1987Thrombosis and HaemostasisRequires access

PROTEIN S AND ANTICARDIOLIPIN ANTIBODIES IN PATIENTS WITH LUPUS ANTICOAGULANT WITH OR WITHOUT THROMBOSIS

Simon Panzer, Ingrid Pabinger, Robert Dudczak, Emanuel Schulz, E Wurz, Klaus Lechner, Katharina Lechner

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Abstract

Arterial and venous thrombosis frequently occur in patients with lupus anticoagulant. We investigated in patients with lupus anticoagulant the possible association between protein S:Ag deficiency and/or anticardiolipin antibodies and a history of thrombosis. In 27 patients (8 with and 19 without a history of thromboembolic disease) free protein S:Ag was determined with immunoelectrophoresis in PEG 8000 precipitated plasma. Anticardiolipin antibodies were measured in 22 patients (10 with thromboembolism) by means of a solid phase radioimmunoassay. Free plasma protein S:Ag was normal or elevated in 25 patients and slightly decreased (protein S:Ag 67%) in 2 patients without thromboembolism. 2-dimensional electrophoresis revealed a normal distribution of the free and of the complexed form of protein S:Ag. Anticardiolipin antibodies were found in 6 out of 10 patients with a history of thrombosis (5 of 7 with venous thrombosis, 1 of 1 with cerebral infarction , none of 2 with combined venous and arterial thromboembolism) and in 4 out of 12 patients without a history of thrombosis. We conclude 1. the thrombophilic state in patients with lupus anticoagulant cannot be explained by a reduction of protein S:Ag, and 2. there seems to be no correlation between the presence or absence of anticardiolipin antibodies and the development of thromboembolic disease.

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What this paper is about

Arterial and venous thrombosis frequently occur in patients with lupus anticoagulant. We investigated in patients with lupus anticoagulant the possible association between protein S:Ag deficiency and/or anticardiolipin antibodies and a history of thrombosis. In 27 patients (8 with and 19 without a history of thromboembolic disease) free protein S:Ag was determined with immunoelectrophoresis in PEG 8000 precipitated plasma. Anticardiolipin antibodies were measured in 22 patients (10 with thromboembolism) by means of a solid phase radioimmunoassay. Free plasma protein S:Ag was normal or elevated in 25 patients and slightly decreased (protein S:Ag 67%) in 2 patients without thromboembolism. 2-dimensional electrophoresis revealed a normal distribution of the free and of the complexed form of protein S:Ag. Anticardiolipin antibodies were found in 6 out of 10 patients with a history of thrombosis (5 of 7 with venous thrombosis, 1 of 1 with cerebral infarction , none of 2 with combined venous and arterial thromboembolism) and in 4 out of 12 patients without a history of thrombosis. We conclude 1. the thrombophilic state in patients with lupus anticoagulant cannot be explained by a reduction of protein S:Ag, and 2. there seems to be no correlation between the presence or absence of anticardiolipin antibodies and the development of thromboembolic disease.

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Available abstract

Arterial and venous thrombosis frequently occur in patients with lupus anticoagulant. We investigated in patients with lupus anticoagulant the possible association between protein S:Ag deficiency and/or anticardiolipin antibodies and a history of thrombosis. In 27 patients (8 with and 19 without a history of thromboembolic disease) free protein S:Ag was determined with immunoelectrophoresis in PEG 8000 precipitated plasma. Anticardiolipin antibodies were measured in 22 patients (10 with thromboembolism) by means of a solid phase radioimmunoassay. Free plasma protein S:Ag was normal or elevated in 25 patients and slightly decreased (protein S:Ag 67%) in 2 patients without thromboembolism. 2-dimensional electrophoresis revealed a normal distribution of the free and of the complexed form of protein S:Ag. Anticardiolipin antibodies were found in 6 out of 10 patients with a history of thrombosis (5 of 7 with venous thrombosis, 1 of 1 with cerebral infarction , none of 2 with combined venous and arterial thromboembolism) and in 4 out of 12 patients without a history of thrombosis. We conclude 1. the thrombophilic state in patients with lupus anticoagulant cannot be explained by a reduction of protein S:Ag, and 2. there seems to be no correlation between the presence or absence of anticardiolipin antibodies and the development of thromboembolic disease.

Key concepts: Lupus anticoagulant, Medicine, Thrombosis, Anticardiolipin antibodies, Anticoagulant, Venous thrombosis, Internal medicine, Gastroenterology

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