Polymorphism of the Fc? Receptor II as a Possible Predisposing Factor for Heparin-Induced Thrombocytopenia

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F15%3A33154990" target="_blank" >RIV/61989592:15110/15:33154990 - isvavai.cz</a>

Výsledek na webu

<a href="http://dx.doi.org/10.7754/Clin.Lab.2015.141207" target="_blank" >http://dx.doi.org/10.7754/Clin.Lab.2015.141207</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.7754/Clin.Lab.2015.141207" target="_blank" >10.7754/Clin.Lab.2015.141207</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Polymorphism of the Fc? Receptor II as a Possible Predisposing Factor for Heparin-Induced Thrombocytopenia

Popis výsledku v původním jazyce

Background: Heparin-induced thrombocytopenia (HIT) represents a serious complication of heparin treatment. IgG antibodies binding platelet factor 4 (PF4) and heparin trigger the clinical manifestations of HIT. However, only a portion of the antibodies have the ability to activate platelets, and these can be identified by a platelet aggregation test (functional testing). However, this expression has been detected to have a molecular cause, which is a mutation of Fc?RIIa. The Fc?RIIa receptor is responsible for the activation of platelets by antibodies in HIT. Methods: To determine HIT, impedance aggregometry using the Multiplate analyzer (MEA) as heparin-induced aggregation technique and the Technozym HIT IgG ELISA test were used. The MEA method uses sensitization of donor platelets with patient plasma in the presence of heparin at a concentration of 0.5 IU/mL. The results were compared with the ELISA test. Mutation of Fc?RIIa was assessed using the asymmetric real-time PCR method that

Název v anglickém jazyce

Polymorphism of the Fc? Receptor II as a Possible Predisposing Factor for Heparin-Induced Thrombocytopenia

Popis výsledku anglicky

Background: Heparin-induced thrombocytopenia (HIT) represents a serious complication of heparin treatment. IgG antibodies binding platelet factor 4 (PF4) and heparin trigger the clinical manifestations of HIT. However, only a portion of the antibodies have the ability to activate platelets, and these can be identified by a platelet aggregation test (functional testing). However, this expression has been detected to have a molecular cause, which is a mutation of Fc?RIIa. The Fc?RIIa receptor is responsible for the activation of platelets by antibodies in HIT. Methods: To determine HIT, impedance aggregometry using the Multiplate analyzer (MEA) as heparin-induced aggregation technique and the Technozym HIT IgG ELISA test were used. The MEA method uses sensitization of donor platelets with patient plasma in the presence of heparin at a concentration of 0.5 IU/mL. The results were compared with the ELISA test. Mutation of Fc?RIIa was assessed using the asymmetric real-time PCR method that

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

FD - Onkologie a hematologie

OECD FORD obor

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Projekt

<a href="/cs/project/NT14394" target="_blank" >NT14394: Vliv exprese tkáňového faktoru na vznik těhotenských komplikací</a><br>

Návaznosti

S - Specificky vyzkum na vysokych skolach

Rok uplatnění

2015

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Clinical Laboratory

ISSN

1433-6510

e-ISSN

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Svazek periodika

61

Číslo periodika v rámci svazku

8

Stát vydavatele periodika

DE - Spolková republika Německo

Počet stran výsledku

6

Strana od-do

1027-1032

Kód UT WoS článku

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EID výsledku v databázi Scopus

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