TY - JOUR
T1 - When heparin causes thrombosis
T2 - Significance, recognition, and management of heparin-induced thrombocytopenia in dialysis patients
AU - Chang, John Jae Young
AU - Parikh, Chirag R.
PY - 2006/7
Y1 - 2006/7
N2 - Heparin-induced thrombocytopenia (HIT) is characterized by thrombocytopenia and paradoxical hypercoagulability. HIT occurs when an antibody ("HIT antibody") produced against the complex of heparin and platelet factor 4 (PF4) causes systemic platelet consumption and activation. Nephrologists encounter HIT in the care of end-stage renal disease (ESRD) patients because heparin is a routine anticoagulant in hemodialysis. The incidence of HIT in ESRD appears to be lower than in other clinical settings. However, HIT is equally life threatening in ESRD patients and therefore demands the same prompt recognition and aggressive treatment. Diagnosing HIT requires the detection of HIT antibodies. A functional assay (e.g., [14C] serotonin release assay) relies on the patient's HIT antibodies to activate donor platelets at pharmacologic heparin concentrations. The more common antigen assay (e.g., enzyme-linked immunosorbent assay [ELISA]) detects the binding of the patient's HIT antibodies to antigens (e.g., heparin-PF4 complex) in a microtiter well and does not involve platelets. The moment HIT is suspected, heparin should be stopped and an alternative anticoagulant initiated immediately, even before the result of a serologic test becomes available. The advent of several new anticoagulants in the last decade, especially argatroban and bivalirudin, has expanded treatment options for HIT in dialysis patients. This review discusses the epidemiology, pathogenesis, clinical features, diagnosis, and treatment of HIT, with special emphasis on concepts relevant to the care of dialysis patients.
AB - Heparin-induced thrombocytopenia (HIT) is characterized by thrombocytopenia and paradoxical hypercoagulability. HIT occurs when an antibody ("HIT antibody") produced against the complex of heparin and platelet factor 4 (PF4) causes systemic platelet consumption and activation. Nephrologists encounter HIT in the care of end-stage renal disease (ESRD) patients because heparin is a routine anticoagulant in hemodialysis. The incidence of HIT in ESRD appears to be lower than in other clinical settings. However, HIT is equally life threatening in ESRD patients and therefore demands the same prompt recognition and aggressive treatment. Diagnosing HIT requires the detection of HIT antibodies. A functional assay (e.g., [14C] serotonin release assay) relies on the patient's HIT antibodies to activate donor platelets at pharmacologic heparin concentrations. The more common antigen assay (e.g., enzyme-linked immunosorbent assay [ELISA]) detects the binding of the patient's HIT antibodies to antigens (e.g., heparin-PF4 complex) in a microtiter well and does not involve platelets. The moment HIT is suspected, heparin should be stopped and an alternative anticoagulant initiated immediately, even before the result of a serologic test becomes available. The advent of several new anticoagulants in the last decade, especially argatroban and bivalirudin, has expanded treatment options for HIT in dialysis patients. This review discusses the epidemiology, pathogenesis, clinical features, diagnosis, and treatment of HIT, with special emphasis on concepts relevant to the care of dialysis patients.
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U2 - 10.1097/00006676-200604000-00010
DO - 10.1097/00006676-200604000-00010
M3 - Review article
C2 - 16893407
AN - SCOPUS:33746265263
SN - 0894-0959
VL - 19
SP - 297
EP - 304
JO - Seminars in dialysis
JF - Seminars in dialysis
IS - 4
ER -