Heparin-induced thrombocytopenia: a prospective study on the incidence, platelet-activating capacity and clinical significance of antiplatelet factor 4/heparin antibodies of the IgG, IgM, and IgA classes.

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Greinacher, A (författare)

Heparin-induced thrombocytopenia : a prospective study on the incidence, platelet-activating capacity and clinical significance of antiplatelet factor 4/heparin antibodies of the IgG, IgM, and IgA classes.

Artikel/kapitelEngelska2007

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Elsevier BV,2007
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LIBRIS-ID:oai:DiVA.org:uu-161357
https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-161357URI
https://doi.org/10.1111/j.1538-7836.2007.02617.xDOI

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Språk:engelska
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INTRODUCTION: Platelet-activating antiplatelet factor 4/heparin (anti-PF4/heparin) antibodies are the major cause of heparin-induced thrombocytopenia (HIT). However, the relative utility of functional (platelet activation) vs. antigen [enzyme-immunoassay (EIA)] assays, and the significance of assay discrepancies remain unresolved. METHODS: Consecutive patient sera (n = 1650) referred for diagnostic HIT testing were screened prospectively by both the heparin-induced platelet activation (HIPA) test and anti-PF4/heparin EIA - including individual classes (IgG, IgA, IgM) - with clinical correlations studied. Platelet microparticle and annexin-V-binding properties of the sera were also investigated. RESULTS: Only 205 (12.4%) sera tested positive in either the HIPA and/or EIA: 95 (46.3%) were positive in both, 109 (53.1%) were only EIA-positive, and, notably, only one serum was HIPA-positive/EIA-negative. Of 185 EIA-positive sera, only 17.6% had detectable IgM and/or IgA without detectable IgG. Among sera positive for EIA IgG, optical density values were higher when the sera were HIPA-positive (1.117 vs. 0.768; P < 0.0001), with widely overlapping values. Two HIPA-positive but EIA-IgG-negative sera became HIPA-negative following IgG depletion, suggesting platelet-activating antibodies against non-PF4-dependent antigens. Clinical correlations showed that HIPA-negative/EIA-positive patients did not develop thrombosis and had reasons other than HIT to explain thrombocytopenia. IgM/A antibodies did not increase microparticle penetration, but increased annexin-V binding. CONCLUSIONS: The anti-PF4/heparin EIA has high ( approximately 99%) sensitivity for HIT. However, only about half of EIA-positive patients are likely to have HIT. Anti-PF4/heparin antibodies of IgM/A class and non-PF4-dependent antigens have only a minor role in HIT.

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MEDICIN OCH HÄLSOVETENSKAP Klinisk medicin hsv//swe
MEDICAL AND HEALTH SCIENCES Clinical Medicine hsv//eng

Biuppslag (personer, institutioner, konferenser, titlar ...)

Juhl, D (författare)
Strobel, U (författare)
Wessel, A (författare)
Lubenow, NorbertDepartment of Transfusion Medicine, Greifswald University, Germany(Swepub:uu)norlu522 (författare)
Selleng, K (författare)
Eichler, P (författare)
Warkentin, T E (författare)
Department of Transfusion Medicine, Greifswald University, Germany (creator_code:org_t)

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Ingår i:Journal of Thrombosis and Haemostasis: Elsevier BV5:8, s. 1666-731538-79331538-7836

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Av författaren/redakt...: Greinacher, A; Juhl, D; Strobel, U; Wessel, A; Lubenow, Norbert; Selleng, K; visa fler...; Eichler, P; Warkentin, T E; visa färre...

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