Significant Association between Subclinical Left Cardiac Dysfunction and Liver Stiffness in Metabolic Syndrome Patients with Diabetes Mellitus and Non-Alcoholic Fatty Liver Disease.

Background and Objectives: Diabetes mellitus (DM) is connected to both cardiovascular disease and non-alcoholic fatty liver disease (NAFLD), and is an important component of metabolic syndrome (MetS). NAFLD can be detected and quantified using the vibration controlled transient elastography (VCTE) and the controlled attenuation parameter (CAP), whereas traditional and two-dimensional speckle tracking echocardiography (2D-STE) can reveal subclinical abnormalities in heart function. We sought to see if there was a link between left cardiac dysfunction and different levels of hepatic fibrosis in MetS patients with DM and NAFLD. Patients and Methods: We recruited successive adult subjects with MetS and a normal left ventricular ejection fraction, who were divided into two groups according to the presence or absence of DM. The presence of NAFLD was established by CAP and VCTE, while conventional and 2D-STE were used to assess left heart's systolic and diastolic function. The mean age of the MetS subjects was 62 ± 10 years, 82 (55%) were men. The distribution of liver steatosis severity was similar among diabetics and non-diabetics, while liver fibrosis grade 2 and 3 was significantly more frequent in diabetics (p = 0.02, respectively p = 0.001). LV diastolic dysfunction was found in 52% of diabetic and in 36% of non-diabetic MetS patients (p = 0.04). 2D-STE identified in the diabetic subjects increased LA stiffness (40% versus 24%, p = 0.03) and reduced global left ventricular longitudinal strain (47% versus 16%, p < 0.0001). Liver fibrosis grade ≥ 2 was identified as an independent predictor of both subclinical LV systolic dysfunction and of LA dysfunction in MetS patients with DM (p < 0.0001). Conclusions: The current investigation confirms the link between liver stiffness and subclinical cardiac dysfunction as detected by 2D-STE in MetS patients with DM. The novel parameters derived from LA and LV 2D-STE have demonstrated greater sensitivity compared to the older measurements, and a substantial connection with hepatic fibrosis.

Dynamic Changes in Liver Stiffness in Patients with Chronic Hepatitis B Undergoing Antiviral Therapy.

This is a retrospective single-center study that included 87 subjects. All subjects had chronic hepatitis B or HBV cirrhosis and underwent nucleos(t)ide analogs (NUC) treatment for more than one year. The study aimed to evaluate the dynamic changes in liver stiffness (LS) measured by transient elastography (TE) during a median interval of 64 months. Patients were assessed prior to starting therapy and followed up annually. Liver stiffness measurements (LSM) were performed annually, and ten valid LSMs were obtained in each session. Reliable LSMs were defined as the median value of 10 measurements with Interquartile range/median (IQR/M) ≤ 30%. A significant decrease in liver stiffness values (p < 0.001) was observed during follow-up. In patients with liver cirrhosis, the LSMs decreased significantly after only one year, 24.6 ± 4.3 kPa vs. 13.5 ± 4.2 kPa (p = 0.007), whereas the decrease in non-cirrhotic patients was not significant, 7.31 ± 3.62 vs. 6.80 ± 2.41 (p = 0.27). Liver stiffness decrease was more significant in patients with initially higher transaminases. Undetectable viral load was achieved in 73.5% of patients in year one, 82.7% in year two, and 90.8% in year three of treatment. In conclusion, our study reveals a decrease in liver stiffness by TE in patients with chronic hepatitis B when undergoing anti-HBV therapy in the first two years. It can be used as a method for follow-up in patients undergoing NUC therapy.

In Vitro and In Ovo Evaluation of the Potential Hepatoprotective Effect of Metformin.

Background and Objectives: Metformin is currently the leading drug of choice for treating type 2 diabetes mellitus, being one of the most widely used drugs worldwide. The beneficial effects of Metformin, however, extend far beyond the reduction of blood glucose. Therefore, this study aimed to evaluate Metformin's effects both in vitro and in ovo. Materials and Methods: Metformin has been tested in five different concentrations in human hepatocytes -HepaRG, in terms of cell viability, morphology, structure and number of nuclei and mitochondria, as well as the effect on cell migration. Through the application of HET-CAM, the biocompatibility and potential anti-irritant, as well as protective effects on the vascular plexus were also assessed. Results: According to the results obtained, Metformin increases cell viability without causing morphological changes to cells, mitochondria, or nuclei. Metformin displayed an anti-irritant activity rather than causing irritation at the level of the vascular plexus. Conclusions: In conclusion, Metformin enhances cell viability and proliferation and, has a protective effect on the vascular plexus. Nonetheless, more studies are required to clarify the mechanism of hepatoprotective effect of metformin.