Scop: Revizuirea dovezilor privind tratamentul endoscopic al EB şi AC precoce.
Material şi metodă: Metaplazia columnară mai sus de joncţiunea esofago-gastrică a fost definită ca esofag columnar metaplaziat (ECM). EB a fost definit la prezenţa metaplaziei intestinale. Examinarea endoluminală - GIF HQ190 (Olympus). Tratamentul endoscopic - GIF 1TH190, unitate electrochirurgicală Vio200D, APC 2 (ERBE). S-au studiat 83 cazuri ECM: 26 displazie minoră (DM),10 displazie avansată (DA), 3 AC precoce. Tactica de tratament - în funcţie de prezenţa şi tipul metaplaziei, gradul displaziei şi neoplaziei. AC şi DA au fost tratate prin REM/DES. DM: 8 cazuri - supraveghere endoscopică, 7 cazuri - REM, 10 cazuri – ablaţie argon-plazmă (AAP). Herniile hiatale (HH) (n=12) au fost tratate prin fundoplicaţie chirurgicală în etapă II. Tratament endoluminal al EB postfundoplicaţie - 4 cazuri.
Rezultate: Reversibilitatea ECM nu s-a determinat. Supraveghere endoscopică 5 ani: progresie DM (n=4) din EB fără displazie, DA (n=3) din DM, AC T1m (n=1) din DA. La toţi 4 pacienţi, după fundoplicaţie (EB netratat preoperator), diagnosticarea s-a apreciat dificilă, regresia EB absentă, tratamentul endoscopic a fost incomplet. EB restant – 1 caz postREM, 2 cazuri post AAP – tratament reablaţie. Supraveghere endoscopică 2-5 ani - recidive absente.
Concluzii: ECM necesită supraveghere endoscopică, EB fără displazie - supraveghere sau AAP. DM poate fi tratată prin AAP. DA şi AC precoce necesită DES/REM cu confirmarea histologică a R0 criteriilor pentru neoplazie. Tratamentul endoluminal trebuie să anticipeze fundoplicaţia chirurgicală.

Introduction: Barrett’s esophagus (BE) is a premalignant condition, the presence of dysplasia is the predictive factor for the development of esophageal adenocarcinoma (AC).
The aim of this study was to review the available evidence of the endoscopic treatment of BE.
Material and methods: Columnar metaplasia above the gastro-esophageal junction was defined as a columnar lined esophagus (CLE). BE is defined as the presence of intestinal metaplasia. Endoluminal examination - GIF HQ190 (Olympus). Endoscopic treatment - GIF 1TH190, electro-surgical unit Vio200D, APC 2 (ERBE). A total of 83 cases were examined CLE: 26 low-grade dysplasia (LGD), 10 high grade dysplasia (HGD), 3 early AC. The treatment tactic – based on the appearance and the type of the metaplasia, the grade of dysplasia and neoplasia. AC and HGD were treated with EMR/ESD. LGD: 8 cases - endoscopic surveillance, 7 cases - EMR, 10 cases – argon plasma coagulation (APC). Hiatal hernias (HH) (n=12) were treated through surgical fundoplication in stage II. Endoluminal treatment of post fundoplication BE - 4 cases.
Results: No reversibility of CLE was found. Endoscopic surveillance 5 years: progression LGD (n=4) of BE without dysplasia, HGD (n=3) of LGD, AC T1m (n=1) of HGD. For all 4 patients, after fundoplication (pre-surgery untreated BE), the diagnosis turned to be difficult, the regression of BE was absent, the endoscopic treatment was incomplete. Residual BE– 1 case after EMR, 2 cases after APC –reablation. Endoscopic surveillance 2-5 years – absent relapses.
Conclusions: CLE necessities endoscopic surveillance, BE without dysplasia - surveillance or APC. LGD can be treated through APC. HGD, early AC necessities ESD/EMR with histologic confirmation of R0 criteria for neoplasia. Endoluminal treatment needs to anticipate surgical fundoplication.