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PubMed · 8793265

A decrease in antiphospholipid antibodies before a thrombotic event.

Abstract

We are reporting a systemic lupus erythematosus patient with antiphospholipid syndrome who developed iliofemoral thrombosis. Before the occurrence of iliofemoral venous thrombosis, antiphospholipid antibodies (aPL) gradually decreased over a period of 18 weeks but were within normal range during its acute phase. In the course of two years following this case of thrombosis, aPL have never returned to the high prethrombotic values. It is therefore most likely that aPL were involved in the process of provoking thrombosis rather than being consumed during its acute phase.

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BibTeXRIS

S Praprotnik, B Bozic. 1996. A decrease in antiphospholipid antibodies before a thrombotic event.. https://doi.org/10.1007/bf02229712

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Monocyte tissue factor induction by activation of beta 2-glycoprotein-I-specific T lymphocytes is associated with thrombosis and fetal loss in patients with antiphospholipid antibodies.

Antiphospholipid (aPL) syndrome (APS) is characterized by thromboembolic events, thrombocytopenia, or recurrent miscarriage associated with aPL Abs with specificity for beta2-glycoprotein-I (beta2GPI). We recently reported that at least 44% of patients with the APS possess circulating type 1 (Th1) CD4+ T cells that proliferate and secrete IFN-gamma when stimulated with beta2GPI in vitro. In this study, we show that stimulation of PBMCs from 20 APS patients with beta2GPI induced substantial monocyte tissue factor (TF) (80 +/- 11 TF stimulation index (TF-SI)), whereas no induction was observed using PBMCs from 13 patients with aPL Abs without APS (6 +/- 1 TF-SI) or 7 normal and 7 autoimmune controls (5 +/- 1 and 3 +/- 1 TF-SI, respectively) (p < 0.0001). TF induction on monocytes by beta2GPI was dose dependent and required CD4+ T lymphocytes and class II MHC molecules. Because monocyte TF induction by beta2GPI was observed in all patients with APS, but not in any patient with aPL Abs without APS, this response is a potentially useful predictor for APS in patients with aPL Abs, as well as providing mechanistic insight into thrombosis and fetal loss in these patients.

Antibodies, Antiphospholipid↗

[Prevalence and clinical significance of antiphospholipid antibodies in chronic hepatitis C].

BACKGROUND: To know the prevalence of antiphospholipid antibodies in chronic hepatitis C and their relationship with disease progression. METHODS: One hundred and twenty-eight patients with chronic hepatitis C and 93 healthy controls were enrolled up. We determined platelets, ALT, gamma GT, RNAHCV in serum and liver and non-organ specific antibodies, grade and stage in liver biopsy, risk factors, duration of disease and alcohol intake were also included. Portal hypertension and liver function parameters were studied. Antiphospholipid antibodies (APA): lupus anticoagulant (LA) and anticardiolipin antibodies (ACA) (IgG and IgM) were measured by EIA. Anti-beta 2 glycoprotein I antibodies were also detected by EIA in ACA positive patients. RESULTS: Thirty one out of 128 (25%; 95% CI: 17.8%-33.4%) showed positive antiphospholipid antibodies. Positive ACA-IgG was higher in patients than controls (22% vs 3.2%; p < 0.05), whereas, ACA-IgM was similar (5% vs 3.2%; p = NS), and LA was absent in both groups. ALT levels, viraemia, viral load in liver, platelets, or ANA titre were similar in patients with and without positive ACA-IgG. Risk factors, duration of disease or alcohol intake were not related yet. Patients with staging F1 showed positive ACA-IgG 4 of 44 (9%; 95% CI: 2.5%-21.7%), in staging F2 7 of 39 (18%; 95% CI: 7.5%-33.5%) and in staging F4 17 of 45 (38%; 95% CI: 23.8%-53.5%; p < 0.005). ACA-IgG was significantly related to portal hypertension, Child-Pugh stage and presence of cirrhosis complications. Anti-beta 2 glycoprotein I antibodies were detected in ten (43.5%; CI 95%: 23.2%-65.5%) out of 23 ACA positive patients. CONCLUSIONS: ACA-IgG seems to be associated with chronic hepatitis C, and could play a potential role in fibrosis progression and liver disease in these patients.

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