Immunologic measurement of antithrombin III-heparin cofactor and α2macroglobulin in disseminated intravascular coagulation and hepatic failure coagulopathy

Damus, Paul S.; Wallace, G. A.

doi:10.1016/0049-3848(75)90148-6

Cited by 70 publications

(27 citation statements)

References 16 publications

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“…Another marker of intravascular coagulation is a reduction in the level of physiological anticoagulants such as antithrombin I11 and protein C. Indeed, lowered concentrations of antithrombin I11 have been described during sickle cell crisis [8], but this finding is not specific, since transient reductions in this protein may occur with alterations in hepatic synthetic capacity [30]. We found reductions in protein C during the steady state and during crisis, but in some patients factor X was proportionately reduced, suggesting compromised hepatic synthesis.…”

Section: Discussionmentioning

confidence: 96%

Is sickle cell crisis a thrombotic event?

Green

Scott

1986

American J Hematol

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Although large vessel thrombi are occasionally reported in patients with homozygous sickle cell disease, the role of intravascular coagulation in typical pain crises is controversial. Therefore, we studied 24 sickle cell patients during and between episodes of pain crisis, using several sensitive tests of hemostasis. Fibrinogen was measured by a clotting assay, beta-thromboglobulin (beta-TG) and fibrinopeptide A (FPA) were quantitated by radioimmunoassay, and protein C was determined by absorbing the zymogen from test plasma, activating it with thrombin-thrombomodulin complex, and measuring activity with a selective synthetic substrate. Fibrinogen was elevated in asymptomatic patients (355 +/- 145 mg/dl) but was no different from the value in these same patients during crisis (333 +/- 180 mg/dl, p greater than 0.1). Similarly, beta-TG 136 +/- 52 ng/ml vs 118 +/- 56; FPA 3.7 +/- 4.8 ng/ml vs 5.2 +/- 4.5, and protein C 71 +/- 20% vs 66 +/- 19 showed no important changes during crisis. However, all these values were significantly different from those in age- and sex-matched healthy controls. beta-TG, fibrinogen, and FPA were elevated (p less than 0.001, 0.005, and 0.05, respectively), and protein C was decreased (p less than 0.003). We conclude that while chronic intravascular coagulation is common in patients with sickle cell disease, there is no evidence that the pain crisis per se is a thrombotic event.

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Section: Discussionmentioning

confidence: 96%

Is sickle cell crisis a thrombotic event?

Green

Scott

1986

American J Hematol

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“…The incidence of venous thromboembolism in AT deficient individuals is 20 times higher [25]. AT deficiency can also be acquired in conditions such as DIC, liver disease and nephritic syndrome [26,27]. Long term management of these cases is by anticoagulant therapy.…”

Section: Discussionmentioning

confidence: 99%

Hypercoagulable State

Jaiprakash¹,

Kumar

Chopra³

et al. 2006

Medical Journal Armed Forces India

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Background : The hypercoagulable state results from a complex interplay of blood coagulation factors, coagulation-inhibitory factors, platelets and the vascular endothelium. Imbalance of the complex interplay between these factors results in thrombosis often complicated by embolism. The causes of thrombosis are varied and maybe congenital or acquired. The current interest is centered on the congenital deficiency of coagulation inhibitors as there is an increasing awareness of their involvement in thrombosis, especially in the young. Methods: A total of 42 patients with thrombosis were studied. The most common clinical presentation was deep vein thrombosis. All the cases were evaluated for coagulation inhibitors Antithrombin, resistance to activated protein C, Protein C and Protein S using standard assay kits. Results: Resistance to activated protein C (n=10) was seen to be the commonest cause of thrombophilia. This was followed by deficiency of Antithrombin (n-4), Protein C (n=3) and Protein S (n=2). Majority of our cases were in the third decade of life. Conclusion: The identification of the underlying aetiology is important for instituting specific therapy and patient management.

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“…It provides results based on a method initially described by Clauss [5]. Antithrombin III levels were measured using MDAR Antithrombin III which is a chromogenic assay based on the amidolytic method for the quantitative determination of antithrombin III in human plasma [6]. MDAR Protein C is a chromogenic assay which measures functional levels of protein C in plasma by an amidolytic method using a synthetic chromogenic substrate [7].…”

Section: Study Protocol and Assaysmentioning

confidence: 99%