David J Kuter1, Barbara A Konkle2, Taye H Hamza3, Lynne Uhl4, Susan F Assmann3, Joseph E Kiss5, Richard M Kaufman6, Nigel S Key7, Bruce S Sachais8, John R Hess9, Paul Ness10, Keith R McCrae11, Cindy Leissinger12, Ronald G Strauss13, Janice G McFarland14, Ellis Neufeld15, James B Bussel16, Thomas L Ortel17. 1. Massachusetts General Hospital, Boston, Massachusetts, USA. 2. Puget Sound Blood Center and University of Washington Medical Center, Seattle, Washington, USA. 3. New England Research Institutes, Watertown, Massachusetts, USA. 4. Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA. 5. University of Pittsburgh, Pittsburgh, Pennsylvania, USA. 6. Brigham and Women's Hospital, Boston, Massachusetts, USA. 7. University of North Carolina, Chapel Hill, North Carolina, USA. 8. New York Blood Center, New York, New York, USA. 9. University of Maryland, Baltimore, Maryland, USA. 10. Johns Hopkins University, Baltimore, Maryland, USA. 11. Cleveland Clinic, Cleveland, Ohio, USA. 12. Tulane University Hospital and Clinics, New Orleans, Louisiana, USA. 13. University of Iowa, Iowa City, Iowa, USA. 14. Froedert Memorial Lutheran Hospital, Milwaukee, Wisconsin, USA. 15. Children's Hospital, Boston, Massachusetts, USA. 16. Weill Cornell Medicine, New York, New York, USA. 17. Duke University, Durham, North Carolina, USA.
Abstract
BACKGROUND: Heparin-induced thrombocytopenia (HIT) is a thrombotic disorder usually prompting treatment with non-heparin anticoagulants. The benefits and risks of such treatments have not been fully assessed. METHODS: We analyzed data for 442 patients having a positive heparin-platelet factor 4 antibody test and recent heparin exposure. The primary outcome was a composite endpoint (death, limb amputation/gangrene, or new thrombosis). Secondary outcomes included bleeding and the effect of anticoagulation. FINDINGS: Seventy-one patients (16%) had HIT with thrombosis (HIT-T); 284 (64%) had HIT without thrombosis (isolated HIT); 87 (20%) did not have HIT. An intermediate or high "4T" score was found in 85%, 58%, and 8% of the three respective groups. Non-heparin anticoagulation was begun in 80%, 56%, and 45%. The composite endpoint occurred in 48%, 36%, and 17% (P = .01) of which 61%, 38%, and 40% were receiving non-heparin anticoagulation. Compared with the no HIT group, the composite endpoint was significantly more likely in HIT-T [HR 2.48 (1.35-4.55), P = .003)] and marginally more likely in isolated HIT [HR 1.66 (0.96-2.85), P = .071]. Importantly, risk increased (HR 1.77, P = .02) after platelet transfusion. Major bleeding occurred in 48%, 36%, and 16% of the three groups (P = .005). Non-heparin anticoagulation was not associated with a reduction in composite endpoint events in either HIT group. INTERPRETATION: HIT patients have high risks of death, limb amputation/gangrene, thrombosis, and bleeding. Non-heparin anticoagulant treatment may not benefit all patients and should be considered only after careful assessment of the relative risks of thrombosis and bleeding in individual patients.
BACKGROUND:Heparin-induced thrombocytopenia (HIT) is a thrombotic disorder usually prompting treatment with non-heparin anticoagulants. The benefits and risks of such treatments have not been fully assessed. METHODS: We analyzed data for 442 patients having a positive heparin-platelet factor 4 antibody test and recent heparin exposure. The primary outcome was a composite endpoint (death, limb amputation/gangrene, or new thrombosis). Secondary outcomes included bleeding and the effect of anticoagulation. FINDINGS: Seventy-one patients (16%) had HIT with thrombosis (HIT-T); 284 (64%) had HIT without thrombosis (isolated HIT); 87 (20%) did not have HIT. An intermediate or high "4T" score was found in 85%, 58%, and 8% of the three respective groups. Non-heparin anticoagulation was begun in 80%, 56%, and 45%. The composite endpoint occurred in 48%, 36%, and 17% (P = .01) of which 61%, 38%, and 40% were receiving non-heparin anticoagulation. Compared with the no HIT group, the composite endpoint was significantly more likely in HIT-T [HR 2.48 (1.35-4.55), P = .003)] and marginally more likely in isolated HIT [HR 1.66 (0.96-2.85), P = .071]. Importantly, risk increased (HR 1.77, P = .02) after platelet transfusion. Major bleeding occurred in 48%, 36%, and 16% of the three groups (P = .005). Non-heparin anticoagulation was not associated with a reduction in composite endpoint events in either HIT group. INTERPRETATION:HITpatients have high risks of death, limb amputation/gangrene, thrombosis, and bleeding. Non-heparin anticoagulant treatment may not benefit all patients and should be considered only after careful assessment of the relative risks of thrombosis and bleeding in individual patients.
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