Roles of protein C, protein S, and antithrombin III in acute leukemia

2006 ◽  
Vol 81 (3) ◽  
pp. 171-174 ◽  
Author(s):  
Ashish Dixit ◽  
Meganathan Kannan ◽  
M. Mahapatra ◽  
Ved P. Choudhry ◽  
Renu Saxena
Keyword(s):  
Acute Leukemia ◽  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
C Protein

Protein C, protein S and antithrombin III in children with portal vein obstruction

1997 ◽  
Vol 27 (1) ◽  
pp. 132-135 ◽  
Author(s):  
Claire Dubuisson ◽  
Catherine Boyer-Neumann ◽  
Martine Wolf ◽  
Dominique Meyer ◽  
Olivier Bernard
Keyword(s):  
Portal Vein ◽  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
C Protein ◽  
Portal Vein Obstruction

scholarly journals Thrombophilia And Arterial Ischemic Stroke

2017 ◽  
pp. 45
Author(s):  
A.A. Abrishamizadeh
Keyword(s):  
Ischemic Stroke ◽  
Vitamin K ◽  
Arterial Thrombosis ◽  
Protein C ◽  
Antithrombin Iii ◽  
Factor V Leiden ◽  
Protein S ◽  
Factor V ◽  
Factor V Leiden Mutation ◽  
C Protein

Ischemic stroke (IS) is a common cause of morbidity and mortality with significant socioeconomic impact especially when it affects young patients. Compared to the older adults, the incidence, risk factors, and etiology are distinctly different in younger IS. Hypercoagulable states are relatively more commonly detected in younger IS patients.Thrombophilic states are disorders of hemostatic mechanisms that result in a predisposition to thrombosis .Thrombophilia is an established cause of venous thrombosis. Therefore, it is tempting to assume that these disorders might have a similar relationship with arterial thrombosis. Despite this fact that 1-4 % of ischemic strokes are attributed to Thrombophillia, this   alone rarely causes arterial occlusions .Even in individuals with a positive thrombophilia screen and arterial thrombosis, the former might not be the primary etiological factor.Thrombophilic   disorders can be broadly divided into inherited or acquired conditions. Inherited thrombophilic states include deficiencies of natural anticoagulants such as protein C, protein S, and antithrombin III (AT III) deficiency, polymorphisms causing resistance to activated protein C(Factor V Leiden mutation), and disturbance in the clotting balance (prothrombin gene 20210G/A variant). Of all the inherited  thrombophilic disorders, Factor V Leiden mutation is perhaps the commonest cause. On the contrary, acquired thrombophilic disorders are more common and include conditions such as the antiphospholipid syndrome, associated with lupus anticoagulant and anticardiolipin antibodies.The more useful and practical approach of ordering various diagnostic tests for the uncommon thrombophilic states tests should be determined by a detailed clinical history, physical examination, imaging studies and evaluating whether an underlying hypercoagulable state appears more likely.The laboratory thrombophilia   screening should be comprehensive and avoid missing the coexisting defect and It is important that a diagnostic search protocol includes tests for both inherited and acquired thrombophilic disorders.Since the therapeutic approach (anticoagulation and thrombolytic therapy) determines the clinical outcomes, early diagnosis of the thrombophilic  disorders plays an important role. Furthermore, the timing of test performance of some of the  thrombophilic  defects (like protein C, protein S, antithrombin III and fibrinogen levels) is often critical since these proteins can behave as acute phase reactants and erroneously elevated levels of these factors may be observed in patients with acute thrombotic events. On the other hand, the plasma levels of vitamin K-dependent proteins (protein C, protein S and APC resistance) may not be reliable in patients taking vitamin K antagonists. Therefore, it is suggested that plasma-based assays for these disorders should be repeated3 to 6 months after the initial thrombotic episode to avoid false-positive results and avoid unnecessary prolonged   anticoagulation therapy. The assays for these disorders are recommended after discontinuation of oral anticoagulant treatment or heparin for at least 2 weeks.    

Protein C, Protein S, and Antithrombin III Levels in Patients on Continuous Ambulatory Peritoneal Dialysis and Hemodialysis

Nephron ◽  
1990 ◽  
Vol 56 (3) ◽  
pp. 271-276 ◽  
Author(s):  
Kar Neng Lai ◽  
Jane A. Yin ◽  
Patrick M.P. Yuen ◽  
Philip K.T. Li
Keyword(s):  
Peritoneal Dialysis ◽  
Continuous Ambulatory Peritoneal Dialysis ◽  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
C Protein

Effect of Hemodialysis on Protein C, Protein S, and Antithrombin III Levels

1991 ◽  
Vol 17 (1) ◽  
pp. 38-42 ◽  
Author(s):  
Kar-Neng Lai ◽  
Jane A. Yin ◽  
Patrick M.P. Yuen ◽  
Philip K.T. Li
Keyword(s):  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
C Protein

Relationship between Maternal Antithrombin III and Protein C/Protein S Levels before, during and after Delivery

1990 ◽  
Vol 30 (2) ◽  
pp. 87-90 ◽  
Author(s):  
T.T. Lao ◽  
J.A. Yin ◽  
W.K. Ng ◽  
P.M.P. Yuen
Keyword(s):  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
C Protein

Thrombosis during Pregnancy and Surgery in Patients with Congenital Deficiency of Antithrombin III, Protein C, Protein S

1994 ◽  
Vol 71 (06) ◽  
pp. 799-800 ◽  
Author(s):  
V De Stefano ◽  
G Leone ◽  
S Mastrangelo ◽  
A Tripodi ◽  
F Rodeghicro ◽  
...  
Keyword(s):  
Protein C ◽  
Antithrombin Iii ◽  
Protein S ◽  
C Protein ◽  
Congenital Deficiency

Protein C, Protein S and c4b-Binding Protein in Severe lnfection and Septic Shock

1991 ◽  
Vol 65 (02) ◽  
pp. 126-129 ◽  
Author(s):  
J F Hesselvik ◽  
J Malm ◽  
B Dahlbäck ◽  
M Blombäck
Keyword(s):  
Septic Shock ◽  
Total Protein ◽  
Protein C ◽  
Blood Donors ◽  
Antithrombin Iii ◽  
Severe Infection ◽  
Protein S ◽  
C Protein ◽  
Normal Value ◽  
Free Protein

SummaryWe measured concentrations of the natural anticoagulant protein C; its cofactor, protein S; and the carrier protein C4bbinding protein (C4BP), in 24 patients with severe infection and 13 with septic shock. Decreased antithrombin III levels were found in 16 of 24 infection patients and all shock patients; high thrombin-antithrombin (TAT) complexes were present in 16 of 24 infection and 12 of 13 shock patients. Protein C concentrations were significantly reduced compared to healthy blood donors, to 60 ± 14% (infection) and 47 ± 20% (septic shock) (mean ± 1 SD). Total protein S levels were not reduced (119 ± 36.7 and 88 ± 20.0%, normal value 96±15%). Free protein S was also normal (27 ± 9.4 and 30 ± 8.7%, normal value 29 ± 9%). The percentage free of total protein S was normal in shock patients (35 ± 8.5%), but significantly reduced in patients without shock (23 ± 5.3%). C4BP was significantly higher than normal in the latter group (135 ± 43%), but not in the shock group (118 ± 40%), possibly due to increased consumption. Thus, no deficiency of total or free protein S was found in these patients, who had evidence of activated coagulation but no clinical DIC.

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