H2 Blockers Revisited: Any Role in Barrett’s Esophagus (BE) Management and Prevention of Esophageal Adenocarcinoma (EAC)?

Abstract

Introduction: Long-term use of H2 blockers or proton pump inhibitors (PPI) was reported to be a marker for increased risk of EAC. This may be due to the underlying disease rather than the drugs per se. In fact, PPI use seems to lower the risk of dysplasia in BE. With the recent concerns raised about harmful consequences of chronic PPI use, there is renewed interest about other means of acid suppression. Henceforth, we aimed to study the effect of H2 blockers in our Barrett’s cohort. Methods: Barrett’s Registry was started in 1979 and included demographic data such as age, sex, race, endoscopic findings such as length of BE, hiatal hernia size and histological findings. We included data from BE registry of patients from 2002 to 2013. Medication use such as PPI, aspirin, H2 blockers, lipid lowering agents was obtained by chart review. Results: The cohort consisted of 2,341 patients with a mean age of 60± 13 years, of which 1756 (75%) were men and 2198 (95.8%) were Caucasians. Mean BE length was 3.2±3.5 cm and hiatal hernia size was 2±2.2 cm. Use of PPIs was observed in 825 (35.2%) and H2 blockers in 360 (15.4%). The histological findings on index biopsy are presented in table. Data from 1,034 patients was available for follow-up. There were 836 patients in no dysplasia group and 198 patients in LGD group. No dysplasia group: Median follow-up time was 47 [24, 90] months during which 22% had progression (134 to LGD, 26 to HGD and 21 to EAC). After adjusting for age, gender, BE length and hernia size, H2 blocker users had 53% lower hazard of progression to HGD/EAC than nonusers HR= 0.47(0.22, 0.97) p=0.042. LGD group: Median follow-up time was 30 [9, 56] months during which time 24% had progression (16 to HGD and 33 to adenocarcinoma). No statistically significant association was observed for progression to HGD/EAC HR=0.65 (0.32, 1.4), p=0.26.Table 1: Baseline Prevalence of DysplasiaConclusion: H2 blocker use was observed less frequently than PPI use in our Barrett’s cohort. HGD/EAC were less prevalent in H2 blocker users than non-users. In patients without dysplasia, H2 blockers had lower risk of progression to HGD/EAC. Hence, it is reasonable to conclude that H2 blockers are associated with lower risk of dysplasia and progression to HGD/EAC in patients with BE.