Visceral hypersensitivity is associated with GI symptom severity in functional GI disorders: consistent findings from five different patient cohorts.

OBJECTIVE: Our aim was to evaluate the association between visceral hypersensitivity and GI symptom severity in large cohorts of patients with functional GI disorder (FGID) and to adjust for psychological factors and general tendency to report symptoms. DESIGN: We included five cohorts of patients with FGIDs (IBS or functional dyspepsia; n=1144), who had undergone visceral sensitivity testing using balloon distensions (gastric fundus, descending colon or rectum) and completed questionnaires to assess GI symptom severity, non-GI somatic symptoms, anxiety and depression. Subjects were divided into sensitivity tertiles based on pain/discomfort thresholds. GI symptom severity was compared between sensitivity tertiles in each cohort and corrected for somatisation, and anxiety and depression. RESULTS: In all five cohorts, GI symptom severity increased gradually with increasing visceral sensitivity, with significant differences in GI symptom severity between the sensitivity tertiles (p<0.0001), with small to medium effect sizes (partial η2: 0.047-0.11). The differences between sensitivity tertiles remained significant in all cohorts after correction for anxiety and depression, and also after correction for non-GI somatic symptom reporting in all of the cohorts (p<0.05). CONCLUSIONS: A gradual increase in GI symptom severity with increasing GI sensitivity was demonstrated in IBS and functional dyspepsia, which was consistent across several large patient groups from different countries, different methods to assess sensitivity and assessments in different parts of the GI tract. This association was independent of tendency to report symptoms or anxiety/depression comorbidity. These findings confirm that visceral hypersensitivity is a contributor to GI symptom generation in FGIDs.

Ablation of Tacr2 in mice leads to gastric emptying disturbance.

BACKGROUND: Tacr2 is one of the G protein-coupled receptors(GPCRs) that mediate the biological actions of tachykinins. It is abundantly expressed in the gastrointestinal (GI) system and is thought to play an important role in GI motility, secretion, and visceral sensitivity. Previously, the physiological and pathophysiological functions of Tacr2 were mainly studied using Tacr2 selective agonists or antagonists. Here, we seek to investigate the effect of Tacr2 disruption in mice to provide further insights. METHODS: The Tacr2 knockout mice were generated by homologous recombination and the phenotypic changes of the Tacr2-null mice were analyzed and compared with their wild type (wt) littermates. KEY RESULTS: Increased food retention was detected in Tacr2-/- mice. The stomach of Tacr2-/- mice had thinner muscularis externa and less neurons in the myenteric plexus. The stomach and small intestine exhibited longer duration of electrical field stimulation (EFS)-induced inhibition in the gastric fundus and decreased frequency of migrating motor complex (MMC), respectively. Neuronal nitric oxide synthase (nNOS) and vasoactive intestinal polypeptide (VIP) were significantly up-regulated due to Tarc2 deficiency, contributing to enhanced nitric oxide (NO) signaling in the stomach of Tacr2-/- mice. Intraperitoneal application of 7-nitroindazole (7-NI) to Tacr2-/- mice effectively relieved the gastric emptying disturbance. Moreover, Creb and NF-κB signalings were involved in the regulation of these physiological changes initiated by Tacr2 deficiency. CONCLUSIONS & INFERENCES: Tacr2 negatively regulated the expression of nNOS and VIP both in vivo and in vitro. Its ablation in mice elevated the expression of nNOS and VIP, enhanced NO signaling and changed the Creb and NF-κB signalings, finally leading to the gastric emptying disturbance of Tacr2-/- mice.

[Paradoxical sphincters and cardinal continence function of the gastric fundus]. / Die paradoxen Sphinkteren und die kardinale Kontinenzfunktion des Magenfundus.

Gastroesophageal reflux disease is a common disorder in humans and has been treated for the last 67 years using fundoplication. However, treatment results have generally not been satisfactory. Physiological and anatomic findings must be taken into account to improve the therapy technique. In this article, these are described using the example of paradoxical sphincters and the effect of NO signal molecules in the gastrointestinal tract.

Impairment of gastric accommodation induced by water-avoidance stress is mediated by 5-HT2B receptors.

BACKGROUND: Psychological stress has been shown to impair gastric accommodation (GA), but its mechanism has not been elucidated. This study was conducted to clarify the role of 5-HT2B receptors in a guinea pig model of stress-induced impairment of GA. METHODS: Gastric accommodation was evaluated by measuring the intrabag pressure in the proximal stomach after administration of a liquid meal. The guinea pigs were subjected to water-avoidance stress. The role of 5-HT2B receptors in impairment of GA was investigated by administering a 5-HT2B receptor agonist (BW723C86) or antagonist (SB215505), the traditional Japanese medicine rikkunshito (RKT), a muscarinic M3 receptor antagonist (1,1-dimethyl-4-diphenylacetoxypiperidium iodide [4-DAMP]), or a nitric oxide synthase inhibitor (Nω -nitro-L-arginine [L-NNA]). KEY RESULTS: In normal animals, liquid meal-induced GA was inhibited by BW723C86, but was not affected by SB215505. The inhibition of GA by BW723C86 was reversed by co-administration of 4-DAMP. Compared to normal animals, GA in stressed animals was significantly inhibited. SB215505 and RKT significantly suppressed stress-induced impairment of GA. After meal administration, the level of cyclic guanosine monophosphate in gastric fundus tissue increased by approximately twofold in normal animals, but did not change in stressed animals. The inhibition of GA by L-NNA was suppressed by SB215505 or RKT. At a dose that did not affect GA in normal animals, BW723C86 exacerbated the impairment of GA in stressed animals. CONCLUSIONS AND INFERENCES: Stress-induced impairment of GA may be mediated by an increased responsiveness of 5-HT2B receptors, and activation of the 5-HT2B receptor signaling pathway may have an inhibitory effect on nitric oxide function.

Noninflammatory upregulation of nerve growth factor underlies gastric hypersensitivity induced by neonatal colon inflammation.

Gastric hypersensitivity is one of the key contributors to the postprandial symptoms of epigastric pain/discomfort, satiety, and fullness in functional dyspepsia patients. Epidemiological studies found that adverse early-life experiences are risk factors for the development of gastric hypersensitivity. Preclinical studies found that neonatal colon inflammation elevates plasma norepinephrine (NE), which upregulates expression of nerve growth factor (NGF) in the muscularis externa of the gastric fundus. Our goal was to investigate the cellular mechanisms by which NE upregulates the expression of NGF in gastric hypersensitive (GHS) rats, which were subjected previously to neonatal colon inflammation. Neonatal colon inflammation upregulated NGF protein, but not mRNA, in the gastric fundus of GHS rats. Western blotting showed upregulation of p110γ of phosphatidylinositol 4,5-bisphosphate 3-kinase (PI3K), phosphoinositide-dependent kinase-1 (PDK1), pAKT(Ser473), and phosphorylated 4E-binding protein (p4E-BP1)(Thr70), suggesting AKT activation and enhanced NGF protein translation. AKT inhibitor MK-2206 blocked the upregulation of NGF in the fundus of GHS rats. Matrix metalloproteinase 9 (MMP-9), the major NGF-degrading protease, was suppressed, indicating that NGF degradation was impeded. Incubation of fundus muscularis externa with NE upregulated NGF by modulating the protein translation and degradation pathways. Yohimbine, an α2-adrenergic receptor antagonist, upregulated plasma NE and NGF expression by activating the protein translation and degradation pathways in naive rats. In contrast, a cocktail of adrenergic receptor antagonists suppressed the upregulation of NGF by blocking the activation of the protein translation and degradation pathways. Our findings provide evidence that the elevation of plasma NE induces NGF expression in the gastric fundus.

The normoglycaemic biobreeding rat: a spontaneous model for impaired gastric accommodation.

OBJECTIVE: Impaired gastric accommodation is reported in patients with functional dyspepsia (FD). Previous findings in postinfectious patients with FD suggest that low-grade inflammation and dysfunction of nitrergic nerves play a role in impaired accommodation. To date, spontaneous animal models to study the relationship between these changes are lacking. We hypothesise that the normoglycaemic BioBreeding diabetes-prone (BB-DP) rat provides an animal model of inflammation-induced impaired gastric motor function. DESIGN: Control diabetes-resistant biobreeding, normoglycaemic and hyperglycaemic BB-DP rats were sacrificed at the age of 30, 70 and 220 days and gastric fundus tissue was harvested to study nitrergic motor control, inflammation and expression of neuronal isoform of nitric oxide synthase (nNOS) and inducible isoform of nitric oxide synthase (iNOS). Nutrient-induced changes in intragastric pressure (IGP) were measured in normoglycaemic BB-DP rats to study accommodation. RESULTS: No differences in nitrergic function and inflammation were observed between BB-DP and control rats at 30 days. The nitrergic component of the fundic muscle relaxation was reduced in BB-DP rats of 70 and 220 days. This was accompanied by a significant loss of nNOS proteins. IGP significantly increased during nutrient infusion in BB-DP rats of 220 days, indicating impaired accommodation. Infiltration of polymorphonuclear cells, increased myeloperoxidase activity and increased expression of iNOS was observed in the fundic mucosa and muscularis propria of 70-day-old and 220-day-old BB-DP rats. CONCLUSIONS: BB-DP rats of 220 days display altered fundic motor control and impaired accommodation, which is least partially explained by loss of nitrergic function. This may be related to inflammatory changes in the neuromuscular layer, suggesting that normoglycaemic BB-DP rats provide a spontaneous model for inflammation-induced impaired gastric accommodation.

[Paradoxical sphincters in the abdomen]. / Paradoxe Sphinkteren im Abdomen.

Nitric oxide molecules serve as neurotransmitters to relax smooth muscle tension in many parts of the body. In humans and other mammals they play an important role for correct smooth muscle function in unusual locations. We previously described this mechanism (Stelzner, Chirurg. doi:10.1007/s00104-014-2777-z, 2014) using the occlusive mechanism of the upper and lower esophageal sphincters as an example. Cells producing nitric oxide can be found in the gastric fundus, the anorectal continence organ, vesicourethraltract and also in the uterine cervix in the final trimester of pregnancy. In all these locations they serve as elements of anatomical sphincter structures that have a paradoxical function. These observations confirm the points made in the introduction of this article on the stretch sphincter mechanism of the lower esophageal sphincter and the treatment of gastroesophageal reflux disease by retensioning of the esophagus in the diaphragmatic hiatus. In particular, high-resolution esophageal manometry of the lower esophageal sphincter can easily detect every functional disturbance caused by gastric plication and such changes were to be expected based on what we described in articles I and II.

Contractile profile of esophageal and gastric fundus strips in experimental doxorubicin-induced esophageal atresia.

Esophageal atresia (EA) is characterized by esophageal and gastric motility changes secondary to developmental and postsurgical damage. This study evaluated the in vitro contractile profile of the distal esophagus and gastric fundus in an experimental model of EA induced by doxorubicin (DOXO). Wistar pregnant rats received DOXO 2.2 mg/kg on the 8th and 9th gestational days. On day 21.5, fetuses were collected, sacrificed, and divided into groups: control, DOXO without EA (DOXO-EA), and DOXO with EA (DOXO+EA). Strips from the distal esophagus and gastric fundus were mounted on a wire myograph and isolated organ-bath system, respectively, and subjected to increasing concentrations of carbamylcholine chloride (carbachol, CCh). The isolated esophagus was also stimulated with increasing concentrations of KCl. In esophagus, the concentration-effect curves were reduced in response to CCh in the DOXO+EA and DOXO-EA groups compared to the control group (P<0.05). The maximum effect values (Emax) for DOXO+EA and DOXO-EA were significantly lower than control (P<0.05), but the half-maximal effective concentration (EC50) values were not significantly different when the three groups were compared (P>0.05). In response to KCl, the distal esophagus samples in the three groups were not statistically different with regard to Emax or EC50 values (P>0.05). No significant difference was noted for EC50 or Emax values in fundic strips stimulated with CCh (P>0.05). In conclusion, exposure of dams to DOXO during gestation inhibited the contractile behavior of esophageal strips from offspring in response to CCh but not KCl, regardless of EA induction. The gastric fundus of DOXO-exposed offspring did not have altered contractile responsiveness to cholinergic stimulation.

A preliminary observation of weight loss following left gastric artery embolization in humans.

BACKGROUND/OBJECTIVES: Embolization of the left gastric artery (LGA), which preferentially supplies the gastric fundus, has been shown to produce weight loss in animal models. However, weight loss after LGA embolization in humans has not been previously established. The aim of this study was to evaluate postprocedural weight loss in patients following LGA embolization. SUBJECTS/METHODS: A retrospective analysis of the medical records of patients who underwent LGA embolization for upper gastrointestinal (GI) bleeding was performed. Postprocedural weight loss in this group was compared to a control group of patients who had undergone embolization of other arteries for upper GI bleeding. RESULTS: The experimental group (N = 19) lost an average of 7.3% of their initial body weight within three months of LGA embolization, which was significantly greater than the 2% weight loss observed in the control group (N = 28) (P = 0.006). No significant differences were seen between the groups in preprocedural body mass index (BMI), age, postprocedural care in the intensive care unit, history of malignancy, serum creatinine, or left ventricular ejection fraction. CONCLUSIONS: The current data suggest that body weight in humans may be modulated via LGA embolization. Continued research is warranted with prospective studies to further investigate this phenomenon.

Effect of liquid meals with different volumes on gastroesophageal reflux disease.

BACKGROUND AND AIM: Patients with gastroesophageal reflux disease (GERD) are often advised to avoid large meals, based on their complaints of increased symptoms after eating too much, and epidemiological evidence of a link between high volume intake and the presence of GERD. However, the precise effects of meal volume on gastroesophageal reflux have not been well studied. We aimed to clarify the effect of meal volume on acid regurgitation and symptoms in patients with GERD. METHODS: Fifteen patients (10 female, 5 male; mean 54 ± 10 years old) with GERD were studied twice each in random order, during 24 h ambulatory pH monitoring. On one day, they consumed a 600 mL liquid test meal three times (breakfast, lunch, and dinner), and on the other, they consumed a 300 mL test meal six times (breakfast, snack, lunch, snack, dinner, and snack). Gastric fundus and antral areas and antral contractions were measured by transabdominal ultrasound. Symptoms were recorded using questionnaires. RESULTS: During the 600 mL regimen, there were more reflux episodes (17 ± 4 vs 10 ± 2, P = 0.03) and a greater total acid reflux time (12.5 ± 5.9% vs 5.5 ± 3.6%; P = 0.045) than the 300 mL regimen. Both the cross-sectional area of the gastric fundus (P = 0.024) and the number of antral contractions (P = 0.014) were greater for the 600 mL regimen. CONCLUSIONS: Larger meals are associated with distension of the gastric fundus and an increase in gastroesophageal reflux when compared with smaller, more frequent meals.

Gastric and lower esophageal sphincter pressures during nausea: a study using visual motion-induced nausea and high-resolution manometry.

Nausea is the subjective unpleasant sensation that immediately precedes vomiting. Studies using barostats suggest that gastric fundus and lower esophageal sphincter (LES) relaxation precede vomiting. Unlike barostat, high-resolution manometry allows less invasive, detailed measurements of fundus pressure (FP) and axial movement of the gastroesophageal junction (GEJ). Nausea was induced in 12 healthy volunteers by a motion video and rated on a visual analog scale. FP was measured as the mean value of the five pressure channels that were clearly positioned below the LES. After intubation, a baseline (BL) recording of 15 min was obtained. This was followed by presentation of the motion video (at least 10 min, maximum 20 min) followed by 30 min recovery recording. Throughout the experiment we recorded autonomic nervous system (ANS) parameters [blood pressure, heart rate (HR), and cardiac vagal tone (CVT), which reflects efferent vagal activity]. Ten out of 12 subjects showed a drop in FP during peak nausea compared with BL (-4.0 ± 0.8 mmHg; P = 0.005), and 8/10 subjects showed a drop in LES pressure (-8.8 ± 2.5 mmHg; P = 0.04). Peak nausea preceded peak fundus and LES pressure drop. Nausea was associated with configuration changes at the GEJ such as LES shortening and esophageal lengthening. During nausea we observed a significantly increased HR and decreased CVT. In conclusion, nausea is associated with a drop in fundus and LES pressure, configuration changes at the GEJ as well as changes in the ANS activity such as an increased sympathetic tone (increased HR) and decreased parasympathetic tone (decreased CVT).

[Adaptive changes of parietal cells of the fundal glands of the stomach after total colonectomy].

The researchers are investigated in 32 white male, rats by means of electron-microscopic methods and morphometric analysis. The sharp reduction acid produceds functions parietal hutches after total colonectomy, her (its) stability at early periods after operation are certainly conditioned inflammatory-distrofic change on the part of secretory membranes, and particularly mitochondria of the device.

Laparoscopic sleeve gastrectomy: symptoms of gastroesophageal reflux can be reduced by changes in surgical technique.

BACKGROUND: Bariatric surgery is the most effective treatment for gastro-esophageal reflux disease (GERD) in obese patients, with the Roux-en-Y gastric bypass being the technique preferred by many surgeons. Published data reporting the results of laparoscopic sleeve gastrectomy (LSG) in patients with GERD are contradictory. In a previous observational study, we found that relative narrowing of the distal sleeve, hiatal hernia (HH), and dilation of the fundus predispose to GERD after LSG. In this study, we evaluated the effects of standardization of our LSG technique on the incidence of postoperative symptoms of GERD. METHODS: This was a concurrent cohort study. Patients who underwent bariatric surgery at our center were followed prospectively. LSG was performed in all patients in this series. RESULTS: A total of 234 patients underwent surgery. There were no cases of death, fistula, or conversion to open surgery. All 134 patients who completed 6-12 months of postoperative follow-up were evaluated. Excess weight loss at 1 year was 73.5%. In the study group, 66 patients (49.2%) were diagnosed with GERD preoperatively, and HH was detected in 34 patients (25.3%) intraoperatively. HH was treated by reduction in three patients, anterior repair in 28, and posterior repair in three. Only two patients (1.5%) had symptoms of GERD at 6-12 months postoperatively. CONCLUSIONS: Our results confirm that careful attention to surgical technique can result in significantly reduced occurrence of symptoms of GERD up to 12 months postoperatively, compared with previous reports of LSG in the literature.

Un insólito caso de síndrome de Kartagener / An unusual case of kartagener syndrome

No disponible

Gastric dysmotility after liquid bolus ingestion in systemic sclerosis: an ultrasonographic study.

Gastric involvement appears quite commonly in systemic sclerosis (SSc). The aim of this study was to evaluate gastric wall motility using ultrasonography, a noninvasive method able to track both filling and emptying of fundus and antrum. The study was performed in 20 SSc patients and 20 healthy control subjects. Gastric filling and emptying were evaluated by transabdominal ultrasonography, measuring changes in fundus and antral areas over a 1-h period after ingestion of a liquid bolus (500 ml of mineral water). Areas of both gastric fundus and antrum at basal evaluation were found to be smaller in SSc patients than in healthy controls. Gastric filling was significantly reduced after ingestion of liquid bolus. Gastric emptying was delayed both in fundus and antrum. No significant differences of gastric wall motility have been observed in different subsets of SSc patients. Our findings show that gastric dysmotility is frequent and severe in SSc patients, contributing to the gastrointestinal disturbances which are very common in this disease.

Review of the pathogenesis, diagnosis, and management of type I gastric carcinoid tumor.

Gastric carcinoid tumors comprise 7% of all gastrointestinal carcinoids and have significantly increased in incidence over the past few decades. Seventy to 80% of gastric carcinoids are type I, which usually are clinically asymptomatic and found incidentally at endoscopic evaluation for abdominal pain or anemia. In this review, advances in understanding the pathophysiology of type I gastric carcinoid are highlighted. In addition, various current diagnostic and treatment options are discussed. Although type I carcinoids generally hold a benign course, rigorous investigation is needed to ensure accurate diagnosis and optimal treatment. This includes appropriate diagnostic procedures and imaging and accurate staging of tumor. Tumor size, depth of invasion, presence of metastasis, and the tumor's gastrin dependency dictate treatment options. Appropriate treatments can consist of endoscopic resection, antrectomy, medical management, or frequent follow-up. This article provides a systematic method of evaluating and treating type I gastric carcinoid.

Changes in the structure and function of ICC networks in ICC hyperplasia and gastrointestinal stromal tumors.

BACKGROUND & AIMS: Gastrointestinal stromal tumors (GISTs) express the receptor tyrosine kinase c-kit. Approximately 90% of GISTs have gain-of-function mutations in the Kit gene, which leads to its constitutive activation and drives malignant behavior of GISTs. Interstitial cells of Cajal (ICC) express c-kit; however, it is unknown whether uncontrolled hyperplasia of ICC is responsible for GISTs. Here, we sought to determine whether gain-of-function mutations in Kit lead to hyperplasia of all classes of ICC, whether ICC hyperplasia begins before birth, and whether functional defects occur in ICC hyperplasia or the development of GISTs. METHODS: Heterozygous mutant Kit(V558Delta)/+ mice that develop symptoms of human familial GISTs and prematurely die from pathology of the gastrointestinal tract were utilized and compared with wild-type controls. C-kit-immunohistochemistry and intracellular electrical recording of spontaneous and nerve-evoked activity were applied to examine the density and functionality of ICC in these mutants. RESULTS: There was considerable hyperplasia in all classes of ICC throughout the GI tract of Kit(V558Delta)/+ mice, except for ICC in the deep muscular plexus of the intestine. Spontaneous electrical activity and postjunctional neural responses in hyperplastic ICC tissues appeared normal but were up-regulated in the cecum, where GISTs were commonly found. CONCLUSIONS: Kit gain-of-function leads to hyperplasia of most classes of ICC throughout the GI tract. ICC retain normal pacemaker function and enteric neural responses well after development of hyperplasia.

Weight loss after laparoscopic adjustable gastric banding is not caused by altered gastric emptying.

BACKGROUND: In order to know the role of gastric emptying in the mechanism of weight loss and early satiety after a restrictive surgical procedure for treatment of morbid obesity, a consecutive series of patients were scintigraphically investigated before and after laparoscopic adjustable gastric banding. METHODS: Sixteen patients undergoing laparoscopic adjustable gastric banding underwent preoperatively, and at 6 months postoperatively, a gastric emptying study (solid meal and single isotope). Esophageal retention time, lag phase, peak activity time, gastric emptying rate, fundus emptying rate, and weight loss were recorded. Upper GI symptom assessment was carried out by using a standardized questionnaire. Gastric emptying parameters were correlated with the upper GI symptoms. RESULTS: Gastric band placement showed no significant influence on postoperative gastric emptying rate [median % (interquartile range): 42 (23.3-59) preoperatively vs 38 (31-71) postoperatively and fundus emptying rate: 59(37-91) preoperatively vs 70 (53-89) postoperatively]; however, an increase in early satiety was found. Neither gastric emptying rate nor fundus emptying rate showed a relation with early satiety or weight loss. Furthermore, no correlation was found between early satiety and lag phase, esophageal retention time, start of activity, and peak activity time in proximal stomach. CONCLUSION: Laparoscopic adjustable gastric banding seems not to affect gastric emptying. Neither a relation between postoperative gastric emptying rate and weight loss nor between early satiety and weight loss was found. Therefore, it is unlikely that gastric emptying plays a role in the mechanism of weight loss following laparoscopic adjustable gastric banding.

Prokinetics and fundic relaxants in upper functional GI disorders.

Gastrointestinal prokinetics are a heterogeneous class of drugs that stimulate smooth muscle contractions to enhance gastric emptying and intestinal transit. Recently studied prokinetics include antidopaminergic agents (itopride), serotonergic agents (tegaserod and others), and motilin receptor agonists and ghrelin receptor agonists (mitemcinal, TZP101). It has been difficult to establish symptomatic benefit with prokinetic drugs in gastroparesis and functional dyspepsia, because of pathophysiological heterogeneity of the patient populations, a lack of well-accepted endpoints, and inconsistent relationships between changes in motor function and symptomatic outcome. Fundic relaxant drugs are a recent different approach to treatment of gastric motility disorders. Recently studied drugs include drugs under investigation including nitrates, serotonin reuptake blockers, 5-HT(1A) receptor agonists (buspirone and R137696), and muscarinc M1/M2 receptor antagonists (acotiamide or Z-338).

Does previous fundoplication alter the surgical approach to esophageal adenocarcinoma?

OBJECTIVE: The primary aim of this study was to test the widespread assumption that the viability of the gastric fundus is compromised by fundoplication, thereby limiting the use of stomach to reconstruct the upper gastrointestinal tract after esophageal resection. METHODS: Between February 1991 and February 2006, a consecutive series of 142 patients with esophageal adenocarcinoma (EADC) underwent esophageal resection. To reconstruct the upper gastrointestinal tract, all patients had a narrow gastric tube (greater curvature of stomach based on the right gastroepiploic artery) transposed through the posterior mediastinum to the left neck where an anastomosis to the cervical esophagus was performed. From a prospective database, 15 patients were identified to have undergone an 'open' fundoplication (transabdominal Nissen, n=11; transthoracic Belsey, n=4) from 12 to 23 years earlier. Outcomes were compared between patients with EADC who had undergone previous fundoplication, and patients with EADC who never had antireflux surgery. RESULTS: Gastric transposition and cervical esophagogastrostomy were technically feasible in all patients. No significant differences in outcome were found between patient groups. Gastric necrosis developed in only one patient, who had not undergone previous fundoplication. Anastomotic leak rates after esophageal resection and reconstruction were not statistically different based on whether patients had undergone previous fundoplication (2/15, 13.3%) or not (16/127, 12.6%; p=0.99). CONCLUSIONS: With careful attention to surgical technique, previous fundoplication does not preclude the use of stomach to reconstruct the foregut after esophageal resection, refuting the notion that previous antireflux surgery is a relative contraindication to, or alters the approach to esophageal cancer surgery.