HEPARIN-INDUCED THROMBOCYTOPENIA (HIT) is a syndrome of thrombocytopenia caused by circulating Ig antibodies ("HIT antibodies") that bind to heparin platelet factor 4 cornplexes.(1) HIT with thrombosis (HITT) is HIT with the clinical syndrome of arterial or venous thrombosis because of platelet activation. The frequency of development of HIT antibodies depends on the type of heparin exposure (higher with unfractionated hepanin [UFH] compared with low-molecular-weight heparin [LMWH]) and the patient population (surgical patients higher than medical patients). Cardiac surgical patients who are exposed to UFH perioperatively have a 50% incidence of detectable HIT antibodies.' In orthopedic surgical patients, the incidence is 15% with exposure to UFH but only 8% with exposure to LMWH.(1) Not all patients who develop HIT antibodies will become thrombocytopenic. Clinical HIT with thrombocytopenia below 100,0001/mu L is uncommon, and thrombosis (HITT) is rare (0%-5% of patients).(2-5) Thrombocytopenia develops generally within 4 to 15 days of exposure to heparin but occasionally call Occur within hours (rapid-onset HIT) because of the presence of circulating HIT antibodies formed after a recent exposure.(6-8) Of 73 patients identified to have had rapid-onset HIT over a period of 15 years, most had received heparin (all UFH) within the previous 3 weeks and all within the previous 100 days.(6) The authors describe a case of fatal rapid-onset HIT in a patient of previously unknown HIT status who had received UFH more than I year and LMWH 8 months before the current admission.

Fatal heparin-induced thrombocytopenia 8 months after prior exposure to heparin

CRIMI C;
2008-01-01

Abstract

HEPARIN-INDUCED THROMBOCYTOPENIA (HIT) is a syndrome of thrombocytopenia caused by circulating Ig antibodies ("HIT antibodies") that bind to heparin platelet factor 4 cornplexes.(1) HIT with thrombosis (HITT) is HIT with the clinical syndrome of arterial or venous thrombosis because of platelet activation. The frequency of development of HIT antibodies depends on the type of heparin exposure (higher with unfractionated hepanin [UFH] compared with low-molecular-weight heparin [LMWH]) and the patient population (surgical patients higher than medical patients). Cardiac surgical patients who are exposed to UFH perioperatively have a 50% incidence of detectable HIT antibodies.' In orthopedic surgical patients, the incidence is 15% with exposure to UFH but only 8% with exposure to LMWH.(1) Not all patients who develop HIT antibodies will become thrombocytopenic. Clinical HIT with thrombocytopenia below 100,0001/mu L is uncommon, and thrombosis (HITT) is rare (0%-5% of patients).(2-5) Thrombocytopenia develops generally within 4 to 15 days of exposure to heparin but occasionally call Occur within hours (rapid-onset HIT) because of the presence of circulating HIT antibodies formed after a recent exposure.(6-8) Of 73 patients identified to have had rapid-onset HIT over a period of 15 years, most had received heparin (all UFH) within the previous 3 weeks and all within the previous 100 days.(6) The authors describe a case of fatal rapid-onset HIT in a patient of previously unknown HIT status who had received UFH more than I year and LMWH 8 months before the current admission.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.11769/552255
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