Abstract
Barrett's esophagus (BE) is a complication of long lasting severe esophageal reflux disease. It is characterised by metaplastic epithelium which contains goblet cells instead of normal squamous esophageal epithelium.
The main clinical importance of BE is its high risk of esophageal adenocarcinoma.The progression of intestinal metaplasia through different grade of dysplasia until invasive carcinoma is supposed. The prediction of the risk of progress of BE is difficult and therefore the authors have been trying to find any prognostic markers to enable the diagnosis, treatment and prognosis of these patients.
During followed-up period of l8 months (from January 2002) 35 patients with BE were examined. In these patients a standard diagnostic-therapeutic protocol was used.
This protocol involved endoscopy checking including chromoendoscopy and sequential biopsy which was evaluated by the only one experienced pathologist, by 24 hours esophageal pH metry and barium swallov. Coincidentally, the biopsy sample for genetic examination was taken for mutation of TP53 gen in 5-9 exon.The patients were divided according to the state of the disease and/or dysplasia and were managed according to that particular way.
BE patients without dysplasia (11 patients = 46%) or with low grade dysplasia (LGD) - 1 patient (4%) were managed by antireflux plastic surgery. When this state progressed the endoscopic mucosectomy was indicated.
In 2 patients after antireflux surgery a regression of histologic finding was seen, but in one patient with a short esophagus managed by classical open surgery fundoplication this surgery failed and progression into LGD was demonstrated. In one patient (4%) BE with high grade dysplasia (HGD) and in 11 patients (46%) esophageal adenocarcinoma in BE was recognised.These patient were indicated for esophageal resection and esophagus was replaced by stomac or colon.
In a patient with HGD after esophageal resection a carcinoma after final histologic examination has been revealed. Three patients with non-operable tumour was managed by stent replacement.
Mutation of the gene TP53 was discovered only in carcinomas in BE (36.4%).This mutation was not seen in any BE patient without carcinoma. According to our results we conclude this mutation cannot serve as a self-factor for early prognosis assesment.