title: Heparin-induced thrombocytopenia (HIT II) - a drug-associated autoimmune disease.
abstract: Autoimmune thrombocytopenia (ITP) is an acquired autoimmune disease characterised by isolated persistent thrombocytopenia and normal megakaryopoiesis. This definition also applies to heparin-induced thrombocytopenia (HIT II), a frequent side effect of heparin treatment. In HIT II, the immunogen is a coagulation active complex of heparin and platelet factor 4 (PF4). By now, diagnostics of HIT II is often material and time consuming. Three groups of patients were investigated for HIT II antibodies (HIT II-AB): 54 hospitalised stroke patients, 87 hospitalised cardiac patients, and 71 patients on chronic haemodialysis, all treated with heparin. Furthermore, 100 healthy volunteers were investigated. For detection of HIT II-AB the innovative whole blood test PADA-HIT (PADA: platelet adhesion assay) was used. PADA-HIT quantifies the interaction of IgG antibodies with FcgammaIIA receptors by comparing the activation state of platelets in citrated and heparinised whole blood. The occurrence of HIT II-AB in blood was very high with 44 % of stroke patients, 69% of cardiac patients and 38% of haemodialysis patients compared to only 15% of healthy volunteers. This demonstrates a high incidence and a rapid onset of HIT II-AB in patients being acutely treated with heparin. HIT II is one of the most frequent and severe autoimmune diseases bearing a great thrombosis risk. PADA-HIT represents an innovative diagnostic method for detection of autoimmune antibodies of IgG type that are directed against platelet factor 4 (PF4)-heparin-complex. By early and fast diagnostics and appropriate treatment severe complications of HIT II can be prevented.
authors.affiliation: University Hospital Jena, Research Group Pharmacological Haemostaseology, 07747 Jena, Germany. AGPHH@med.uni-jena.de
authors.forename: Götz
authors.initials: G
authors.lastname: Nowak
mesh_terms: D000328:Adult; D000368:Aged; D000925:Anticoagulants / Q000009:adverse effects* / Q000276:immunology / Q000494:pharmacology / Q000627:therapeutic use; D001323:Autoantibodies / Q000096:biosynthesis / Q000097:blood* / Q000276:immunology; D002951:Citrates / Q000494:pharmacology; D042241:Early Diagnosis; D005260:Female; D006331:Heart Diseases / Q000150:complications / Q000188:drug therapy / Q000276:immunology; D006493:Heparin / Q000009:adverse effects* / Q000276:immunology / Q000494:pharmacology / Q000627:therapeutic use; D006801:Humans; D007074:Immunoglobulin G / Q000032:analysis* / Q000096:biosynthesis / Q000276:immunology; D007676:Kidney Failure, Chronic / Q000150:complications / Q000188:drug therapy / Q000276:immunology; D008297:Male; D018448:Models, Immunological; D010973:Platelet Adhesiveness; D010976:Platelet Count / Q000379:methods*; D010978:Platelet Factor 4 / Q000187:drug effects / Q000276:immunology*; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000139:chemically induced* / Q000150:complications / Q000175:diagnosis / Q000276:immunology; D017452:Receptors, IgG / Q000276:immunology; D006435:Renal Dialysis; D000077559:Sodium Citrate; D020521:Stroke / Q000150:complications / Q000188:drug therapy / Q000276:immunology
chemical_list: D000925:Anticoagulants; D001323:Autoantibodies; D002951:Citrates; C080568:Fc gamma receptor IIA; D007074:Immunoglobulin G; D017452:Receptors, IgG; D000077559:Sodium Citrate; D010978:Platelet Factor 4; D006493:Heparin