Recurrent Peptic Ulcers in Patients Following Successful <i>Helicobacter pylori</i> Eradication: A Multicenter Study of 4940 Patients

Miwa, Hiroto; Sakaki, Nobuhiro; Sugano, Kentaro; Sekine, Hitoshi; Higuchi, Kazuhide; Uemura, Naomi; Kato, Mototsugu; Murakami, Kazunari; Kato, Chieko; Shiotani, Akiko; Ohkusa, Toshifumi; Takagi, Atsushi; Aoyama, Nobuo; Haruma, Ken; Okazaki, Kazuichi; Kusugami, Kazuo; Suzuki, Masayuki; Joh, Takashi; Azuma, Takeshi; Yanaka, Akinori; Suzuki, Hidekazu; Hashimoto, Hiroshi; Kawai, Takashi; Sugiyama, Toshiro

doi:10.1111/j.1083-4389.2004.00194.x

Cited by 109 publications

(62 citation statements)

References 26 publications

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“…Furthermore, over 4,000 multicenter studies spent 4 years in Japan indicated that the recurrence ratio of gastric ulcer or duodenal ulcer is only 1-2 % per annum after eradication [47]. We found NSAID meditation records and habit of smoking or drinking alcohol more significantly in the recurrence cases of gastric ulcer; 93.1 % of gastric ulcer recurred as gastric ulcer, and all duodenal ulcers recurred as duodenal ulcers.…”

Section: Ulcer Recurrence After Eradicationmentioning

confidence: 67%

“…In contrast, in the unsuccessfully eradicated group, it showed a significantly higher rate of each of 65 and 85 %. Also, over 4,000 multicenter studies spent 4 years in Japan [47] indicated that the recurrence ratio of gastric ulcer or duodenal ulcer is only 1-2 % per annum after eradication. Therefore, we should conduct an infection diagnosis on the cases of gastric or duodenal ulcer which have neither active hemorrhage nor are associated with NSAID, and also we should conduct eradication treatment on the cases infected by H. pylori.…”

Section: Prevention Of Ulcer Recurrencementioning

confidence: 99%

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Evidence-based clinical practice guidelines for peptic ulcer disease 2015

et al. 2016

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The Japanese Society of Gastroenterology (JSGE) revised the evidence-based clinical practice guidelines for peptic ulcer disease in 2014 and has created an English version. The revised guidelines consist of seven items: bleeding gastric and duodenal ulcers, Helicobacter pylori (H. pylori) eradication therapy, non-eradication therapy, drug-induced ulcer, non-H. pylori, non-nonsteroidal anti-inflammatory drug (NSAID) ulcer, surgical treatment, and conservative therapy for perforation and stenosis. Ninety clinical questions (CQs) were developed, and a literature search was performed for the CQs using the Medline, Cochrane, and Igaku Chuo Zasshi databases between 1983 and June 2012. The guideline was developed using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system. Therapy is initially provided for ulcer complications. Perforation or stenosis is treated with surgery or conservatively. Ulcer bleeding is first treated by endoscopic hemostasis. If it fails, surgery or interventional radiology is chosen. Second, medical therapy is provided. In cases of NSAID-related ulcers, use of NSAIDs is stopped, and anti-ulcer therapy is provided. If NSAID use must continue, the ulcer is treated with a proton pump inhibitor (PPI) or prostaglandin analog. In cases with no NSAID use, H. pylori-positive patients receive eradication and anti-ulcer therapy. If first-line eradication therapy fails, second-line therapy is given. In cases of non-H. pylori, non-NSAID ulcers or H. pyloripositive patients with no indication for eradication therapy, non-eradication therapy is provided. The first choice is PPI therapy, and the second choice is histamine 2-receptor antagonist therapy. After initial therapy, maintenance therapy is provided to prevent ulcer relapse.

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Section: Ulcer Recurrence After Eradicationmentioning

confidence: 67%

Section: Prevention Of Ulcer Recurrencementioning

confidence: 99%

Evidence-based clinical practice guidelines for peptic ulcer disease 2015

et al. 2016

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“…Helicobacter pylori is a gram-negative bacterium known as a common pathogen associated with atrophic and metaplastic changes in the stomach, and peptic ulcer disease [1][2][3]. Antibiotic treatment for H. pylori commonly includes a combination of proton pump inhibitors (PPIs) and one or several antibacterial agents such as amoxicillin, clarithromycin, and metronidazole [4].…”

Section: Introductionmentioning

confidence: 99%

Phenotypic and genotypic correlation as expressed in Helicobacter pylori resistance to clarithromycin and fluoroquinolones

Binyamin

Pastukh

et al. 2017

Gut Pathog

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Background:Helicobacter pylori susceptibility to clarithromycin and fluoroquinolone can be determined through Etest or molecular assays. We examined the correlation between phenotypic susceptibility (MIC results) and genotypic susceptibility in H. pylori strains isolated from gastric biopsies. Results:Out of 85 duplicate biopsies obtained from patients from northern Israel who underwent endoscopy, 70 were positive for H. pylori using the CUTest (urease test). These biopsies were cultured for H. pylori and Etest breakpoints were determined for levofloxacin and clarithromycin. H. pylori detection, characterization of wild type (WT) or mutant alleles, and antibiotic resistance were determined molecularly using GenoType HelicoDR kit. Phenotypic and genotype results were compared. The molecular method had higher sensitivity for detection of H. pylori than culture (94.3% vs. 77.1%). Resistance to clarithromycin was higher than to levofloxacin by both methods. Levofloxacin resistance was found in 21.2 and 0% using genotypic and phenotypic methods, respectively. Clarithromycin resistance was found in 66.7 and 62.9% by genotypic and phenotypic methods, respectively. Some samples were found susceptible by Etest and resistant by GenoType HelicoDR (13/53 samples) and some vice versa (10/53 samples). Conclusion:GenoType HelicoDR kit has high sensitivity rate for H. pylori detection. It has the ability to detect many mutations and can help to determine initial antibiotic treatment at the beginning of therapy. However, there were a few cases where there was a phenotype-genotype mismatch result that could derive from possible causes. For example, a resistance mechanism that is not tested in the kit.

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“…[6][7][8][9][10][11] H. Pylorinin duodenal ülser oluşumunda ve nükste etkili olmadığı-na yönelik görüşler de bildirilmiştir. [12][13][14] Kalach ve ark.nın Avrupa çapında yaptıkları 694 olgunun incelendiği ileriye yönelik çok merkezli bir çalışmada H. Pylori enfeksiyonunun, peptik ülser gelişmiş olan çocukların %27'sinde görüldüğü bildirilmiştir. [15] Bu çalışmada duodenal ülser nedeniyle perforasyon oluşmuş olguların hiçbirinde yüksek gastrin düzeyi saptanmadı ancak yine de ameliyat sonrası dönemde minimum altı hafta proton pompa inhibitörü kullandık.…”

Section: Discussionunclassified

Duodenum perforations in children

Emre

Aydın

Özcan

et al. 2016

Ulus Travma Acil Cerrahi Derg

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ÖZETKliniğimizde duodenal perforasyon nedeniyle takip ve tedavisi yapılan olgular incelendi. Duodenal perforasyon tanısı ile 1990-2014 yılları arasında tedavi edilen 14 olgunun kayıtları geriye dönük olarak değerlendirildi. On dört olgunun (sekiz erkek, altı kız) ort. başvuru yaşı 6.2 yıl (25 gün-16 yıl) dı. İki olgu primer olarak başvuruda bulunurken, 12 olgu dış merkezlerden yönlendirilmişti. Ortalama başvuru süresi 3.2 (bir gün-bir hafta) gündü. Perforasyon nedeni 10 olguda duodenal ülser, üç olguda travmatik perforasyon, ichtiosisli iki aylık bir olguda ise idiyopatik idi. Bir olguda nesidioblastozis nedeniyle totale yakın pankreatektomi sonrasında hiperbilüribineminin devam etmesi üzerine yapılan laparotomide duodenal perforasyon saptanarak hastaya duodenum birinci ve ikinci kıtalara rezeksiyon, pilor rezeksiyonu, koledekojejunostomi, gastrojejunostomi ve jejunojejunostomi uygulandı. Kalan 13 hastada primer onarım yapıldı. Primer onarım yapılan hastaların birinde ek olarak gastrostomi açılırken dokuz olguya omentoplasti yapıldı. Takipte 12 olgunun herhangi bir klinik yakınması yokken, iki olgu kaybedilmiştir. Duodenal perforasyonlar çocuk cerrahlarının nadir karşılaştıkları cerrahi problemlerden biridir. Bu nedenle karın ağrısının ayırıcı tanısında akılda tutulmalıdır. Cerrahi sağaltımda primer onarım (duodenorafi ± omentoplasti), etkin ve güvenli bir cerrahi yöntemdir.

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Recurrent Peptic Ulcers in Patients Following Successful Helicobacter pylori Eradication: A Multicenter Study of 4940 Patients

Abstract: Curative treatment of H. pylori infection is useful in preventing ulcer recurrence. Gastric ulcer is more likely to relapse than duodenal ulcer. Recurrent ulcer tended to recur at the site of the original ulcers.

Cited by 109 publications

References 26 publications

Evidence-based clinical practice guidelines for peptic ulcer disease 2015

Evidence-based clinical practice guidelines for peptic ulcer disease 2015

Phenotypic and genotypic correlation as expressed in Helicobacter pylori resistance to clarithromycin and fluoroquinolones

Duodenum perforations in children

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