Non-alcoholic fatty liver disease (NAFLD) covers a range of liver lesions of various severity, from isolated steatosis to non-alcoholic steatohepatitis (NASH) with or without fibrosis, liver cirrhosis and hepatocellular carcinoma (HCC). NAFLD has reached the scale of a pandemic that affects approximately 25 % of the world’s population and approximately 60 % of patients with type 2 diabetes mellitus (DM2) worldwide. Diabetes mellitus is also considered a risk factor for the development of NAFLD/NASH and is a strong predictor of the development and progression of fibrosis, HCC and associated mortality. Despite a clear link between NAFLD and DM2, it is still unclear how glycemic control affects the severity and associated risk of progression of NAFLD and NASH.
 The aim of the study. To investigate the relationship between glycemic control (using the mean hemoglobin A1c [HbA1c] levels) and development and severity of NAFLD and hepatic fibrosis.
 Materials and methods. Investigations involved 113 patients who met the following criteria: age ≥ 18 years, diagnosis of NAFLD/NASH, confirmed by multimodal ultrasound and/or sustained increase in transaminases, and at least one documented value of HbA1c within 90 days before the clinical diagnosis of NAFLD/NASH. All patients underwent clinical and anamnestic, general clinical, biochemical studies to determine liver functional tests and lipid spectrum, HbA1c and fasting glucose, multimodal ultrasound to determine steatosis (steatometry) and liver fibrosis (elastography). Depending on the average level of HbA1c before the diagnosis of NAFLD/NASH, 3 subgroups of patients were identified — with good, moderate and poor glycemic control (average HbA1c values were 6.5 %, 7.6 % and 10.0 %, respectively).
 Results. In the majority of patients (76.9 %) with established NASH, the previous glycemic control determined by the level of HbA1c was moderate (57.7 %) or poor (19.2 %). In contrast, in most patients (62.3 %) with good glycemic control, simple steatosis was detected, and NASH was not confirmed by clinical and biochemical criteria. Relevant data were obtained for elevated levels of ALA and alkaline phosphatase, as well as triglycerides, which in patients with good glycemic control did not exceed normal values. Liver fibrosis (F1—F4) was detected in only 20 % with good glycemic control, while in moderate and poor glycemic control it was detected in most patients (80 %; p < 0.001). In addition, advanced liver fibrosis (F3—F4) was diagnosed only in patients with moderate and poor glycemic control.
 Conclusions. Poor glycemic control as determined by HbA1c can be considered as a potential modifier of the risk of progression of NAFLD/NASH.
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