The thrombotic diathesis associated with the presence of phospholipid antibodies may be due to low levels of free protein S

Parke, Ann L.; Weinstein, Ralph E.; Bona, Robert; Maier, Donald; Walker, Frederick J.

doi:10.1016/0002-9343(92)90679-6

Cited by 69 publications

(27 citation statements)

References 26 publications

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“…Protein S dcficicncies (7,14,15) and the inhibition of fibrinolysis (22,23) can also be excluded, since we used normal blood with the investigated aCL in the absence of viable endothelial cells. In addition, in this system, most of the mechanisms related to protein C or protein S activity (4,5,(24)(25)(26) can be reasonably discarded.…”

Section: Discussionmentioning

confidence: 99%

“…A number of mechanisms have been proposed to explain how aPL cause the clinical manifestations of APS, but none of the proposed mechanisms can individually explain all of the available data. The mechanisms of aPL activity that have been evaluated include fibrinolysis (22,23), as well as interaction with cndothelial cells (3,12), proteins C and S (4,5,(24)(25)(26), platelets (3,6,27), and more recently, monocytes (7,8,28). Some aCL bind cardiolipin only in the presence of their cofactor, P,-glycoprotein I (P,GPI) (29,30), and this &GPT dependence seems to be related to the ability of aCL to produce the clinical manifestations of A P S .…”

mentioning

confidence: 99%

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Effects of human monoclonal anticardiolipin antibodies on platelet function and on tissue factor expression on monocytes

Reverter

Tàssies

Font

et al. 1998

Arthritis & Rheumatism

102

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Effects of human monoclonal anticardiolipin antibodies on platelet function and on tissue factor expression on monocytes

Reverter

Tàssies

Font

et al. 1998

Arthritis & Rheumatism

102

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“…Various potential mechanisms have been proposed to explain the increased risk of thrombosis in SLE and APL syndrome. These include a decrease in the plasma level of free protein S [69], and the occurrence of a plasma inhibitor of endothelial activation of protein C [70]. A plasma inhibitor of factor Va degradation [71], increased plasma level of PAI-1 [72], and a plasma factor which inhibits endothelial cell release and/or production of PGI 2 [73] have also been reported.…”

Section: Antiphospholipid Antibodiesmentioning

confidence: 99%

The role of thrombosis in severe pulmonary hypertension

Chaouat¹,

Weitzenblum²,

Higenbottam³

1996

Eur Respir J

116

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Considering the important surface in pulmonary circulation where blood can interact with the endothelium, the maintenance of blood fluidity through the lung, by antithrombotic pathways and products of the endothelium, is essential. This function appears to be ineffective in primary pulmonary hypertension and in severe secondary pulmonary hypertension. Thrombotic lesions are frequently found in pulmonary arteries in these diseases.Thrombin activity appears to be increased in severe pulmonary hypertension. Antithrombotic pathway disorders may account for this abnormality, particularly in chronic thromboembolic pulmonary hypertension and primary pulmonary hypertension. Injured endothelium, a constant feature in severe pulmonary hypertension, either primary or secondary, enhances thrombus formation in pulmonary vessels. This is probably related to thrombomodulin and tissue factor imbalance, impairment of prostacyclin and nitric oxide release, as well as inefficiency of fibrinolysis. Moreover, platelets appear to be activated in the pulmonary circulation of these patients. They release several mediators acting on vascular tone and as mitogenic agents, and may also contribute to thrombin and clot generation. Long-term oral anticoagulant and continuous infusion of prostacyclin, treatments which impede thrombosis, are known to improve the survival rate in patients with primary pulmonary hypertension.These are the strongest arguments, so far, in favour of the role of thrombosis in severe pulmonary hypertension. However, we do not know whether these abnormalities result from a previous vascular injury or represent the primary disturbance.

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“…In several studies, acquired free protein-S deficiency was associated with both antiphospholipid antibodies and procoagulant laboratory measures in patients with SLE and the APS [21,46,50,51]. Acquired deficiency of free protein-S results from enhanced binding of protein S by its circulating plasma inhibitor, C4BP.…”

Section: Acquired Protein-s Deficiencymentioning

confidence: 98%

Clinical trials for the antiphospholipid syndrome

Merrill

2000

Curr Rheumatol Rep

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The thrombotic diathesis associated with the presence of phospholipid antibodies may be due to low levels of free protein S

Cited by 69 publications

References 26 publications

Effects of human monoclonal anticardiolipin antibodies on platelet function and on tissue factor expression on monocytes

Effects of human monoclonal anticardiolipin antibodies on platelet function and on tissue factor expression on monocytes

The role of thrombosis in severe pulmonary hypertension

Clinical trials for the antiphospholipid syndrome

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