Effects of the Lupus Anticoagulant in Patients with Systemic lupus Erythematosus on Endothelial Cell Prostacyclin Release and Procoagulant Activity

Rustin, M.H.A.; Bull, Helen A.; Machin, Samuel J.; Isenberg, David; Snaith, M L; Dowd, Pauline M.

doi:10.1111/1523-1747.ep12560947

Cited by 64 publications

(25 citation statements)

References 36 publications

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“…[18] studied the clinical and serological findings in 24 patients with PH. The frequency of antiphospholipid antibodies (lupus anti coagulant and aCL) of these 24 patients was 68% in their re port, which is higher than the 30-40% generally found in patients with SLE [19]. Two of the twenty-four patients de scribed above clearly suffered from thromboembolic PH, 1 with SLE and the other with an antiphospholipid syn drome.…”

Section: Discussionmentioning

confidence: 76%

Anticardiolipin Antibodies Are Associated with Pulmonary Hypertension in Patients with Mixed Connective Tissue Disease or Systemic Lupus Erythematosus

Miyata

Suzuki

Sakuma

et al. 1993

Int Arch Allergy Immunol

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Anticardiolipin antibodies (aCL) were studied in relation to pulmonary hypertension (PH) in 22 patients with mixed connective tissue disease (MCTD) or systemic lupus erythematosus (SLE). The mean pulmonary arterial pressure (mPAP) values were similar in the 12 MCTD and 10 SLE patients: 26 ± 11 and 25 ± 11 mm Hg, respectively. However, the frequency of PH was higher in SLE (60%) than in MCTD patients (33%). The titers of aCL were significantly higher in SLE (38 ± 27 IU/ml) than in MCTD (17 ± 7 IU/ml; p < 0.02). Two SLE patients with high titers of aCL had multiple cerebral infarction and transverse myelitis, and deep vein thrombosis, respectively. A significant correlation between the titers of aCL and mPAP was observed in patients with MCTD (p < 0.05), but not in patients with SLE.

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Section: Discussionmentioning

confidence: 76%

Anticardiolipin Antibodies Are Associated with Pulmonary Hypertension in Patients with Mixed Connective Tissue Disease or Systemic Lupus Erythematosus

Miyata

Suzuki

Sakuma

et al. 1993

Int Arch Allergy Immunol

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“…The mechanism of pathogenicity is uncertain, but a procoagulant activity is likely. No definitive explanation of aPL mechanism yet exists, although many possible mechanisms have been proposed, including crossreactivity with antiendothelial cell antibodies (I0, 11), inhibition of arachidonic acid release (12,13), and interference with thrombomodiulin (14,15), tissue plasminogen activator activity (16), protein S (I7), or antithrombin III (18). Evidence supporting each of these proposals is not definitive.…”

Section: Introductionmentioning

confidence: 99%

Phospholipid binding of antiphospholipid antibodies and placental anticoagulant protein

et al. 1992

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“…Investigators speculate that a prothrombotic state may be induced by aPL antibodies activating platelets 8 -10 or endothelial cells (ECs) or by inhibition of protein C activation. [11][12][13][14][15][16][17][18][19][20][21] aPL antibodies may bind phospholipids or ␤ 2 -glycoprotein 1 (␤ 2 GP1) in the membranes of ECs or platelets, resulting in their activation. 8 -10,16,22 EC activation by aPL antibodies has been demonstrated in vitro in several ways, including enhanced adhesion molecule expression and monocyte adherence 22,23 ; however, no in vivo studies have shown such activation.…”

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confidence: 99%

Antiphospholipid Antibodies From Antiphospholipid Syndrome Patients Activate Endothelial Cells In Vitro and In Vivo

et al. 1999

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Background —Antiphospholipid (aPL) antibodies are associated with thrombosis in patients diagnosed with antiphospholipid syndrome (APS) and enhance thrombus formation in vivo in mice, but the mechanism of thrombosis by aPL is not completely understood. Although aPL antibodies have been shown to inhibit protein C activation and activate endothelial cells (ECs) in vitro, no study has examined whether these antibodies activate ECs in vivo. Therefore, human affinity-purified aPL (ap aPL) antibodies from APS patients were tested in a mouse model of microcirculation using the cremaster muscle that allows direct microscopic examination of thrombus formation and adhesion of white blood cells (WBCs) to ECs as an indication of EC activation in vivo. Adhesion molecule expression on human umbilical vein endothelial cells (HUVECs) after aPL exposure was performed to confirm EC activation in vitro. Methods and Results —All 6 ap aPL antibodies significantly increased the expression of VCAM-1 (2.3- to 4.4-fold), with one of the antibodies also increasing the expression of E-selectin (1.6-fold) on HUVECs in vitro. In the in vivo experiments, each ap aPL antibody except for 1 preparation increased WBC sticking (mean number of WBCs ranged from 22.7 to 50.6) compared with control (14.4), which correlated with enhanced thrombus formation (mean thrombus size ranged from 1098 to 6476 versus 594 μm 2 for control). Conclusions —Activation of ECs by aPL antibodies in vivo may create a prothrombotic state on ECs, which may be the first pathophysiological event of thrombosis in APS.

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Effects of the Lupus Anticoagulant in Patients with Systemic lupus Erythematosus on Endothelial Cell Prostacyclin Release and Procoagulant Activity

Cited by 64 publications

References 36 publications

Anticardiolipin Antibodies Are Associated with Pulmonary Hypertension in Patients with Mixed Connective Tissue Disease or Systemic Lupus Erythematosus

Anticardiolipin Antibodies Are Associated with Pulmonary Hypertension in Patients with Mixed Connective Tissue Disease or Systemic Lupus Erythematosus

Phospholipid binding of antiphospholipid antibodies and placental anticoagulant protein

Antiphospholipid Antibodies From Antiphospholipid Syndrome Patients Activate Endothelial Cells In Vitro and In Vivo

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