Val Metko

Association Between Helicobacter pylori and Barrett's Esophagus, Erosive Esophagitis, and Gastroesophageal Reflux Symptoms

BACKGROUND & AIMS Infection with Helicobacter pylori, particularly the cytotoxin-associated gene A (cagA)+ strain, is believed to protect against Barretts esophagus, but it is not clear if it protects against gastroesophageal reflux disease (GERD). We aimed to determine whether H pylori infection is associated with GERD symptoms, erosive esophagitis, and Barretts esophagus within the same cohort. METHODS We analyzed data from a case-control study of 533 men (ages, 50-79 y) who underwent colorectal cancer screening at 2 tertiary medical centers in Michigan between 2008 and 2011 and who also were recruited to undergo upper endoscopy. We assessed 80 additional men found to have Barretts esophagus during clinically indicated upper-endoscopy examinations. Logistic regression was used to estimate the associations between serum antibodies against H pylori or cagA and GERD symptoms, esophagitis, and Barretts esophagus, compared with randomly selected men undergoing colorectal cancer screens (n = 177). RESULTS H pylori infection was associated inversely with Barretts esophagus (odds ratio [OR], 0.53; 95% confidence interval [CI], 0.29-0.97), particularly the cagA+ strain (OR, 0.36; 95% CI, 0.14-0.90). There was a trend toward an inverse association with erosive esophagitis (H pylori OR, 0.63; 95% CI, 0.37-1.08; and cagA+ OR, 0.47; 95% CI, 0.21-1.03). However, GERD symptoms were not associated with H pylori infection (OR, 0.948; 95% CI, 0.548-1.64; and cagA+ OR, 0.967; 95% CI, 0.461-2.03). CONCLUSIONS Based on a case-control study, infection with H pylori, particularly the cagA+ strain, is associated inversely with Barretts esophagus. We observed a trend toward an inverse association with esophagitis, but not with GERD symptoms.

Associations of Diabetes Mellitus, Insulin, Leptin, and Ghrelin With Gastroesophageal Reflux and Barrett's Esophagus

BACKGROUND & AIMS Insulin and leptin have proliferative and anti-apoptotic effects. Ghrelin promotes gastric emptying and secretion of growth hormone and inhibits inflammation. We assessed whether diabetes mellitus and serum levels of insulin, leptin, and ghrelin are associated with gastroesophageal reflux disease (GERD) and Barretts esophagus. METHODS We conducted a case-control study in 822 men undergoing colorectal cancer screening who were recruited to also undergo upper endoscopy. We identified 70 with Barretts esophagus; 80 additional men with Barretts esophagus were recruited shortly after their clinical diagnoses. Serum levels of insulin, leptin, and ghrelin were assayed in all 104 fasting men with Barretts esophagus without diabetes and 271 without diabetes or Barretts esophagus. Logistic regression was used to estimate the effects of diabetes and levels of insulin, leptin, and ghrelin on GERD and Barretts esophagus. RESULTS Among men with GERD, diabetes was inversely associated with Barretts esophagus (adjusted odds ratio [OR] = 0.383; 95% confidence interval [CI]: 0.179-0.821). Among nondiabetics, hyperinsulinemia was positively associated with Barretts esophagus, but the association was attenuated by adjustment for leptin and ghrelin. Leptin was positively associated with Barretts esophagus, adjusting for obesity, GERD, and levels of insulin and ghrelin (OR for 3(rd) vs 1(st) tertile = 3.25; 95% CI: 1.29-8.17); this association was stronger in men with GERD (P = .01 for OR heterogeneity). Ghrelin was positively associated with Barretts esophagus (OR for an increment of 400 pg/mL = 1.39; 95% CI: 1.09-1.76), but inversely associated with GERD (OR for 3(rd) vs 1(st) tertile = 0.364; 95% CI: 0.195-0.680). CONCLUSIONS Based on a case-control study, leptin was associated with Barretts esophagus, particularly in men with GERD. Serum insulin level was associated with Barretts esophagus, but might be mediated by leptin. Serum ghrelin was inversely associated with GERD, as hypothesized, but positively associated with Barretts esophagus, contrary to our hypothesis. Additional studies are needed in men and women to replicate these findings.

Protective role of gluteofemoral obesity in erosive oesophagitis and Barrett's oesophagus

Objective Abdominal obesity has been associated with erosive oesophagitis (EO) and Barretts oesophagus (BO). As gluteofemoral obesity protects against diabetes mellitus and cardiovascular disease, we hypothesised that gluteofemoral obesity would be inversely associated with EO and BO. Design We conducted a cross-sectional study on 822 male colorectal cancer screenees who were recruited to also undergo upper endoscopy. An additional 80 patients with BO clinically detected by upper endoscopy referred for clinical indications were recruited shortly after their diagnoses of BO. Logistic regression was used to estimate the effects of abdominal obesity (waist circumference), gluteofemoral obesity (hip circumference) and waist-to-hip ratio (WHR) on EO and BO (vs neither condition). Results There were 225 cases of either BO or EO and 675 controls. After adjustment for potential confounders, a positive association was observed between waist circumference and BO and/or EO, which became stronger with further adjustment for hip circumference. In contrast, hip circumference was inversely associated with BO and/or EO. Compared with the lowest quartile of WHR, the adjusted ORs were 1.32 (95% CI 0.747 to 2.33) for the 2nd quartile, 1.54 (95% CI 0.898 to 2.63) for the 3rd quartile, and 2.68 (95% CI 1.57 to 4.55) for the highest quartile. Similar results were obtained for BO and EO treated as separate outcomes. Conclusions In a population of older, mostly overweight men, the distribution of obesity is associated with the presence of EO and BO. Abdominal obesity appears to increase the risk of these outcomes, whereas gluteofemoral obesity may be protective.

Use of Appropriate Surveillance for Patients With Nondysplastic Barrett’s Esophagus

BACKGROUND & AIMS: Barrett’s esophagus (BE) is a precursor to esophageal adenocarcinoma (EAC). Guidelines recommend that patients with nondysplastic BE (NDBE) undergo surveillance endoscopy every 3–5 years. We aimed to identify factors associated with surveillance endoscopy of patients with NDBE and identify trends in appropriate surveillance endoscopy of NDBE at a large tertiary care center. METHODS: We performed a retrospective analysis of data from a Barrett’s Esophagus Registry, identifying patients with NDBE who underwent endoscopy in 2002 or later. We identified patients with NDBE and collected data on length of BE segment, esophageal lesions, demographic features, medications, histology findings, comorbidities, development of EAC, and dates of follow‐up endoscopies. We defined appropriate surveillance as 3–5 years between 2nd and 3rd endoscopies, over‐utilizers as patients who had less than 3 years between their 2nd and 3rd endoscopies, under‐utilizers as patients who had more than 5 years between their 2nd and 3rd endoscopies; and never‐surveilled as patients who never received a 2nd endoscopy. The primary outcomes were effects of patient factors, year, and referring providers on appropriateness of surveillance intervals. RESULTS: We identified 477 patients with NDBE. Only 15.9% had appropriate surveillance; 37.9% were over‐utilizers 15.7% were under‐utilizers and 30.4% were never surveilled. Patients were less likely to be over‐surveilled if their primary care physician referred them for their 3rd endoscopy instead of a gastroenterologist (adjusted odds ratio, 0.51; 95% CI, 0.27–0.95). Male patients or those with an increased number of comorbidities were more likely to be under‐surveilled or never‐surveilled, whereas patients with long BE segment were more likely to be over‐surveilled. CONCLUSIONS: In a retrospective analysis of data from a registry of patients with BE, we found that less than 16% receive appropriate surveillance for NDBE. A primary care provider in the same health system as the endoscopy clinic reduced risk of over‐surveillance. This could reflect better coordination of care between specialists and primary care providers.

Sa1982 Association of Serum Leptin With Barrett's Esophagus

methylation patterns in the H. pylori-positive stomach. (A) Phenotypic and epigenetic differences between the antrum and the body. (B) Age-related patterns of concurrent overmethylation. Age-related methylation patterns were evaluated using the average overmethylation frequencies of Alu-adjacent housekeeping genes (CDH1 and ARRDC4) (full lines), LTRadjacent housekeeping genes (MMP2, CDKN2A, RUNX2, and RUNX3) (broken lines), and stomach-specific genes (TFF2, ATP4B, PGC, and TFF1) (dotted lines) respectively.