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J Thorac Cardiovasc Surg 2007;134:1284-1291
© 2007 The American Association for Thoracic Surgery

General Thoracic Surgery

Impact of obesity on outcomes in the management of localized adenocarcinoma of the esophagus and esophagogastric junction

Laura A. Healy, BSc, Aoife M. Ryan, BSc, Bussa Gopinath, FRCS, Suzanne Rowley, MSc, Patrick J. Byrne, PhD, John V. Reynolds, MD*

Departments of Clinical Surgery, St James’s Hospital, and Trinity College Dublin, Dublin 8, Ireland.

Received for publication December 12, 2006; revisions received May 16, 2007; accepted for publication June 1, 2007.

* Address for reprints: John V. Reynolds, MD, Department of Clinical Surgery and Dublin Molecular Medicine Center, Trinity Center for Health Sciences, St James’s Hospital, Dublin 8, Ireland. (Email: reynoljv{at}tcd.ie).


   Abstract
Top
 Abstract
Introduction
 Materials and Methods
 Statistical Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
Objective: Obesity trends in the Western world parallel the increased incidence of adenocarcinoma of the esophagus and esophagogastric junction. The implications of obesity on standard outcomes in the management of localized adenocarcinoma, particularly operative risks, have not been systematically addressed.

Methods: This retrospective analysis of prospectively collected data included 150 consecutive patients (36 [24%] obese [body mass index > 30] and 114 nonobese), of whom 43 were normal weight (body mass index 20–25) and 71 were overweight (body mass index 25–30). Eighty-one patients underwent multimodal therapy. The primary end points were in-hospital mortality and morbidity, and median and overall survivals.

Results: Thirty of 36 obese patients (84%) had a body mass index from 30 to 35. Compared with those of the nonobese cohort, obese patients had significantly increased respiratory complications (P = .037), perioperative blood transfusions (P = .021), anastomotic leaks (P = .009), and length of stay (P = .001), but no difference in mortality (P = .582) or major respiratory complications (P = .171). Median and overall survivals were equivalent (P = .348) in both groups.

Conclusions: Obesity was associated with increased respiratory complications and anastomotic leak rates but not with major respiratory complications, mortality, or survival. These outcomes suggest that the added risks of obesity on standard outcomes in esophageal cancer surgery are modest and should not independently have a significant impact on risk assessment in esophageal cancer management.

Abbreviations and Acronyms ARDS = acute respiratory distress syndrome; BMI = body mass index; TRG = tumor regression grade


   Introduction
Top
 Abstract
 Introduction
Materials and Methods
 Statistical Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
The pattern of esophageal cancer in Europe and North America has changed dramatically in recent decades, with a marked increase in the incidence of adenocarcinoma of the esophagus and esophagogastric junction.1Go The explanation for this increase is unclear, but several risk factors, including chronic gastroesophageal reflux disease, obesity/diet, and Helicobacter pylori eradication, are plausibly linked with this emerging trend.1,2Go Increasing epidemiologic evidence strongly links obesity and both the incidence of adenocarcinoma at these sites and death from this cancer.3-9Go

Consequently, the esophageal surgeon today is presented increasingly with the challenge of managing obese patients with adenocarcinoma of the esophagus or junction. The risk of operative mortality is up to 10%, with an approximate 50% risk of morbidity. Some evidence suggests that these risks may be further increased by neoadjuvant therapy, particularly combination chemotherapy and radiation therapy.10-12Go The management of localized disease has a major impact on quality of life over several months.13,14Go Studies of the implications of obesity, defined by World Health Organization criteria15Go as a body mass index (BMI) of greater than 30 kg/m2, are therefore important, particularly with regard to risk assessment for esophageal surgery. A combination of factors, including the association of obesity with existing comorbidities and medical complications, the complexity and duration of anesthesia and surgery, and insulin resistance, hormonal alterations, and chronic inflammation,16Go permit the speculative thesis that obesity may increase the incidence of complications.

The principal risks after esophagectomy relate to respiratory complications. Intuitively, obese patients may be at higher risk, because pulmonary function in obese patients is characterized by reductions in functional residual capacity, expiratory reserve volume, and alveolar oxygen partial pressure, and an increase in the alveolar–arterial oxygen difference.17,18Go The obese patient may consequently be more vulnerable to significant hypoxia from common postoperative problems, such as atelectasis. Abnormalities in control of breathing are also common, obstructive sleep apnea may occur in up to 40% of men with morbid obesity, and obstructive hypoventilation syndrome may also occur.19Go Intraoperative or postoperative ventilation may be impaired by reduced compliance of the lung and chest wall and an increase in airway resistance. Moreover, when ventilator support is required postoperatively, weaning may be delayed because of this reduced chest wall compliance, and obese patients compared with nonobese patients have an up to a 5-fold increase in oxygen uptake when changing from positive pressure ventilation to spontaneous breathing as a result of the increased work of breathing.16,17Go

Notwithstanding theoretic concerns, there is currently no reported systematic assessment of the relationship between obesity and standard outcomes in the management of localized cancer of the esophagus and esophagogastric junction. We report the experience of this unit and highlight the largely equivalent outcomes at this time between obese and nonobese cohorts.


   Materials and Methods
Top
 Abstract
 Introduction
 Materials and Methods
Statistical Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 
We performed a retrospective analysis of a prospectively compiled database of patients with histologically proven adenocarcinoma of the esophagus or esophagogastric junction who underwent surgery in St James Hospital, Dublin, between January of 1998 and December of 2005. This study was approved by the hospital’s ethics committee. Severely malnourished patients with a BMI less than 20 kg/m2 (n = 5) and patients who underwent an emergency esophagectomy were excluded from the analysis. Preoperative weight and height were used to calculate BMI. The preoperative medical comorbidities and presenting symptoms were noted, as well as the reported and actual weight loss at time of diagnosis. The patients’ age, cigarette and alcohol consumption, performance status, initial routine blood results, and pulmonary function test scores were also noted. Obesity was defined as a BMI greater than 30 kg/m2 per World Health Organization and National Institutes of Health Clinical Guidelines on the Identification, Evaluation, and Treatment of Overweight and Obesity in Adults.15,20Go

All patients had localized disease according to clinical, endoscopic, and computed tomography assessments. Endoscopic ultrasound was not routinely used. Fluorodeoxyglucose–positron emission tomography scanning has been routinely used since 2004. By using computed tomography criteria, the mediastinal, left gastric, and celiac lymph nodes were classified as N1 (invaded) if the maximal transverse diameter of these nodes was larger than 1 cm. Localized disease was defined as T1-3, N0-1. All tumors of the esophagogastric junction were assigned as type I, II, or III, per Siewert and Stein.21Go Type I is adenocarcinoma of the distal esophagus, usually arising in specialized intestinal metaplasia; type II is a true adenocarcinoma of the cardia arising immediately at the esophagogastric junction; and type III is a subcardial gastric carcinoma infiltrating the esophagogastric junction and distal esophagus from below.

Patients with type I and II tumors were considered for multimodal therapy involving a regimen of chemotherapy (cisplatin and fluorouracil) and radiation therapy (40–44 Gy in 15–20 fractions) as previously described.22Go The majority (97%) of patients undergoing an esophagectomy had a thoracotomy as a component of their surgical management, combined with the following: an abdominal and neck exploration (3-stage) for mid and upper-esophageal cancers or cancer arising in long-segment Barrett’s esophagus, an abdominal exploration (2-stage) for most lower third and junctional tumors, or a total gastrectomy for junctional tumors with significant gastric extension (type III). All intrathoracic and cervical anastomoses were performed with interrupted single-layer 3-0 polydioxanone (Ethicon, Dublin, Ireland). A 2-field lymphadenectomy (abdominal and thoracic) was performed in all transthoracic cases. The length of the operation, intraoperative blood loss, and blood products given were all noted.

Unit protocol states that all patients receive epidural analgesia, be extubated immediately after surgery, and be managed in a high-dependency unit. All patients are fed enterally through a needle catheter jejunostomy from 12 hours postoperatively. A Gastrografin contrast study is performed routinely on day 8 postoperatively before initiating oral fluids. Throughout the hospitalization and at the 3-month follow-up, a dietitian monitored nutritional intake, complications, and body weight changes.

All complications from surgery to discharge from hospital were prospectively documented. Respiratory failure was defined as the requirement for mechanical ventilation more than 24 hours after surgery. Acute respiratory distress syndrome (ARDS) and multiple organ failure were defined per Bone and colleagues,23Go sepsis required evidence of systemic inflammatory response syndrome with microbiological evidence of infection, and pneumonia required positive sputum cultures or clear clinical and radiographic evidence of consolidation.

Major respiratory complications for the purpose of this analysis were defined as pneumonia, empyema, respiratory failure, and ARDS. Any patient who experienced more than 1 major complication was only included in the analysis once.

The tumor stage was defined according to the TNM staging system and the American Joint Committee on Cancer classification.24Go Fat-clearing methods were not used to increase lymph node yield. The definition of a curative resection was that all visible tumor was removed and that proximal, distal, and circumferential margins were free of tumor on histologic examination. In patients undergoing neoadjuvant therapy, the extent of residual carcinoma in the esophagectomy specimen was assigned to 1 of 5 tumor regression grade (TRG) categories per Mandard and colleagues:25Go TRG1 represents fibrosis within the esophageal wall with no identifiable residual cancer cells, pathological complete response; TRG2 represents rare residual cancer cells scattered throughout the fibrosis; TRG3 represents an increase in the number of residual cancer cells, but fibrosis still predominant; TRG4 represents residual cancer cells outgrowing fibrosis; and TRG5 represents a complete absence of regression change. A TRG of 1 or 2 is deemed a good response, and a TRG of 3 to 5 is deemed a poor response.


   Statistical Methods
Top
 Abstract
 Introduction
 Materials and Methods
 Statistical Methods
Results
 Discussion
 Limitations
 Conclusions
 References
 
Statistical analysis was performed using the Statistical Package for the Social Sciences Version 11.0 for Windows (SPSS Inc, Chicago, Ill). Analysis of variance was used to identify significant differences between BMI categories. Postoperative complications were compared using univariate chi-square tests. The primary comparison was between obese and nonobese cohorts, but some comparisons were also made between 3 cohorts: obese, overweight, and normal weight. Multinominal logistic regression models were used to account for potential confounding factors associated with postoperative complications. The models included age, sex, heavy alcohol intake, and current smokers. We obtained hazard ratios and 95% confidence interval levels from the models for the obese and nonobese groups. Actuarial survival was calculated from the date of first treatment by the Kaplan–Meier method, and comparisons between the groups were made by the log–rank test.


   Results
Top
 Abstract
 Introduction
 Materials and Methods
 Statistical Methods
 Results
Discussion
 Limitations
 Conclusions
 References
 
Patient Demographics
During this period, resection for localized disease with curative intent (anticipated clear margins, R0) was undertaken in 150 patients, 81 of whom (54%) had neoadjuvant chemoradiation therapy before surgery according to the unit protocol. Forty-three patients (29%) were of normal weight (BMI 20-25 kg/m2), with a weight range between 50 and 85 kg; 70 patients (47%) were overweight (BMI 25-30 kg/m2), with a weight range of 80 and 130 kg; and 36 patients (24%) were obese (BMI > 30 kg/m2), with a weight range between 80 and 130 kg. The median BMI was 27 kg/m2. In the obese group, 30 patients (83%) had a BMI between 30 and 35 kg/m2 (80–115 kg), 4 patients (11%) had a BMI between 35 and 40 kg/m2 (101–125 kg), and 2 patients (5%) had a BMI greater than 40 kg/m2 (131 kg) (Table 1).


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  		TABLE 1 Demographics of obese and nonobese groups
 
The clinical pattern of presentation was similar in both groups. There was no significant difference between obese and nonobese patients in known type 2 diabetes, respiratory disease, or performance status. The incidence of cardiovascular disease was influenced by BMI; 7 of 43 patients (16%) with a BMI between 20 and 25 kg/m2 had a history of cardiovascular disease, compared with 28 of 70 patients (40%) with a BMI between 25 and 30 kg/m2 and 17 of 36 patients (47%) with a BMI more than 30 kg/m2 (P = .003).

In obese patients, preoperative forced expiratory volume in 1 second (P = .046) and the forced expiratory volume in 1 second/forced vital capacity ratio (P = .014) were significantly inferior compared with those of the nonobese group. This did not relate to tobacco consumption; the highest percentage of current smokers (40%) was in the normal weight groups compared with the overweight (14%) and obese (19%) groups (P = .042).

Treatment Characteristics
There was no significant difference in esophagogastric junction classification among the BMI categories. Some 67% of obese patients received multimodal therapy compared with 50% of nonobese patients (P = .018). The majority of patients in both groups underwent a 2-stage esophagectomy (Table 2).


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  		TABLE 2 Tumor type, treatment details, and pathology
 
Pathologic Analysis
The R0 resection rate was 83% and 84% in the obese and nonobese groups, respectively (P = .198). In patients undergoing multimodal therapy, the complete pathologic response rate was 12% in the obese group compared with 21% in the nonobese group (P = .425), and there were no differences between groups in terms of achieving a major histomorphologic response (TRG1 or 2) at the primary site, observed in 42% and 45% in the obese and nonobese groups, respectively (P = .495). In this cohort, nonobese patients had more advanced cancer according to pathologic stage, with 46% of patients presenting with stage 3 disease versus 25% of obese patients (P = .013). There was no significant difference in nodal status; the majority of patients were node-positive: 53% in the obese group versus 61% in the nonobese group (P = .082). The median nodal yield was significantly (P = .008) greater in the nonobese group at 15 (5–46), compared with 10 (4–28) in the obese patient. Nonobese patients had a significantly greater number of positive nodes than obese patients: 3 (0–25) versus 1 (0–8) (P = .037). Barrett’s epithelium was present in 56% of resected specimens in the obese group and 44% in the nonobese group (P = .180).

Surgery and In-hospital Complications
There was no significant difference (P = .150) between the mean duration of surgery in the obese group (350 minutes) and nonobese group (320 minutes). The use of blood products intraoperatively and in the first 48 hours after surgery in the obese group (P = .021) was increased, with 24% of patients requiring over 2 units of blood compared with 7% in the nonobese group (Table 3).


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  		TABLE 3 In-hospital postoperative morbidity and mortality
 
In-hospital mortality was 6% in both groups. Twenty-one of 36 obese patients (58%) had a respiratory complication, compared with 43 of 114 nonobese patients (38%) (P = .037); however, there was no significant difference between obese and nonobese groups in major respiratory complications, including pneumonia (P = .502), ARDS (P = .630), and respiratory failure (P = .299). There were 2 cases of empyema, both in the obese group (P = .057). An anastomotic leak (3 radiologic and 2 clinical) developed in 5 patients in the obese group, compared with 1 clinical and 1 radiologic leak in the nonobese group (P = .009). All were managed nonoperatively, and 1 clinical leak in both groups was managed with endoprosthesis. There were no significant differences between groups with respect to venous thromboembolism (P = .436), major wound problems (P = .760), arrhythmias (P = .168), and renal dysfunction (P = .482). The median stay in the high-dependency unit postoperatively was 4 days (0–14 days) in the obese group compared with 4 days (0–32 days) in the nonobese group (P = .937). The median hospital stay was significantly (P = .001) greater at 23 days (13–94 days) in the obese group compared with 18 days (1–61 days) in the nonobese group.

On multivariate analysis (Table 4), obese patients were 2.6 times more likely to have any respiratory complication (P = .014), 2.7 times more likely to have a pleural effusion (P = .019), and 11 times more likely to have an anastomotic leak (P = .006) than nonobese patients.


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  		TABLE 4 Relative hazard ratios for obesity and postoperative complication
 
Postoperative Nutrition
All patients were nutritionally supported via a feeding jejunostomy in the postoperative period. The median duration of postoperative nutrition support (full feeding or overnight feeding) was 16 days (10–80 days) in the obese group and 15 days (2–53 days) in the nonobese group (P = .128). Obese patients lost more weight postoperatively as in-patients compared with nonobese patients (4.7 [0–26] kg vs 2.8 [0–14] kg; P = .048).

Survival
At a median follow-up of 39 months, the median survival (Figure 1) in the obese group was 27 months, compared with 25 months in the nonobese group (P = .348). The 1, 3, and 5-year survivals were 75%, 46%, and 46%, respectively, in the obese group, and 75%, 34%, and 22%, respectively, in the nonobese group.


Figure 1
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  		Figure 1. Survival.

 

   Discussion
Top
 Abstract
 Introduction
 Materials and Methods
 Statistical Methods
 Results
 Discussion
Limitations
 Conclusions
 References
 
Obesity, defined as a BMI greater than 30 kg/m2, has increased in incidence in the developed world in the last decade. Approximately 30% of the population are obese in the United States, and more than 100,000 operations were performed for morbid obesity in 2004.26,27Go The increased incidence of adenocarcinoma of the esophagus and esophagogastric junction in recent decades parallels the increasing prevalence of obesity. In an Irish cohort we recently reported that 82% of patients with adenocarcinoma of the esophagus or esophagogastric junction were overweight or obese, and that obesity in males was associated with a 4-fold increase risk of adenocarcinoma.8Go The explanation for this association is unclear. One possible mechanism links the typical male central adiposity with chronic gastroesophageal reflux disease, both of which are independently associated with adenocarcinoma of the esophagus and junction.28Go In addition to a mechanical link, the pleiotropic properties of the adipocyte have come under scrutiny, because adipocytes from central fat may have endocrine, paracrine, and immunologic properties.29Go This may be manifested in the metabolic syndrome, which is a constellation of atherogenic dyslipidemia, elevated blood pressure, and elevated blood glucose associated with insulin resistance. The proinflammatory response associated with central adiposity and the metabolic syndrome may, at least theoretically, promote inflammation and tumorigenic pathways that are relevant to esophageal adenocarcinoma and other tumor types.16Go

Surgery for esophageal cancer is associated with a significant risk of morbidity and mortality, and has a major impact on quality of life.1Go A recent review of 70,000 patients reported a mortality of 6.7% between 1990 and 2000.30Go The combined Veterans Administration experience for the same period reported a major morbidity rate of approximately 50% and a mortality rate of 10%.10Go In the United Kingdom, McCulloch and colleagues31Go reported a 12% in-hospital mortality rate from a multicenter series. The recent advent of multimodality regimens, particularly neoadjuvant combination chemotherapy and radiation therapy, may further increase operative risks.11,12Go It is unassailable that there is no common elective cancer surgery that carries the same risks. In an era of risk stratification and informed consent, data on the impact of obesity on outcomes after esophagectomy are increasingly important, and to our knowledge this is the first report specifically addressing the relationship of obesity to the standard outcome indicators of an esophageal unit.

In this study, no increase in in-hospital mortality was observed in the obese cohort. Respiratory complications were rigorously recorded, and an increased incidence of complications was observed in the obese cohort. There was, however, no increase in the more major complications of postoperative pneumonia, respiratory failure, or ARDS in the obese group. The incidence of anastomotic leaks was increased in the obese group; however, the incidence of clinically evident leaks was not significantly different. The incidence of anastomotic leak was low (3%), compared with the reported incidence of up to 10% post-esophagectomy.32,33Go On univariate analysis, obesity was the only factor associated with anastomotic leak, and there was no relationship to incidence and age, sex, American Surgical Association grade, smoking, or alcohol use. Obesity was associated with the risk of anastomotic leak after resection and primary anastomosis for left-sided colonic emergencies.34Go The factors involved in the increased leaks observed in the obese group in this study are unclear, but we speculate that the dependence of touch and judgment rather than clear visibility of the right gastroepiploic vessels, as well as increased tension of the conduit in the high thorax or the cervical site, may compromise the vascularity of the gastric anastomotic site. Other factors, such as diabetes and cardiovascular disease, may also be contributory, but this was not evident in this analysis.

The concern that obese patients would have a higher incidence of wound infections and dehiscence could not be verified, and the incidence of clinical venous thromboembolism was low in this study in which all patients received prophylactic low molecular weight heparin. Blood transfusion requirements were significantly increased in the obese group, and obesity was associated with a significantly longer duration of postoperative hospital stay.

Esophagectomy is associated with significant metabolic, endocrine, and immunoinflammatory changes. A similar spectrum of response is seen after major blunt trauma. In studies of patients with blunt trauma, however, and in contrast with this study, Smith–Choban and colleagues35Go reported a 42% mortality in obese patients versus 7% for nonobese patients, and respiratory failure as the result of ARDS was the primary cause. In a study by Neville and colleagues36Go on 242 patients admitted to the intensive care unit after blunt trauma, 62 were obese and the odds ratio of mortality was 5.7 compared with the nonobese cohort. In a study of patients undergoing liver transplantation, obesity was associated with an increased incidence of multiple organ failure.37Go The lack of major added risks associated with obesity in this study is consistent with reports of equivalent complication rates in obese and nonobese patients undergoing cardiac surgery, in which the increased risk of complications seems to be evident only in patients with extreme obesity (BMI > 40 kg/m2).38Go Only 2 patients in this study had a BMI greater than 40 kg/m2; both patients had sleep apnea and 1 patient had obesity hypoventilation syndrome, but both survived without major complications. It is clear that risk assessment in the morbidly obese patient cannot be inferred from this study of predominantly patients with a BMI from 30 to 35 kg/m2.

Frequent symptoms of reflux are associated with increased risks of Barrett’s esophagus, and these risks are substantially elevated by obesity and smoking.39Go In a population-based study39Go in obese patients (BMI > 30), the risk of Barrett’s esophagus was minimal with no reflux symptoms (odds ratio: 0.7 95% confidence interval 0.2–2.4) and increased dramatically with weekly reflux symptoms (odds ratio: 34.4 95% confidence interval 6.3–188). There was no difference in the reported incidence of gastroesophageal reflux disease in this population, which may explain the lack of association between obesity and Barrett’s esophagus. This study also addressed the standard oncologic indicators, and there was no differences in RO resection rate, tumor response rate, and survival. Nodal yield was less in the obese cohort, perhaps reflecting the lack of routine fat-clearing mechanisms by pathologists.


   Limitations
Top
 Abstract
 Introduction
 Materials and Methods
 Statistical Methods
 Results
 Discussion
 Limitations
Conclusions
 References
 
The limitations of the study are acknowledged, particularly the retrospective nature of the analysis. Prospective study in this unit now encompasses assessment of the metabolic syndrome, comprehensive respiratory physiology analysis pretreatment, documentation on intraoperative and early postoperative dynamics in respiratory physiology, and studies of immune function and metabolism in the perioperative period. Underweight patients (BMI < 20 kg/m2) were also excluded because of the small number (n = 5) of the cohort and the fact that they represent a high-risk group. When all patients were included and the population was divided into quintiles or tertiles, a significant association of the highest quintile or tertile with anastomotic leaks and respiratory complications remained evident (data not shown).


   Conclusions
Top
 Abstract
 Introduction
 Materials and Methods
 Statistical Methods
 Results
 Discussion
 Limitations
 Conclusions
References
 
This study shows that obese patients undergoing surgical or multimodality management of localized adenocarcinoma of the esophagus or esophagogastric junction have a longer hospital stay, an increased incidence of respiratory complications and radiologic anastomotic leaks, and greater requirements for blood products compared with nonobese patients. There was no difference in mortality or major complications, and the cancer survival outcomes are equivalent. Risk stratification is the ultimate motivation for establishing complication rates in obese patients undergoing esophageal surgery, and this study shows that surgery was undertaken in an obese population, predominantly patients with a BMI between 30 and 35 kg/m2, with no major increased risk of serious morbidity or mortality.


   References
Top
 Abstract
 Introduction
 Materials and Methods
 Statistical Methods
 Results
 Discussion
 Limitations
 Conclusions
 References
 

  1. Enzinger PC, Mayer RJ. Esophageal cancer. N Engl J Med. 2003;349:2241-2252.[Medline]
  2. Devesa SS, Blot WJ, Fraumeni JF. Changing patterns in the incidence of esophageal and gastric carcinoma in the United States. Cancer 1998;83:2049-2053.[Medline]
  3. Engel LS, Chow WH, Vaughan TL, Gammon, MD, Risch HA, Stanford JL, et al. Population attributable risks of esophageal and gastric cancers. J Natl Cancer Inst. 2003;95:1404-1413.[Abstract/Free Full Text]
  4. Brown LM, Swanson CA, Gridley G, Swanson GM, Schoenberg JB, Greenberg RS, et al. Adenocarcinoma of the esophagus: role of obesity and diet. J Natl Cancer Inst. 1995;87:104-109.[Abstract/Free Full Text]
  5. Vaughan TL, Davis S, Kristal A, Thomas DB. Obesity, alcohol, and tobacco as risk factors for cancers of the esophagus and gastric cardia: adenocarcinoma versus squamous cell carcinoma. Cancer Epid Biomark Prev. 1995;4:85-92.[Abstract]
  6. Chow WH, Blot WJ, Vaughan TL, Risch HA, Gammon, MD, Stanford JL, et al. Body mass index and risk of adenocarcinoma of the esophagus and gastric cardia. J Natl Cancer Inst. 1998;90:150-155.[Abstract/Free Full Text]
  7. Lagergren J, Bergström R, Nyrén O. Association between body mass index and adenocarcinoma of the esophagus and gastric cardia. Ann Intern Med. 1999;130:883-890.[Abstract/Free Full Text]
  8. Ryan AM, Rowley SP, Fitzgerald AP, Ravi N, Reynolds JV. Adenocarcinoma of the esophagus and gastric cardia: male preponderance in association with obesity. Eur J Cancer 2006;42:1151-1158.[Medline]
  9. Calle EE, Rodriguez C, Walker-Thurmund K, Thun MJ. Overweight, obesity and mortality from cancer in a prospectively studied cohort of U.S. adults. N Engl J Med. 2003;348:1625-1638.[Medline]
  10. Bailey SH, Bull DA, Harpole DH, Rentz JJ, Neumayer LA, Pappas TN, et al. Outcomes after esophagectomy: a ten-year prospective cohort. Ann Thorac Surg. 2003;75:217-222.[Abstract/Free Full Text]
  11. Fiorica F, DiBona D, Schepis F, Licata A, Shahied L, Venturi A, et al. Preoperative chemoradiotherapy for esophageal cancer: a systematic review and meta-analysis. Gut 2004;53:925-930.[Abstract/Free Full Text]
  12. Reynolds JV, Ravi N, Hollywood D, Kennedy MJ, Rowley S, Ryan A, et al. Neoadjuvant chemoradiation may increase the risk of respiratory complications and sepsis after transthoracic esophagectomy. J Thorac Cardiovasc Surg. 2006;132:549-555.[Abstract/Free Full Text]
  13. Blazeby JM, Sandford E, Falk SJ, Alderson D, Donovan JL. Health related quality of life during neoadjuvant therapy and surgery for localised esophageal cancer. Cancer 2005;103:1791-1799.[Medline]
  14. Reynolds JV, Mc Laughlin R, Moore J, Rowley S, Ravi N, Byrne PJ. Prospective evaluation of quality of life in patients with localised esophageal cancer treated by multimodality therapy or surgery alone. Br J Surg. 2006;93:1084-1090.[Medline]
  15. World Health Organisation Consultation on Obesity Preventing and managing the global epidemic: report of a WHO consultation on Obesity, Geneva, 3-5 June 1997, 1-276. Geneva, Switzerland: World Health Organization; 1998.
  16. Balkwill F, Mantovani A. Inflammation and cancer: back to Virchow?. Lancet 2001;357:539-545.[Medline]
  17. Adams JP, Murphy PG. Obesity in anaesthesia and intensive care. Br J Anaesth. 2000;85:91-108.[Free Full Text]
  18. Flanchbaum L, Choban PS. Surgical implications of obesity. Ann Rev Med. 1998;49:215-234.[Medline]
  19. Brooks-Brumm JA. Predictors of postoperative pulmonary complications following abdominal surgery. Chest 1997;111:564-571.[Medline]
  20. National Institutes of Health Clinical Guidelines on the Identification, Evaluation and Treatment of Overweight and Obesity in Adults: The Evidence Report. Obes Res. 1998;6(suppl 2):51S-209S.[Medline]
  21. Siewert JR, Stein HJ. Classification of adenocarcinoma of the esophagogastric junction. Br J Surg. 1998;85:1457-1459.[Medline]
  22. Walsh T, Noonan N, Hollywood D, Kelly A, Keeling N, Hennessy TPJ. A comparison of multimodal therapy and surgery for esophageal adenocarcinoma. N Engl J Med. 1996;335:462-467.[Medline]
  23. Bone RC, Sibbald WJ, Spring CL. The ACCP-SCCM consensus conference on sepsis and organ failure. Chest 1992;101:1481-1483.[Medline]
  24. In: Greene FL, Page DL, Fleming ID, Fritz A, Balch CM, Haller DG, et al. editors. American Joint Committee on Cancer. AJCC Cancer Staging Manual. 6th ed.. New York: Springer-Verlag; 2002.
  25. Mandard AM, Dalibard F, Mandard JC, Marnay J, Henry Amar M, Petiot JF, et al. Pathologic assessment of tumor regression after preoperative chemoradiotherapy of esophageal carcinoma. Cancer 1994;73:2680-2686.[Medline]
  26. National Task Force on the Prevention and Treatment of Obesity Overweight, obesity, and health risk. Arch Intern Med. 2000;160898-94.
  27. Steinbrook R. Surgery for severe obesity. N Engl J Med. 2004;350:1075-1079.[Medline]
  28. Lagergren J. Controversies surrounding body mass, reflux, and risk of esophageal adenocarcinoma. Lancet Oncol. 2006;7:347-349.[Medline]
  29. Kershaw EE, Flier JS. Adipose tissue as an endocrine organ. J Clin Endocrinol Metab. 2004;89:2548-2556.[Abstract/Free Full Text]
  30. Jamieson GG, Mathew G, Ludeman R, Wayman J, Myers JC, Devitt PG. Postoperative mortality after esophagectomy and problems in reporting its rate. Br J Surg. 2004;91:943-947.[Medline]
  31. McCulloch P, Ward J, Tekkis P. Mortality and morbidity in gastro-esophageal cancer surgery: initial results of ASCOT multicenter prospective study. BMJ 2003;327:1192-1197.[Abstract/Free Full Text]
  32. Junemann-Ramirez M, Awan MY, Khan ZM, Rahmamim JS. Anastomotic leakage post esophagectomy for esophageal carcinoma: retrospective analysis of predictive factors, management and influence on longterm survival in a high volume centre. Eur J Cardiothorac Surg. 2005;27:3-7.[Abstract/Free Full Text]
  33. Briel JW, Tamhanker AP, Hagen JA, DeMeester SR, Johansson J, Choustoulakis E, et al. Prevalence and risk factors for ischaemia, leak, and stricture of esophageal anastomosis: gastric pull up versus colonic interposition. J Am Coll Surg. 2004;198:536-541.[Medline]
  34. Bionda S, Pares D, Kreisler E, Marti Rague J, Fraccalvieri D, Garcia Ruiz A, et al. anastomotic dehiscence after resection and primary anastomosis in left sided colonic emergencies. Dis Colon Rectum 2005;48:2272-2280.[Medline]
  35. Smith-Choban P, Weireter LJ, Maynes C. Obesity and increased mortality in blunt trauma. J Trauma. 1991;31:1253-1257.[Medline]
  36. Neville AL, Brown CVR, Weng J, Demetriades D, Velmahos GC. Obesity is an independent risk factor of mortality in severely injured blunt trauma patients. Arch Surg. 2004;139:983-987.[Abstract/Free Full Text]
  37. Sawyer RG, Pelletier SJ, Pruett TL. Increased early morbidity and mortality with acceptable long-term function in severely obese patients undergoing liver transplantation. Clin Transplant. 1999;13:126-130.[Medline]
  38. Wigfiled CH, Lindsey JD, Munoz A, Chopra PS, Edwards NM, Love RB. Is extreme obesity a risk factor for cardiac surgery?. An analysis of patients with a BMI > 40. Eur J Cadiothorac Surg. 2006;29:434-440.[Abstract/Free Full Text]
  39. Smith KJ, O’Brien SM, Smithers BM, Gotley DC, Webb PM, Green AC, et al. Interactions among smoking, obesity, and symptoms of acid reflux in Barrett’s esophagus. Cancer Epidemiol Biomarkers Prev. 2005;14:2481-2486.[Abstract/Free Full Text]



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