hematology-2018-posters-abstracts

Page 35

allied

academies

August 23-24, 2018 | London, UK

Hematology and Oncology

International Conference on

Journal of Hematology and Blood Disorder | Volume 2

Chronic liver disease and hemostatic disturbances

Olfat M Hendy

Menoufia University, Egypt

he liver is the primary site of synthesis of most of the clotting

factors and the proteins involved in the fibrinolytic system.

These include all the vitamin K-dependent coagulation proteins

(factors II, VII, IX, X, ATIII, protein C, protein S and protein Z), as

well as factor V, XIII, fibrinogen, antithrombin, and plasminogen.

Decreased plasma concentrations for all proteins except for

factor VIII are observed in patients with hepatic failure. Besides

low levels of clotting factors due to impaired synthesis capacity,

also dysfunctional proteins are found in patients with liver

failure. Additionally, liver plays a vital role in the regulation of

anticoagulation. Removal and clearance of activated clotting

and fibrinolytic factors, especially tissue plasminogen activator

(tPA), is mediated through the hepatic reticuloendothelial

system. Multiple alterations in platelet number and function

can be found in patients with liver disease. Amild tomoderately

reduced platelet count is frequently present in patients

with acute or chronic liver failure. The net outcome of these

alterations in the hemostatic system is a bleeding diathesis,

although thrombosis of the portal vein is also frequently seen in

patients with cirrhosis. As liver disease has multiple effects on

the hemostatic system, it is difficult to determine which factors

contributemost to the bleeding diathesis. No single coagulation

test is predictive of hemorrhage or thrombosis in patients with

chronic liver disease. AprolongedPTor international normalized

ratio(INR)isakeyindicatorofhepaticdysfunctionandcommonly

used as a trigger for liver transplantation. Thrombophilia tests:

levels of the naturally occurring anticoagulants (ATIII, protein

C, protein S) may all be reduced as a consequence of liver

disease. In conclusion: Because of the hemostatic problem of

liver disease is multifactorial, the follow up and management

of chronic liver disease may ameliorate the bad prognosis.