Barrett's esophagus can and does regress after antireflux surgery: a study of prevalence and predictive features

BACKGROUND: To investigate the factors leading to histologic regression of metaplastic and dysplastic Barrett's esophagus (BE). STUDY DESIGN: The study sample consisted of 91 consecutive patients with symptomatic Barrett's esophagus. Pre- and posttreatment endoscopic biopsies from 77 Barrett's patients treated surgically and 14 treated with proton pump inhibitors (PPI) were reviewed. An expert pathologist confirmed the presence of intestinal metaplasia (IM) with or without dysplasia. Posttreatment histology was classified as having regressed if two consecutive biopsies taken more than 6 months apart plus all subsequent biopsies showed loss of IM or loss of dysplasia. Clinical factors associated with regression were studied by multivariate analysis, as was the time course of its occurrence. RESULTS: Histopathologic regression occurred in 28 of 77 patients (36.4%) after antireflux surgery and in 1 of 14 patients (7.1%) treated with PPIs alone (p < 0.03). After surgery, regression from low-grade dysplastic to nondysplastic BE occurred in 17 of 25 patients (68%) and from IM to no IM in 11 of 52 (21.2%). Both types of regression were significantly more common in short (< 3 cm) than long (> 3 cm) segment Barrett's esophagus; 19 of 33 (58%) and 9 of 44 (20%) patients, respectively (p = 0.0016). Eight patients progressed, five from IM alone to low-grade dysplasia and three from low- to high-grade dysplasia. All those who progressed had long segment BE. On multivariate analysis, presence of short segment Barrett's and type of treatment were significantly associated with regression; age, gender, surgical procedure, and preoperative lower esophageal sphincter and pH characteristics were not. The median time of biopsy-proved regression was 18.5 months after surgery, with 95% occurring within 5 years. CONCLUSIONS: This study refutes the widely held assumption that once established, Barrett's esophagus does not change. More than one-third of patients with visible segments of Barrett's esophagus undergo histologic regression after antireflux surgery. Regression is dependent on the length of the columnar-lined esophagus and time of followup after antireflux surgery.     

Barrett's esophagus. Comparison of benign and malignant cases.

Using strict criteria for diagnosis, 23 patients having benign Barrett's esophagus, and 20 patients with adenocarcinoma arising in this epithelium have been analyzed. Evidence supports severe gastroesophageal reflux as a cause of Barrett's esophagus. Successful antireflux surgery leads to stabilization and possibly regression of the dysplasia in Barrett's epithelium, and can be followed by squamous epithelial regeneration in some. Antireflux surgery is advocated in all patients with Barrett's esophagus demonstrated to have abnormal reflux regardless of symptoms. The malignant potential of the columnar epithelium is higher in men who smoke, in patients with intestinal-type metaplasia who continue to have severe reflux, and in patients who develop dysplasia. In those with high grade dysplasia, the probability of carcinoma is high and esophagectomy should be seriously considered in the hopes that the pathological stage of the neoplasm is still favorable.     

Long-term clinical and pathologic response of Barrett's esophagus after antireflux surgery

BACKGROUND: The impact of antireflux surgery on outcome in Barrett's esophagus, in particular its effect on both the regression of metaplasia and the progression of metaplasia through dysplasia to adenocarcinoma, remains unclear. This long-term follow-up study evaluated clinical, endoscopic, histopathologic, and physiologic parameters in patients with Barrett's esophagus who underwent antireflux surgery in a specialist unit. METHODS: Between 1985 and 2001, 58 patients with Barrett's esophagus (49 long-segment and 9 short-segment) underwent a Rossetti-Nissen fundoplication, 32 via open procedure and 26 laparoscopically. Symptomatic follow-up with a detailed questionnaire was available in 58 (100%) and follow-up endoscopy and histology in 57 (98%) patients, and 41 patients (71%) underwent preoperative and postoperative 24-hour pH monitoring. RESULTS: At a median follow-up of 59 months, 52 patients (90%) had excellent symptom control, whereas 6 patients (10%) had significant recurrent symptoms and were on regular proton pump inhibitor medication. Seventeen of 41 patients having preoperative and postoperative pH monitoring (41%) had a persistent increase of acid reflux above normal. Thirty-five percent (20 of 57) of patients showed either partial or complete regression of Barrett's epithelium. Six of 8 patients with preoperative low-grade dysplasia showed evidence of regression. Dysplasia developed after surgery in 2 patients, and 2 patients developed adenocarcinoma at 4 and 7 years after surgery. All 4 of these patients had abnormal postoperative acid scores. CONCLUSIONS: Nissen fundoplication provides excellent long-lasting relief of symptoms in patients with Barrett's esophagus and may promote regression of metaplasia and dysplasia. Control of symptoms does not concord fully with abolition of acid reflux. Progression of Barrett's to dysplasia and tumor was only evident in patients with abnormal postoperative acid scores, suggesting that pH monitoring has an important role in the follow-up of surgically treated patients.     

Treatment of Barrett''s esophagus by endoscopic laser ablation and antireflux surgery.

OBJECTIVE: The regeneration of intestinal metaplasia by squamous epithelium in 17 patients with Barrett's esophagus after endoscopic laser ablation in a reflux-free environment after successful antireflux surgery was prospectively examined. METHODS: All patients had antireflux surgery, and healing of reflux was verified at postoperative endoscopy and 24-hour esophageal pH monitoring. Thereafter, in 11 patients, the whole Barrett's epithelium was ablated using endoscopic Nd-YAG laser energy in 1 to 8 sessions (mean, 4). The needed energy was 965 to 11,173 joules (mean 4709), or about 1000 joules per centimeter of Barrett's esophagus. Six patients had no laser ablation but were treated by antireflux surgery and served as a control group. RESULTS: In all laser-treated patients, the regenerated epithelium was histologically of squamous type in the tubular esophagus, but two patients still had intestinal metaplasia in the gastric cardia. In controls, the length of Barrett's esophagus and intestinal metaplasia remained unchanged. The length of follow-up was 26 months after the last laser session and 21 months in the control group. CONCLUSIONS: The regenerated esophageal epithelium arising after laser ablation in reflux-free environment surgery is of squamous type. This treatment may have a role in preventing the development of esophageal adenocarcinoma arising in Barrett's esophagus.     

The impact of an antireflux procedure on intestinal metaplasia of the cardia.

OBJECTIVE: The aim of this study was to determine whether antireflux surgery is more effective in producing loss of intestinal metaplasia located only at the gastroesophageal junction than it has been in patients with intestinal metaplasia extending up into the distal esophagus. SUMMARY BACKGROUND DATA: Biopsies of a normal appearing gastroesophageal junction will demonstrate cardiac mucosa containing goblet cells--the hallmark of intestinal metaplasia--in 10% to 15% of patients who are evaluated for symptoms of gastroesophageal reflux. The incidence of adenocarcinoma of the esophagus and cardia is rising faster than any other cancer in America, and most of these cancers are found adjacent to areas of intestinal metaplasia. Antireflux surgery in patients with Barrett's esophagus may provide protection from progression to dysplasia and cancer; however, it does not reliably cause regression of the intestinal metaplasia. Less is known about the potential for intestinal metaplasia limited to the cardia (CIM) to regress. METHODS: Sixty patients with intestinal metaplasia of the esophagus or cardia had antireflux surgery. Patients in the intestinal (CIM) group (n = 15) had no endoscopically visible segment of columnar epithelium. Patients in the Barrett's group (n = 45) had columnar epithelium visible within the esophagus. Median follow-up was 25 months in each group. RESULTS: Postoperative biopsies showed complete loss of intestinal metaplasia in 73% of the patients with CIM compared with 4.4% of the patients with Barrett's. Low-grade dysplasia, present in 10 patients preoperatively, regressed in 7 patients (70%). No patient progressed to high-grade dysplasia or cancer. CONCLUSIONS: Loss of intestinal metaplasia after antireflux surgery is rare in patients with Barrett's, but occurred in most patients with CIM. This suggests that cardiac epithelium is dynamic and that microscopic areas of intestinal metaplasia are able to regress much more frequently than longer, visible segments of intestinal metaplasia.     

Clinical and histologic follow-up after antireflux surgery for Barrett's esophagus.

There are few prospective studies that document the histologic follow-up after antireflux surgery in patients with Barrett's esophagus, as defined by the recently standardized criteria. We report the clinical, endoscopic, and histologic results of patients with Barrett's esophagus followed postoperatively for at least 2 years. Diagnosis of Barrett's esophagus required preoperative endoscopic evidence of columnar-lined epithelium in the esophagus and a biopsy demonstrating specialized intestinal metaplasia, which stains positively with Alcian blue stain. Between April 1993 and November 1998, a total of 104 patients meeting these criteria underwent fundoplication (laparoscopic [n = 84] or open [n = 6] nissen, laparoscopic Toupet [n = 11], laparoscopic Collis-Nissen [n = 1], Collins-Toupet [n = 1] or open Dor [n = 1]). Short-segment Barrett's esophagus (length of intestinal metaplasia <3 cm) was found preoperatively in 34% and low-grade dysplasia in 4% of patients. All patients were contacted yearly by mail, phone, or clinic visit. At a mean follow-up of 4.6 years (range 2 to 7.5 years), 81% of patients had stopped taking antisecretory medications and 97% were satisfied with the results of their operations. Eight patients have undergone reoperation for recurrence of symptoms. Two patients have died and two were excluded from endoscopic biopsy because of portal hypertension. Sixty-six patients complied with the surveillance protocol, and their histologic results were returned to our center. Symptomatic follow-up of the 34 patients who refused surveillance esophagogastro and duodenoscopy revealed two patients who were taking medication for reflux symptoms. None of the patients have developed high-grade dysplasia or esophageal carcinoma during surveillance endoscopy (337 total patient-years of follow-up). The incidence of regression of intestinal metaplasia to cardiac-fundic-type metaplasia after successful antireflux surgery is greater than previously reported. We suspect that this is a result of longer follow-up and the inclusion of patients with short-segment Barrett's esophagus. A substantial number of patients with Barrett's esophagus who are asymptomatic after antireflux surgery refuse surveillance endoscopy.     

Efficacy of laparoscopic antireflux surgery in patients with Barrett's esophagus

BACKGROUND: Laparoscopic antireflux surgery (LARS) corrects significant physiologic and anatomic abnormalities in patients with gastroesophageal reflux disease (GERD); however, debate exists whether LARS prevents recurrent symptoms and malignant transformation in patients with Barrett's esophagus (BE). This study compared clinical outcomes after LARS in patients with and without BE. METHODS: From 1994 to 2001, 448 patients who underwent LARS were studied. Of these, 68 (15%) had preoperative evidence of BE with low-grade dysplasia in 3 (4%), and 380 (85%) were without BE. Mean postoperative follow-up was more than 30 months in each group. RESULTS: After LARS, there was equivalent reduction in acid reduction medication use and typical GERD symptoms in both groups. Anatomic failures developed in 12% of patients with BE and in 5% of those without BE (P = 0.05). Upper endoscopy with biopsies was obtained in 50 of 68 patients (74%) with BE at 37 +/- 22 months postoperatively. Intestinal metaplasia was no longer present in 7 of 50 (14%) BE patients, and low-grade dysplasia regressed to nondysplastic Barrett's in 2 of 3 patients. New low-grade dysplasia developed in 1 BE patient (2%) at postoperative endoscopic surveillance. No BE patients developed high-grade dysplasia or adenocarcinoma. CONCLUSIONS: After LARS, patients with BE have symptomatic relief and reduction in medication use equivalent to non-BE patients. Regression of intestinal metaplasia and the absence of progression to high-grade dysplasia or adenocarcinoma suggest that LARS is an effective approach for the management of patients with Barrett's esophagus. The higher failure rate of LARS in BE is of concern and mandates ongoing follow-up of these patients.     

Diagnosis and treatment of Barrett's oesophagus. A general survey

Barrett's oesophagus is an acquired condition with columnar metaplasia of the distal oesophagus. This condition represents the most serious consequence of chronic gastro-oesophageal reflux as it is associated with an increased incidence of oesophageal adenocarcinoma. Since the exact pathophysiology is not known, prevention is not possible. The diagnosis of Barrett's oesophagus requires the presence of intestinal metaplasia in at least one biopsy specimen from the lower oesophagus. Barrett's oesophagus is considered a premalignant condition and some cases progress from dysplasia to invasive adenocarcinoma. Medical or surgical antireflux treatment controls symptoms and oesophagitis, but Barrett's oesophagus remains. Patients are usually followed up by endoscopy for detection of dysplasia or early cancer. Several reports in the literature have assessed the effects of H2-blocker and proton pump inhibitors treatment on Barrett's epithelium, but none has clearly documented a significant and consistent regression of the metaplastic epithelium. Even with high doses of proton pump inhibitors given for a prolonged period of time, it does not appear that a significant regression of Barrett's epithelium can be achieved. Various studies have assessed the effects of antireflux surgery on the regression of columnar epithelium and dysplasia and its potential protective effect on the subsequent development of carcinoma. Overall, it appears from these reports that antireflux surgery, despite adequate symptomatic results, does not significantly and consistently lead to a reduction in length or disappearance of the Barrett's mucosa, and does not prevent the development of dysplasia and its progression to carcinoma. Recently, numerous reports have documented the regression of Barrett's mucosa by using various experimental techniques: these thermal therapies focus on the removal of the columnar epithelium with restoration of the squamous epithelium. Technological advances including laser and especially photodynamic therapy have allowed for endoscopic mucosal ablation. Long-term results are more encouraging when this mucosal ablation is associated with antireflux medical or surgical therapy. Currently, none of these approaches can obviate the need for continued endoscopic surveillance; however the photodynamic therapy seems to be a promising alternative in the future.     

Dysplasia and Adenocarcinoma After Classic Antireflux Surgery in Patients With Barrett’s Esophagus: The Need for Long-Term Subjective and Objective Follow-Up

OBJECTIVE: To assess the clinical, endoscopic, and functional results in a group of patients with Barrett's esophagus undergoing classic antireflux surgery in whom dysplasia and adenocarcinoma were found at a late objective follow-up. SUMMARY BACKGROUND DATA: There have been isolated reports of patients with Barrett's esophagus undergoing antireflux surgery who show dysplasia or even adenocarcinoma on follow-up. METHODS: Of 161 patients undergoing surgery, dysplasia developed in 17 (10.5%) at late follow-up and adenocarcinoma developed in 4 (2.5%). These 21 patients represent the group assessed and were compared with 126 surgical patients with long-segment Barrett's in whom dysplasia did not develop. They were evaluated by clinical questionnaire, multiple endoscopic procedures and biopsy specimens, 24-hour pH studies, and 24-hour bilirubin monitoring. RESULTS: Of the 17 patients with dysplasia, 3 were asymptomatic at the time that dysplastic changes appeared; all patients with adenocarcinoma had symptoms. Two patients (12%) in the dysplasia group had short-segment Barrett's; all patients with adenocarcinoma had long-segment Barrett's. Manometric studies revealed an incompetent lower esophageal sphincter in 70% of the dysplasia group, similar to nondysplasia patients with recurrence, and in 100% of the adenocarcinoma group. The 24-hour pH study showed pathologic acid reflux in 94% of the patients with dysplasia, similar to patients with recurrence without dysplasia, whereas bilirubin monitoring showed duodenal abnormal reflux in 86% of the patients. Among patients with dysplasia, three different histologic patterns were identified. All patients with adenocarcinoma had initially intestinal metaplasia, with appearance of this tumor 6 to 8 years after surgery. CONCLUSIONS: Patients with Barrett's esophagus who undergo antireflux surgery need close and long-term endoscopic and histologic surveillance because dysplasia or even adenocarcinoma can appear at late follow-up. Metaplastic changes from fundic to cardiac mucosa and then to intestinal metaplasia and later to dysplasia or adenocarcinoma can clearly be documented. There were no significant differences in terms of clinical, endoscopic, manometric, 24-hour pH, and bilirubin monitoring studies between patients with recurrence of symptoms without dysplastic changes, and patients with dysplasia. Therefore, the high-risk group for the development of dysplasia is mainly the group with failed antireflux surgery.     

Effect of duodenal diversion on low-grade dysplasia in patients with Barrett’s esophagus: Analysis of 37 patients

It is well known that in patients with Barrett’s esophagus (BE), even after antireflux surgery, intestinal metaplasia can progress to dysplasia or even adenocarcinoma. However, the opposite—that is regression of dysplastic changes to intestinal metaplasia after antireflux surgery—has been documented in only a few reports. The objective of this study was to determine the effect of a duodenal diversion operation on lowgrade dysplasia in patients with BE. Thirty-seven patients with either short-segment (n = 12) or longsegment (n = 25) BE underwent antireflux surgery plus either a duodenal switch procedure (13 patients) or a partial distal gastrectomy with Roux-en-Y gastrojejunal anastomosis (24 patients). All of them were subjected to complete clinical, endoscopic, histologic, manometric, and 24-hour pH testing, and 24-hour monitoring of the bile exposure in distal esophagus. There were no deaths in this series, and morbidity occurred in only one patient (2.7%). Manometric assessment after surgery showed a significant increase in sphincter pressure, abdominal length, and total length (P < 0.001). Acid reflux showed a significant decrease after surgery, and duodenal reflux was completely abolished in all except one patient. Follow-up in all patients was longer than 24 months (mean 60 months). Three to four endoscopic procedures were performed after surgery in each patient, and several biopsy specimens were taken distal to the squamo-columnar junction during each endoscopic procedure. Eleven patients (91%) with short-segment BE demonstrated histologic regression to either cardiac mucosa or nondysplastic intestinal metaplasia. Among the 25 patients with long-segment BE, there was a 62.5% rate of histologic regression to nondysplastic epithelium when the length of BE measured between 31 and 99 mm and 33 % histologic regression when the length of BE was 101 mm or more. There were no cases of progression to high-grade dysplasia or adenocarcinoma. The endoscopic length of the columnar-lined esophagus did not change late after surgery. In 65% of patients with BE, antireflux surgery, gastric acid reduction, and duodenal diversion produced histologic regression of low-grade dysplasia to nondysplastic mucosa. This effect was even more pronounced when the length of BE was shorter. It seems to be permanent, and no progression to high-grade dysplasia or adenocarcinoma has occurred.     

Laparoscopic surgical treatment for patients with short- and long-segment Barrett's esophagus: which technique in which patient?

Laparoscopic antireflux surgery is very successful in patients with short-segment Barrett's esophagus (BE), but in patients with long-segment BE, the results remain in discussion. In these patients, during the open era of surgery, we performed acid suppression + duodenal diversion procedures added to the antireflux procedure (fundoplication + vagotomy + antrectomy + Roux-en-Y gastrojejunostomy) to obtain better results at long-term follow-up. The aim of this prospective study is to present the results of 3 to 5 years' follow-up in patients with short-segment and long-segment or complicated BE (ulcer or stricture) who underwent fundoplication or the acid suppression-duodenal diversion technique, both performed by a laparoscopic approach. One hundred eight patients with histologically confirmed BE were included: 58 patients with short-segment BE, and 50 with long-segment BE, 28 of whom had complications associated with severe erosive esophagitis, ulcer, or stricture. After surgery, among patients treated with fundoplication with cardia calibration, endoscopic erosive esophagitis was observed in 6.9% of patients with short-segment BE, while 50% of patients with long-segment BE presented with positive acid reflux, persistence of endoscopic esophagitis with intestinal metaplasia, and progression to dysplasia (in 5% of cases; P = 0.000). On the contrary, after acid suppression-duodenal diversion surgery in patients with long-segment BE, more than 95.6% presented with successful results regarding recurrent symptoms and endoscopic regression of esophagitis. Regression of intestinal metaplasia to the cardiac mucosa was observed in 56.9% of patients with short-segment BE who underwent fundoplication and in 61% of those with long-segment BE treated with the acid suppression-duodenal diversion procedure. Patients with long-segment BE who experienced fundoplication alone presented no regression of intestinal metaplasia; on the contrary, progression to dysplasia was observed in 1 case (P = 0.049). Patients with short-segment BE can be successfully treated with fundoplication, but for patients with long-segment BE, we suggest performance of fundoplication plus an acid suppression-duodenal diversion procedure.     

Regression of intestinal metaplasia to cardiac or fundic mucosa in patients with Barrett's esophagus submitted to vagotomy, partial gastrectomy and duodenal diversion. A prospective study of 78 patients with more than 5 years of follow up

BACKGROUND: Regression of intestinal metaplasia to cardiac mucosa in patients with Barrett's (BE) esophagus could alter the natural history of BE. OBJECTIVE: To determine the regression of intestinal metaplasia to cardiac mucosa in patients followed more than 5 years after operation, by repeated endoscopy with biopsy. MATERIAL AND METHODS: This prospective study included 78 patients with BE submitted to combined vagotomy, antrectomy (an antireflux procedure), and Roux-en-Y gastrointestinal reconstruction with more than 60 months follow up. Patients were divided in 3 groups: (1) 31 with short-segment BE (< or =30 mm length); (2) 42 with long-segment BE (31 to 99 mm length); and (3) 5 with extra-long-segment BE (> or =100 mm). Each patient had at least three endoscopic procedures with multiple biopsies during a mean follow up of 95 months (range, 60-220 months). Acid and duodenal reflux were also evaluated. RESULTS: Sixty-four percent of patients with short segment BE had regression to cardiac mucosa at a mean of 40 months after operation. Sixty-two percent of patients with long segment BE had regression to cardiac mucosa at a mean of 47 months postoperatively. No regression occurred in the 5 patients with extra-long segment BE. In 20% of patients, regression to fundic mucosa occurred between 78 to 94 months after surgery. One patient progressed to low grade dysplasia, but no patient progressed to high-grade dysplasia or adenocarcinoma. Acid and duodenal reflux studies demonstrated that in asymptomatic patients, reflux was abolished; 90% of the patients had a Visick grade of 1 or 2. CONCLUSIONS: Vagotomy and antrectomy combined with duodenal bile diversion abolish acid and duodenal reflux into the distal esophagus in patients with BE, which is accompanied by a regression of BE from intestinal to cardiac or fundic mucosa in about 60% of patients. This regression is time dependent and varies directly with the length of BE. The potential for an antineoplastic effect, especially in young patients with long segment BE, suggests that this operation may become an attractive option as a definitive surgical treatment. Patients with short segment BE submitted to this procedure behave similar to patients submitted to Nissen fundoplication, and therefore in these patients, we do not advocate this complex operation.     

Impact of antireflux operation on columnar-lined esophagus

BACKGROUND: The effect of antireflux operation on the natural history of columnar-lined esophagus (CLE) is not fully understood. The aim of this study was to assess a single center's experience and review the literature on the impact of antireflux operation on CLE without high-grade dysplasia. STUDY DESIGN: The medical records of 26 patients with CLE but without high-grade dysplasia who underwent antireflux operation in our unit were retrospectively analyzed at longterm followup with detailed endoscopic investigation. Thirteen patients presented with intestinal metaplasia (6 had short segments, and 1 had preoperative laser ablation) and 13 without intestinal metaplasia.For the group of 13 patients presenting with intestinal metaplasia, the mean endoscopic followup was 74.7 months (median 46 months). Three of six with short-segment lesion and two of seven with circumferential involvement had complete regression of intestinal metaplasia (one after laser therapy). None had progression to dysplasia or carcinoma. RESULTS: For the group of 13 patients without intestinal metaplasia, mean endoscopic followup was 43.9 months (median 28 months). One had complete regression of CLE, and none developed intestinal metaplasia during surveillance. CONCLUSIONS: Our study suggests that antireflux operation can alter the natural history of CLE, allowing disease stabilization in a substantial proportion of patients. After antireflux operation, total regression of CLE is possible, but in an unpredictable manner.     

Barrett's epithelium after antireflux surgery.

Barrett's epithelium (BE), defined as endoscopically visible, histologically proved intestinal-type epithelium in the esophagus, is considered the ultimate consequence of long-standing gastro(duodeno)esophageal reflux disease (GERD). Recent reports suggest that effective antireflux therapy may promote the regression of this metaplastic process. This study aimed to establish whether antireflux surgery (laparoscopic fundoplication) can induce any endoscopic and/or histologic changes in BE. Thirty-five consecutive cases of BE (11 short-segment [SBE] and 24 long-segment [LBE]) were considered. All patients underwent extensive biopsy sampling before and after surgery (mean follow-up, 28 months; range, 12-99 mo). In all cases, (a) intestinal metaplasia (IM) extension (H&E), (b) IM phenotype (high-iron diamine [HID]), and (c) Cdx2 immunohistochemical expression were histologically scored in the biopsy material obtained before and after fundoplication. After surgery, a significant decrease in IM extension and a shift from incomplete- to complete-type IM were documented in SBE. No significant changes occurred in the LBE group in terms of IM extension or histochemical phenotype. A drop in the immunohistochemical expression of Cdx2 protein was also only documented in the SBE group. Antireflux surgery significantly modifies the histologic phenotype of SBE, but not of LBE.     

Effect of gastric bypass on barrett’s esophagus and intestinal metaplasia of the cardia in patients with morbid obesity

Gastric bypass in patients with morbid obesity should be an excellent antireflux procedure, because no acid is produced at the small gastric pouch and no duodenal reflux is present, due to the long Roux-en-Y limb. Five hundred fifty-seven patients with morbid obesity submitted to resectional gastric bypass, and routine preoperative upper endoscopy with biopsy samples demonstrated 12 patients with Barrett’s esophagus (2.1%) and three patients with intestinal metaplasia of the cardia (CIM). An endoscopic procedure was repeated twice after surgery, producing seven patients with short-segment Barrett’s esophagus (BE) and five patients with long-segment BE. Body mass index (BMI) decreased significantly, from 43.2 kg/m² to 29.4 kg/m² 2 years after surgery. Symptoms of reflux esophagitis, which were present in 14 of the 15 patients, disappeared in all patients 1 year after surgery. Preoperative erosive esophagitis and peptic ulcer of the esophagus healed in all patients. There was regression from intestinal metaplasia to cardiac mucosa in four patients (57%) with short-segment BE, and in one patient (20%) with long-segment BE. Two (67%) of three cases with CIM had regression to cardiac mucosa. There was no progression to low- or high-grade dysplasia. Gastric bypass in patients with Barrett’s esophagus and morbid obesity is an excellent antireflux operation, proved by the disappearance of symptoms and the healing of endoscopic esophagitis or peptic ulcer in all patients, which is followed by an important regression to cardiac mucosa that is length-dependent and time-dependent.     

Esophageal adenocarcinoma after Nissen’s fundoplication for Barrett’s esophagus: report of a case

It remains unclear whether surgical treatment of gastro-esophageal reflux disease (GERD) and Barrett’s esophagus (BE) decreases the long-term risk of lower esophagus malignancy; yet, proposed reductions in Barrett’s epithelial transformation have been used as a rationale for antireflux surgery. We report the case of a 63-year-old woman with a 40-year history of GERD, whose symptoms returned after a Nissen fundoplication. A gastroscopy done 3 years later revealed BE. Despite close surveillance, adenocarcinoma of the lower esophagus was diagnosed 8 years after the original surgery. Thus far, there is insufficient evidence to convince practitioners that surgery should be the first line of treatment to prevent malignant change in BE. Further well-standardized, prospective trials are required. Our case demonstrates that antireflux surgery in a patient with GERD and BE cannot be relied upon to prevent adenocarcinoma.     

Results of laparoscopic antireflux operations in patients who have Barrett's esophagus

In most patients who have Barrett's esophagus and who are undergoing open or laparoscopic antireflux surgery, there is a significant improvement in symptom control that is equivalent to that in patients who have uncomplicated gastroesophageal reflux disease. The requirement for reoperation in patients with Barrett's esophagus may be slightly higher, although in the two laparoscopic series published to date, the rate is still only approximately 6%. How much this will increase with longer follow-up, time alone will tell, but given the good results in approximately 95% of patients operated to date, the authors do not believe that the diagnosis of Barrett's esophagus should be considered a blanket contraindication for laparoscopic antireflux surgery. Clearly, in most patients with Barrett's esophagus, an antireflux operation will not result in regression of Barrett's mucosa. It is still unclear whether antireflux surgery provides any protection against subsequent development of esophageal adenocarcinoma. What is clear, however, is that after antireflux surgery, patients who have Barrett's esophagus are still at risk for developing adenocarcinoma and should remain in surveillance programs. The authors believe that laparoscopic antireflux surgery is a safe and effective approach for the cure of reflux-related symptoms in patients who have Barrett's esophagus.     

The influence of Barrett's esophagus on the clinical signs and postoperative results of GERD

AIM OF THE STUDY: Was to estimate the influence of the Barrett's esophagus on the clinical signs and post-surgical results of the GERD. PATIENTS AND METHODS: Within 1998-2001 193 patients have been operated upon in our clinic due to GERD, 81 male and 112 female. Mean patient age was 55 years (from 16 to 84 years). All patients had complaints on heartburn and regurgitation. We assessed the severity of heartburn, regurgitation, dysphagia with the help of a special scale ranging from 1 (absence of symptoms) to 5 (most severe symptoms). All patients underwent gastric and esophageal radiological investigation with barium contrast as well as esophago-gastro-duodenoscopy (EGDS) with biopsy. In 190 cases esophageal hernia was found. The reflux-esophagitis was classified according to Savary-Miller after endoscopic examination. Esophagitis of degree I-III was diagnosed presurgically in 176 cases, Barrett's esophagus in 16 (9.1%) cases. In 13 cases we found a short metaplastic segment (< 3 cm), in 3 cases a long segment (> 3 cm). In 15 cases we found metaplasia without dysplasia, in 1 case low-grade dysplasia. In order to assess the presence of BM influence on presurgical clinical signs, the severity of esophagitis, and the regression rate of symptoms after surgery, we divided the patients into two groups and compared them: group I (with Barrett's metaplasia), and group II (without Barrett's metaplasia). All patients underwent laparoscopic Nissen or Toupet fondoplications. For group I patients we performed 14 Nissen and 2 Toupet procedures, in group II 148 Nissen and 29 Toupet interventions. The regression of clinical and endoscopic symptoms was assessed 6 months after surgery by re-questioning the patients and with the help of EGDS. In cases of Barrett's esophagus endoscopic biopsies from all 4 esophageal segments were performed. The patients of group I were followed-up by performing EGDS every 6 months. The mean follow-up period after surgery was 28 months. RESULTS: No statistically significant difference was found when comparing the groups for age (group I--59/SD 11, and group II--54/SD 13.2), gender, disease duration (group I--13.2/SD 13.7 years, group II--8.2/SD 10.5 years), radiologically determined hernial size or preoperative severity of esophagitis. The regression of the severity of heartburn and regurgitation was prominent in both groups with no significant difference between the groups. Dysphagia before and after surgery was comparable in both groups. Esophagitis confirmed by EGDS remained in 3 of 16 cases in group I and in 9 of 164 cases in group II. The metaplastic changes in group I were followed every 6 months for 16-36 months (mean 28 months). In 13 cases the metaplastic segment demonstrated no changes, it became shorter in 3 cases. We didn't observe any complete regression of metaplasia. In the case with preoperative low grade dysplasia, the length of the segment did not change, we observed neither histological progression or regression. CONCLUSIONS: Barrett's metaplasia had no influence on the regression of symptoms of GERD and esophagitis after antireflux surgery. No histological progression of Barrett's metaplasia has been observed after antireflux surgery. The EGDS follow-up should not be very frequent in cases of Barrett's esophagus without dysplasia and good postsurgical regression of symptoms.     

Barrett's esophagus and antireflux surgery: a study of a series of 26 patients]

STUDY AIM: The aim of this study was to report the results of a retrospective series of 26 patients with Barrett's esophagus treated by antireflux surgery. PATIENTS AND METHODS: From 1979 to 1998, 21 men and five women (mean age: 53 years) with histologically proven Barrett's esophagus underwent an antireflux procedure. The mean length of Barrett's epithelium was 5.9 cm for 19 patients (73.1%). Six patients (23.1%) had tongue lesions of Barrett's epithelium, and one (3.8%) had ectopic gastric mucosa. None of the patients had a preoperative esophageal biopsy that revealed high-grade dysplasia or carcinoma. Laparotomy was performed in 17 cases and laparoscopy in nine cases. Preoperative endoscopic local treatment with argon coagulation was performed in one patient. RESULTS: Clinical mean follow-up was 78 months and endoscopic mean follow-up was 59.3 months. No increase in the length of the Barrett's epithelium was observed. Seven patients (27%) had complete or partial regression (among them three patients with tongue lesions and one patient preoperatively treated by argon). No patients developed high-grade dysplasia or carcinoma. CONCLUSION: Regression of Barrett's esophagus is possible but not frequent and unpredictable after antireflux procedure. However, endoscopic and histological surveillance should be continued postoperatively.     

Barrett's oesophagus: place of antireflux surgery

The aim of this study was to review the literature about the effect of antireflux surgery on the metaplasia-dysplasia-adenocarcinoma sequence in patients with Barrett's oesophagus. Antireflux operations (by laparotomy or laparoscopy) can alter the natural history of Barrett's oesophagus, allowing disease stabilization in a substantial proportion of patients without high grade dysplasia at time of surgery. It also may induce complete or partial regression of Barrett's epithelium, especially for short segment of Barrett's oesophagus, but in unpredictable manner. While regression of low-grade dysplasia is commonly observed, histologic progression is rarely observed after effective antireflux surgery. However, ineffective antireflux surgery expose to histologic progression to high-grade dysplasia or adenocarcinoma. These data support the need for a long-term clinical, endoscopic, and histologic follow-up program after antireflux surgery in patients with Barrett's oesophagus.