MANAGEMENT OF BARRETT'S ESOPHAGUS - CME Conferences
MANAGEMENT OF BARRETT'S ESOPHAGUS - CME Conferences MANAGEMENT OF BARRETT'S ESOPHAGUS - CME Conferences
3 rd Annual Essentials in Primary CareSummer Conference: Session 1Thursday, July 26, 2012PRIOR ACID SUPPRESSION THERAPYRELATED TO SHORTER BARRETT’S• Retrospective analysis of 340 BE patients– Diagnosis made between 1981-2000• Mean length of BE at initial Dx: 4.4 cm (range: 0.5-16)– 201(59%) no prior Rx: 4.8 cm– 63(19%) H2RA only: 4.6 cm p=0.55– 35(10%) PPI only: 3.4 cm p=0.0013– 41(12%) both PPI & H2RA: 3.1 cm p=0.002• Conclusions:– Provides a rationale for aggressive therapy of GERD– Counters the concept that antisecretory therapyincreases risk of esophageal adenocarcinoma(El-Serag et al(Sampliner): Aliment Pharmacol Ther 2004; 19: 1255)NORMALIZATION OF INTESTINALMETAPLASIA WITH ACID CONTROLN = 101; average FU = 4 yrsDysplasia or cancer: 13% LSBE; 3% SSBE; 0% EGJSIM(Horwhat et al: Am J Gastroenterol 2007; 102: 497)Donald Castell, MDManagement of Barrett’s Esophagus
3 rd Annual Essentials in Primary CareSummer Conference: Session 1Thursday, July 26, 2012MAXIMAL ACID CONTROL FORBARRETT’S ESOPHAGUS• Not achieved in prior studies• pH monitoring required (i.e. can not rely on Sx)• May produce endoscopic regression• Does it affect progression to dysplasia or cancer?PPI DELAYS DEVELOPMENT OFDYSPLASIA IN BARRETT’S• BE surveillence program from 1981-2001• PPI began in 1989• 350 patients with Barrett’s (intestinal metaplasia)– 1422 surveillance endoscopies– Median FU = 4.7 years• Delayed PPI use(>2 yrs) compared to PPI in 1 st year– 5.6X greater risk of LGD– 20.9X greater risk of HGD or adenocarcinoma• Conclusion: “PPI therapy appeared beneficial in theprevention of dysplasia & adenocarcinoma. Wesuggest that all patients with this condition, eventhose with no esophagitis or symptoms, should beencouraged to continue long term PPI therapy”.(Hillman AC et al: Med J Australia 180: 387, 2004)Donald Castell, MDManagement of Barrett’s Esophagus
- Page 1 and 2: 3 rd Annual Essentials in Primary C
- Page 3 and 4: 3 rd Annual Essentials in Primary C
- Page 5 and 6: 3 rd Annual Essentials in Primary C
- Page 7 and 8: 3 rd Annual Essentials in Primary C
- Page 9: 3 rd Annual Essentials in Primary C
- Page 13 and 14: 3 rd Annual Essentials in Primary C
- Page 15 and 16: 3 rd Annual Essentials in Primary C
- Page 17 and 18: 3 rd Annual Essentials in Primary C
- Page 19 and 20: 3 rd Annual Essentials in Primary C
3 rd Annual Essentials in Primary CareSummer Conference: Session 1Thursday, July 26, 2012MAXIMAL ACID CONTROL FORBARRETT’S <strong>ESOPHAGUS</strong>• Not achieved in prior studies• pH monitoring required (i.e. can not rely on Sx)• May produce endoscopic regression• Does it affect progression to dysplasia or cancer?PPI DELAYS DEVELOPMENT <strong>OF</strong>DYSPLASIA IN BARRETT’S• BE surveillence program from 1981-2001• PPI began in 1989• 350 patients with Barrett’s (intestinal metaplasia)– 1422 surveillance endoscopies– Median FU = 4.7 years• Delayed PPI use(>2 yrs) compared to PPI in 1 st year– 5.6X greater risk of LGD– 20.9X greater risk of HGD or adenocarcinoma• Conclusion: “PPI therapy appeared beneficial in theprevention of dysplasia & adenocarcinoma. Wesuggest that all patients with this condition, eventhose with no esophagitis or symptoms, should beencouraged to continue long term PPI therapy”.(Hillman AC et al: Med J Australia 180: 387, 2004)Donald Castell, MDManagement of Barrett’s Esophagus
Change language