Laboratory diagnosis of the antiphospholipid syndrome

Wisløff, Finn; Jacobsen, Einar; Liestøl, Sigurd

doi:10.1016/s0049-3848(02)00400-0

Cited by 81 publications

(40 citation statements)

References 84 publications

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“…127 The upper reference limit for the screening tests is determined as the mean clotting time plus two or three standard deviations or the 97.5th or 99th percentile of a normal population. 128 For dRVVT and for KCT, clotting time ratios (test plasma/normal plasma) >1.1 and >1.2, respectively, have been used as cut-off values for a positive test. 129…”

Section: Elongation Of Clotting Timementioning

confidence: 99%

Antiphospholipid Antibodies: Laboratory and Pathogenetic Aspects

Vlachoyiannopoulos

Samarkos

Sikara

et al. 2007

Critical Reviews in Clinical Laboratory Sciences

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Antiphospholipid antibodies (aPL) constitute a heterogeneous group of autoantibodies that share the ability to bind phospholipids (PL) alone, protein-PL complexes, or PL-binding proteins. They have been detected in isolation, in association with autoimmune diseases such as systemic lupus erythematosus (SLE), and during the course of different infections. aPL have been associated with an array of clinical manifestations in virtually every organ, although deep vein and arterial thrombosis as well as pregnancy morbidity are predominant. The co-occurrence of these clinical findings with aPL constitutes the so-called antiphospholipid syndrome (APS). aPL can be detected by immunological methods [e.g., anticardiolipin antibodies (aCL)] or by functional methods that exploit the effect of aPL on blood coagulation [lupus anticoagulant (LA)]. Since aPL are heterogeneous, numerous immunological and coagulation assays have been developed. These assays have not been fully standardized, and, therefore, problems such as high interlaboratory variation are relatively frequent. Recently, recommendations have been published regarding LA and aCL testing. Not all aPL are pathogenic. However, when they are not associated with infections, they have a role in the pathogenesis of APS. Clinical and experimental data have shown that aPL exert their pathogenic activity by interfering with the function of coagulation factors, such as thrombin and factors X, XI and XII, and with the function of anticoagulant proteins of the protein C system. In addition, aPL interaction with platelets and endothelial cells induces a pro-adhesive activated phenotype.

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Section: Elongation Of Clotting Timementioning

confidence: 99%

Antiphospholipid Antibodies: Laboratory and Pathogenetic Aspects

Vlachoyiannopoulos

Samarkos

Sikara

et al. 2007

Critical Reviews in Clinical Laboratory Sciences

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“…Interpretation of laboratory tests for lupus anticoagulants can be difficult in the presence of anticoagulant therapy, particularly heparin. 6 Primary antiphospholipid syndrome refers to patients with the syndrome who do not have any other rheumatologic or autoimmune conditions, whereas secondary antiphospholipid syndrome refers to patients who also have systemic lupus erythematosus (SLE) or other conditions. In general, the clinical manifestations of the antiphospholipid syndrome are similar for primary and secondary forms of the disease.…”

Section: Thrombosis and The Antiphospholipid Syndromementioning

confidence: 99%

“…6 • Lupus anticoagulant, diagnosed by the ISTH criteria, † detected in the blood on 2 or more occasions separated by at least 6 weeks.…”

Section: 2mentioning

confidence: 99%

Thrombosis and the Antiphospholipid Syndrome

Ortel¹

2005

Hematology

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The antiphospholipid syndrome is an antibodymediated hypercoagulable state characterized by recurrent venous and arterial thromboembolic events. Several studies have determined that the frequency of antiphospholipid syndrome in patients presenting with a venous thromboembolic event is between 4% and 14%. Because of the high risk for recurrent thromboembolism in these patients, current recommendations suggest a longer, potentially lifelong, course of antithrombotic therapy following an initial event. Although most authorities agree on an extended course of therapy, considerable controversy surrounds the optimal target therapeutic INR for patients with antiphospholipid syndrome. For an initial venous thromboembolic event, a target INR of 2.0 to 3.0 is supported by two prospective, randomized clinical trials. In contrast, relatively limited data exist for an initial arterial thromboembolic event in patients who have the antiphospholipid syndrome, and therapeutic recommendations range from aspirin to warfarin with a high target INR. Recurrent thromboembolic events can be extremely difficult to treat, and some patients may benefit from the addition of immunosuppressive therapies. Importantly, as many as 50% of the initial thromboembolic events sustained by patients with antiphospholipid antibodies occur in the setting of additional, coincident prothrombotic risk factors, indicating the importance of addressing any additional risk factors, such as hypercholesterolemia, in these patients. Prospective studies are needed to address the role of thromboprophylactic strategies in asymptomatic individuals with antiphospholipid antibodies in the absence of additional risk factors.

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“…LAC was detected using activated partial thromboplastin time (APTT -Diagnostica Stago, France) and diluted Russell's viper venom time (dRVVT -Trinity Biotech, Wiclow, Ireland, UK) according to international guidelines. 26 Serum IgG and IgM anti-β 2 GPI were detected by ELISA (The Binding Site, Birmingham, UK), according to the manufacturer's instructions with cutoff values of 10 U/mL for IgM and 20 U/mL for IgG.…”

Section: Antibody Assaysmentioning

confidence: 99%

Anticorpos antinucleossomo e síndrome antifosfolipídica: estudo observacional

Souza

Keusseyan

Silva

et al. 2012

Rev. Bras. Reumatol.

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Objective: To study the association of anti-nucleosome (anti-NCS) antibodies in primary antiphospholipid syndrome (APS) and the development of systemic lupus erythematosus (SLE) during follow-up. Materials and methods: Thirty-six women with primary APS were evaluated prospectively for clinical features of systemic autoimmune diseases and for the presence of antiphospholipid antibodies, antinuclear antibodies and anti-NCS/chromatin antibodies. Results: After a mean follow-up period of 45.7 months, anti-NCS/chromatin antibodies were detected in only one patient (2.8%), who developed features of SLE including polyarthritis, lymphopenia, optic neuritis, multiple sclerosis-like lesions, and an autoantibody profi le suggestive of SLE. Conclusion: The frequency of anti-NCS/chromatin antibodies in primary APS patients is very low, and they may be associated with the development of SLE manifestations.

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Laboratory diagnosis of the antiphospholipid syndrome

Cited by 81 publications

References 84 publications

Antiphospholipid Antibodies: Laboratory and Pathogenetic Aspects

Antiphospholipid Antibodies: Laboratory and Pathogenetic Aspects

Thrombosis and the Antiphospholipid Syndrome

Anticorpos antinucleossomo e síndrome antifosfolipídica: estudo observacional

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