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Koroy P.V., Yagoda A.V. Stavropol State Medical Academy, Russia The aim of study was to estimate relationship between parameters of platelets and liver fibrosis in chronic viral liver diseases. Materials and methods. We have examined 47 patients with chronic viral hepatitis and 10 patients with liver cirrhosis viral etiology, and 10 healthy volunteers. Contents of platelets, spontaneous and induced (by epinephrine and collagen) platelet aggregation, concentration of β-thromboglobulin and platelet factor 4 in platelet-poor citrate plasma were determined in all patients in a day of liver biopsy. The patients were divided into 3 groups according by index Desmet F0-F1, F2-F3, and F4. Results. We have found reliable increase in levels of spontaneous platelet aggregation, β-thromboglobulin, platelet factor 4, and decrease in contents of platelets and induced platelet aggregation in patients with chronic viral hepatitis. The obtained results showed the intravascular platelet’s activation. Table Parameters of platelets in patients with different expressiveness of liver fibrosis ()

Parameters	Control	Patients with fibrosis’s index
		F0-F1	F2-F3	F4
Contents of platelets (*109/l)	n=10 272,08,04	n=15 233,817,73 *	n=32 202,089,64 */**	n=10 139,913,88 */**/***
Epinephrine-induced platelet aggregation (%)	n=32 64,701,94	n=13 76,922,92 *	n=30 40,354,43 */**	n=10 20,265,95 */**/***
Collagen-induced platelet aggregation (%)	n=32 60,011,35	n=13 73,682,12 *	n=30 43,583,54 */**	n=10 17,926,66 */**/***
Spontaneous platelet aggregation (%)	n=10 0,670,07	n=17 1,640,25 *	n=21 2,300,17 */**	n=6 1,180,21 ***
β- thromboglobulin (IU/ml)	n=10 146,128,13	n=17 176,826,91 *	n=21 206,107,68 */**	n=6 168,226,04 ***
Platelet factor 4 (sec)	n=10 3,020,57	n=17 5,160,65 *	n=21 7,300,51 */**	n=6 4,450,35 ***

* – p<0,05 in comparison with control parameters; ** – p<0,05 in comparison with parameters of patients with index Desmet F0-F1; *** – p<0,05 in comparison with parameters of patients with index Desmet F2-F3. In group patients with index Desmet F0-F1 the parameters of spontaneous and induced platelet aggregation and serum levels of thrombocyte-specific peptides were increased and contents of platelet were decreased (tab.). In group with index Desmet F2-F3 induced platelet aggregation and contents of platelet were reduced, whereas spontaneous platelet aggregation, beta-thromboglobulin and platelet factor 4 were significantly higher than in controls and group patients with index Desmet F0-F1. The more pronounced decrease of platelets levels and induced platelet aggregation were in group with index Desmet F4 (liver cirrhosis without clinical signs). In this group the concentrations of components of α-granules and levels of spontaneous platelet aggregation were lower than in patients with index Desmet F2-F3. Conclusion. Platelets dysfunction correspondes to fibrosis degree in chronic viral liver diseases. The associations of parameters of platelets and expressiveness of liver fibrosis are demonstrated the participation of platelets in hepatic remodelling and infringement of liver’s architectonics. The platelets parameters may be use as non-invasive markers for diagnosis of liver fibrosis progression without liver biopsy.