UNLABELLED: The aim of the study was to highlight correlations between serum biochemical markers and different degrees of liver inflammation or fibrosis revealed by liver biopsy in morbidly obese patients. We also wanted to emphasize that the occurrence of hepatocellular carcinoma (HCC) is increasingly associated with obesity, metabolic syndrome and nonalcoholic fatty liver disease. MATERIAL AND METHODS: A clinical retrospective study was carried out on a series of 13 patients operated for morbid obesity in our surgical unit. Included in this study were only the obese patients referred for bariatric surgery without other risk factors for liver disease and in whom a liver biopsy was taken during metabolic surgery. RESULTS: The pathology report revealed different stages of nonalcoholic fatty liver disease in all 13 patients: pathological features of steatohepatitis (7 patients), hepatic steatosis (5 patients) and lesions specific for evolving cirrhosis (1 patient). Regardless of the pathological changes of the liver, except the patient with evolving cirrhosis, none of these patients showed changes in classical liver function blood tests. DISCUSSIONS: Hepatic alteration in obese patients, ranging from simple steatosis to steatohepatitis or even cirrhosis, is not always correlated with the values of classical biological liver function tests. Literature data suggest the involvement of adipokines in the development and progression of steatosis as the hepatic expression of metabolic and chronic inflammation syndrome occurring in obese patients. Furthermore, these proteins secreted by adipose tissue seem to be related to the HCC occurrence. However, none of these studies show the exact pathway followed by the hepatic cell from simple fatty liver to hepatocellular carcinoma. CONCLUSIONS: finding and selecting the population at risk for fatty liver disease progression and for HCC development among obese patients is mandatory.
UNLABELLED: The aim of the study was to highlight correlations between serum biochemical markers and different degrees of liver inflammation or fibrosis revealed by liver biopsy in morbidly obesepatients. We also wanted to emphasize that the occurrence of hepatocellular carcinoma (HCC) is increasingly associated with obesity, metabolic syndrome and nonalcoholic fatty liver disease. MATERIAL AND METHODS: A clinical retrospective study was carried out on a series of 13 patients operated for morbid obesity in our surgical unit. Included in this study were only the obesepatients referred for bariatric surgery without other risk factors for liver disease and in whom a liver biopsy was taken during metabolic surgery. RESULTS: The pathology report revealed different stages of nonalcoholic fatty liver disease in all 13 patients: pathological features of steatohepatitis (7 patients), hepatic steatosis (5 patients) and lesions specific for evolving cirrhosis (1 patient). Regardless of the pathological changes of the liver, except the patient with evolving cirrhosis, none of these patients showed changes in classical liver function blood tests. DISCUSSIONS: Hepatic alteration in obesepatients, ranging from simple steatosis to steatohepatitis or even cirrhosis, is not always correlated with the values of classical biological liver function tests. Literature data suggest the involvement of adipokines in the development and progression of steatosis as the hepatic expression of metabolic and chronic inflammation syndrome occurring in obesepatients. Furthermore, these proteins secreted by adipose tissue seem to be related to the HCC occurrence. However, none of these studies show the exact pathway followed by the hepatic cell from simple fatty liver to hepatocellular carcinoma. CONCLUSIONS: finding and selecting the population at risk for fatty liver disease progression and for HCC development among obesepatients is mandatory.