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Sažeci 2. Hrvatskog kongresa medicinske biokemije SEKCIJSKA PREDAVANJA S5/5 HEMOREOLOGIJA U POREMEĆAJIMA HEMOSTAZE V. Lipovac Klinika za dijabetes, endokrinologiju i bolesti metabolizma "Vuk Vrhovac", Zagreb Glavni hemoreološki parametri koji određuju viskoznost krvi su hematokrit, viskoznost plazme, agregacija i sklonost eritrocita promjenama oblika te broj i sklonost leukocita promjenama oblika. Poremećaj jednog ili više hemoreoloških čimbenika ima za posljedicu povećanje viskoznosti krvi. Nastale promjene mehanizmom povratne sprege dalje povećavaju hiperviskoznost krvi i pogoršavaju početne poremećaje te postupno dovode do pojave ishemije, tromboze, gangrene itd. Brojna klinička i epidemiološka ispitivanja potvrdila su povezanost između hemoreoloških promjena i bolesti s poremećajima hemostaze. Znatan utjecaj na stupanj hemoreoloških promjena imaju i genetski čimbenici, stres, lijekovi i dr. Većina se hemoreoloških poremećaja danas može in vitro mjeriti specifičnim i preciznim metodama, ali širu primjenu u kliničkoj praksi jedino je steklo određivanje viskoznosti plazme. U posljednje vrijeme postignut je znatan napredak u ispitivanju mehanizama nastanka hemoreoloških poremećaja na molekularnoj razini, što omogućuje bolje razumijevanje interakcije između pojedinih krvnih stanica kao i učinka medijatora i njihovog djelovanja na stanice endotela. Djelotvornost pojedinih postupaka i farmakoloških agensa na poboljšanje hemoreoloških svojstava krvi potvrđena su u raznim in vitro ili u kratkoročnim in vivo ispitivanjima, ali još nedostaju dugoročna ispitivanja koja bi pokazala uspješnost terapijskih postupaka u prevenciji hemoreoloških poremećaja. 48 BIOCHEMIA MEDICA god. 6, br. 1, 1996.
SEKCIJSKA PREDAVANJA Sažeci 2. Hrvatskog kongresa medicinske biokemije S5/6 SELECTED TOPICS IN HEMATOLOGICALPRACTICE: FOCUS ON THROMBOPHILIA AND ACTIVATED PROTEIN C RESISTANCE I. Vučenik Department of Medical and Research Technology, University of Maryland School of Medicine, Baltimore, Maryland, USA Thrombophilia is a hemostatic disorder characterized by thromboembolism and thrombosis. Factors causing thrombophilia may be inherited or acquired. Inherited alterations of coagulation proteins clearly associated with a prethrombotic state are: antithrombin III deficiencv, protein C deficiency, protein S deficiencv, dysfibrinogenemias, and recently discovered, activated protein resistance (APCresistance). Alternately, acquired risk factors include surgery, pregnancy, immobilization, oral contraceptives, and inflammatory states. In 1993 APC-resistance was described as a newly recognized cause of thrombophilia. Soon it has become apparent that APC-resistance in Western societies is the most frequent genetic risk factor for familiar thrombophilia, and that it is at least tenfold more common than any of the other genetic causes of thromboembolic disease, despite the fact that its prevalence may vary significantly between different populations. It affects an estimated 5% of the general population, and it was found in up to 60% of patients with venous thrombosis. The mode of inheritance is suggested to be autosomal dominant. The pathogenesis of APC-resistance is associated with a single point mutation in the factor V gene, which predicts substitution of an arginine at position 506 with a glutamine. This abnormality was found in more than 90% of patients with APC-resistance. Mutated factor V is also known as factor V Leiden. Thrombin and factor Xa activate mutated factor V normally, while its impaired inactivation by APC results in life-long hypercoagulability. Laboratory determination of APC-resistance can be made with a functional, APTT-based, APC-resistance test and with factor V gene mutation analysis. Because these two methods provide complementary information, both the functional APCresistance test and the factor V gene mutation analysis are required for optimal evaluation of a single patient. This approach is not always possible for practical and economic reasons. The suggested management of APC-resistant patients is prophylactic treatment in situations known to provoke thrombosis, such as major surgery, pregnancy, or usage of oral contraception. BIOCHEMIA MEDICA god. 6, br. 1, 1996 49
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