Hamostaseologie 2021; 41(S 01): S37
DOI: 10.1055/s-0041-1728156
Poster
Coagulation and fibrinolysis

Hepatic Disorders Contribute to Platelet Dysfunction

C Bacher
1   Pathology, Loyola University Medical Center, Maywood
,
A Farooqui
1   Pathology, Loyola University Medical Center, Maywood
,
F Siddiqui
1   Pathology, Loyola University Medical Center, Maywood
,
B Daravath
1   Pathology, Loyola University Medical Center, Maywood
,
D Hoppensteadt
1   Pathology, Loyola University Medical Center, Maywood
,
O Iqbal
1   Pathology, Loyola University Medical Center, Maywood
,
J Fareed
1   Pathology, Loyola University Medical Center, Maywood
,
M George
1   Pathology, Loyola University Medical Center, Maywood
,
D Van Thiel
1   Pathology, Loyola University Medical Center, Maywood
› Author Affiliations
 
 

    Objective The role of platelets in hemostasis involves their adherence to sites of vessel injury, aggregation to form plugs. Agents that physiologically activate platelets in vivo include adenosine diphosphate (ADP), epinephrine, collagen, thromboxane A2 (TxA2) and serotonin. Vascular and platelet dysfunction represent complications of hepatic disease. The purpose of this study is to investigate the effect of various agonists on platelet aggregation profile of patient with hepatic disease.

    Material and Methods Icteric Samples from the clinical lab from Loyola University medical center were randomly selected for this study (n=25). Blood samples from the healthy donors were included to prepare platelet rich plasma (PRP) and platelet poor plasma (PPP). PRP and PPP from various donors were separated to make pools. Four different pools were made namely Normal PRP, Icteric PRP, Icteric PRP + Normal PPP 1:1, Normal PRP + Icteric PPP1:1. Agonists such as ADP, arachidonic acid (AA), epinephrine and collagen were used to activate the platelets. The final assay concentration for ADP is 20 uM, AA is 500 ug/ml, collagen is 190 ug/ml and epinephrine is 10 ug/ml.

    Results All results were compiled in terms of percent aggregation of platelets and represented as mean ± standard deviation. Normal PRP showed platelet aggregation response reaching a peak aggregation of 93.± 27.70 with ADP agonist. Icteric PRP, and two different pools did not show any significant platelet aggregation with ADP. Varying degrees of the inhibition of platelet aggregation was noted with different agonists.

    Conclusion On the basis of the results we concluded that normal PRP showed platelet aggregation response. Icteric PRP and different pools (as shown above) did not show any platelet aggregation response. This data suggests that the icteric plasma contains an endogenous substance which produces the inhibitory effect on agonist induced platelet aggregation.


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    Publication History

    Article published online:
    18 June 2021

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