Prevalence of Heparin-Associated Antibodies Without Thrombosis in Patients Undergoing Cardiopulmonary Bypass Surgery

Bauer, Thomas; Arepally, Gowthami M.; Konkle, Barbara A.; Mestichelli, Bernadette; Shapiro, Sandor S.; Cines, Douglas B.; Poncz, Mortimer; McNulty, Stephen E.; Amiral, Jean; Hauck, Walter W.; Edie, Richard N.; Mannion, John D.

doi:10.1161/01.cir.95.5.1242

Cited by 311 publications

(215 citation statements)

References 22 publications

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“…The differences in the reported frequencies of anti-H/PF4 antibodies may be due in part to the spontaneous disappearance of these antibodies, as described in previous series [19,20]. In a series of 243 patients, heparin-induced antibody titers fell below the detection threshold within a median of 50 days if a platelet serotonin-release assay was used and within 85 days if an antigen assay was used [21].…”

Section: Discussionmentioning

confidence: 86%

A prospective study of the prevalence of heparin‐induced antibodies and other associated thromboembolic risk factors in pediatric patients undergoing hemodialysis

et al. 2006

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Heparin, which is used at high doses in hemodialysis patients, may induce antibodies favoring thromboembolic complications. We prospectively investigated the prevalence of heparininduced platelet-reactive antibodies in a cohort of 38 pediatric hemodialysis patients, by means of heparin/platelet factor 4 (H/PF4) ELISA and heparin-induced platelet activation assay (HIPA). We also assessed other acquired and congenital hypercoagulable states. Heparin-induced antibodies were detected in 13 and 21% of patients with HIPA and ELISA, respectively. Anti-H/PF4 antibodies were negatively correlated with the number of hemodialysis sessions. These antibodies disappeared after a median time of 6 months despite continuing heparin treatment. The prevalence of antiphospholipid antibodies was 21% (anticardiolipin 10.5%, anti-b2GPI 13%, and lupus anticoagulant 5%). Blood levels of homocysteine, factor VIII, and fibrinogen were significantly higher and factor II levels were significantly lower in hemodialysis patients than in controls, whereas factor VII, factor IX, and natural coagulation inhibitor levels were similar in patients and controls. Overall, 26 of 38 patients had at least one biomarker of hypercoagulability, but only 1 patient, without anti-H/PF4 antibodies, presented with thrombosis. In conclusion, heparin induces the transient production of anti-H/PF4 antibodies in children undergoing hemodialysis, but other abnormalities probably contribute to hypercoagulability. These findings may help to improve the diagnosis and management of thrombotic events in hemodialysis patients. Am. J. Hematol. 81:328-334, 2006. V V C 2006 Wiley-Liss, Inc.

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Section: Discussionmentioning

confidence: 86%

A prospective study of the prevalence of heparin‐induced antibodies and other associated thromboembolic risk factors in pediatric patients undergoing hemodialysis

et al. 2006

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“…Yet, antibodies with this specificity are produced by 10-50% of patients treated with heparin [12,41,44,45]. Most of these antibodies are weak and may not be clinically significant.…”

Section: What Is the Basis For The Immune Response To Heparin?mentioning

confidence: 99%

Heparin‐induced thrombocytopenia and thrombosis

Davoren

Aster

2005

American J Hematol

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Heparin, employed clinically for more than 50 years, is still a widely used anticoagulant. Unfortunately, some patients given this agent develop thrombocytopenia and thrombosis. Because this side effect can have catastrophic consequences, it is imperative that all clinicians caring for patients who receive heparin have at least a basic understanding of its pathogenesis, diagnosis, and management. Am. J. Hematol. 81:36-44, 2006Hematol. 81:36-44, . ª 2005 Wiley-Liss, Inc.

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“…First, a major decrease in platelet count of approximately 40-50% occurs universally during the first 72 h after cardiac surgery [3]. Second, as many as 25-70% of patients develop anti-platelet factor 4 (PF4)-heparin antibodies detectable by immunoassays, and 4-20% test positive by platelet activation assay, during the first 10 days post-cardiac surgery [4][5][6][7][8]. However, only a minority of these patients develop clinically evident HIT, characterized by a second episode of thrombocytopenia beginning within a narrow ÔwindowÕ between postoperative days 5 and 10 (the ÔP1 patternÕ reported by Pouplard et al [9]).…”

Section: Introductionmentioning

confidence: 99%

Early‐onset and persisting thrombocytopenia in post‐cardiac surgery patients is rarely due to heparin‐induced thrombocytopenia, even when antibody tests are positive

Selleng

Malowsky²,

Strobel

et al. 2010

Journal of Thrombosis and Haemostasis

158

123

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thrombocytopenia in post-cardiac surgery patients is rarely due to heparin-induced thrombocytopenia, even when antibody tests are positive. See also Gruel Y, Pouplard C. Post-operative platelet count profile: the most reliable tool for identifying patients with true heparin-induced thrombocypenia after cardiac surgery. This issue, pp 27-9.Summary. Background: The high frequency of thrombocytopenia in post-cardiac surgery patients makes it challenging to diagnose heparin-induced thrombocytopenia (HIT). Two platelet count profiles are reported as indicating possible HIT in these patients: profile 1 describes a platelet count fall that begins between postoperative days 5 and 10, whereas profile 2 denotes early-onset thrombocytopenia that persists beyond day 5. Objectives: Toexaminehowthese platelet count profiles correlate withantibodystatusandHITpost-cardiacsurgery.Methods:We prospectively screened 581 cardiac surgery patients for heparindependent antibodies by platelet factor 4 (PF4)-heparin immunoassay and platelet-activation test, and performed daily platelet counts (until day 10) with 30-day follow-up. Results: All three patients with platelet count profile 1 tested positive for platelet-activating anti-PF4-heparin IgG antibodies [odds ratio (OR) 521.7, 95% confidence interval (CI) 3.9-34 000, P = 0.002], and were judged to have HIT. In contrast, none of 25 patients with early-onset and persisting thrombocytopenia (profile 2) was judged to have HIT, including five patients testing positivefor platelet-activating anti-PF4-heparin IgG antibodies. In these patients, the frequency of heparin-dependent antibodies didnot differfromthat in non-thrombocytopeniccontrols, either for anti-PF4-heparin IgG (OR 1.7, 95% CI 0.7-4.1, P = 0.31) or for platelet-activating antibodies (OR 1.9, 95% CI 0.6-5.7, P = 0.20). Multivariate analysis revealed that type of cardiac surgery, but not HIT antibody status, predicted early-onset and persisting thrombocytopenia. Together, these findings show that HIT was uncommon in this study population [overall frequency, 3/581 (0.5%), 95% CI 0.1-1.5%]. Conclusions: Thrombocytopenia that begins between 5 and 10 days post-cardiac surgery is highly predictive for HIT. In contrast, early-onset and persisting thrombocytopenia is usually caused by non-HIT factors with coinciding heparin-dependent antibody seroconversion.

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Prevalence of Heparin-Associated Antibodies Without Thrombosis in Patients Undergoing Cardiopulmonary Bypass Surgery

Cited by 311 publications

References 22 publications

A prospective study of the prevalence of heparin‐induced antibodies and other associated thromboembolic risk factors in pediatric patients undergoing hemodialysis

A prospective study of the prevalence of heparin‐induced antibodies and other associated thromboembolic risk factors in pediatric patients undergoing hemodialysis

Heparin‐induced thrombocytopenia and thrombosis

Early‐onset and persisting thrombocytopenia in post‐cardiac surgery patients is rarely due to heparin‐induced thrombocytopenia, even when antibody tests are positive

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