Metabolic syndrome and hepatic resection: improving outcome

Abstract

Objective: A review of the peri-operative risk associated with hepatic resection in patients with metabolic syndrome (MetS) and identification of measures for the improvement of cardiometabolic disturbances and liver-related mortality.

Background: MetS and its hepatic manifestation non-alcoholic fatty liver disease (NAFLD) are associated with an increased operative mortality in spite of a significant improvement in peri-operative outcome after hepatic resection.

Methods: A review of the English literature on MetS, liver resection and steatosis was performed from 1980 to 2011 using the MEDLINE and PubMed databases.

Results: MetS is a predictor of NAFLD and patients with multiple metabolic risk factors may harbour non-alcoholic steatohepatitis (NASH) predictive of operative and cardiovascular mortality. Pre-operative diagnosis of unsuspected NASH with the selective use of a liver biopsy can modify the operative strategy by limiting the extent of hepatic resection, avoiding or altering the pre-operative chemotherapy regimen and the utilization of portal vein embolization. Thiazolidinediones are therapeutic for MetS and NASH and Vitamin E for active NASH; however, their utility in improving the peri-operative outcome after hepatic resection is unknown. A short-term regimen for weight loss improves post-operative patient and liver-related outcomes in patients with >30% steatosis. Cardiovascular disease associated with MetS or NAFLD should be managed aggressively. Peri-operative measures to minimize thrombotic events and acute renal injury secondary to the pro-inflammatory, prothrombotic state of MetS may further improve the outcome.

Conclusion: Potential candidates for hepatic resection should be screened for MetS as the pre-operative identification of NASH, short-term treatment of significant steatosis, cardiovascular risk assessment and optimization of each component of MetS may improve the peri-operative outcome in this high-risk subset of patients.

Figure 1

The channelling of surplus calories from excess dietary consumption and sedentary lifestyle into insulin-sensitive subcutaneous adipose tissue will protect against the development of metabolic syndrome. However, in the presence of dysfunctional adipose tissue, genetic predisposition and a neuroendocrine profile related to a maladaptive response to stress, the triacylglycerol surplus will be deposited at undesirable sites such as the liver, heart, skeletal muscle and visceral adipose tissue – a phenomenon known as ectopic fat deposition. Metabolic consequences of this defect in energy partitioning include visceral obesity, insulin resistance, atherogenic dyslipidemia and a prothrombotic proinflammatory profile the defining features of metabolic syndrome. Reprinted by permission from Macmillan Publishers Ltd: Després & Lemieux, copyright 2006.