Key result
Each 1% HbA1c increase is linked to ~0.8 kPa higher liver stiffness in hypertension.
Why the study?
Non-alcoholic fatty liver disease increases cardiovascular risk, motivating the evaluation of liver steatosis, liver fibrosis, and body composition in patients with arterial hypertension with and without carbohydrate metabolism disorders.
Does the presence of impaired carbohydrate metabolism (impaired glucose tolerance or type 2 diabetes mellitus) increase indicators of liver steatosis and liver fibrosis in patients with arterial hypertension?
Cross-Sectional (n=100)
Does the presence of impaired carbohydrate metabolism (impaired glucose tolerance or type 2 diabetes mellitus) increase indicators of liver steatosis and liver fibrosis in patients with arterial hypertension?
In patients with arterial hypertension, impaired glucose tolerance and type 2 diabetes mellitus are associated with significantly higher indicators of liver steatosis and stiffness, with each 1% increase in HbA1c predicting a 0.78 kPa increase in liver stiffness.
Answers are grounded in this paper and cite their sources.
HbA1c rise may flag higher fibrosis risk in hypertensive patients; leaves open whether glycemic control alters stiffness.
Non-alcoholic fatty liver disease is one of the most common chronic liver diseases that has been proven to increase the risk of cardiovascular disease. The aim of the study: to study the characteristics of steatosis and liver fibrosis, as well as to analyze the body composition in patients with and without carbohydrate metabolism disorders and arterial hypertension (AH). Materials and methods . The study included 100 patients (31 men and 69 women) with AH aged 25 to 80 years with and without carbohydrate metabolism disorders. In addition to standard studies, all patients underwent determination of parameters of fatty hepatosis and liver fibrosis by transient elastometry (TE), determination of the compositional composition of the body. Liver steatosis was diagnosed according to the ultrasound attenuation parameter (UAP) of more than 244 dB/m, liver fibrosis was diagnosed according to the liver stiffness index Fs of more than 7.3 kPa. Results . The patients were divided into 3 groups: without carbohydrate metabolism disorders (50 people), with impaired glucose tolerance (IGT) (18 people), with type 2 diabetes mellitus (DM) (32 patients). The UAP value in patients with IGT significantly exceeded the value in patients without carbohydrate metabolism disorders. The Fs values in the groups with carbohydrate metabolism disorders were comparable, significantly exceeding the values in patients without carbohydrate metabolism disorders. In the group of patients with type 2 diabetes mellitus with non-target HbA1c, liver fibrosis was diagnosed in all examined. A direct correlation was found between the HbA1c level and the Fs indicator. Using linear regression analysis, it was found that an increase in HbA1c by 1% is associated with an increase in liver stiffness by 0.78 kPA. Conclusion . In patients with AH and IGT, the indicators of steatosis and liver stiffness were higher than in patients without carbohydrate metabolism disorders. The level of HbA1c is not only an indicator of carbohydrate metabolism, but also has predictive significance in relation to the development of liver fibrosis. Our study showed the need for a comprehensive examination of patients with carbohydrate metabolism disorders, including transient elastometry, for the timely diagnosis of steatosis and liver fibrosis.
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Евгеньевна et al. (2026) conducted a cross-sectional in Arterial hypertension with and without carbohydrate metabolism disorders (n=100). Carbohydrate metabolism disorders (IGT and type 2 DM) and HbA1c level vs. Patients with arterial hypertension without carbohydrate metabolism disorders was evaluated on Liver steatosis (UAP >244 dB/m) and liver fibrosis (liver stiffness index Fs >7.3 kPa) assessed by transient elastometry (0.78 kPa per 1% HbA1c increase). Carbohydrate metabolism disorders in hypertensive patients were associated with higher liver steatosis and stiffness, with each 1% HbA1c increase linked to a 0.78 kPa rise in liver stiffness.
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