scholarly journals Relationship between time-varying status of reflux esophagitis and Helicobacter pylori and progression to long-segment Barrett’s esophagus: time-dependent Cox proportional-hazards analysis

2020 ◽  
Author(s):  
Genki Usui ◽  
Tomohiro Shinozaki ◽  
Toyohisa Jinno ◽  
Kazutoshi Fujibayashi ◽  
Teppei Morikawa ◽  
...  

Abstract Background: Reflux esophagitis (RE) and absence of Helicobacter pylori (non-H. pylori) are considered to be associated with the progression to long-segment Barrett’s esophagus (LSBE). However, it is difficult to assess this association because RE and H. pylori status can change during follow-up. Additionally, the association between H. pylori eradication and LSBE remains unclear.Methods: A total of 11,493 asymptomatic Japanese subjects who underwent medical check-ups and were endoscopically diagnosed with short-segment Barrett’s esophagus (SSBE) between May 2006 and December 2015 were enrolled. The hazards of progression to LSBE were compared between time-varying RE and H. pylori infection/eradication by time-dependent multivariable Cox proportional hazards models.Results: A total of 7,637 subjects who underwent additional medical check-ups after being diagnosed with endoscopic SSBE were analyzed. Subjects with RE and without current/past H. pylori infection were strongly associated with a higher rate of progression to LSBE (adjusted hazard ratio [HR]: 7.17, 95% confidence interval [CI]: 2.48-20.73, p<0.001 for RE and non-H. pylori vs. non-RE and H. pylori groups). Subjects with H. pylori had a lower rate of progression to LSBE (adjusted HR: 0.48, 95% CI: 0.22-1.07, p=0.07 for H. pylori vs. non-H. pylori). Hazards of progression to LSBE were still lower in the H. pylori eradication group than that of the non-H. pylori group (adjusted HR: 0.51, 95% CI: 0.18-1.46, p=0.21).Conclusions: RE and non-H. pylori were associated with the progression to LSBE, considering the changes in exposures. H. pylori infection was associated with the prevention of the development of LSBE irrespective of RE. The environment preventive of the development of LSBE persists for at least a few years after H. pylori eradication.

2020 ◽  
Author(s):  
Genki Usui ◽  
Tomohiro Shinozaki ◽  
Toyohisa Jinno ◽  
Kazutoshi Fujibayashi ◽  
Teppei Morikawa ◽  
...  

Abstract Background: Reflux esophagitis (RE) and absence of Helicobacter pylori (non-H. pylori) are considered to be associated with the progression to long-segment Barrett’s esophagus (LSBE). However, it is difficult to assess this association because RE and H. pylori status can change during follow-up. Additionally, the association between H. pylori eradication and LSBE remains unclear. Methods: A total of 11,493 asymptomatic Japanese subjects who underwent medical check-ups and were endoscopically diagnosed with short-segment Barrett’s esophagus (SSBE) between May 2006 and December 2015 were enrolled. The hazards of progression to LSBE were compared between time-varying RE and H. pylori infection/eradication by time-dependent multivariable Cox proportional hazards models. Results A total of 7,637 subjects who underwent additional medical check-ups after being diagnosed with endoscopic SSBE were analyzed. Subjects with RE and without current/past H. pylori infection were strongly associated with a higher rate of progression to LSBE (adjusted hazard ratio [HR]: 7.17, 95% confidence interval [CI]: 2.48–20.73, p < 0.001 for RE and non-H. pylori vs. non-RE and H. pylori groups). Subjects with H. pylori had a lower rate of progression to LSBE (adjusted HR: 0.48, 95% CI: 0.22–1.07, p = 0.07 for H. pylori vs. non-H. pylori). Hazards of progression to LSBE were still lower in the H. pylori eradication group than that of the non-H. pylori group (adjusted HR: 0.51, 95% CI: 0.18–1.46, p = 0.21). Conclusions RE and non-H. pylori were associated with the progression to LSBE, considering the changes in exposures. H. pylori eradication may not increase the rate of progression to LSBE.


2020 ◽  
Author(s):  
Genki Usui ◽  
Tomohiro Shinozaki ◽  
Toyohisa Jinno ◽  
Kazutoshi Fujibayashi ◽  
Teppei Morikawa ◽  
...  

Abstract Background: Reflux esophagitis (RE) and absence of Helicobacter pylori (non-H. pylori) are considered to be associated with the progression to long-segment Barrett’s esophagus (LSBE). However, it is difficult to assess this association because RE and H. pylori status can change during follow-up. Additionally, the association between H. pylori eradication and LSBE remains unclear.Methods: A total of 11,493 asymptomatic Japanese subjects who underwent medical check-ups and were endoscopically diagnosed with short-segment Barrett’s esophagus (SSBE) between May 2006 and December 2015 were enrolled. The hazards of progression to LSBE were compared between time-varying RE and H. pylori infection/eradication by time-dependent multivariable Cox proportional hazards models.Results: A total of 7,637 subjects who underwent additional medical check-ups after being diagnosed with endoscopic SSBE were analyzed. Subjects with RE and without current/past H. pylori infection were strongly associated with a higher rate of progression to LSBE (adjusted hazard ratio [HR]: 7.17, 95% confidence interval [CI]: 2.48-20.73, p<0.001 for RE and non-H. pylori vs. non-RE and H. pylori groups). Subjects with H. pylori had a lower rate of progression to LSBE (adjusted HR: 0.48, 95% CI: 0.22-1.07, p=0.07 for H. pylori vs. non-H. pylori). Hazards of progression to LSBE were still lower in the H. pylori eradication group than that of the non-H. pylori group (adjusted HR: 0.51, 95% CI: 0.18-1.46, p=0.21).Conclusions: RE and non-H. pylori were associated with the progression to LSBE, considering the changes in exposures. H. pylori infection was associated with the prevention of the development of LSBE irrespective of RE. The environment preventive of the development of LSBE persists for at least a few years after H. pylori eradication.


2011 ◽  
Vol 2011 ◽  
pp. 1-4 ◽  
Author(s):  
Yeong Yeh Lee ◽  
Sharifah Emilia Tuan Sharif ◽  
Syed Hassan Syed Abd Aziz ◽  
S. Mahendra Raj

Objective. This study was undertaken to gain an insight into the relationship between Helicobacter pylori (H. pylori) infection, Barrett's esophagus and reflux esophagitis in an area of exceptionally low prevalence of H. pylori infection. Methods. A total of 1895 consecutive upper endoscopies performed between January 2005 and July 2007 were reviewed. 120 cases of columnar-lined esophagus and endoscopic esophagitis were evaluated. H. pylori infection was determined using the urease test and/or histology. Results. The rate of endoscopic esophagitis was 5.49% (80 Malays, 24 non-Malays) while histological reflux esophagitis was found in 3.75% (56 Malays, 15 non-Malays). Barrett's esophagus was present in 0.79% (11 Malays, 4 non-Malays). H. pylori infection was present in 8/120 or 6.67% subjects. Conclusion. The low rate of Barrett's esophagus in this population does not support the hypothesis that the absence of H. pylori infection is more than a minor risk factor for Barrett's esophagus.


Nutrients ◽  
2019 ◽  
Vol 11 (8) ◽  
pp. 1874
Author(s):  
Jeung Hui Pyo ◽  
Hyuk Lee ◽  
Sung Chul Choi ◽  
Soo Jin Cho ◽  
Yoon-Ho Choi ◽  
...  

Helicobacter pylori (H. pylori) may be involved in diabetes and other insulin-related processes. This study aimed to investigate the associations between H. pylori infection and the risks of type 2 diabetes, impaired glucose tolerance (IGT), diabetic nephropathy, and poor glycemic control. We retrospectively evaluated 16,091 subjects without diabetes at baseline who underwent repeated health examinations. Subjects were categorized according to whether they were seropositive and seronegative for H. pylori infection. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazard models. The serological results were validated using an independent cohort (n = 42,351) based on a histological diagnosis of H. pylori infection. During 108,614 person-years of follow-up, 1338 subjects (8.3%) developed newly diagnosed diabetes, although the cumulative incidence of diabetes was not significantly related to serological H. pylori status. The multivariate Cox proportional-hazards regression models revealed that H. pylori seropositivity was not significantly associated with diabetes (HR: 1.01, 95% CI: 0.88–1.16; p = 0.854), IGT (HR: 0.98, 95% CI: 0.93–1.04; p = 0.566), diabetic nephropathy (HR: 0.99, 95% CI: 0.82–1.21; p = 0.952), or poor glycemic control (HR: 1.05, 95% CI: 0.90–1.22; p = 0.535). Similarly, histopathological findings of H. pylori infection were not significantly associated with diabetes (p = 0.311), diabetic nephropathy (p = 0.888), or poor glycemic control (p = 0.989). The findings from these large Korean cohorts indicate that there does not appear to be a role for past H. pylori infection in the development of diabetes, IGT, diabetic nephropathy, or poor glycemic control.


Digestion ◽  
2000 ◽  
Vol 62 (2-3) ◽  
pp. 95-99 ◽  
Author(s):  
R.J.L.F. Loffeld ◽  
B.F.M. Werdmuller ◽  
J.G. Kuster ◽  
G.I. Pérez-Pérez ◽  
M.J. Blaser ◽  
...  

2003 ◽  
Vol 124 (4) ◽  
pp. A636 ◽  
Author(s):  
angel Lanas ◽  
Rafael Benito ◽  
Maria Asuncion Garcia-Gonzalez ◽  
Juan Arenas ◽  
Angel Ferrandez ◽  
...  

2021 ◽  
Vol 162 (51) ◽  
pp. 2040-2046

Összefoglaló. Az 1970-es évek előtt a nyelőcsőrákok csupán 1–3%-a volt adenocarcinoma. A 70-es évek közepétől a nyelőcső-adenocarcinoma mutatta a legnagyobb növekedést az összes malignus daganat közül, és a 90-es évek közepétől már meghaladta a laphámrákok előfordulási gyakoriságát a nyugati világban. Ma a nyelőcső-adenocarcinoma relatív incidenciája Magyarországon 34,7%, míg a nyugati világban már 60% körül van. A nyelőcső-adenocarcinoma etiológiájában meghatároztak néhány kockázati tényezőt, így a gastrooesophagealis refluxot, a Barrett-nyelőcsövet, a kóros kövérséget, a dohányzást és a csökkenő Helicobacter pylori fertőzöttséget. Ezek a tényezők azonban jelen voltak már a 70-es évek előtt is. A kövérség előfordulásának gyakorisága és a következményes gastrooesophagealis reflux megduplázódott az elmúlt 40 évben, de ez egyedül nem magyarázza az adenocarcinomák szaporodásának ütemét. Egy új, hatékony savcsökkentő gyógyszercsoportnak, a H2-receptor-blokkolóknak a bevezetésére 1976-ban került sor, és ez egybeesik a szokatlanul nagy incidencianövekedéssel. Tom DeMeester teóriája szerint a savcsökkentő kezelés által létrehozott pH-változás okozhatja a refluxátum carcinogenitasának fokozódását. A Barrett-oesophagus és a nyelőcső-adenocarcinoma etiológiájában, megelőzésében és kezelésében számos ellentmondás és vitás kérdés tapasztalható, különösen a protonpumpagátló gyógyszerek (PPI-k) hosszú távú használata körül. A PPI-k hatásossága a gyógyszer túlzott alkalmazásához vezetett nem mindig megfelelő indikációban, kitéve a betegeket potenciális kockázatoknak. Összefoglalva, a nyelőcső-adenocarcinoma drámai növekedésében biztosan szerepet játszik az elhízás és a refluxbetegség ezzel párhuzamos terjedése. Fontos továbbá a H. pylori fertőzöttség csökkenése, és új szempont a hatásos savcsökkentő szerek széles körű alkalmazása, melyek a refluxátumban okozott pH-változással erősíthetik a carcinogenesist. Orv Hetil. 2021; 162(51): 2040–2046. Summary. Before the 1970s, only 1–3% of esophageal cancers were adenocarcinoma. Since the mid-70s, the incidence of esophageal adenocarcinoma has shown the greatest increase compared to all other cancer types and overtook squamous carcinoma incidence in the mid-90s in the Western countries. Today, the relative incidence of esophageal adenocarcinoma in Hungary is 34.7% and around 60% in the Western countries. Some risk factors for esophageal adenocarcinoma have been identified such as gastroesophageal reflux disease, Barrett’s esophagus, obesity, smoking and decreased prevalence of Helicobacter pylori infection, but these risk factors were already present before the 70s. The prevalence of obesity and the consequentially developed gastroesophageal reflux has doubled during the last 40 years, but it does not explain alone the dramatic rise in the esophageal adenocarcinoma incidence. The H2 blockers, as new effective antisecretory medication, were introduced in 1976, coinciding in time with the substantial rise of esophageal adenocarcinoma. According to the DeMeester theory, the change in the pH of gastric refluxate caused by acid suppression enhances its carcinogenic potential. There are a lot of controversies among the prevention, etiology and treatment of Barrett’s esophagus and esophageal adenocarcinoma, especially regarding the long-term use of proton pump inhibitors (PPIs), an even more effective group of acid suppressors. The effectiveness of PPIs has led to an overuse exceeding its regular indications with little benefit, exposing patients to a number of potential risks. In conclusion, in the dramatic rise of the esophageal adenocarcinoma incidence, obesity accompanied by reflux disease and the decreased incidence of H. pylori infection certainly play important roles. The introduction of modern antisecretory drugs in the treatment of acid-related diseases promoting carcinogenesis, arises as a new consideration. Orv Hetil. 2021; 162(51): 2040–2046.


2019 ◽  
Vol 32 (8) ◽  
Author(s):  
Ali Soroush ◽  
John M Poneros ◽  
Charles J Lightdale ◽  
Julian A Abrams

SUMMARY Quality indicators have been proposed for endoscopic eradication therapy of Barrett's esophagus (BE). One such measure suggests that complete eradication of intestinal metaplasia (CE-IM) should be achieved within 18 months of starting treatment. The aim of this study was to assess whether achievement of CE-IM within 18 months is associated with improved long-term clinical outcomes. This was a retrospective cohort study of BE patients who underwent endoscopic eradication. Time to CE-IM was recorded and categorized as ≤ or > 18 months. The main outcome measures were recurrence of IM and of dysplasia after CE-IM, defined as a single endoscopy without endoscopic evidence of BE or histologic evidence of intestinal metaplasia. Recurrence was analyzed using the Kaplan–Meier method and multivariable Cox proportional hazards modeling. A total of 290 patients were included in the analyses. The baseline histology was high-grade dysplasia or intramucosal carcinoma in 74.2% of patients. CE-IM was achieved in 85.5% of patients, and 54.1% of the cohort achieved CE-IM within 18 months. Achieving CE-IM within 18 months was not associated with reduced risk of recurrence of IM or dysplasia in both unadjusted and adjusted analyses. In this cohort, older age and increased BE length were associated with IM recurrence, and increased hiatal hernia size was associated with dysplasia recurrence. Compared to longer times, achieving CE-IM within 18 months was not associated with a reduced risk of recurrence of IM or dysplasia. Alternative evidence-based quality metrics for endoscopic eradication therapy should be identified.


Medicina ◽  
2011 ◽  
Vol 47 (8) ◽  
pp. 434 ◽  
Author(s):  
Laimas Jonaitis ◽  
Darius Kriukas ◽  
Gediminas Kiudelis ◽  
Limas Kupčinskas

Objective. To establish the prevalence and risk factors of erosive esophagitis (EE) and Barrett’s esophagus (BE) among patients routinely referred for upper endoscopy. Material and Methods. A total of 4032 consecutive patients referred to a regional hospital for upper endoscopy due to upper gastrointestinal and/or “alarm” symptoms were examined. Analysis was performed on the prospectively selected patients (40 in each group) with EE of different grades and BE. Results. EE was diagnosed in 474 patients (11.75%): grade A, in 194 (41%); grade B, in 167 (35%); grade C, in 65 (14%); and grade D, in 48 patients (10%). Increasing severity of erosive esophagitis and presence of its complication – Barrett’s esophagus – were associated with the decreasing prevalence of H. pylori and increasing hiatal hernia size (P<0.05). Male gender (OR, 3.57; 95% CI, 1.12 to 10.62), hiatal hernia >2 cm (OR, 3.73; 95% CI, 1.60 to 8.68), and absence of H. pylori (OR, 4.24; 95% CI, 1.07 to 16.84) were the factors found to be associated with severe EE. The factors associated with BE were as follows: ulcer and/or stricture of esophagus (OR, 11.94; 95% CI, 2.51 to 41.37), age >60 years (OR, 1.06; 95% CI, 1.01 to 1.20), smoking >10 cigarettes per day (OR, 4.62; 95% CI, 1.01 to 12.50), hiatal hernia >2 cm (OR, 5.22; 95% CI, 1.86 to 14.64), and absence of H. pylori (OR, 5.60; 95% CI, 1.38 to 22.72). Conclusions. The prevalence of EE was found to be low, and the prevalence of BE was found to be very low among routinely endoscoped patients in primary and secondary care settings in a Lithuanian rural area with high H. pylori prevalence. Increasing severity of gastroesophageal reflux disease was associated with the decreasing prevalence of Helicobacter pylori.


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