Mild hepatic steatosis is not a major risk factor for hepatectomy and regenerative power is not impaired
Department of Surgery, Seoul National University, Sŏul, Seoul, South Korea Surgery
(Impact Factor: 3.38).
05/2006; 139(4):508-15. DOI: 10.1016/j.surg.2005.09.007
An understanding of the regeneration power and operative risk of steatotic livers after hepatectomy is still unclear. We evaluated the volume regeneration and outcome of steatotic livers after donor hepatectomy.
Fifty-four, consecutive living liver donors from September 2002 to December 2003 were evaluated prospectively by volumetric analysis, liver-spleen ratio, and liver attenuation index; the latter has been shown by serial computed tomographic scanning to be correlated strongly with histologic steatosis. Donors were followed up completely for at least 1 year (460-915 days) and were allocated according to histologic degree of macrovesicular steatosis: group 1, <5% (n = 36); group 2, 5%-30% (n = 18).
No mortality or hepatic failure was observed, and no donor required reoperation or intraoperative transfusion. The results of serial liver function tests, and major and minor morbidities were comparable between groups. Liver-spleen ratio and liver attenuation index remained at a constant level above normal values postoperatively in group 1, but increased rapidly above normal values in group 2. No difference in the rate of liver regeneration at 10 days after hepatectomy was found between the groups (P = .487), but the liver regeneration rate at 3 months after hepatectomy in group 1 was slightly higher than that in group 2 (P < .044). However, no difference was observed between the 2 groups at 1 year after hepatectomy (P = .4).
Mild hepatic steatosis is cleared immediately after hepatectomy, and early regeneration power is impaired, but the long-term regenerative power is comparable. Hepatectomy in donors with mild steatosis can be performed with low morbidity.
Available from: Ahmed Mostafa Sira
- "It has been shown that the risk of postoperative complications in patients with any degree of steatosis undergoing partial hepatectomy was double that of their non-steatotic counterparts, and that those with severe steatosis had an almost 3-fold increased risk of death . In addition, a study of patients undergoing liver resection for living-related liver donation showed reduced recovery of liver volume over the initial 3 months following surgery in patients with mild steatosis versus no steatosis . "
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ABSTRACT: The liver is a major metabolic organ, essentially controlling glucose and fat metabolism. Because lipids are water-insoluble, they need to be transported in the circulation in association with proteins in the form of lipoproteins. These lipoproteins play a key role in the absorption and transport of dietary lipids by the small intestine, in the transport of lipids from the liver to peripheral tissues, and in the transport of lipids from peripheral tissues to the liver and intestine. Upon feeding, energy is provided by glycolysis and the unused glucose is stored as glycogen in the liver. Excess glucose is used to synthesize fatty acids through de novo lipogenesis. Fatty acids are incorporated into triacylglycerol, phospholipids, or cholesterol esters in hepatocytes. These complex lipids are stored in lipid droplets or secreted into the circulation as very low-density lipoprotein particles. Upon fasting, after consumption of stored glycogen, the liver secretes glucose through gluconeogenesis. Fasting also promotes lipolysis in adipose tissue, resulting in release of free fatty acids which are metabolized in hepatic mitochondria though beta-oxidation for energy production, while excess fatty acids are stored by the liver leading to hepatic steatosis. Disturbances in lipid metabolism, as in alcoholic and non-alcoholic steatohepatitis, obesity and diabetes, will affect liver performance and function. Likewise, disturbed liver functions by acute or chronic liver disease, as in viral hepatitis, will affect lipid homeostasis. This may carry an increased risk of atherosclerosis and ischemic heart disease which may endanger life. Dietary restriction or fasting was found to have a positive impact on restoring lipid homeostasis leading to improved quality of life.
Available from: Lucas McCormack
- "While these results are valid for deceased donor liver transplantation , the experience of using fatty liver grafts for living donor liver transplantation is scarce and hepatic steatosis is usually regarded as a contraindication for living donation in most centers . However, the regeneration ability of the fatty liver is controversially discussed  . Whether potential donors with mild steatosis should be completely denied from live donation depends, therefore, also on graft volume and donor age. "
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ABSTRACT: Steatotic liver grafts represent the most common type of "extended criteria" organs that have been introduced during the last two decades due to the disparity between liver transplant candidates and the number available organs. A precise definition and reliable and reproducible method for steatosis quantification is currently lacking and the potential influence of the chemical composition of hepatic lipids has not been addressed. In our view, these shortcomings appear to contribute significantly to the inconsistent results of studies reporting on graft steatosis and the outcome of liver transplantation. In this review, various definitions, prevalence and methods of quantification of liver steatosis will be covered. Ischemia/reperfusion injury of the steatotic liver and its consequences on post-transplant outcome will be discussed. Selection criteria for organ allocation and a number of emerging protective strategies are suggested.
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ABSTRACT: Early postoperative graft function assessments are essential after living donor liver transplantation (LDLT) to predict patient and graft outcome. Computed tomography (CT) is usually used to evaluate various complications and parenchymal abnormalities after LDLT. Here, we attempted to determine the prognostic values of CT attenuation changes of grafts for predicting 1-year patient survival. Liver attenuation indices (LAIs), derived from differences between hepatic and splenic attenuations, were calculated on unenhanced CT images obtained 10 days after LDLT in 62 adult LDLT recipients between September 2002 and August 2004. Patients were assigned to 1 of 2 groups according to LAI value on the 10th postoperative day, as follows: group L (LAI < or = 5, n = 14) or group H (LAI > 5, n = 48). Parenchymal dysfunction scores, summed parameters for histological dysfunction including both portal tract and centrilobular features, were also assessed on the 10th postoperative day using liver biopsy specimens. Histological parenchymal dysfunction, especially in the centrilobular area, in terms of cholestasis, centrilobular necroinflammation, central vein fibrosis, steatosis, mononuclear infiltrates, and hepatocyte ballooning, was more prominent in group L than in group H, while that in the portal area was similar between the 2 study groups. Significant negative linear correlations were observed between LAI and parenchymal dysfunction scores (r = 0.486, P < 0.001). Group L patients showed lower 1-year survival (69.7%) than group H patients (95.8%; P = 0.0002). Moreover, group H patients died with a functioning graft (n = 3), whereas group L patients died of graft failure (n = 6). After multivariate analysis, LAI alone remained independently associated with 1-year mortality (P = 0.014; odds ratio = 0.845; 95% confidence interval, 0.739-0.967). The sensitivity and specificity of LAI were 84.6% and 75%, respectively, and LAI outperformed MELD score as a predictor of 1-year mortality after LDLT by receiver operating characteristic curve analysis. In conclusion, LAI, as determined by unenhanced CT 10 days after LDLT, well predicts 1-year patient survival after LDLT.
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