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O Amengual

Publications and source records attributed to O Amengual.

29 records · Page 2Linked to original sources
PubMed1998

The role of the tissue factor pathway in the hypercoagulable state in patients with the antiphospholipid syndrome.

The antiphospholipid syndrome (APS) is characterised by both arterial and venous thrombosis, recurrent pregnancy loss and thrombocytopaenia in association with antiphospholipid antibodies (aPL). To explore further the pathogenesis of thrombosis in APS, we evaluated the behaviour of tissue factor (TF) pathway in patients with APS. Plasma antigen levels of soluble TF and tissue factor pathway inhibitor (TFPI), a physiological regulator of TF dependent coagulation activation, were measured in 57 APS patients (36 primary and 21 secondary to systemic lupus erythematosus). Significantly elevated levels of both TF and TFPI were found in APS patients compared with 25 healthy controls (279 +/- 15 vs. 217 +/- 17 pg/ml, p = 0.01; 56.24 +/- 2.00 vs. 47.92 +/- 2.22 ng/ml, p = 0.01, respectively), suggesting in vivo upregulation of TF pathway in patients with APS. By flow-cytometry, monocytes from a healthy donor displayed higher TF antigen expression when incubated in the presence of APS plasmas than in control plasmas (24.23 +/- 3.11 vs. 12.78 +/- 1.57%, p = 0.002). Peripheral blood mononuclear cells (PBMC) also expressed more procoagulant activity (PCA) when incubated in the presence of APS plasmas than in control plasmas (1.80 +/- 0.12 vs. 1.35 +/- 0.054, p = 0.001) implying that TF up-regulation in APS was reproducible in vitro. Human monoclonal anticardiolipin antibodies induced PCA on PBMC and also TF mRNA on both PBMC and human umbilical vein endothelial cells shown by reverse-transcription polymerase chain reaction. These data strongly suggest that the TF pathway is implicated in the pathogenesis of aPL related thrombosis.

Adult↗
PubMed1998

Advances in antiphospholipid (Hughes') syndrome.

Fifteen years have passed since Hughes reported the detailed clinical description of antiphospholipid syndrome (APS), and it is now recognised as one of the most common prothrombotic disorders. Its main clinical features are recurrent thrombosis (both venous and arterial), recurrent pregnancy loss and thrombocytopenia associated with the presence of antiphospholipid antibodies (aPLs). aPLs are a heterogeneous group of autoantibodies detected by either clotting or immunological assays. They include lupus anticoagulant (LA), anticardiolipin antibodies (aCL) and antibodies against other phospholipids (PLs). Recently the aPLs family has expanded to include antibodies whose specificity are claimed to be directed not only towards PLs, but also towards plasma proteins and their complex with PLs. Animal models are providing important new data on clinical and pathogenic aspects of APS. The detection of antibodies against beta 2 glycoprotein I by a simple and rapid enzyme-linked immunosorbent assay (ELISA) may facilitate the recognition of "pathogenic" aCL in APS. Regarding the treatment of APS, long-term anticoagulation therapy is needed to prevent recurrences.

Adult↗
PubMed1998

Fcgamma receptor IIA H/R131 polymorphism in patients with antiphospholipid antibodies.

A role for Fcgamma receptor in the pathophysiology of thrombosis in APS has been hypothesized. The polymorphism of this receptor, FcgammaRIIA H/R131, is associated with the binding affinity for human IgG2 (i.e. FcgammaRIIA-H131 isoform has a higher affinity than FcgammaRIIA-R131). Since anti-beta2 glycoprotein I antibodies (anti beta2GPI), which play a major pathogenic role in APS, show IgG2 dominant distribution, we investigated the prevalence of receptor isoforms in patients with antiphospholipid antibodies (aPL) by a PCR-RFLP method. We studied 100 Caucasian patients with aPL (57 primary APS, 32 secondary APS to SLE and 11 other diseases with aPL) and 41 healthy controls. H131/H131, H131/R131 and R131/R131 genotypes were found in 21 (21%), 50 (50%) and 29 (29%) in the patient group, and 9 (22%), 23 (56%) and 9 (22%) in control group, respectively. Thus there was no statistically significant difference in the prevalence of each genotype in these groups. None of the clinical manifestations of primary APS (arterial/venous thrombosis, recurrent pregnancy loss and thrombocytopenia) was significantly correlated with any FcgammaRIIA genotype. In conclusion, FcgammaRIIA polymorphism did not correlate with the manifestations of APS, and FcgammaRIIA genotype is not a genetic marker of APS.

Adolescent↗
PubMed1998

Autoantibodies to human prothrombin and clinical manifestations in 207 patients with systemic lupus erythematosus.

OBJECTIVE: Prothrombin (factor II) is one of the phospholipid binding proteins with a procoagulant property. Some publications have shown the presence of autoantibodies against prothrombin (aPT) in patients with antiphospholipid antibodies (aPL). We assessed the clinical significance of aPT in thrombotic events in patients with systemic lupus erythematosus (SLE). METHODS: IgG and IgM aPT were tested by ELISA in 207 patients with SLE. RESULTS: Fifty-eight patients (28%) had positive aPT (> mean + 3 SD of 100 controls). Twenty-eight (14%) had IgG alone, 21 (10%) IgM alone, and 9 (4%) had both IgG and IgM. Patients with aPT had a history of thrombosis more frequently than those without aPT [31/58 (53%) vs 47/149 (32%), chi-squared=7.6, p=0.006]. No correlation was found between the presence of aPT and clinical features of SLE. CONCLUSION: aPT are frequently found in patients with SLE, and are a potential marker for thrombosis.

Abortion, Spontaneous↗
PubMed1998

Antibodies to beta2-glycoprotein I: a potential marker for clinical features of antiphospholipid antibody syndrome in patients with systemic lupus erythematosus.

OBJECTIVE: To clarify risk factors for the development of clinical features of antiphospholipid syndrome (APS) in patients with anticardiolipin antibodies (aCL) in systemic lupus erythematosus (SLE). METHODS: We studied 65 SLE patients, all with positive IgG and/or IgM aCL. Patients were divided into 2 groups; I: 29 SLE patients with features of APS (SLE/APS) and II: 36 aCL positive SLE patients without any feature of APS (SLE/aCL). Serum samples were collected from our serum bank. Anti-beta2-glycoprotein I (anti-beta2-GPI) were tested by ELISA using irradiated plates in the absence of cardiolipin. Anti-dsDNA antibodies were tested by standard Farr assay. RESULTS: There were no major differences between SLE clinical manifestations in both groups. However, the frequency of IgG anti-beta2-GPI was markedly increased in SLE/APS (18/29, 62%) than in SLE/aCL (4/36, 11%) (chi-squared 18.6, p=0.0001). The levels of anti-dsDNA antibodies in the same samples were slightly lower in SLE/APS. CONCLUSION: Our data suggest that increased levels of IgG anti-beta2-GPI may be a specific feature of SLE/APS patients rather than reflecting a polyclonal B cell activation.

Adult↗
PubMed1997

Autoantibodies against oxidized low-density lipoprotein in antiphospholipid syndrome.

The prevalence and clinical significance of anti-oxidized low-density lipoprotein antibodies (anti-ox-LDL) were evaluated in patients with the antiphospholipid syndrome (APS). Anti-ox-LDL were measured in the sera of 107 patients with APS (64 primary APS, 43 secondary to systemic lupus erythematosus) by enzyme-linked immunosorbent assay (ELISA) utilizing malondialdehyde (MDA)-modified LDL as antigen. In the same patients, anticardiolipin antibodies (aCL) and anti-beta2-glycoprotein I antibodies (anti-beta2GPI) were also measured. A positive titre of anti-ox-LDL was detected in 22% of patients, but only in 6% of control subjects (chi2 = 12, P = 0.0005). Levels of anti-ox-LDL were higher in patients with arterial thrombosis (n = 58) than in those without (n = 49) (P = 0.0001). Anti-ox-LDL levels correlated weakly with those of aCL (r = 0.196, P = 0.043), but not with those of anti-beta2GPI (r = 0.076). Our findings suggest that elevated levels of anti-ox-LDL may represent another potential marker of APS, particularly of patients prone to arterial thrombosis.

Adult↗
PubMed1996

Specificity of ELISA for antibody to beta 2-glycoprotein I in patients with antiphospholipid syndrome.

The clinical significance of anti-beta 2 glycoprotein I (beta 2-GPI) antibodies was evaluated in patients with antiphospholipid syndrome (APS), primary and secondary to systemic lupus erythematosus (SLE). Anti-beta 2-GPI were tested in 120 patients (39 primary APS, 32 APS with SLE and 49 SLE without APS) by ELISA utilizing irradiated plates in the absence of cardiolipin. Anticardiolipin antibodies (aCL) and antiphosphatidylserine antibodies were also measured in the same patients using standardized assays. Anti-beta 2-GPI titres correlated strongly to those of aCL (r = 0.816, P = 0.0001), and to those of antiphosphatidylserine antibodies (r = 0.841, P = 0.0001). Anti-beta 2-GPI were detected in 53.5% of APS patients (38/71), but only in 4.1% of SLE patients without APS (2/49). In the latter group, 24.5% (12/49) of patients had a positive titre of aCL. The anti-beta 2-GPI assay showed higher specificity for APS than the aCL in APS (96 vs 75%, respectively, chi 2 = 6.75, P = 0.00094). Our findings suggest that the assay of anti-beta 2-GPI may improve the specificity for APS.

Adult↗
PubMed1996

Clinical significance of anti-beta 2-glycoprotein I antibodies.

Antiphospholipid antibodies are a heterogeneous group of autoantibodies with clinical importance because of their strong association with thrombotic events. Recent evidence have shown that antiphospholipid antibodies are not directed against phospholipids, as has previously been thought, but are a part of a large family of autoantibodies against phospholipid-binding plasma proteins. So far, one of the most common and best characterized antigenic target is beta 2-glycoprotein I (beta 2-GPI), which plays an important role in the binding of anticardiolipin antibodies (aCLA) to cardiolipin. The detection of anti-beta 2-GPI antibodies by using a simple and rapid ELISA may facilitate the recognition of alpha "pathogenic" alpha aCL in antiphospholipid syndrome.

Antibodies, Anticardiolipin↗
PubMedDate not supplied

Antiphospholipid antibodies in leprotic patients: a correlation with disease manifestations.

OBJECTIVES: Previous studies showed that antiphospholipid antibodies (aPL) are frequent in the sera of leprosy patients and are most probably directed against body tissue cardiolipins. Some groups have demonstrated differences between the binding specificity of "autoimmune-aPL" and "non-autoimmune-aPL". It is widely accepted that a plasma protein, beta 2-Glycoprotein I (beta 2-GPI), is required for the binding of autoimmune anticardiolipin antibodies (aCL) to cardiolipin. However, some reports suggested heterogeneity of leprosy aCL with respect to their beta 2-Glycoprotein I (beta 2GPI) dependency, although no thromboembolic complications have been reported. This study was designed to assess the specificity of aPL by investigating the prevalence of aCL, anti-phosphatidylserine (aPS), anti-phosphatidylinositol (aPI), anti-beta 2GPI and antiprothrombin (aPT) antibodies, and evaluate their clinical significance in a group of patients with lepromatous leprosy. PATIENTS AND METHODS: 35 lepromatous leprosy patients were selected randomly from an Egyptian leprosarium as a study group. 35 normal household contact controls were selected matching the study group for both sex and age. aCL, aPS, aPI, aPT, anti-beta 2GPI and beta 2-dependent aCL antibodies were investigated by ELISA in all patients and controls. RESULTS: aCL antibodies were more frequent in leprosy patients than in controls [13/35 (37%) vs. 3/35 (9%), respectively, p = 0.02] and significantly correlated with Raynaud's phenomenon, skin nodules, chronic skin ulcers and urticarial skin rash. No association was found with hypopigmentation, hyperpigmentation and saddle nose. None of the patients presented aPS nor aPI. Only 1 subject from the control group presented aPI along with aCL. aPT were present in 2/35 (5.7%) and anti-beta 2GPI in 1/35 (2.9%) leprotic patients. None of the individuals from the control group presented aPT nor anti-beta 2GPI. CONCLUSIONS: An association was found between the presence of aCL and certain dermatological manifestations of leprosy, such as Raynaud's phenomenon, skin nodules, chronic skin ulcers and urticarial skin rash. As in other infectious diseases, there was a lack of beta 2GPI-dependency and an absence of thrombotic complications.

Adult↗