a period of 7 days. Successful eradication was assessed by culture and gastric histology 1 month after completion of the ulcer treatment.
RESULTS: The eradication rates of H. pylori in the full analysis set were 0% in Group A-LPZ-only, 87.5% in Group B-LAC200 and 89.2% in Group C-LAC400 for gastric ulcer and, 4.4% in Group A-LPZ-only, 91.1% in Group B-LAC200 and 83.7% in Group C-LAC400 for duodenal ulcer. The eradication rates of Group B-LAC200 and Group C-LAC400 were 89.2% (95% CI: 84.8-93.7%) and 86.4% (95%CI: 81.5-91.3%) in total in the full analysis set, 89% (95% CI: 84.3-93.7%) and 85.3% (95%CI: 80.1-90.5%) in the per protocol set. The eradication rates in Groups B-LAC200 and group C-LAC400 were statistically significantly higher than the rate in Group A-LPZ-only for both gastric ulcer and duodenal ulcer patients (p <.0001 for both).
CONCLUSION: A satisfactorily high H. pylori eradication rate was obtained in Japanese ulcer patients with the triple therapy regimen consisting of LPZ 30 mg, AMPC 750 mg, and CAM 200 mg b.i.d.

PMID 11683930  Helicobacter. 2001 Sep;6(3):254-61.
著者: H Kuwayama, M Asaka, T Sugiyama, Y Fukuda, N Aoyama, Y Hirai, T Fujioka, Japan Rabeprazole Study Group
雑誌名: Aliment Pharmacol Ther. 2007 May 1;25(9):1105-13. doi: 10.1111/j.1365-2036.2007.03298.x.
Abstract/Text BACKGROUND: Large-scale studies of rabeprazole-based Helicobacter pylori eradication therapy have not been reported in Japan.
AIMS: To evaluate H. pylori eradication by rabeprazole-based therapy with reference to antibiotic susceptibility, CYP2C19 genotype, and rabeprazole and clarithromycin dosages.
METHODS: From 35 centres 479 H. pylori-positive patients with gastric or duodenal ulcer were randomized to four treatment groups: Group 1 (10 mg rabeprazole + 750 mg amoxicillin + 200 mg clarithromycin twice daily for 7 days); Group 2 (10 mg, 750 mg, 400 mg); Group 3 (20 mg, 750 mg, 200 mg) and Group 4 (20 mg, 750 mg, 400 mg).
RESULTS: Eradication rates were 86% (102 of 119), 89% (97 of 109), 91% (106 of 116) and 90% (104 of 115) for Groups 1-4, respectively. The eradication rate was 95% (360 of 379) for clarithromycin-susceptible strains, and 50% (30 of 60) for clarithromycin-resistant strains. The eradication rates were 88% (332 of 379) and 96% (77 of 80) in extensive metabolizers and poor metabolizers, respectively.
CONCLUSIONS: Rabeprazole-based therapies achieved 50% eradication of clarithromycin-resistant H. pylori, and even achieved good rates in extensive metabolizers. Accordingly, rabeprazole can be recommended as part of a first-line proton pump inhibitor-based triple therapy for H. pylori.

PMID 17439512  Aliment Pharmacol Ther. 2007 May 1;25(9):1105-13. doi: ・・・
著者: Hajime Kuwayama, Gordon Luk, Shunichi Yoshida, Takefumi Nakamura, Mitsuhiko Kubo, Naomi Uemura, Shigeru Harasawa, Mitsuru Kaise, Eiko Sanuki, Ken Haruma, Masaki Inoue, Tomohiko Shimatani, Hiroshi Mieno, Masahiro Kawanishi, Hidenobu Watanabe, Mituyoshi Nakashima, Saburo Nakazawa
雑誌名: Clin Drug Investig. 2005;25(5):293-305.
Abstract/Text OBJECTIVES: To investigate the efficacies of two different triple-therapy regimens (standard versus low doses), and the influence of cytochrome P450 enzyme (CYP) genetic polymorphism on these efficacies, in Japanese patients undergoing Helicobacter pylori eradication treatment.
METHODS: All patients received 1 week of triple therapy. Patients in group A (low-dose regimen) received omeprazole 40 mg/day + amoxicillin 1500 mg/day + clarithromycin 800 mg/day; patients in group B (standard-dose regimen) received omeprazole 40 mg/day + amoxicillin 2000 mg/day + clarithromycin 1000 mg/day.
RESULTS: A total of 225 patients (113 in group A and 112 in group B) were randomised to one of the two triple-therapy regimens. The eradication rates were 78.8% (89/113 patients; 95% CI 70.1, 85.9) in group A and 83.0% (93/112 patients; 95% CI 74.8, 89.5) in group B. Genetic polymorphism of CYP2C19, a major metabolic enzyme of omeprazole, did not affect eradication rates, while susceptibility to clarithromycin greatly affected the success of eradication. The cumulative ulcer relapse rate at 24 weeks after endoscopically documented ulcer healing (30 weeks after completion of the drug regimen) was 8.3% for group A and 12.5% for group B (log rank test: p = 0.6248). However, comparison of the cumulative relapse rate of 6.7% in patients after successful H. pylori eradication with the relapse rate of 27.3% in those who failed H. pylori eradication revealed a significant difference in the remission-time curve (log rank test: p = 0.0047). This finding suggested the existence of a relationship between H. pylori eradication failure and ulcer relapse. Both drug regimens were well tolerated. Endoscopically proven reflux esophagitis developed in about 10% of patients after eradication, but was not clinically significant.
CONCLUSIONS: One week of triple therapy with a low-dose regimen provides adequate H. pylori eradication in Japanese patients. CYP genetic polymorphism is of minimal clinical significance with both triple-therapy regimens.

PMID 17532667  Clin Drug Investig. 2005;25(5):293-305.
著者: Kazuhide Higuchi, Takama Maekawa, Koichiro Nakagawa, Shinji Chouno, Takanobu Hayakumo, Naomi Tomono, Akio Orino, Hirohisa Tanimura, Kan Asahina, Naotaka Matsuura, Motohiko Endo, Masanori Hirano, Choitsu Sakamoto, Tsutomu Inomoto, Tetsuo Arakawa
雑誌名: Clin Drug Investig. 2006;26(7):403-14.
Abstract/Text OBJECTIVE: Seven-day administration of omeprazole 40 mg/day + amoxicillin 1500 mg/day + clarithromycin 800 mg/day is currently approved in Japan for the eradication of Helicobacter pylori infection. We investigated the efficacy and safety of an omeprazole-based triple therapy regimen in combination with amoxicillin and low-dose clarithromycin in Japanese patients.
METHODS: Patients were randomly assigned to either the low-dose group (omeprazole 40 mg/day + amoxicillin 1500 mg/day + clarithromycin 400 mg/day) or the high-dose group (omeprazole 40 mg/day + amoxicillin 1500 mg/day + clarithromycin 800 mg/day). A total of 288 patients were allocated to the low-dose (143) and high-dose (145) groups and were treated twice daily for 1 week.
RESULTS: For the full-analysis set, H. pylori eradication rates were 81.1% (116/143 patients, 90% confidence interval [CI] 74.9, 86.3) in the low-dose group and 80.0% (116/145 patients, 90% CI 73.7, 85.3) in the high-dose group. Per-protocol eradication rates were 81.7% (103/126 patients, 90% CI 75.1, 87.2) and 84.1% (90/107 patients, 90% CI 77.1, 89.6), respectively. When patients with non-susceptibility to clarithromycin were excluded, eradication rates were >80% for both gastric and duodenal ulcers in the two groups. The results suggested that eradication rates were affected more by susceptibility to clarithromycin than to amoxicillin. Both regimens were well tolerated.
CONCLUSION: This study demonstrated that an omeprazole-based triple-therapy regimen with clarithromycin 400 mg/day was as effective as that with clarithromycin 800 mg/day for H. pylori eradication.

PMID 17163273  Clin Drug Investig. 2006;26(7):403-14.
著者: Kazunari Murakami, Yuuichi Sakurai, Madoka Shiino, Nobuo Funao, Akira Nishimura, Masahiro Asaka
雑誌名: Gut. 2016 Sep;65(9):1439-46. doi: 10.1136/gutjnl-2015-311304. Epub 2016 Mar 2.
Abstract/Text OBJECTIVE: The objective of this study was to assess the efficacy, safety and tolerability of vonoprazan, a novel potassium-competitive acid blocker, as a component of Helicobacter pylori eradication therapy.
DESIGN: A randomised, double-blind, multicentre, parallel-group study was conducted to verify the non-inferiority of vonoprazan 20 mg to lansoprazole 30 mg as part of first-line triple therapy (with amoxicillin 750 mg and clarithromycin 200 or 400 mg) in H pylori-positive patients with gastric or duodenal ulcer history. The first 50 patients failing first-line therapy with good compliance also received second-line vonoprazan-based triple therapy (with amoxicillin 750 mg and metronidazole 250 mg) as an open-label treatment.
RESULTS: Of the 650 subjects randomly allocated to either first-line triple therapy, 641 subjects completed first-line therapy and 50 subjects completed second-line therapy. The first-line eradication rate (primary end point) was 92.6% (95% CI 89.2% to 95.2%) with vonoprazan versus 75.9% (95% CI 70.9% to 80.5%) with lansoprazole, with the difference being 16.7% (95% CI 11.2% to 22.1%) in favour of vonoprazan, thus confirming the non-inferiority of vonoprazan (p<0.0001). The second-line eradication rate (secondary end point) was also high (98.0%; 95% CI 89.4% to 99.9%) in those who received second-line therapy (n=50). Both first-line triple therapies were well tolerated with no notable differences. Second-line triple therapy was also well tolerated.
CONCLUSION: Vonoprazan is effective as part of first-line triple therapy and as part of second-line triple therapy in H pylori-positive patients with a history of gastric or duodenal ulcer.
TRIAL REGISTRATION NUMBER: NCT01505127.

Published by the BMJ Publishing Group Limited. For permission to use (where not already granted under a licence) please go to http://www.bmj.com/company/products-services/rights-and-licensing/
PMID 26935876  Gut. 2016 Sep;65(9):1439-46. doi: 10.1136/gutjnl-2015-3・・・
著者: H Isomoto, K Inoue, H Furusu, A Enjoji, C Fujimoto, M Yamakawa, Y Hirakata, K Omagari, Y Mizuta, K Murase, S Shimada, I Murata, S Kohno
雑誌名: Aliment Pharmacol Ther. 2003 Jul 1;18(1):101-7.
Abstract/Text BACKGROUND: There is currently no optimal second-line treatment after failure of Helicobacter pylori triple therapy.
AIM: To determine effective salvage therapy after failure of lansoprazole-amoxicillin-clarithromycin.
METHODS: After failure of lansoprazole-amoxicillin-clarithromycin 123 out-patients were randomized to receive either 2-week rabeprazole (20 mg b.d.) + amoxicillin (1000 mg b.d.) (RA group) or 1-week rabeprazole (10 mg b.d.) + amoxicillin (750 mg twice b.d.) + metronidazole (250 mg b.d.) (RAM group). Eradication was assessed by the 13C-urea breath test. We also evaluated cytochrome p450 (CYP) 2C19 genotype status, determined by polymerase chain reaction - restriction fragment length polymorphism, and susceptibility to clarithromycin and metronidazole.
RESULTS: On an intention-to-treat basis, H. pylori infection cure was achieved in 37 of 63 (59%) patients in the RA group and in 49 of 60 (82%) patients in the RAM group. Per protocol-based eradication rates in the RA and RAM groups were 66% (37/56) and 88% (49/56), respectively. In both analytic sets there were significant differences between the treatment groups (P < 0.01 in each). Mild adverse events were observed in eight and five patients from the RA and RAM groups, respectively. Genetic predisposition of CYP2C19 and antibiotic resistance did not influence the treatment outcome either regimen.
CONCLUSIONS: The rabeprazole + amoxicillin + metronidazole therapy yielded satisfactory results. In contrast, the cure rate in high-dose rabeprazole + amoxicillin was below an acceptable level.

PMID 12848631  Aliment Pharmacol Ther. 2003 Jul 1;18(1):101-7.
著者: Takeshi Matsuhisa, Takashi Kawai, Tatsuhiro Masaoka, Hidekazu Suzuki, Masayoshi Ito, Yo Kawamura, Kengo Tokunaga, Masayuki Suzuki, Tetsuya Mine, Shin-ichi Takahashi, Nobuhiro Sakaki
雑誌名: Helicobacter. 2006 Jun;11(3):152-8. doi: 10.1111/j.1523-5378.2006.00394.x.
Abstract/Text BACKGROUND: With the increase in the frequency of clarithromycin-resistant Helicobacter pylori (H. pylori), there is rising concern about the decline of the eradication rate of this infection following treatment. The Tokyo Hp Study Group examined the eradication rate in response to a second-line regimen consisting of proton pump inhibitor (PPI), amoxicillin, and metronidazole by conducting a multicenter study in the Tokyo Metropolitan Area.
MATERIALS AND METHODS: Two hundred and twenty-eight patients with H. pylori infection, in whom the first-line therapy with a PPI, amoxicillin, and clarithromycin administered for 1 week had failed to eradicate the infection, were enrolled in this study. These cases were randomly assigned to one of the two second-line regimens containing metronidazole (PPI/AM500 or PPI/AM750) administered for 1 week. 13C-urea breath test was performed as a diagnostic method test for H. pylori infection not earlier than 8 weeks after the second-line therapy.
RESULTS: Intention-to-treat (ITT) and per-protocol (PP) analyses revealed an eradication rate of 87.6 and 90.6%, respectively, following PPI/AM500 treatment, and 86.9 and 88.6%, respectively, following PPI/AM750 treatment. Neither analysis revealed any significant difference in the eradication rate between PPI/AM500 and PPI/AM750 (p = .876 and .621, respectively). According to ITT and PP analyses, the eradication rates following treatment with PPI/AM500 were 85.2 and 88.5% with the use of lansoprazole, 62.5 and 62.5% with the use of omeprazole, and 93.2 and 96.5% with the use of rabeprazole, respectively. There was a significant difference in the eradication rates between PPI (omeprazole)/AM500 and PPI (rabeprazole)/AM500. In the case of PPI/AM750, the corresponding eradication rates were 84.8 and 87.0% with the use of lansoprazole, 92.9 and 92.9% with the use of omeprazole, and 92.9 and 92.9% with the use of rabeprazole, respectively. There were no significant differences in the eradication rates obtained with the use of the three PPIs.
CONCLUSIONS: Both PPI/AM500 and PPI/AM750 administered for 1 week appeared to be highly effective second-line regimens for the treatment of H. pylori infection in Japanese patients. From the viewpoint of adverse events, PPI/AM500 appeared to be safe compared with PPI/AM750.

PMID 16684262  Helicobacter. 2006 Jun;11(3):152-8. doi: 10.1111/j.1523・・・
著者: E M el-Omar, I D Penman, J E Ardill, R S Chittajallu, C Howie, K E McColl
雑誌名: Gastroenterology. 1995 Sep;109(3):681-91.
Abstract/Text BACKGROUND & AIMS: The mechanism by which Helicobacter pylori predisposes to duodenal ulcers (DUs) remains unclear. The aim of this study was to investigate the effect of the infection on acid secretion.
METHODS: Acid output was examined basally and in response to gastrin-releasing peptide (GRP) and gastrin in healthy volunteers with and without H. pylori infection and in patients with DUs before and after eradication of the infection.
RESULTS: Compared with H. pylori-negative healthy volunteers, patients with DUs with H. pylori had the following abnormalities of acid secretion: (1) threefold increase in basal acid output, (2) sixfold increase in acid response to GRP, (3) increased maximal acid response to exogenous gastrin, (4) increased ratio of basal acid output to maximal gastrin-stimulated output, and (5) increased ratio of maximal GRP-stimulated acid output to maximal gastrin-stimulated output. All of these abnormalities resolved fully after H. pylori eradication except for increased maximal acid output to gastrin, which was unchanged. Infected healthy volunteers showed a threefold increase in acid response to GRP that resolved after eradication of H. pylori infection.
CONCLUSIONS: These disturbances in acid secretion caused by H. pylori infection are consistent with impaired inhibitory control and are likely to be relevant to the mechanism by which the infection predisposes to DU.

PMID 7657096  Gastroenterology. 1995 Sep;109(3):681-91.
著者: Y Yasunaga, Y Shinomura, S Kanayama, M Yabu, T Nakanishi, Y Miyazaki, Y Murayama, J J Bonilla-Palacios, Y Matsuzawa
雑誌名: Gut. 1994 Nov;35(11):1571-4.
Abstract/Text This study examined the effects of eradication of Helicobacter pylori (H pylori) infection on gastric mucosal morphology and acid secretion. Sixteen H pylori positive patients with enlarged gastric body folds were divided into two groups: (a) patients with moderate enlargement (fold width: 6 to 10 mm, n = 8) and (b) patients with severe enlargement (> 10 mm, n = 8). After successful treatment, gastric body fold width was reduced in both groups (p < 0.01) with an associated decrease in inflammatory infiltrates in the body mucosa (p < 0.01 and p < 0.05). Basal acid output and tetragastrin stimulated maximal acid output (mean (SEM)) in all 16 patients significantly increased from 1.1 (0.5) to 2.9 (0.9) mmol/h (p < 0.05) and from 5.4 (1.3) to 18.7 (2.3) mmol/h (p < 0.01), respectively, with a significant decrease in fasting serum gastrin concentrations, from 127.1 (16.1) to 59.6 (3.8) pg/ml (p < 0.01). The increase in acid secretion after eradication of H pylori was more noticeable in the severe group, who had shown lower acid secretion and higher serum gastrin concentrations (p < 0.05) before eradication, than the increase seen in the moderate group. The decreases in ammonia nitrogen content seen after eradication were significant in basal (from 0.91 (0.17) to 0.37 (0.08) mmol/h, p < 0.05) and stimulated gastric secretions (from 1.57 (0.19) to 0.37 (0.13) mmol/h, p < 0.01), although these changes were too small to explain the increases in basal acid output and maximal acid output. These results suggest that inflammation of the gastric body mucosa caused by H pylori infection is associated with enlarged gastric body folds and inhibition of acid secretion in H pylori positive patients with enlarged gastric body folds.

PMID 7828975  Gut. 1994 Nov;35(11):1571-4.
著者: Masahiro Kawanishi
雑誌名: J Gastroenterol. 2005 Nov;40(11):1024-8. doi: 10.1007/s00535-005-1685-x.
Abstract/Text BACKGROUND: We aimed to determine the incidence and causative factors of reflux esophagitis following Helicobacter pylori eradication in Japanese patients.
METHODS: In patients in whom reflux esophagitis could not be detected endoscopically, we conducted an annual follow-up observation in 326 H. pylori-cured patients, 199 H. pylori-positive patients, and 151 H. pylori-negative patients, to study the incidence and causative factors of reflux esophagitis.
RESULTS: Development of reflux esophagitis was observed in 74 (22.7%) of the H. pylori-cured patients during a median follow-up period of 6.0 years, in 16 (8.0%) of the H. pylori-positive patients during a median follow-up period of 5.0 years, and in 29 (19.2%) of the H. pylori-negative patients during a median follow-up period of 5.4 years. The results, after correction for sex and age, showed that H. pylori-cured patients had a significantly higher risk of reflux esophagitis than H. pylori-positive patients (risk ratio, 2.43; P < 0.01), but their risk did not differ from that in the H. pylori-negative patients. It was also shown that hiatal hernia (risk ratio, 4.01; P < 0.01) and smoking history (risk ratio, 1.77; P < 0.05) were significant risk factors for the development of reflux esophagitis.
CONCLUSIONS: With regard to the development of reflux esophagitis following H. pylori eradiation therapy, we observed that the frequency was higher in H. pylori-cured patients than in H. pylori-positive patients, but the frequency in H. pylori-cured patients and H. pylori-negative patients was the same. We elucidated that hiatal hernia and smoking history are important risk factors for reflux esophagitis.

PMID 16322945  J Gastroenterol. 2005 Nov;40(11):1024-8. doi: 10.1007/s・・・
著者: T Furuta, S Baba, M Yamade, T Uotani, T Kagami, T Suzuki, S Tani, Y Hamaya, M Iwaizumi, S Osawa, K Sugimoto
雑誌名: Aliment Pharmacol Ther. 2018 Aug;48(3):370-377. doi: 10.1111/apt.14849. Epub 2018 Jun 19.
Abstract/Text BACKGROUND: Although autoimmune gastritis (AIG) is generally considered relatively rare, we frequently encounter AIG among patients at to our hospital who have experienced at least two episodes of Helicobacter pylori eradication failure.
AIMS: We investigated the incidence of AIG in consecutive patients who consulted our department for H. pylori eradication with reference to eradication history.
METHODS: A total of 404 consecutive patients who visited the H. pylori-specific out-patient unit of our hospital from June 2015 to June 2017 were enrolled. Of these, 137 were treatment-naive, 47 had failed treatment once (single failure), and 220 had failed treatment twice or more (multiple failures) by 13 C-UBT. Gastroscopy was performed in all patients. Culture tests of gastric mucosal samples were performed for H. pylori and other bacteria positive for urease activity. Anti-parietal cell antibody (APCA) was measured. Patients with severe atrophy in the gastric corpus and positivity for APCA were diagnosed as having AIG.
RESULTS: A total of 43 patients were diagnosed as having AIG, of whom two were treatment-naive (1.5%, 2/137), 1 failed eradication once (2.1% 1/47), and 40 failed treatment at least twice (18.2%, 40/220). The incidence of AIG was significantly higher in the multiple failure group than in the single failure or treatment-naive groups. Urease-positive bacteria, such as Klebsiella pneumoniae and alpha-streptococcus, were identified in 33 of the 35 AIG patients who underwent culture testing.
CONCLUSION: AIG patients were often misdiagnosed as refractory to eradication therapy, probably because achlorhydria in AIG might allow urease-positive bacteria other than H. pylori to colonise the stomach, causing positive 13 C-UBT results.

© 2018 John Wiley & Sons Ltd.
PMID 29920721  Aliment Pharmacol Ther. 2018 Aug;48(3):370-377. doi: 10・・・
著者: Tadayoshi Okimoto, Kazunari Murakami, Ryugo Sato, Hajime Miyajima, Masaru Nasu, Jiro Kagawa, Masaaki Kodama, Toshio Fujioka
雑誌名: Helicobacter. 2003 Jun;8(3):186-91.
Abstract/Text BACKGROUND: Reinfection of Helicobacter pylori after eradication is rare in developed countries but most often occurs within 1 year. In the present study, we attempted to differentiate between reinfection and recrudescence of H. pylori strains between 6 months and 6 years after successful eradication in Japan, a country with a high prevalence of H. pylori infection.
MATERIALS AND METHODS: After successful eradication of H. pylori, 274 patients were followed up by endoscopy and urea breath test. In recurrent patients, H. pylori strains isolated initially and after recurrence were compared using PCR-based restriction fragment length polymorphism (RFLP) analysis.
RESULTS: Recurrence of H. pylori occurred in 15 of 274 patients (5.5%) at 6 months after eradication and the annual recurrence rate was 2.0% per patient year (between 1 and 6 years). PCR-based RFLP analysis of H. pylori strains isolated initially and after recurrence showed that 62.5% (at 6 months) and 100% (after 1 years) of bacteria were of different strains.
CONCLUSION: Reinfection of H. pylori was not as rare at 6 months after eradication as reported previously, and up to 6 years after eradication, the annual reinfection rate is 2.0% per patient year in Japan.

PMID 12752730  Helicobacter. 2003 Jun;8(3):186-91.
著者: Masayasu Adachi, Motowo Mizuno, Kenji Yokota, Masatsugu Miyoshi, Yasuhiro Nagahara, Toshirou Maga, Kunihara Ishiki, Tomoki Inaba, Hioyuki Okada, Keiji Oguma, Takao Tsuji
雑誌名: J Gastroenterol Hepatol. 2002 Jan;17(1):27-31.
Abstract/Text BACKGROUND AND AIM: In developed countries, reinfection of Helicobacter pylori (H. pylori) after eradication of the bacterium is unusual, while the reinfection rate in developing countries is variable. In this study, we determined the reinfection rate after successful H. pylori eradication in Japan, a country with a high prevalence of H. pylori infection.
METHODS: After successful eradication, 377 patients were followed up by endoscopy and urea breath test annually. In reinfected patients, H. pylori strains isolated initially and after reinfection were compared by using random amplification of polymorphic DNA fingerprinting.
RESULTS: H. pylori became positive in four of 337 patients (1.2) 1 year after eradication and in two of 133 patients (1.5) 2 years after eradication. One patient experienced an ulcer relapse 2 years after eradication therapy. Random amplification of polymorphic DNA fingerprinting of the isolated strains from four of the six patients showed two had identical strains (at 1 year) while the other two had different strains (one at 1 year and one at 2 years). When infection in the two patients reinfected with identical strains is considered a recrudescence, the true reinfection rate is < 0.8 per patient year.
CONCLUSIONS: The reinfection rate after eradication of H. pylori is low in Japan despite the country's high prevalence of H. pylori infection.

PMID 11987263  J Gastroenterol Hepatol. 2002 Jan;17(1):27-31.
著者: Douglas R Morgan, Javier Torres, Rachael Sexton, Rolando Herrero, Eduardo Salazar-Martínez, E Robert Greenberg, Luis Eduardo Bravo, Ricardo L Dominguez, Catterina Ferreccio, Eduardo C Lazcano-Ponce, Maria Mercedes Meza-Montenegro, Edgar M Peña, Rodolfo Peña, Pelayo Correa, María Elena Martínez, William D Chey, Manuel Valdivieso, Garnet L Anderson, Gary E Goodman, John J Crowley, Laurence H Baker
雑誌名: JAMA. 2013 Feb 13;309(6):578-86. doi: 10.1001/jama.2013.311.
Abstract/Text IMPORTANCE: The long-term effectiveness of Helicobacter pylori eradication programs for preventing gastric cancer will depend on recurrence risk and individual and community factors.
OBJECTIVE: To estimate risk of H. pylori recurrence and assess factors associated with successful eradication 1 year after treatment.
DESIGN, SETTING, AND PARTICIPANTS: Cohort analysis of 1463 randomized trial participants aged 21 to 65 years from 7 Latin American communities, who were treated for H. pylori and observed between September 2009 and July 2011.
INTERVENTIONS: Randomization to 1 of 3 treatment groups: 14-day lansoprazole, amoxicillin, and clarithromycin (triple therapy); 5-day lansoprazole and amoxicillin followed by 5-day lansoprazole, clarithromycin, and metronidazole (sequential); or 5-day lansoprazole, amoxicillin, clarithromycin, and metronidazole (concomitant). Participants with a positive (13)C-urea breath test (UBT) 6 to 8 weeks posttreatment were offered voluntary re-treatment with 14-day bismuth-based quadruple therapy.
MEASUREMENTS: Recurrent infection after a negative posttreatment UBT and factors associated with successful eradication at 1-year follow-up.
RESULTS: Among participants with UBT-negative results who had a 1-year follow-up UBT (n=1091), 125 tested UBT positive, a recurrence risk of 11.5% (95% CI, 9.6%-13.5%). Recurrence was significantly associated with study site (P = .03), nonadherence to initial therapy (adjusted odds ratio [AOR], 2.94; 95% CI, 1.31-6.13; P = .01), and children in the household (AOR, 1.17; 95% CI, 1.01-1.35 per child; P = .03). Of the 281 with positive posttreatment UBT results, 138 completed re-treatment, of whom 93 tested UBT negative at 1 year. Among the 1340 who had a 1-year UBT, 80.4% (95% CI, 76.4%-83.9%), 79.8% (95% CI, 75.8%-83.5%), and 77.8% (95% CI, 73.6%-81.6%) had UBT-negative results in the triple, sequential, and concomitant groups, respectively (P = .61), with 79.3% overall effectiveness (95% CI, 77.1%-81.5%). In a single-treatment course analysis that ignored the effects of re-treatment, the percentage of UBT-negative results at 1 year was 72.4% (95% CI, 69.9%-74.8%) and was significantly associated with study site (P < .001), adherence to initial therapy (AOR, 0.26; 95% CI, 0.15-0.42; P < .001), male sex (AOR, 1.63; 95% CI, 1.25-2.13; P < .001), and age (AOR, 1.14; 95% CI, 1.02-1.27 per decade; P = .02). One-year effectiveness among all 1463 enrolled participants, considering all missing UBT results as positive, was 72.7% (95% CI, 70.3%-74.9%).
CONCLUSIONS AND RELEVANCE: One year after treatment for H. pylori infection, recurrence occurred in 11.5% of participants who had negative posttreatment UBT results. Recurrence determinants (ie, nonadherence and demographics) may be as important as specific antibiotic regimen in determining the long-term success of H. pylori eradication interventions. Study findings are relevant to the feasibility of programs for the primary prevention of gastric cancer in high-incidence regions of Latin America.
TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT01061437.

PMID 23403682  JAMA. 2013 Feb 13;309(6):578-86. doi: 10.1001/jama.2013・・・

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