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1 cardiac foramen ovale, or elevated levels of antiphospholipid antibody.
2 ctive protein (CRP), and the presence of any antiphospholipid antibody.
3 hrombotic risk in asymptomatic patients with antiphospholipid antibodies.
4 recurrent pregnancy failure associated with antiphospholipid antibodies.
5 al anticoagulant and fibrinolytic systems by antiphospholipid antibodies.
6 tion on noncellular phospholipid surfaces by antiphospholipid antibodies.
7 the reduction of surface-bound annexin V by antiphospholipid antibodies.
8 of lupus pregnancy, especially in women with antiphospholipid antibodies.
9 factor VII mutation, factor II mutation, and antiphospholipid antibodies.
10 ished by the 13th International Committee on Antiphospholipid Antibodies.
11 or at risk of, thrombosis in the setting of antiphospholipid antibodies.
12 cular complications of lupus associated with antiphospholipid antibodies.
13 ffective for nonthrombotic manifestations of antiphospholipid antibodies.
14 coprotein I (beta2GPI), the main antigen for antiphospholipid antibodies.
15 ity in the presence of persistently positive antiphospholipid antibodies.
16 disease activity, emotional disturbance, and antiphospholipid antibodies.
17 w that ApoER2 is involved in pathogenesis of antiphospholipids antibodies.
21 mbocytopenia associated with the presence of antiphospholipid antibodies and persistently positive an
22 lar endothelial cell dysfunction mediated by antiphospholipid antibodies and subsequent complement sy
23 mbotic status of APS patients induced by IgG-antiphospholipid antibodies and the beneficial effects o
24 ress with regard to the relationship between antiphospholipid antibody and its target, beta-2-glycopr
25 n I (beta2GPI; the major autoantigen for the antiphospholipid antibodies) and the homologous catalyti
26 c lupus erythematosus (SLE), 2 patients with antiphospholipid antibodies, and 3 other patients, but a
27 re corticosteroid treatment, the presence of antiphospholipid antibodies, and acute thrombocytopenia.
28 limitations of existing laboratory tests for antiphospholipid antibodies, and the absence of evidence
29 levant risk factors including renal disease, antiphospholipid antibody, and anti-Ro/SS-A and anti-La/
31 erosclerosis have an increased prevalence of antiphospholipid antibodies (aPL) and antibodies to oxid
40 phospholipid syndrome (APS), suggesting that antiphospholipid antibodies (aPL) may bind platelets, ca
42 ients had APS, 24 patients were positive for antiphospholipid antibodies (aPL), and 19 patients had S
43 ion with these mutations and the presence of antiphospholipid antibodies (aPL), lupus anticoagulant (
44 a condition characterized by the presence of antiphospholipid antibodies (aPL), often suffer pregnanc
48 to PON1 activity, SLE risk, lupus nephritis, antiphospholipid antibody (aPL) positivity, and carotid
49 action of WIG in an in vivo murine model of antiphospholipid antibody (aPL)-induced thrombosis and e
50 sis prevention in asymptomatic, persistently antiphospholipid antibody (aPL)-positive individuals (th
51 y was to evaluate the safety of rituximab in antiphospholipid antibody (aPL)-positive patients with n
59 There are few data on the relationship of antiphospholipid antibodies (aPLs) to pathologically pro
63 d detected in clinical laboratory assays for antiphospholipid antibodies are directed against prothro
64 (n = 513; LMWH + LDA) and women negative for antiphospholipid antibodies as controls (n = 791; no tre
65 utcome in women with a history of refractory antiphospholipid antibody-associated pregnancy loss(es)
66 n with aspirin is justified in patients with antiphospholipid antibodies but without a prior history
69 a component and suggest that the epitopes of antiphospholipid antibodies could include CL or oxidized
70 bset of periodontitis patients with elevated antiphospholipid antibodies could represent a subgroup a
72 y of stroke, migraine with aura, circulating antiphospholipid antibodies, discontinuation of antiplat
74 the mechanism of thrombosis associated with antiphospholipid antibodies found in the rheumatic disea
77 gs of yellow scleral plaques and circulating antiphospholipid antibodies have been proposed as marker
78 rophoblasts and endothelial cells exposed to antiphospholipid-antibody IgG as compared with control I
79 rophoblasts and endothelial cells exposed to antiphospholipid-antibody IgG had faster mean (+/- SE) p
82 PS) is defined by the persistent presence of antiphospholipid antibodies in patients with a history o
83 een conducted to determine the prevalence of antiphospholipid antibodies in patients with retinal vas
87 thrombosis, fetal loss, and the presence of antiphospholipid antibodies, including anti-beta2-glycop
89 patients with key clinical manifestations of antiphospholipid antibodies, including patients with ant
90 ion discusses novel pathogenic mechanisms of antiphospholipid antibodies, including the activation of
91 ll lines, wherein HCQ reduced the binding of antiphospholipid antibodies, increased cell-surface AnxA
92 Delineation of the epitopes recognized by antiphospholipid antibodies induced by HIV-1 offers insi
94 of thrombosis and gestational morbidity with antiphospholipid antibodies is termed antiphospholipid s
95 n of disease, hypertension, body mass index, antiphospholipid antibodies, kidney disease, acute throm
96 (P = 0.04) and were also more likely to have antiphospholipid antibodies (lupus anticoagulant) (P = 0
97 e setting of persistently positive levels of antiphospholipid antibodies measured on 2 different occa
102 otein I (beta(2)-GPI) is a major antigen for antiphospholipid antibodies present in patients with the
106 r assessment in the management of refractory antiphospholipid antibody-related pregnancy loss(es), al
108 antibody-positive patients, although lacking antiphospholipid antibodies, shared an amino acid epitop
110 r V Leiden, prothrombin 20210A mutation, and antiphospholipid antibodies significantly increases a pa
111 the first direct evidence that a particular antiphospholipid antibody specificity may contribute to
113 End-stage renal disease (ESRD) patients with antiphospholipid antibody syndrome (APAS) remain at high
115 optimal clinical management of patients with antiphospholipid antibody syndrome (APS) is uncertain be
118 es that were all isolated from patients with antiphospholipid antibody syndrome (APS); testing was al
120 wledge of the clinical syndrome that we call antiphospholipid antibody syndrome has also progressed.
121 understanding of the pathophysiology behind antiphospholipid antibody syndrome has led to novel appr
122 idelines for the treatment and management of antiphospholipid antibody syndrome have been established
126 rment within SLE and related conditions (eg, antiphospholipid antibody syndrome, active vs inactive S
127 iolipin (anti-CL) antibodies, diagnostic for antiphospholipid antibody syndrome, are associated with
128 d cause valvular vegetations associated with antiphospholipid antibody syndrome, which would be a new
134 d IgG fractions from three patients with the antiphospholipid-antibody syndrome and from normal contr
138 reincubation of healthy monocytes before IgG-antiphospholipid antibody treatment decreased oxidative
139 the molecular and intracellular events that antiphospholipid antibodies trigger in target cells, as
140 actions and the intracellular signaling that antiphospholipid antibodies trigger, new therapeutic and
141 rrent pregnancy loss includes measurement of antiphospholipid antibodies under the perception that th
146 olytic anemia, anti-double-stranded DNA, and antiphospholipid antibody were associated with thrombocy
147 pus erythematosus occurs in association with antiphospholipid antibodies, which also are associated w
148 or V antibody not related to the presence of antiphospholipid antibodies, which is responsible for th
150 ion on biopsy as compared with patients with antiphospholipid antibodies who were not receiving sirol
151 patients, and 0 of 5 cycles in 2 women with antiphospholipid antibody (without SLE or primary APS) r
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