Endocrine Abstracts

Obesity and the metabolic syndrome show increased morbidity and mortality, by inducing morphological and functional alterations of several organs, the liver included (non-alcoholic fatty liver disease – NAFLD). They start with minimal alterations ranging to terminal liver disease (non-alcoholic steatohepatitis – NASH – and cirrhosis).

We intended to identify the histological aspects in NAFLD and to examine the correlations between the histological aspect, the biochemical features and the characteristics of the metabolic syndrome.

Material and method: The study group consisted of 35 patients diagnosed with hepato-steatosis who had no history of alcohol consumption or hepatitis B or C. We analyzed the parameters: sex, age, body weight, BMI, Waist circumference, blood pressure, blood glucose (± Diabetes Mellitus/Metabolic Syndrome), Insuline, IR–HOMA, blood lipids, ALT, AST, CRP, liver ultrasound, liver biopsy. The identification of the metabolic syndrome was made considering the ATP III diagnostic criteria. We performed liver biopsy in 20 patients.

Results: Aminotransferases were elevated in the studied patients, while the CRP was moderately elevated in the obese patients. The patients with mild steatosis showed a lower level of the triglycerides compared to those with fibrosis (steatohepatitis) 99±43 vs 169±85 mg/dl. HOMA-IR was lower in the patients with simple steatosis compared to those with severe steatosis and fibrosis (2.54±0.9 vs 4.5±2.5 P=0.002). TG>180 mg/dl or HOMA-IR>4.5 were associated with NASH. The main characteristic of NASH was the presence of the fatty cells in the liver parenchyma, together with inflammatory cells and degenerative lesions.

Conclusions: The NAFLD requires careful histological and clinical evaluation. Insulin resistance is present in the majority of the patients with non-alcoholic steatosis. The HOMA-IR Index >4.5 and the TG level >180 mg/dl can be predictive (risk factors) for the presence of steatohepatitis and fibrosis. Insulin resistance could play a role in the pathogenesis of the fibrosis’ progression in the NAFLD patients (non-alcoholic steatosis).