Acquired Protein S Deficiency, Likely due to Anti-PS Autoantibodies, following a Thrombotic Event in a Patient with a Systemic Lupus erythematosus

1997 ◽  
Vol 78 (05) ◽  
pp. 1416-1417 ◽  
Author(s):  
P E Morange ◽  
M C Alessi ◽  
M C Barthet ◽  
M F Aillaud ◽  
J R Harlé ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Thrombotic Event ◽  
Protein S ◽  
Protein S Deficiency ◽  
Systemic Lupus ◽  
S Deficiency

Free Protein S Deficiency May Be Found in Patients with Antiphospholipid Antibodies who Do not Have Systemic Lupus Erythematosus

1996 ◽  
Vol 76 (05) ◽  
pp. 689-691 ◽  
Author(s):  
M A Crowther ◽  
M Johnston ◽  
J Weitz ◽  
J S Ginsberg
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Antiphospholipid Antibodies ◽  
Protein S ◽  
Antiphospholipid Antibody ◽  
Protein S Deficiency ◽  
Systemic Lupus ◽  
Free Protein ◽  
S Deficiency ◽  
History Of

SummaryIn order to determine if there is a relationship between antiphospholipid antibodies and reduced free protein S levels, we evaluated 21 patients who had an antiphospholipid antibody but had neither a history of venous thromboembolism nor systemic lupus erythematosus (cases) and 55 matched controls, who did not have an antiphospholipid antibody, a history of thrombosis or systemic lupus erythematosus. Cases and controls had similar protein C and antithrombin levels. Six of 21 cases had reduced free protein S antigen levels, compared to 5 of 55 controls (x 2 = 5.823 p <0.025). In addition, the mean free protein S level was significantly lower in cases than in controls (0.30 ± 0.09 units vs 0.39 ± 0.13 units, p <0.01, two-tailed Student’s t-test). We conclude that antiphospholipid antibodies are associated with a significant decrease in free protein S levels, and that this acquired free protein S deficiency may contribute to the thrombotic diathesis seen in patients with antiphospholipid antibodies.

Protein S deficiency revealed by skin necrosis in a patient with lupus

Lupus ◽  
2019 ◽  
Vol 28 (7) ◽  
pp. 903-905 ◽  
Author(s):  
A Plana-Pla ◽  
I Bielsa Marsol ◽  
C Ferrandiz Foraster
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Venous Thromboembolism ◽  
Lupus Erythematosus ◽  
Arterial Thrombosis ◽  
Skin Necrosis ◽  
Protein S ◽  
Protein S Deficiency ◽  
Systemic Lupus ◽  
Skin Ulcers ◽  
S Deficiency

Protein S deficiency is rare in systemic lupus erythematosus (SLE) and is generally associated with the presence of antiphospholipid (APL) antibodies. Lack of protein S can cause skin necrosis, but when it does it is generally in response to warfarin exposure. In this article, we describe the case of a patient who had not received warfarin and without APL antibodies who developed extensive skin necrosis due to protein S deficiency. It is important to investigate protein S deficiency in patients with lupus and extensive skin ulcers as it is a sign of arterial thrombosis and venous thromboembolism.

scholarly journals Insights into the Procoagulant Profile of Patients with Systemic Lupus Erythematosus without Antiphospholipid Antibodies

2020 ◽  
Vol 9 (10) ◽  
pp. 3297
Author(s):  
Elena Monzón Manzano ◽  
Ihosvany Fernández-Bello ◽  
Raúl Justo Sanz ◽  
Ángel Robles Marhuenda ◽  
Francisco Javier López-Longo ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Lupus Erythematosus ◽  
Antiphospholipid Antibodies ◽  
Thrombin Generation ◽  
Thrombotic Event ◽  
Systemic Lupus ◽  
Activation Markers ◽  
Global Tests ◽  
Platelet Aggregates ◽  
Pai 1

We aimed to identify the key players in the prothrombotic profile of patients with systemic lupus erythematosus (SLE) not mediated by antiphospholipid antibodies, as well as the potential utility of global coagulation tests to characterize hemostasis in these patients. Patients with SLE without antiphospholipid antibodies and without signs of thrombosis were included. The kinetics of clot formation were determined by ROTEM®. Platelet activation markers were determined by flow cytometry. Thrombin generation associated with Neutrophil Extracellular Traps (NETs) and microparticles (MPs) was measured by calibrated automated thrombogram (CAT). The plasma levels of PAI-1 were also determined. ROTEM® showed a procoagulant profile in SLE patients. SLE patients had activated platelets and more leukocyte/platelet aggregates at basal conditions. The plasma PAI-1 and platelet aggregates correlated with several ROTEM® parameters. The thrombin generation associated withthe tissue factor (TF) content of MPs and with NETs was increased. Our results suggest the utility of global tests for studying hemostasis in SLE patients because they detect their procoagulant profile, despite having had neither antiphospholipid antibodies nor any previous thrombotic event. A global appraisal of hemostasis should, if possible, be incorporated into clinical practice to detect the risk of a thrombotic event in patients with SLE and to consequently act to prevent its occurrence.

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