555 Visceral Obesity: Prevalence, and Impact on Operative and Oncologic Outcomes in the Curative Management of Esophageal Cancer

Abstract

Obesity, in particular visceral obesity, is a risk factor for esophageal cancer, but its prevalence and impact on operative and oncologic outcomes is unclear. The aim of this study was to study adipose distribution in esophageal cancer (EC), and to assess its independent impact. Methods 11 consecutive patients undergoing treatment with curative intent for esophageal cancer were studied. Total (TFA), subcutaneous (SFA) and visceral fat areas (VFA), and fat mass (FM), were determined pre-treatment, preoperatively, and 1 year postoperatively. Visceral obesity was defined by CT at L3 as VFA greater than 163.8 cm2 for men and 80.1 cm2 for women. All complications were recorded prospectively, including comprehensive complications index, Clavien-Dindo, and pulmonary complications (PPC). Multivariable logistic and Cox proportional hazards regression were utilized to determine independent predictors of operative and oncologic outcome. Results Visceral obesity (VO) was evident in 290 patients (47.5%), and was associated with BMI-defined obesity, diabetes, metabolic syndrome, Barrett’s esophagus (P = 0.001), well-differentiated tumors (P = 0.027), and lower cN stage (P = 0.012). VO did not impact tumor regression grade (TRG) after neoadjuvant therapy. Postoperatively, VO independently predicted anastomotic leak (P = 0.033, OR2.42 [1.07-5.45]) and pneumonia (P = 0.046, OR1.53 [1.01–2.32]), but not in-hospital mortality (P = 0.466), which was 1% overall. VO was associated with significantly improved overall and disease-specific survival on univariable (P = 0.005, Figure), and multivariable analysis (P = 0.026, 0.74 [0.57–0.97]). In survivorship, VO significantly declined, and was evident in just 15.3% at one year postoperatively. Conclusion VO is linked with Barrett’s associated EC, and less aggressive tumour biology. Although it negatively impacted operative outcomes, VO was associated with improved oncologic outcomes, independent of BMI or fat mass, indicating a distinct biologic phenotype, and highlighting the importance of research elucidating the interaction between the visceral fat microenvironment, metabolic dysfunction, and the tumor microenvironment.

Cardiopulmonary exercise testing has greater prognostic value than sarcopenia in oesophago‐gastric cancer patients undergoing neoadjuvant therapy and surgical resection

“…This is at odds with recently published meta‐analyses that show that preoperative sarcopenia is an independent unfavorable prognostic factor for oesophageal and gastric cancer patients after oesophagectomy and gastrectomy 54,55 . Nevertheless, there is conflicting evidence from multiple studies that, similar to us, have been unable to find an association between sarcopenia and postoperative outcomes in an OG cancer cohort undergoing curative therapy 16–18 . Another recently published meta‐analysis found sarcopenia was only significantly associated with overall morbidity and had no effect on overall mortality or major morbidity (CD3‐5) 56 .…”

“…During NAT, a reduction in skeletal muscle mass is observed, leading to an increase in the rate of sarcopenia 14–18 . Sarcopenia in OG cancer has been associated with increased dose‐limiting chemotherapy toxicity, 14,19 increased circumferential resection margin positivity 18 and increased mortality 15,20 .…”

Acute Kidney Injury After Esophageal Cancer Surgery

“…The association of visceral obesity and new-onset postoperative atrial dysrhythmia may suggest common pathways relevant to other perfusion-related complications, including AKI. 39 Although severe postoperative complications may impact on oncologic outcomes, postoperative AKI was not found to independently impact OS or DFS. A Clavien-Dindo classification of 3 or greater was; however, significant, consistent with other studies.…”

Addressing the changing rehabilitation needs of patients undergoing thoracic surgery

“…[35][36][37][38] Impairments of physical fitness and HRQoL already present before surgery can be further exacerbated by the surgical procedure, adjuvant chemotherapy and persistent malnutrition. 39 It has been observed that impairments of cardiorespiratory fitness persist for up to 2 years after surgical treatment, 40 muscle mass may continue to decline for up to 1 year after treatment, 41 and HRQoL can remain impaired for years. 42 While this again provides a strong rationale for post-surgery rehabilitation the (promising) evidence in this area is so far limited.…”