PubMed Health⌕ Search

Biomedical subjects

S R DeMeester

Publications and source records attributed to S R DeMeester.

At least 19 recordsLinked to original sources

Bravo capsule induction of esophageal hypercontractility and chest pain.

BACKGROUND: The Bravo catheter-free pH monitoring system uses a capsule attached to the esophageal mucosa to detect acid exposure. Placement of the Bravo capsule is associated with intermittent chest pain in 50% of normal volunteers. The authors hypothesized that chest pain in this setting may be attributable to hypertensive esophageal contractions induced by the Bravo capsule. METHODS: The study population consisted of 40 consecutive patients with reflux symptoms who had stationary esophageal manometry within 1 h after Bravo capsule placement. The control group consisted of 40 patients with symptomatic gastroesophageal reflux disease (GERD) from a population of patients with foregut symptoms who were computer matched to the study group for age, sex, lower esophageal sphincter (LES) pressure, LES length, and 24-h pH composite score. The patients in the control group had manometry before Bravo capsule placement. The occurrence of chest pain was assessed before and during the monitoring period by interview and review of the patient's diary. Mean contraction amplitudes in the distal third of the esophagus after 10 wet swallows were averaged. The prevalence of patients with esophageal contraction amplitudes in the distal third that exceeded the 95th percentile of normal (180 mmHg) and the mean amplitude of distal third esophageal contractions in the study and control populations were compared. In the study group, the incidence of chest pain among the patients with hypercontractility of the esophagus was compared with the incidence among those without hypercontractility. RESULTS: The mean contraction amplitude was higher in the study group (144.7 vs 105.5 mmHg; p = 0.002). The number of patients with a mean distal esophageal contraction amplitude exceeding the 95th percentile of normal also was significantly higher in the study group (13/40 vs 5/40; p = 0.03). A total of 10 patients experienced new onset of chest pain with the Bravo capsule in place, and 6 patients experienced hypertensive esophageal contractions. CONCLUSIONS: The intraesophageal Bravo capsule can cause hypertensive esophageal contractions, which may lead to chest pain.

Adult↗

Predictive factors of coexisting cancer in Barrett's high-grade dysplasia.

BACKGROUND: Identification of high-grade dysplasia (HGD) in Barrett's esophagus has been considered an indication for esophagectomy because of the high risk for coexisting cancer. However, rigorous endoscopic surveillance programs recently have been recommended, reserving esophagectomy for patients whose cancer is identified on biopsy. This approach risks continued surveillance for patients who already have cancer unless reliable markers for the presence of occult cancer are identified. This study aimed to determine the endoscopic, histologic, and demographic features associated with the presence of occult cancer in patients with HGD. METHODS: Endoscopic, histologic, and demographic findings for 31 patients who underwent esophagectomy for HGD were reviewed. The presence of an ulcer, nodule, stricture, or raised area on preoperative endoscopy was noted. The results of endoscopic biopsies taken before resection every 1 to 2 cm along the Barrett's segment were reviewed. The HGD was categorized as unilevel if the dysplasia was limited to one level of biopsy and as multilevel if more than one level was involved. Patients were divided into two groups according to the presence or absence of cancer in the resected specimens, and these variables were compared. RESULTS: The prevalence of coexisting cancer in patients with HGD was 45% (14/31). Of the 31 patients in this study, 9 had a visible lesion. Cancer was found in the resected specimens from 7 (78%) of 9 patients with a visible lesion and 7 (32%) of 22 patients without a visible lesion (p = 0.019). Of 22 patients without a visible lesion, 10 had multilevel and 12 had unilevel HGD. The findings showed that 6 (60%) of 10 patients with multilevel HGD and 1 (8.3%) of 12 patients with unilevel HGD had cancer in the resected esophagus (p = 0.009). CONCLUSION: For patients with HGD, a lesion visible on endoscopy and/or HGD at multiple biopsy levels is associated with an increased risk for coexisting cancer. These patients should be considered for early esophagectomy.

Adenocarcinoma↗

Cdx-2 expression in squamous and metaplastic columnar epithelia of the esophagus.

The molecular pathogenesis of Barrett's esophagus is poorly understood. Evidence suggests that at a phenotypic level, the metaplastic process begins with the transformation of squamous epithelium in the distal esophagus to cardiac mucosa, which subsequently becomes intestinalized. The homeobox gene Cdx-2 has been shown to be an important transcriptional regulator of embryonic differentiation and maintenance of adult intestinal type epithelium. We hypothesized that Cdx-2 gene expression levels increase with the phenotypic transformation of normal squamous mucosa to the intestinalized columnar mucosa of Barrett's esophagus. Endoscopic biopsies were obtained at the gastroesophageal junction in patients with symptoms of gastroesophageal reflux disease and classified according to histology: normal squamous mucosa (n = 62), cardiac mucosa (n = 19), oxynto-cardiac mucosa (n = 14), and intestinal metaplasia (n = 15). Duodenal biopsies (n = 26) served as the columnar control. After laser capture microdissection and RNA isolation, gene expression levels of Cdx-2 were measured in each tissue type by quantitative reverse transcription polymerase chain reaction. Consistent with its known function, Cdx-2 gene expression levels were highest in duodenal mucosa and nearly absent in squamous epithelium. There was a stepwise increase in Cdx-2 gene expression from cardiac to Barrett's epithelium (P < 0.001). Expression levels of Cdx-2 in cardiac and oxynto-cardiac mucosa were 40-70 times higher and Barrett's mucosa 400 times higher than that found in squamous epithelium. Relative expression of the homeobox gene Cdx-2, known to induce differentiation of intestinal type epithelium, increases in a stepwise fashion during the phenotypic transformation of distal esophageal squamous mucosa to cardiac columnar mucosa and to the intestinalized columnar mucosa of Barrett's esophagus. Therefore, Cdx-2 may be a potential biomarker to detect the early transition to Barrett's esophagus.

Adolescent↗

Can clinical and endoscopic findings accurately predict early-stage adenocarcinoma?

BACKGROUND: The presentation and management of esophageal cancer are changing, as more patients are diagnosed at an earlier stage of the disease in which endoscopic treatment methods may be contemplated. Therefore, we conducted a study to determine whether symptomatic and endoscopic findings can accurately identify node-negative early-stage adenocarcinoma. METHODS: A total of 213 consecutive patients (171 men and 42 women) with resectable esophageal adenocarcinoma seen from 1992 to 2002 were evaluated. None of these patients received neoadjuvant chemotherapy or radiation therapy. Using a multivariable model, model-based probabilities of early-stage disease (T1 im/sm N0) were calculated for each combination of the following three features: no dysphagia as main symptom at presentation, tumor length <or=2 cm, and noncircumferential lesion. RESULTS: Eighty-two percent of the patients with all three characteristics presented with early-stage disease. Even in the setting of small, visible, noncircumferential tumors/nodules in patients without dysphagia, 14% of the patients harbored node metastasis. CONCLUSIONS: Simple clinical and endoscopic findings predicted early-stage disease in 82% of cases, whereas a small but significant percentage had node metastasis. Because node metastasis predisposes to local failure in nonresectional treatment options such as endoscopic mucosal resection and photodynamic therapy, such findings should have a significant bearing on treatment decisions.

Adenocarcinoma↗

The safety and usefulness of endoscopy for evaluation of the graft and anastomosis early after esophagectomy and reconstruction.

BACKGROUND: Although rare, graft ischemia and necrosis after esophagectomy is a devastating complication. The aim of this study was to review our experience with early endoscopy for evaluation of the graft and anastomosis after esophagectomy and reconstruction. METHODS: From a population of 479 patients who underwent esophagectomy during the years 1996-2003, we identified 102 patients who had endoscopy within 21 days of operation. RESULTS: Endoscopy was performed a median of 9 days after operation. Graft ischemia, anastomotic leak, or both were found in 63 of the 102 patients. Reoperation was necessary in 27% of these patients, including graft removal in nine patients. In 39 patients, endoscopy demonstrated a healthy graft; only one of these patients (2.6%) required reoperation. No patient with ischemia judged insufficient to warrant graft removal on initial endoscopy subsequently lost their graft. There were no complications or anastomotic injuries associated with early endoscopy. CONCLUSION: Endoscopy early after esophagectomy is safe and provides accurate and reliable identification of graft ischemia that can be used to guide the treatment of these patients.

Aged↗

Etiology of intestinal metaplasia at the gastroesophageal junction.

BACKGROUND: Intestinal metaplasia occurs in the esophagus as a consequence of gastroesophageal reflux disease and in the stomach secondary to H. pylori infection. The etiology of intestinal metaplasia limited to the gastroesophageal junction or cardia (CIM) is disputed. We hypothesized that CIM has dual etiologies: gastroesophageal reflux in some, H. pylori infection in others, and that cytokeratin immunostaining can help to differentiate between these two etiologies. METHODS: We defined CIM as the presence of intestinal metaplasia within cardiac mucosa on biopsy from an endoscopically normal-appearing gastroesophageal junction. Thirty patients with CIM who had multiple biopsy specimens taken from the esophagus, gastroesophageal junction, and stomach were identified. Tissue blocks from biopsy specimens taken at the gastroesophageal junction were sectioned and immunostained for cytokeratins 7 and 20. The cytokeratin 7/20 staining of the CIM in each patient was determined to be either a Barrett's or non-Barrett's pattern. H. pylori infection was assessed by Giemsa staining of antral biopsy specimens. RESULTS: H. pylori infection was present in 16 patients. A Barrett's cytokeratin 7/20 staining pattern in the CIM was present in only 46% of the H. pylori-positive patients, as compared to 86% in the 14 patients with CIM and no H. pylori (p = 0.025). Objective evidence of reflux disease was present in 71% of patients with CIM and no H. pylori, as compared to 31% of patients with H. pylori. CONCLUSIONS: The two different patterns of cytokeratin 7/20 staining found in patients with CIM support the concept of dual etiologies for CIM. A Barrett's staining pattern was associated with objective evidence of gastroesophageal reflux and the absence of H. pylori, suggesting that cytokeratin 7/20 immunostaining is useful to determine the likely etiology of CIM.

Biopsy↗

Risk factors and the prevalence of trocar site herniation after laparoscopic fundoplication.

BACKGROUND: Although there have been case reports describing trocar site herniation after laparoscopic fundoplication, its overall prevalence and the risk factors for its development are unclear. METHODS: The records of 320 patients undergoing primary laparoscopic fundoplication as treatment for gastroesophageal reflex disease (GERD) or hiatal hernia between 1991 and 1999 were reviewed retrospectively. Placement of the initial supraumbilical trocar was by the open Hassan technique in all patients. RESULTS: Nine patients (five male) with a mean age 54 years (range, 37-75) developed trocar site herniation, for an overall prevalence of 3%. The mean interval between surgery and diagnosis was 12 months (range, 4-21). In all patients, the hernia occurred at the supraumbilical camera port site. Patients with trocar hernias tended to have a higher body mass index (BMI) than those without hernias (mean BMI, 29.4 kg/m2 vs 27.2 kg/m2, p = 0.13). None of the patients developed intestinal obstruction as a consequence of herniation. To date, all but one of the hernias have been repaired. Six of them required the insertion of a prosthetic mesh. CONCLUSIONS: The prevalence of trocar site herniation after laparoscopic fundoplication was minimal at 3%. All hernias occurred at the midline supraumbilical port, the only site where open trocar insertion was employed. As a consequence of these observations, we have developed a new method of open trocar placement. This method utilizes a paramedian skin incision and separate fascial incisions through anterior and posterior rectus sheathes, with retraction of the rectus abdominis muscle laterally.

Abdomen↗

Epigenetic patterns in the progression of esophageal adenocarcinoma.

Esophageal adenocarcinoma (EAC) arises after normal squamous mucosa undergoes metaplasia to specialized columnar epithelium (intestinal metaplasia or Barrett's esophagus), which can then ultimately progress to dysplasia and subsequent malignancy. Epigenetic studies of this model have thus far been limited to the DNA methylation analysis of a few genes. In this study, we analyzed a panel of 20 genes using a quantitative, high-throughput methylation assay, METHYLIGHT: We used this broader approach to gain insight into concordant methylation behavior between genes and to generate epigenomic fingerprints for the different histological stages of EAC. Our study included a total of 104 tissue specimens from 51 patients with different stages of Barrett's esophagus and/or associated adenocarcinoma. We screened 84 of these samples with the full panel of 20 genes and found distinct classes of methylation patterns in the different types of tissue. The most informative genes were those with an intermediate frequency of significant hypermethylation [ranging from 15% (CDKN2A) to 60% (MGMT) of the samples]. This group could be further subdivided into three classes, according to the absence (CDKN2A, ESR1, and MYOD1) or presence (CALCA, MGMT, and TIMP3) of methylation in normal esophageal mucosa and stomach, or the infrequent methylation of normal esophageal mucosa accompanied by methylation in all normal stomach samples (APC). The other genes were less informative, because the frequency of hypermethylation was below 5% (ARF, CDH1, CDKN2B, GSTP1, MLH1, PTGS2, and THBS1), completely absent (CTNNB1, RB1, TGFBR2, and TYMS1), or ubiquitous (HIC1 and MTHFR), regardless of tissue type. Each class undergoes unique epigenetic changes at different steps of disease progression of EAC, suggesting a step-wise loss of multiple protective barriers against CpG island hypermethylation. The aberrant hypermethylation occurs at many different loci in the same tissues, suggestive of an overall deregulation of methylation control in EAC tumorigenesis. However, we did not find evidence for a distinct group of tumors with a CpG island methylator phenotype. Finally, we found that normal and metaplastic tissues from patients with evidence of associated dysplasia or cancer had a significantly higher incidence of hypermethylation than similar tissues from patients with no further progression of their disease. The fact that the samples from these two groups of patients were histologically indistinguishable, yet molecularly distinct, suggests that the occurrence of such hypermethylation may provide a clinical tool to identify patients with premalignant Barrett's who are at risk for further progression.

Adenocarcinoma↗

Predictive factors of Barrett esophagus: multivariate analysis of 502 patients with gastroesophageal reflux disease.

HYPOTHESIS: Risk factors for the presence and extent of Barrett esophagus (BE) can be identified in patients with gastroesophageal reflux disease (GERD). DESIGN: Case-comparison study. SETTING: University tertiary referral center. PATIENTS: Five hundred two consecutive patients with GERD documented by 24-hour esophageal pH monitoring and with complete demographic, endoscopic, and physiological evaluation, divided in groups according to the presence and extent of BE (328 patients without BE and 174 with BE [67 short-segment BE and 107 long-segment BE]). MAIN OUTCOME MEASURES: Clinical, endoscopic, and physiological data, studied by multivariate analysis, to identify the independent predictors of the presence and extent of BE. RESULTS: Seven factors were identified as predictors of BE. They were abnormal bile reflux (odds ratio [OR], 4.2; 95% confidence interval [CI], 1.9-9.7), hiatal hernia larger than 4 cm (OR, 4.1; 95% CI, 2.1-8.0), a defective lower esophageal sphincter (OR, 2.7; 95% CI, 1.4-5.4), male sex (OR, 2.6; 95% CI, 1.6-4.3), defective distal esophageal contraction (OR, 2.2; 95% CI, 1.4-3.5), abnormal number of reflux episodes lasting longer than 5 minutes (OR, 2.2; 95% CI, 1.1-4.6), and GERD symptoms lasting for more than 5 years (OR, 2.1; 95% CI, 1.4-3.2). Only abnormal bile reflux (OR, 4.8; 95% CI, 1.7-13.2) was identified as a predictor of short-segment BE (baseline, no BE). Three factors were identified as predictors of long-segment BE (baseline short-segment BE). They were hiatal hernia larger than 4 cm (OR, 17.8; 95% CI, 4.1-76.6), a defective lower esophageal sphincter (OR, 16.9; 95% CI, 1.6-181.4), and an abnormal longest reflux episode (OR, 8.1; 95% CI, 2.8-24.0). CONCLUSIONS: Among patients with GERD, specific factors are associated with the presence and extent of BE. Elimination of reflux with an antireflux operation in patients with 1 or more of these factors may prevent the future development of BE.

Adolescent↗

Curative resection for esophageal adenocarcinoma: analysis of 100 en bloc esophagectomies.

OBJECTIVE: To document what can be accomplished with surgical resection done according to the classical principles of surgical oncology. METHODS: One hundred consecutive patients underwent en bloc esophagectomy for esophageal adenocarcinoma. No patient received pre- or postoperative chemotherapy or radiation therapy. Tumor depth and number and location of involved lymph nodes were recorded. A lymph node ratio was calculated by dividing the number of involved nodes by the total number removed. Follow-up was complete in all patients. The median follow-up of surviving patients was 40 months, with 23 patients surviving 5 years or more. RESULTS: The overall actuarial survival rate at 5 years was 52%. Survival rates by American Joint Commission on Cancer (AJCC) stage were stage 1 (n = 26), 94%; stage 2a (n = 11), 65%; stage 2b (n = 13), 65%; stage 3 (n = 32), 23%; and stage 4 (n = 18), 27%. Sixteen tumors were confined to the mucosa, 16 to the submucosa, and 13 to the muscularis propria, and 55 were transmural. Tumor depth and the number and ratio of involved nodes were predictors of survival. Metastases to celiac (n = 16) or other distant node sites (n = 26) were not associated with decreased survival. Local recurrence was seen in only one patient. Latent nodal recurrence outside the surgical field occurred in 9 patients and systemic metastases in 31. Tumor depth, the number of involved nodes, and the lymph node ratio were important predictors of systemic recurrence. The surgical death rate was 6%. CONCLUSION: Long-term survival from adenocarcinoma of the esophagus can be achieved in more than half the patients who undergo en bloc resection. One third of patients with lymph node involvement survived 5 years. Local control is excellent after en bloc resection. The extent of disease associated with tumors confined to the mucosa and submucosa provides justification for more limited and less morbid resections.

Adenocarcinoma↗

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.

Adolescent↗

Is adenocarcinoma following esophagoduodenostomy without carcinogen in the rat reflux-induced?

BACKGROUND: A widely used rat model for reflux-induced esophageal adenocarcinoma in the absence of carcinogens involves induction of duodenoesophageal reflux by performance of esophagoduodenostomy. The aim of this study was to test the hypothesis that acid reflux reduces the incidence of adenocarcinoma in this animal model. METHODS: One hundred ninety 8-week-old male Sprague-Dawley rats were studied. The animals were randomly divided into four groups with a different type of reflux established in each group. Group 1 had an esophagoduodenostomy for duodenogastroesophageal reflux (n = 59), group 2 had an esophagoduodenostomy and a total gastrectomy for duodenoesophageal reflux (n = 54), group 3 had an esophagoduodenostomy and a total gastrectomy with acid supplementation with acidified water to control for the effect of the gastrectomy (n = 50), and group 4 had a total gastrectomy with Roux-en-Y reconstruction to eliminate all reflux (n = 25). One hundred eighty-eight surviving animals were sacrificed at 36 weeks of age and the resected esophagi were examined. RESULTS: All animals except the no reflux control group had severe reflux esophagitis. The frequency of tumor development was similar in all study groups. All of the tumors were well-differentiated adenocarcinomas that were located on the external surface of the bowel either at or immediately distal to the esophagoenteric anastomosis. The tumors appeared to arise from the submucosa and did not involve the overlying mucosa. There was no definite evidence of columnar lining of the esophagus but an admixture of squamous and columnar epithelium was found microscopically in all groups. This finding was unrelated to the presence and composition of reflux. CONCLUSIONS: Adenocarcinomas in this animal model are not reflux-induced and do not arise from the mucosa. Despite previous reports to the contrary, we suggest that this model may not be valid for the study of reflux-induced esophageal adenocarcinoma.

Adenocarcinoma, Mucinous↗

Determinants of intestinal metaplasia within the columnar-lined esophagus.

HYPOTHESIS: The clinical and physiological features of patients with short segments of columnar-lined esophagus (CLE) with and without intestinal metaplasia (IM) are distinct. DESIGN: Retrospective case series. SETTING: University tertiary referral center. PATIENTS: Sixty-five consecutive patients with a 2-cm or shorter length of endoscopically visible CLE. INTERVENTIONS: The type of CLE and the presence of Helicobacter pylori were determined by histopathologic examination of esophageal and gastric antrum biopsy specimens. All patients underwent esophageal manometry and simultaneous 24-hour pH and bilirubin monitoring. MAIN OUTCOME MEASURES: Clinical and physiological data were compared in patients with and without IM. RESULTS: Thirty-six patients had IM and 29 had cardiac-type mucosa without IM in biopsy specimens from the CLE. There was no significant difference in age or sex distribution, but the duration of symptoms was significantly longer in patients with IM (10 vs 5 years; P = .03). Abnormal esophageal acid exposure was found in 30 (83%) of 36 patients with IM and 23 (79%) of 29 patients without IM. The prevalence of abnormal bilirubin exposure was significantly higher in patients with IM (75% [27/36]) than in those without IM (41% [12/29]; P = .01). There was no significant difference in the prevalence of H pylori infection between the 2 groups (8% vs 10%; P >.99). CONCLUSIONS: Patients with short segments of CLE and IM have similar esophageal acid exposure but significantly higher frequency of abnormal bilirubin exposure and longer median duration of reflux symptoms than patients without IM. Therefore, CLE, regardless of histological type, is a manifestation of gastroesophageal reflux disease. The presence of duodenoesophageal reflux and the duration of reflux seem to be important in the pathogenesis of IM.

Barrett Esophagus↗

Laparoscopic repair of large type III hiatal hernia: objective followup reveals high recurrence rate.

BACKGROUND: Recent studies based on symptomatic outcomes analyses have shown that laparoscopic repair of large type III hiatal hernias is safe, successful, and equivalent to open repair. These outcomes analyses were based on a relatively short followup period and lack objective confirmation that the hernia has not recurred. The aim of this study was to compare the outcomes of laparoscopic and open repair of large type III hiatal hernia using both symptomatic evaluation and barium study to assess the integrity of the repair. STUDY DESIGN: Fifty-four patients underwent repair of a large type III hiatal hernia between 1985 and 1998. The surgical approach was laparotomy in 13, thoracotomy in 14, and laparoscopy in 27. An antireflux procedure was included in all patients. Symptomatic outcomes were assessed using a structured questionnaire at a median of 24 months and was complete in 51 of 54 patients (94%). A single radiologist, without knowledge of the operative procedure, assessed the integrity of the repair using video esophagram. Videos were performed at a median of 27 months (35 months open and 17 laparoscopic) and were completed in 41 of 54 patients (75%). RESULTS: Symptomatic outcomes were similar in both groups with excellent or good outcomes in 76% of the patients after laparoscopic repair and 88% after an open repair. Reherniation was present in 12 patients and was asymptomatic in 7. A recurrent hernia was present in 12 of the 41 patients (29%) who returned for a followup video esophagram. Forty-two percent (9 of 21) of the laparoscopic group had a recurrent hernia compared with 15% (3 of 20) of the open group (p < 0.001 log-rank value on recurrence-free followup). CONCLUSIONS: Laparoscopic repair of type III hiatal hernias is associated with a disturbingly high (42%) prevalence of recurrent hernia. More than half such recurrences have few, if any, symptoms.

Adult↗

Columnar mucosa and intestinal metaplasia of the esophagus: fifty years of controversy.

OBJECTIVE: To outline current concepts regarding etiology, diagnosis, and treatment of intestinal metaplasia of the esophagus and cardia. SUMMARY BACKGROUND DATA: Previously, endoscopic visualization of columnar mucosa extending a minimum of 3 cm into the esophagus was sufficient for the diagnosis of Barrett's esophagus, but subsequently the importance of intestinal metaplasia and the premalignant nature of Barrett's have been recognized. It is now apparent that shorter lengths of intestinal metaplasia are common, and share many features of traditional 3-cm Barrett's esophagus. METHODS: Themes and concepts pertaining to intestinal metaplasia of the esophagus and cardia are developed based on a review of the literature published between 1950 and 1999. RESULTS: Cardiac mucosa is the precursor of intestinal metaplasia of the esophagus. Both develop as a consequence of gastroesophageal reflux. Intestinal metaplasia, even a short length, is premalignant, and the presence of dysplasia indicates progression on the pathway to adenocarcinoma. Antireflux surgery, as opposed to medical therapy, may induce regression or halt progression of intestinal metaplasia. The presence of high-grade dysplasia is frequently associated with an unrecognized focus of adenocarcinoma. Vagal-sparing esophagectomy removes the diseased esophagus and is curative in patients with high-grade dysplasia. Invasion beyond the mucosa is associated with a high likelihood of lymph node metastases and requires lymphadenectomy. CONCLUSIONS: Despite improved understanding of this disease, controversy about the definition and best treatment of Barrett's esophagus continues, but new molecular insights, coupled with careful patient follow-up, should further enhance knowledge of this disease.

Barrett Esophagus↗

Helicobacter pylori is not associated with the manifestations of gastroesophageal reflux disease.

HYPOTHESIS: Helicobacter pylori is not associated with gastroesophageal reflux disease and its complications, including adenocarcinoma of the esophagus and the gastroesophageal junction (GEJ). DESIGN: Retrospective analysis. SETTING: University tertiary referral center. PATIENTS: Two hundred twenty-nine patients with symptoms suggestive of foregut disease underwent esophageal manometry, 24-hour pH monitoring, and upper gastrointestinal tract endoscopy, with biopsy specimens obtained from the gastric antrum, the GEJ, and the distal esophagus. In these and in an additional 114 patients with adenocarcinoma of the esophagus and the GEJ, the presence of H. pylori was determined by Giemsa stain. The presence of gastroesophageal reflux disease, defined by abnormal esophageal acid exposure, and its manifestations (carditis, erosive esophagitis, intestinal metaplasia limited to the GEJ, Barrett esophagus, and adenocarcinoma of the esophagus and GEJ) were correlated with the presence of H. pylori. RESULTS: Helicobacter pylori was found on the biopsy specimens of the gastric antrum in 14.0% (32/229) of the patients with benign disease. It was not related to the features of gastroesophageal reflux disease, including abnormal esophageal acid exposure, erosive esophagitis, or Barrett esophagus. The presence of inflamed cardiac mucosa at the GEJ or carditis was inversely related to H. pylori infection and strongly associated with increased esophageal acid exposure. There was no association between the presence of intestinal metaplasia and H. pylori infection. Helicobacter pylori was found in 22 (19.3%) of the 114 patients with esophageal adenocarcinoma, which was not different from the prevalence of H. pylori in patients with benign disease. CONCLUSION: Helicobacter pylori plays no role in the pathogenesis of gastroesophageal reflux disease or its complications.

Adolescent↗