EMR for intramucosal adenocarcinoma of the esophagus: does one size fit all?
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Adenocarcinoma↗
Biomedical subjects
Steven R DeMeester
Publications and source records attributed to Steven R DeMeester.
Increasing cyclooxygenase-2 (cox-2) gene expression in the progression of Barrett's esophagus to adenocarcinoma correlates with that of Bcl-2.
Previous studies from our laboratory and others have suggested that increased expression of cox-2 is important in the genesis of esophageal adenocarcinoma. In vitro studies suggest that cox-2 regulates expression of the anti-apoptotic protein bcl-2, thus possibly accounting for reduced apoptosis in carcinogenesis. The aim of this study was to investigate the relationship of these 2 genes in the development of Barrett's-associated adenocarcinoma. Histologic sections from endoscopic biopsies or esophagectomy specimens were classified as non-dysplastic Barrett's (n = 30), intraepithelial neoplasia (n = 12) and adenocarcinoma (n = 48). The desired tissue was isolated by laser capture microdissection and expression levels of cox-2 and bcl-2 were measured by quantitative real-time PCR (Taqman). Gene expression levels were compared to samples of the distal esophageal squamous epithelium (n = 55) and reflux-esophagitis (n = 25), without Barrett's or cancer. Expression of both bcl-2 and cox-2 were increased in non-dysplastic Barrett's (p = 0.0077, p = 0.0037), intraepithelial neoplasia (p = 0.0053, p = 0.0220) and adenocarcinoma (p < 0.0001, p < 0.0001) compared to squamous epithelium or reflux-esophagitis. Furthermore, there is a significant correlation between these two genes, especially in carcinoma (p < 0.0001).
Adenocarcinoma↗
Adenocarcinoma of the esophagus and cardia: a review of the disease and its treatment.
BACKGROUND: Over the past 50 years there has been a remarkable change in the epidemiology of esophageal cancer. Previously rare, adenocarcinoma of the esophagus and gastroesophageal junction is now the most common esophageal cancer, and in the United States the incidence is increasing faster than that of any other malignancy. Surveillance in patients with Barrett's esophagus is identifying adenocarcinoma at an earlier, more curable stage in many patients, and at the same time new endoscopic and surgical options are available for the therapy of these localized tumors. METHODS: This article is a review of the epidemiology, diagnosis, staging, and treatment options for esophageal and gastroesophageal junction adenocarcinoma. RESULTS: The epidemiology, prognosis, patterns of lymphatic metastasis, and survival for esophageal and gastroesophageal junction adenocarcinoma suggest that these tumors are similar. New options for therapy, as well as the results of surgical resection with and without chemoradiotherapy, are reviewed. CONCLUSIONS: Surveillance programs for Barrett's are identifying patients with early, curable adenocarcinoma of the esophagus or gastroesophageal junction. Therapy for more advanced tumors hinges on local control of the disease and the eradication of systemic metastases.
Adenocarcinoma↗
Molecular determinants in targeted therapy for esophageal adenocarcinoma.
HYPOTHESIS: Cyclooxygenase 2 (COX-2), vascular endothelial growth factor (VEGF), and epidermal growth factor receptor (EGFR) are useful biological determinants in targeted therapy for esophageal adenocarcinoma. DESIGN: Prospective analysis. SETTING: University tertiary referral center. PATIENTS: Sixteen patients with squamous mucosa and normal results of a pH study without mucosal injury (control group), 15 with Barrett esophagus (metaplasia group), and 44 with adenocarcinoma (carcinoma group). INTERVENTIONS: Biopsy specimens were obtained 3 cm above the gastroesophageal junction. Dysplastic tissue was additionally isolated from 9 of the patients in the carcinoma group. After laser-capture microdissection, quantitative real-time polymerase chain reaction was used to measure gene expression across the spectrum of the metaplasia-dysplasia-carcinoma sequence. MAIN OUTCOME MEASURES: Expression of COX-2, VEGF, and EGFR in each patient group. RESULTS: Expression of both COX-2 and VEGF was significantly up-regulated in patients with metaplasia, dysplasia, and cancer compared with controls (P<.01). Expression levels of both were significantly higher in cancer than in the metaplasia group (P<.05) and increased sequentially from metaplasia to dysplasia to cancer. Expression of VEGF was significantly higher in the dysplastic tissue than in nondysplastic Barrett epithelium (P<.05). No change in expression levels of EGFR was seen in the histologic progression to esophageal adenocarcinoma. CONCLUSION: Gene expression data suggest that pharmacologic inhibition of COX-2 and VEGF may be useful adjuncts in targeted therapy for esophageal adenocarcinoma.
Adenocarcinoma↗
Modern 5-year survival of resectable esophageal adenocarcinoma: single institution experience with 263 patients.
BACKGROUND: Surgery, as the mainstay of treatment for localized esophageal cancer, is currently being challenged by the assumed high risk of esophagectomy and the poor longterm survival after resection. Epidemiologic and clinical changes over the past decade indicate that these assumptions should be reevaluated. The aim of this study was to assess the modern outcomes of esophagectomy for adenocarcinoma. STUDY DESIGN: We studied 263 consecutive patients (215 men, 48 women), who had esophagectomy for adenocarcinoma from 1992 to 2002. Ninety-seven (37%) were stage I, 63 (24%) were stage II, 93 (35%) were stage III, and 10 (4%) were stage IV. Forty-five percent (119 of 263) had curative en bloc resection, 52% (138 of 263) had node involvement, and 18% (48) received neoadjuvant therapy. RESULTS: Seventeen percent (44 of 263) of the patients were identified in a Barrett's surveillance program. The frequency of T1N0 adenocarcinoma increased over the study period (p=0.024). The overall 5-year survival was 46.5%, and for the last 5 years of the study was 50.4%. The overall 5-year survival for stage I was 81%; for stage II, 51%; for stage III, 14%; and for stage IV, 0%. Complications occurred in 61% and there were 12 perioperative deaths (4.5%). Cox proportional hazard analysis identified tumor stage and type of resection as independent predictors of survival. CONCLUSIONS: Nearly half of patients undergoing esophagectomy for adenocarcinoma survive >or=5 years. Improvements in survival are associated with increased detection of early stage disease, and a liberal use of en bloc resection. Nonsurgical treatments should be compared with these contemporary outcomes measures.
Adenocarcinoma↗
Complications of achalasia surgery.
The development of minimally invasive techniques have revolutionized the surgical therapy of achalasia and made myotomy with or without partial fundoplication the treatment of choice for most patients. Complications do occur, however, and every effort must be made to minimize their occurrence and identify and treat them effectively when they occur to maximize the likelihood of an excellent outcome in these patients who have a benign but incurable disorder. Further studies on the best location for the myotomy as well as the best type of fundoplication will help refine the procedure for future generations of patients.
Deglutition Disorders↗
Antireflux surgery normalizes cyclooxygenase-2 expression in squamous epithelium of the distal esophagus.
BACKGROUND: In some patients GERD presents with heartburn and regurgitation symptoms but a relative paucity of endoscopic and clinical findings, while in others symptoms may be minor or absent yet there is significant mucosal damage on endoscopy including the presence of Barrett's esophagus. The initial injury of gastroesophageal reflux is to the squamous esophageal mucosa, but while substantial research has been devoted to determining which genes are involved in the progression of Barrett's to dysplasia and cancer, little is known about the gene expression alterations in the squamous mucosa of patients with reflux. We hypothesized that the expression of cyclooxygenase-2 (Cox-2) might be increased in the squamous esophageal mucosal of patients with reflux, and might be a molecular indicator of reflux injury. Further, we hypothesized that Cox-2 expression in the squamous mucosa would be reduced following the elimination of reflux with an antireflux operation. METHODS: Biopsies of the distal esophageal squamous mucosa were taken 3 cm above the squamocolumnar junction (SCJ) in 28 GERD patients before and after Nissen fundoplication. Following microdissection and RNA isolation, quantitative real-time PCR was used to measure Cox-2 gene expression in paraffin-embedded (N = 16) and fresh frozen (N = 12) tissue. Biopsies from patients (paraffin N = 15, frozen N = 14) with normal acid exposure and no evidence of mucosal injury were analyzed as controls. RESULTS: Median Cox-2 expression in the squamous epithelium from paraffin embedded biopsies in patients with reflux disease was significantly increased compared to controls (p = 0.04). The presence of esophagitis or Barrett's esophagus did not significantly alter the expression of Cox-2 compared to patients with nonerosive reflux disease (NERD). After antireflux surgery median Cox-2 expression values were significantly reduced (p = 0.0003) and were normalized to levels similar to controls without reflux (p = 0.74). Similar results were observed in the prospectively obtained fresh frozen tissue. CONCLUSIONS: Cox-2 gene expression is increased in the distal esophageal squamous mucosa of most patients with GERD, and the elevation was similar whether there was mucosal injury in the form of esophagitis or Barrett's or no visible mucosal injury. This suggests that increased Cox-2 expression may serve as a molecular marker of reflux disease. The increased Cox-2 expression in patients with reflux was usually normalized following antireflux surgery. These findings demonstrate for the first time that gene expression can be altered by surgical correction of reflux. Thus, in addition to symptom control and improvement in the quality of life, perhaps future studies assessing the efficacy of antireflux therapy should also focus on the impact of the therapy on gene expression in the esophageal squamous mucosa.
Adult↗
Indications and technique of colon and jejunal interpositions for esophageal disease.
Esophageal replacement is a significant undertaking for both surgeon and patient. Because eating and drinking are some of life's great pleasures, the outcome of this undertaking has a direct impact on a patient's quality of life. The primary esophageal replacement organs are the stomach and colon, and each has advantages and disadvantages. As such, the choice of the graft should be tailored to the patient and the disease process in order to maximize the likelihood that the disease will be effectively treated, and that the patient's ability to enjoy a meal with family and friends will be restored.
Colon↗
Increased CDX2 and decreased PITX1 homeobox gene expression in Barrett's esophagus and Barrett's-associated adenocarcinoma.
BACKGROUND: The CDX2 (caudal-related homeobox gene 2) and PITX1 (pituitary homeobox 1) genes have essential roles in human development. Forced expression of Cdx2 alone in the murine stomach results in gastric intestinal metaplasia (IM). This study was undertaken to investigate the expression pattern of these critical morphogenesis genes in the Barrett's multistage carcinogenesis model. METHODS: CDX2 and PITX1 messenger RNA (mRNA) expression levels, relative to the control gene beta-actin, were measured by reverse transcription-polymerase chain reaction in specimens of Barrett's IM (n = 21), dysplasia (n = 18), adenocarcinoma (n = 20), and matching normal squamous esophagus tissues (n = 39) collected from 19 patients with Barrett's esophagus and 20 patients with esophageal adenocarcinoma. CDX2 protein expression was assessed by immunohistochemistry in specimens of normal squamous esophagus (n = 13), IM (n = 10), dysplasia (n = 8,) and adenocarcinoma (n = 5). RESULTS: The median relative CDX2 mRNA expression was approximately 200 times higher in Barrett's esophagus tissues (0.83) than in matching normal squamous esophagus (0.004) in the patients with Barrett's esophagus (P < .001). The mRNA expression in cancer tissues (0.49) was also higher than in matching normal squamous esophagus specimens (0.009, P < .001). There was no significant difference between the mRNA expression levels in Barrett's esophagus and adenocarcinoma. There was no CDX2 protein expression in normal squamous esophagus, but moderate to strong protein expression was seen in all Barrett's tissues and in a majority of the dysplasia and adenocarcinoma cells. Relative median PITX1 mRNA expression was decreased in Barrett's esophagus (8.02 for all specimens), compared with normal esophagus specimens (47.46 for all specimens, P < .001), and was further reduced in cancer specimens (2.21), compared with either Barrett's esophagus or normal esophagus (both P < .001). Wilcoxon testwas used for all P values shown. CONCLUSIONS: CDX2 mRNA and CDX2 protein expression are upregulated in Barrett's IM tissues, compared with normal squamous esophagus, and remain elevated in dysplasia and adenocarcinoma tissues. In contrast, PITX1 mRNA expression is decreased in Barrett's esophagus, compared with matching normal squamous esophagus specimens, and is further decreased in Barrett's-associated cancer. These descriptive findings suggest a possible role for these genes in the Barrett's metaplasia-dysplasia-adenocarcinoma sequence.
Adenocarcinoma↗
Surgical therapy for Barrett's esophagus.
Given the anatomic and functional defects almost universally present in patients who have BE, antireflux surgery is the most reliable means of stopping acid and nonacid (alkaline) reflux. Because patients who have BE have end-stage GERD, they require durable and reliable control of reflux, and the Hill procedure and partial fundoplication are associated with unacceptably high failure rates. In addition, there is mounting evidence that the success rates for Nissen fundoplication are lower in patients who have BE than in patients who have less severe GERD. Given that the most common mode of failure of a laparoscopic Nissen fundoplication is herniation of the fundoplication into the chest, patients who have BE must be considered at risk for having a short esophagus. The failure rate may be reduced by the liberal addition of a Collis gastroplasty, but the long-term consequences of acid-secreting mucosa left above the fundoplication in patients who have BE remain unclear. Patients suspected of having a short esophagus on the basis of a large hiatal hernia, stricture, or long-segment BE should be considered for a transthoracic approach to their fundoplication, as this affords good esophageal mobilization and may obviate the need for a gastroplasty. Surgeons must pay particular attention to their own and published results and continue to refine the operation to maximize the likelihood of a good outcome in this difficult group of patients. It is only with excellent control of reflux that any differences in the risk of progression to dysplasia and cancer become apparent, and significant, between medically and surgically treated patients.
Barrett Esophagus↗
Endoscopic mucosal resection and vagal-sparing esophagectomy for high-grade dysplasia and adenocarcinoma of the esophagus.
Once a rare tumor, adenocarcinoma of the esophagus is currently the cancer with the fastest rising incidence in America. In addition to the increasing prevalence of the disease, surveillance programs for patients with Barrett's have led to the identification of increasing numbers of patients with high-grade dysplasia or early-stage esophageal adenocarcinomas. Although traditional esophagectomy is curative in the majority of these patients, associated morbidity and mortality remains a hurdle for patient acceptance of the procedure. New endoscopic and surgical therapies offer the potential of decreased morbidity, but do not include a lymphadenectomy, and consequently, are not appropriate in patients that have a significant risk of lymph node metastases. Endoscopic mucosal resection allows precise determination of the depth of tumor invasion and facilitates accurate local staging of early esophageal cancers. A vagal-sparing esophagectomy accomplishes the goal of removing the diseased esophagus while minimizing the physiologic impact of an esophagectomy in patients with early-stage esophageal cancer.
Adenocarcinoma↗
En bloc vs transhiatal esophagectomy for stage T3 N1 adenocarcinoma of the distal esophagus.
HYPOTHESIS: En bloc esophagectomy (EBE) provides improved survival over transhiatal esophagectomy (THE) in patients with similarly sized transmural tumors (T3) and lymph node metastases (N1). DESIGN: A retrospective case-control study of 2 methods of esophageal resection for cancer. SETTING: University hospital (tertiary referral center for esophageal disease). PATIENTS: There were 49 patients (27 who underwent EBE and 22 who underwent THE) with similar T3 N1 disease and the following matched criteria: tumors of similar size and location, more than 20 lymph nodes in the surgical specimen, R0 resection, no previous chemotherapy or radiation therapy, and follow-up until death or for a minimum of 5 years. Main Outcome Measure Survival adjusted for differences in demographic and patient characteristics. RESULTS: The number of nodes harvested was greatest after EBE vs THE (median, 52 vs 29 [range, 21-85 vs 20-60]; P<.001). The median number of involved nodes was similar after EBE vs THE (median, 5 vs 7 [range, 1-19 vs 1-16]). The only 2 independent factors that affected survival in a Cox analysis were the number of involved lymph nodes (P =.01) and the type of resection (P =.03). Patients who underwent EBE had a survival benefit over those who underwent THE (P =.01). The survival benefit of EBE was seen only in patients with fewer than 9 involved lymph nodes (P<.001). CONCLUSION: En bloc esophagectomy confers a better survival than THE in patients with T3 N1 disease and fewer than 9 lymph node metastases.
Adenocarcinoma↗
Increased acid exposure in patients with gastroesophageal reflux disease influences cyclooxygenase-2 gene expression in the squamous epithelium of the lower esophagus.
HYPOTHESIS: Although genetic changes associated with the progression to Barrett esophagus and adenocarcinoma have been identified, changes in gene expression associated with gastroesophageal reflux disease have not been reported. We examined expression levels of several genes important in carcinogenesis and compared expression levels with alterations in esophageal acid exposure. PATIENTS, DESIGN, AND SETTING: Prospective analysis of 61 patients initially seen with reflux symptoms at a private academic hospital. INTERVENTIONS: Paired esophageal biopsy specimens of squamous epithelium 3 cm above the squamocolumnar junction. All patients had 24-hour pH monitoring performed. MAIN OUTCOME MEASURES: Cyclooxygenase (COX) 1, COX-2, thymidylate synthase, human telomerase reverse transcriptase (hTERT), Bcl-2 protein, survivin protein, secreted protein acidic and rich in cysteine (SPARC), tetraspan (TSPAN), and caudal-type homeobox transcription factor 2 (CDX2) messenger RNA expression analysis was performed on snap-frozen, microdissected tissue using a quantitative reverse transcriptase-polymerase chain reaction method. Linear regression and the Pearson product moment correlation were used to relate gene expression to parameters of the 24-hour pH record. RESULTS: Expression levels of COX-2 correlated positively with the 24-hour pH score (r = 0.25, P =.05). There was no correlation between the expression of other tested genes and esophageal acid exposure. There was also no significant increase in COX-2 expression in patients with esophagitis or in those who used nonsteroidal anti-inflammatory drugs. CONCLUSIONS: To our knowledge, these data provide among the first reported correlation of genetic changes and increased esophageal acid exposure in patients with gastroesophageal reflux symptoms. The changes in gene expression occur before any metaplastic changes in the tissue are apparent, and may in the future be useful in predicting which patients will progress through a metaplasia-dysplasia carcinoma sequence.
Adult↗
The prognostic importance of immunohistochemically detected node metastases in resected esophageal adenocarcinoma.
BACKGROUND: The number or ratio of lymph node metastases detected by hematoxylin & eosin (H&E) staining is the most important predictor of survival in esophageal cancer. The survival effect of lymph node metastases detected on immunohistochemistry (IHC) is controversial. My colleagues and I hypothesized that the extent of nodal disease determined by both H&E and IHC examination would more accurately predict survival than either technique alone. METHODS: The study population consisted of 37 patients who underwent en bloc esophagectomy as primary therapy for esophageal adenocarcinoma 5 or more years ago. All had mediastinal and upper abdominal lymphadenectomy. No patient received neoadjuvant or adjuvant therapy. Tissue blocks were sectioned for H&E staining to confirm the initial histology, and a second slide was stained with monoclonal antibodies AE1 and CAM 5.2, which are directed at a number of cytokeratin antigens. The slides were reviewed by an investigator blinded to clinical outcome. The effect of IHC staining on prognosis was assessed by comparing 5-year survival based on H&E and IHC findings. RESULTS: A total of 1,970 nodes were examined in the 37 patients. Routine H&E staining detected metastases in 29 patients (78%); the remaining 8 with N0 disease all survived at least 5 years after operation (median not reached). In the 29 patients with N1 disease, survival was 41% at 5 years. In 20 of the 29 N1 patients, metastases were detected by H&E in less than 10% of the nodes removed; 55% of the patients survived 5 years, and 39% survived 8 years. Nine of the 29 patients had metastases detected in more than 10% of the nodes removed, and all died at a median of 17 months. IHC staining was performed on the nodes from the 8 N0 patients and the 20 patients with less than 10% nodal involvement (a total of 28 patients). Additional nodal metastases, not identified on H&E examination, were found in 51 nodes from 17 patients (60.7%). Of the 8 patients who were node negative on H&E examination, 3 had metastases detected by IHC, and all survived 5 years or more free of disease. Of the 20 patients with less than 10% nodal metastases on H&E, 14 (70%) had additional metastases detected by IHC (median, 2 nodes per patient). When combined with the results of H&E staining, the node ratio remained less than 10% in 13 patients and exceeded 10% in 7. Survival in patients whose ratio remained less than 10% was significantly better than in those whose ratio exceeded 10% (actual 5-year survival, 77% vs 14%; chi2 = 4.662; p = 0.03). CONCLUSIONS: IHC staining techniques can identify nodal metastases missed by routine H&E examination in a large number of patients. The combination of H&E and IHC examination is useful in patients with less than 10% nodal involvement by H&E examination in that IHC detection of micrometastases allows classification into low-risk (> 75% survival) and high-risk (< 15% survival) groups. IHC-detected micrometastases are not of prognostic importance in N0 patients or those with greater than 10% nodal metastases on H&E.
Adenocarcinoma↗
Endoscopic mucosal resection as a staging technique to determine the depth of invasion of esophageal adenocarcinoma.
BACKGROUND: Endoscopic ablation and vagal-sparing esophagectomy offer the potential for reduced morbidity in patients with high-grade dysplasia or early esophageal adenocarcinoma, but neither includes a lymphadenectomy. Although adequate for intramucosal tumors, both are potentially inadequate for patients with submucosal tumor invasion given the high prevalence of nodal metastases with these lesions. Currently there is no test including endoscopic ultrasound that can accurately determine whether a small tumor is confined to the mucosa or has penetrated into the submucosa. The aim of this study was to compare the pathologic depth of invasion by endoscopic mucosal resection with findings and outcome after surgical resection to assess the accuracy and reliability of endoscopic mucosal resection for staging early esophageal adenocarcinoma. METHODS: From 2001 to 2003, 7 patients presented with small, endoscopically visible adenocarcinomas. All underwent endoscopic mucosal resection followed by surgical resection. RESULTS: Analysis of the resected specimens confirmed that the endoscopic mucosal resection had accurately determined the depth of tumor invasion in all patients, and had completely excised the lesion in all but 1 patient (86%). Lymph node dissection was included as part of the resection in 2 patients with submucosal invasion by endoscopic mucosal resection, and a vagal-sparing esophagectomy was used in the 5 patients with only intramucosal tumors. All patients are alive and disease-free at a median follow-up of 7 months. CONCLUSIONS: Endoscopic mucosal resection accurately determines the depth of tumor invasion, and should be used as a staging procedure in patients with early esophageal cancer when therapies that do not include a lymphadenectomy are considered.
Adenocarcinoma↗
Prevalence and risk factors for ischemia, leak, and stricture of esophageal anastomosis: gastric pull-up versus colon interposition.
BACKGROUND: Reports of esophageal anastomotic complications often involve more gastric than colonic reconstructions and are incomplete because of fragmented followup by physicians unfamiliar with the surgical procedure. STUDY DESIGN: Three hundred ninety-three consecutive esophagectomy patients had prevalence and risk factors determined for graft ischemia and anastomotic leak; 363 of these patients followed for more than 1 month (median 15 months) had prevalence and risk factors determined for anastomotic stricture. RESULTS: Conduit ischemia occurred in 36 (9.2%) and anastomotic leak in 43 patients (10.9%). Risk factor for ischemia was comorbid conditions requiring therapy (Odds ratio [OR]: 2.2 [95% CI 1.1-4.3]), and for leak were ischemia (OR: 5.5 [95% CI 2.5-12.1]), neoadjuvant therapy (OR: 2.2 [95% CI 1.1-4.5]), and comorbid conditions (OR: 2.1 [95% CI 1.1-3.9]). A stricture developed in 80 patients (22.0%). Risk factors were ischemia (OR: 4.4 [95% CI 2.0-9.6]), anastomotic leak (OR: 3.8 [95% CI 1.9-7.6]), and increasing preoperative weight (p = 0.022). The prevalence of ischemia was similar after gastric (10.4%) versus colonic (7.4%) reconstruction; leak and stricture were more common (14.3% versus 6.1%, p = 0.013, 31.3% versus 8.7%, p < 0.0001, respectively) and strictures were more severe (11.2% versus 2%, p = 0.001) after gastric pull-up. Patients free of ischemia and leak who developed stricture were more likely to have had a gastric pull-up (25% versus 7%, p < 0.0001). Dilatation was effective treatment in 93% of patients. CONCLUSIONS: After esophagectomy 10% of patients will develop conduit ischemia or an anastomotic leak and 22% will develop anastomotic stricture. Anastomotic leak and strictures are more common and the strictures are more severe after gastric pull-up compared with colon interposition. Dilatation is a safe and effective treatment.
Anastomosis, Surgical↗
Barrett's esophagus.
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Barrett Esophagus↗
Surgical management of hypertensive lower esophageal sphincter with dysphagia or chest pain.
Hypertensive lower esophageal sphincter (LES) is an uncommon manometric abnormality found in patients with dysphagia and chest pain, and is sometimes associated with gastroesophageal reflux disease (GERD). Preventing reflux by performing a fundoplication raises concerns about inducing or increasing dysphagia. The role of myotomy in isolated hypertensive LES is also unclear. The aim of this study was to determine the outcome of surgical therapy for isolated hypertensive LES and for hypertensive LES associated with GERD. Sixteen patients (5 males and 11 females), ranging in age from 39 to 89 years, with hypertensive LES (>26 mm Hg; i.e., >95th percentile of our control population) who had surgical therapy between 1996 and 1999 were reviewed. Patients with a diagnosis of achalasia and diffuse esophageal spasm were excluded. All patients had dysphagia or chest pain. Eight of 16 patients had symptoms of GERD, four had a type III hiatal hernia, and four had isolated hypertensive LES pain. Patients with hypertensive LES and GERD or type III hiatal hernia had a Nissen fundoplication, and those with isolated hypertensive LES had a myotomy of the LES with partial fundoplication. Outcome was assessed as follows: excellent if the patient was asymptomatic; good if symptoms were present but no treatment was required; fair if symptoms were present and required treatment; and poor if symptoms were unimproved or worsened. All patients were contacted by telephone for symptom assessment at a median of 3.6 years (range 3 to 6.1 years) after surgery. Patients with hypertensive LES and GERD or type III hiatal hernia had significantly lower LES pressure than those with isolated hypertensive LES (29.9 vs. 47.4 mm Hg; P=0.013). Dysphagia and chest pain were relieved in all patients at long-term follow up. Outcome was excellent in 10 of 16, good in 3 of 16, and fair in 3 of 16. All patients but one were satisfied with their outcome. Patients with hypertensive LES are a heterogeneous group in regard to symptoms and etiology. Treatment of patients with hypertensive LES should be individualized. A Nissen fundoplication for hypertensive LES with GERD or type III hiatal hernia relieves dysphagia and chest pain suggesting reflux as an etiology. A myotomy with partial fundoplication for isolated hypertensive LES relieves dysphagia and chest pain suggesting a primary sphincter dysfunction.
Adult↗