Abstract
Brain iron deposition correlates with clinical manifestations of cerebral small vessel disease. Excessive iron load leads to the formation of free radicals, and nervous tissue damage. The main damaging effect of hydroxyl radicals is due to conversion of soluble fibrinogen to insoluble fibrin. There is also a possible relationship between the functional state of the liver and the early manifestations of cardiovascular disease. Objective: to investigate the relationship between the parameters of coagulation system, liver functional state, fat and protein metabolism, and brain iron deposition in patients with cerebral small vessel disease in the presence of hypertension and cerebral atherosclerosis. Materials and methods: 80 patients with diagnosed cerebral small vessel disease were selected. Patients were divided into two groups, depending on the severity of brain iron deposition. All patients underwent MRI in the T1-WI, T2-WI, TIRM, DWI, and SWI sequences. Determination of the coagulation system parameters and the biochemical analysis were carried out during routine blood test. Results: using a double-sample t test, it was determined that patients with severe brain iron deposition had higher levels of urea, triglycerides, and prolonged thrombin time. With the logistic regression analysis adjusted by the age and sex, levels of urea and the length of thrombin time were determined as the independent risk factors for severe brain iron deposition. For urea OR 1.87, CI 95% 1.31-2.65 (p = 0.02), for thrombin time OR 1.55, CI 95% 1.06-2.26 (p = 0.02). For these parameters, the risk increased when assessing only patients with ALT levels> 15 U / l. For such patients, the relationship between thrombin time and brain iron deposition increased significantly: OR 2.11, CI 95% 1.20-3.71 (p = 0.01). In this study no relationship was found between the indicators of fat metabolism, levels of fibrin and iron deposition. There is a probable relationship between the brain iron deposition and the state of coagulation system, protein metabolism and liver functional state in patients with cerebral small vessel disease.
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