ENDOTHELIUM LESION MARKERS AND THROMBOCYTE AGGREGATION IN CHRONIC HEPATITIS AND HEPATIC CIRRHOSIS
https://doi.org/10.17650/1818-8338-2012-1-31-35
Abstract
Aim — to estimate endothelium lesion, quantity and thrombocyte aggregation function correlation in viral chronic hepatitis C (CHC) and hepatic cirrhosis (HC).
Materials and methods. 50 CHC patients and 28 HC patients were examined. Using IFA method the total nitric oxide, endothelin‑1, vasculoendothelial growth factor levels, Willebrand factor (vWF) activity were investigated, blood plasma desquamated endotheliocyte (DEC)
number was calculated with Hladovec method, 1978, thrombocyte aggregation (TA) with ADP, collagen, ristocetine was determined.
Results. DEC and vWF demonstrated correlation in CHC (p = 0.014) and HC (p = 0.000004). In HC patients reliable correlation of all the investigated indices of endothelium lesion with the thrombocyte number and TA was detected, but in CHC patients no correlations were revealed. Thus, significant elevation of TA with ristocetine was noted only in CHC. Decrease in thrombocyte amount among CHC patients and,
especially in HC, and heightened vWF activity could change true TA indices. The corrected TA, whose indices in hepatic diseases significantly
increased, was calculated taking into account the correction factor vWF / thrombocytes that in CHC did not differ from that of healthy patients and in HC was essentially higher.
Conclusion. Endothelium dysfunction markers in CH and HC demonstrate correlation with thrombocyte reduction and TA elevation. Determination
of corrected TA permits to reveal disturbances of thrombocyte hemostasis in the form of elevated aggregation in all CHC and HC patients.
About the Author
A. P. Shchekotova
SBEI HPE Perm State Academy of Medicine named after Academician E.A.Wagner of Ministry of Health and Social Development of Russia
Russian Federation
Russian Federation
References
1. Meigs J.B., Hu F.B., Rifai N., Manson J.E. Biomarkers of endothelial dysfunction and risk of type 2
2. diabetes mellitus. JAMA 2004;297:1978−86.
3. Долгов В.В., Свирин П.В. Лабораторная диагностика нарушений гемостаза. М.: Триада, 2005.
4. Marx О.D, Christophep J., Leating А., et al. Altered thrombus formation in von Willebrand factor-deficient mice expressing von Willebrand factor variants with defective binding to collagen or GPIIbIIIa. Blood 2008;112(3):603−9.
5. Helmy A., Newby D.E., Jalan R., et al. Enhanced vasodilatation to endothelin antagonism in patients with compensated cirrhosis and the role of nitric oxide. Gut 2003;52:410−5.
6. Коломоец М.Ю., Хухлина О.С., Зоевидка О.С. Состояние системы гемостаза у больных хроническим гепатитом и холециститом. Украинский медицинский журнал 2004;(4):42−5.
7. Соринсон С.Н. Вирусные гепатиты в клинической практике. СПб.: ТЕЗА, 1996.
8. Le Couter J., Moritz D.R., Li B., et al. Angiogenesis-independent endothelial protection of liver: role of VEGFR‑1. Science 2003;299:890−3.
9. Щёкотова А.П. Дисфункция и повреждение эндотелия при гепатобилиарной патологии. Уральский медицинский журнал 2010;(1):96−9.
10. Баркаган З.С., Момот А.П. Диагностика и контролируемая терапия нарушений гемостаза. М.: Ньюамед, 2001.
11. Gabbasov Z.A., Popov E.G., Gavrilov I.Y., Pozin EYa. Platelet aggregation: the use of optical density fluctuations to study microaggregate formаtion in platelet suspension. Thromb Res 1989;54(3):215−23.
Review
For citations:
Shchekotova A.P. ENDOTHELIUM LESION MARKERS AND THROMBOCYTE AGGREGATION IN CHRONIC HEPATITIS AND HEPATIC CIRRHOSIS. The Clinician. 2012;6(1):31-35. (In Russ.) https://doi.org/10.17650/1818-8338-2012-1-31-35
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