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 columnarlined 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. Presented at the Forty-Second Annual Meeting of The Society for Surgery of the Alimentary Tract, Atlanta, Georgia, May 20–23, 2001 (oral presentation).     

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.     

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.     

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.     

Long-term outcome of antireflux surgery in patients with Barrett's esophagus

OBJECTIVE: To assess the long-term outcome of antireflux surgery in patients with Barrett's esophagus. SUMMARY BACKGROUND DATA: The prevalence of Barrett's esophagus is increasing, and its treatment is problematic. Antireflux surgery has the potential to stop reflux and induce a quiescent mucosa. Its long-term outcome, however, has recently been challenged with reports of poor control of reflux and the inability to prevent progression to cancer. METHODS: The outcome of antireflux surgery was studied in 97 patients with Barrett's esophagus. Follow-up was complete in 88% (85/97) at a median of 5 years. Fifty-nine had long-segment and 26 short-segment Barrett's. Patients with intestinal metaplasia of the cardia were excluded. Fifty patients underwent a laparoscopic procedure, 20 a transthoracic procedure, and 3 abdominal Nissen operations. Nine had a Collis-Belsey procedure and three had other partial wraps. Outcome measures included relief of reflux symptoms (all), patients' perception of the result (all), upper endoscopy and histology (n = 79), and postoperative 24-hour pH monitoring (n = 21). RESULTS: At a median follow-up of 5 years, reflux symptoms were absent in 67 of 85 patients (79%). Eighteen (20%) developed recurrent symptoms; four had returned to taking daily acid-suppression medication. Seven patients underwent a secondary repair and were asymptomatic, increasing the eventual successful outcome to 87%. Recurrent symptoms were most common in patients undergoing Collis-Belsey (33%) and laparoscopic Nissen (26%) procedures and least common after a transthoracic Nissen operation (5%). The results of postoperative 24-hour pH monitoring were normal in 17 of 21 (81%). Recurrent hiatal hernias were detected in 17 of 79 patients studied; 6 were asymptomatic. Seventy-seven percent of the patients considered themselves cured, 22% considered their condition to be improved, and 97% were satisfied. Low-grade dysplasia regressed to nondysplastic Barrett's in 7 of 16 (44%), and intestinal metaplasia regressed to cardiac mucosa in 9 of 63 (14%). Low-grade dysplasia developed in 4 of 63 (6%) patients. No patient developed high-grade dysplasia or cancer in 410 patient-years of follow-up. CONCLUSIONS: After antireflux surgery, most patients with Barrett's enjoy long-lasting relief of reflux symptoms, and nearly all patients consider themselves cured or improved. Mild symptoms recur in one fifth. Importantly, dysplasia regressed in nearly half of the patients in whom it was present before surgery, intestinal metaplasia disappeared in 14% of patients, and high-grade dysplasia and adenocarcinoma were prevented in all.     

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.     

Combination of endoscopic argon plasma coagulation and antireflux surgery for treatment of barrett’s esophagus

Columnar-lined epithelium with specialized intestinal metaplasia of the esophagus (i.e., Barrett’s esophagus) is a premalignant condition caused by chronic gastroesophageal reflux disease. Progression of intestinal metaplasia may be avoided by antirefiux surgery, whereas regeneration of esophageal mucosa could be achieved by endoscopic argon plasma coagulation (EAPC). The aim of this prospective study was to show the early results of a combination of EAPC and antireflux surgery. Thirty patients with Barrett’s esophagus were treated between August 1996 and December 1999. Regeneration of esophageal mucosa was achieved with several sessions of EAPC under general anesthesia. All patients were receiving a double dose of proton pump inhibitors. Endoscopic follow-up was performed 6 to 8 weeks after the last session. Antireflux surgery (Nissen [n = 26] or Toupet In = 4] fundoplication) followed complete regeneration of the squamous epithelium in the esophagus. One year after laparoscopic fundopfication and EAPC follow-up with endoscopy and quadrant biopsies of the esophagus, 24-h0ur pH monitoring and esophageal manonletry were performed. All 30 patients showed complete regeneration of the squamous epithelium after a median of two sessions (range 1 to 7) of EAPC. Twenty-two patients underwent 1-year follow-up studies. All showed endoscopically an intact fundic wrap. Recurrence of a 1 cm segment of Barrett’s epithelium without dysplasia was present in two patients, both of whom had recurrent acid reflux due to failure of their antireflux procedure. Our results indicate that the combination of EAPC and antireflux surgery is an effective treatment option in patients with Barrett’s esophagus with gastroesophageal reflux disease. Long-term follow-up of this therapy is necessary to evaluate its effect on cancer risk in Barrett’s esophagus. Presented at the Forty-First Annual Meeting of The Society for Surgery of the Alimentary Tract, San Diego, Calif., May 21–24, 2000.     

KTP laser ablation of Barrett's esophagus after anti-reflux surgery results in long-term loss of intestinal metaplasia

Background: Efforts to ablate Barrett's epithelium have met with mixed results. We report the long-term follow-up evaluation of the preliminary cohort of patients who underwent thermal ablation of Barrett's epithelium with the potassium–titanyl–phosphate (KTP) laser after anti-reflux surgery. Methods: Nine patients with intestinal metaplasia (IM) of the esophagus underwent fundoplication (7 laparoscopic Nissen, 1 laparoscopic Toupet, 1 open Nissen) between May 1993 and October 1994. Three patients had an IM less than 3 cm long (33%). One year after the operation, all the patients were symptom free, had discontinued medications, and had a normal 24-h pH study. From June 1995 to February 1996, these patients underwent a median of two (range, 1–5) endoscopic procedures with directed mucosal ablation using the KTP laser. A comparative cohort of 21 patients (IM length, <3cm; 38%) treated during the same period with fundoplication alone served as a control. The patients were followed prospectively with annual or biennial endoscopy and biopsy. All the patients were contacted by mail, telephone, or clinic visit annually to determine symptomatic and quality-of-life outcome of antireflux surgery. Results: The mean follow-up period was 6.8 years (range, 6–7.5 years). At this writing, the study patients are alive and well. Eight of the patients have experienced histologic loss of IM (89%) according to their last biopsy result. One patient has had regression of low-grade dysplasia to IM. The patients treated with fundoplication alone had a mean follow-up period of 5.6 years (range, 4.7–7.2 years). On the basis of the last biopsy result, 7 of 21 patients (33%) had no evidence of IM. Conclusions: A program of tailored antireflux surgery followed by thermal mucosal ablation causes a loss of IM in a majority of patients with Barrett's esophagus. This may represent a significant improvement in histologic outcome over that of treatment with fundoplication alone (p = 0.007 Fisher's exact test).     

Antireflux surgery for Barrett's oesophagus

Barrett's oesophagus is usually the result of severe reflux disease. Relief of reflux symptoms is the primary aim of treatment in patients with Barrett's oesophagus who do not have high-grade dysplasia. Some studies with medium-term (2-5 years) follow up show that antireflux surgery can provide good or excellent symptom control, with normal oesophageal acid exposure, in more than 90% of patients with Barrett's oesophagus. Antireflux surgery, but not medical therapy, can also reduce duodenal nonacid reflux to normal levels. There is no conclusive evidence that antireflux surgery can prevent the development of dysplasia or cancer, or that it can reliably induce regression of dysplasia, and patients with Barrett's oesophagus should therefore remain in a surveillance programme after operation. Some data suggest that antireflux surgery can prevent the development of intestinal metaplasia (IM) in patients with reflux disease but no IM. The combination of antireflux surgery plus an endoscopic ablation procedure is a promising treatment for patients with Barrett's oesophagus with low-grade dysplasia.     

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.     

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.     

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.     

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.     

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.     

Gastroesophageal reflux and cancer

The causal relationship between GERD and esophageal adenocarcinoma, although unclear just a few decades ago, now is established fairly well. The physiologic changes and the biocellular alterations of the damaged esophageal mucosa are documented better. Despite this knowledge, the dramatic increase in the incidence of esophageal cancer cannot be explained. The absolute risk of esophageal adenocarcinoma arising from GERD is low, and, at present, does not justify population-screening programs. Still, with the notion that adenocarcinoma of the esophagus is an aggressive cancer once documented, important questions still are in need of answers for patients suffering from reflux symptoms. Patients who have reflux disease are not necessarily symptomatic. It remains unclear if patients experiencing reflux symptoms should undergo mandatory endoscopy with biopsies at the esophagogastric junction. Furthermore, metaplasia of the lower esophagus often is not readily recognizable at endoscopy, and only biopsies can document abnormal histology. A severe and prolonged history of reflux always should orient to the possibility of a reflux-related columnar-lined esophagus. Once documented, Barrett's esophagus needs to be seen as a premalignant condition not necessarily leading to adenocarcinoma formation; despite their increased risk of tumor formation, most patients who have Barrett's esophagus die of other causes. During regular endoscopic follow-up, multilevel circumferential biopsies should document the evolution of the histologic changes in the lower esophagus and at the gastroesophageal junction of these patients. It is the only method available to document the appearance of dysplasia. It still is unclear if medicine or surgery provides the best quality of life and the best protection against the development of dysplasia and the possible progression toward adenocarcinoma formation when intestinal metaplasia is present in the esophagus.     

Laparoscopic Nissen fundoplication and esophageal intestinal metaplasia: preliminary observations

The aim of this preliminary study conducted in a few cases was the retrospective evaluation of the effects of laparoscopic Nissen fundoplication on oesophageal intestinal metaplasia. Seventy-seven patients with hiatal hernia underwent digital videofluorography, endoscopy with biopsies, motility studies and 24-h oesophageal pH-monitoring. On the basis of the results of the diagnostic procedures and considering the patients' ages and response to proton-pump inhibitor treatment, 8 patients underwent laparoscopic Nissen fundoplication; in 5 cases intestinal metaplasia was present at histopathological examination. Two of these had Barrett's oesophagus at endoscopy and intestinal metaplasia was associated with low-grade dysplasia in both at histology; the other 3 did not present a columnar mucosa at endoscopy and 1 had low-grade dysplasia. In all 5 patients, at 1 year postoperative histopathological control, disappearance or decrease of metaplastic epithelium and regression of dysplasia were noted, with excellent results in terms of reflux symptoms at clinical control. On the basis of these preliminary data, it is our opinion that antireflux surgery is not only a suitable treatment in the management of Barrett's oesophagus but also has a favourable effect on intestinal metaplasia regression when a normal oesophageal mucosa is present.     

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.     

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 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.