title: Serum from patients with chronic idiopathic thrombocytopenic purpura frequently affect the platelet function.
abstract: In most, but not all, cases of chronic idiopathic thrombocytopenic purpura (ITP), bleeding complications are known to occur when the platelet count is low. The present study investigates the effect of ITP sera on the in vitro platelet function of donor platelets. Sera from 58 ITP patients were investigated. Using an indirect monoclonal antibody specific immobilisation of platelet antigen (MAIPA) technique, GPIIb/IIIa and GPIb/IX specific antibodies were found in 23 and 20 patients, respectively. Twelve of them had antibodies against both glycoprotein (GP) complexes. The ITP sera's effect on donor platelets was investigated by aggregometry and the results were compared with the ones of 26 healthy donor sera. Grouped together, the ITP sera significantly impaired the ADP-induced platelet aggregation of donor platelets compared to the control sera; the mean relative aggregation response (T(max)) seen for the ITP and control sera were 82 +/- 21% and 92 +/- 7%, respectively (p = 0.0157). However, 6 ITP sera gave an enhanced aggregation response, whereas 17 ITP sera resulted in an impaired platelet aggregation, when using the mean +/- 2 S.D. recorded for the controls as the normal range. There was not any correlation between aggregation response, platelet number or the presence of GPIb/IX or GPIIb/IIIa specific antibodies, other than the fact that all ITP sera causing an enhanced aggregation were from patients with a platelet number less then 100 x 10(9)/l at the time of blood sampling. It is concluded that some ITP sera can either enhance or impair the platelet aggregation response, but in most cases, a normal response is obtained.
authors.affiliation: Department of Internal Medicine, Haematology Section and the Coagulation Centre, Sahlgrenska Hospital, University of Göteborg, SE-413 45 Göteborg, Sweden. anna.olsson@medic.gu.se
authors.forename: Anna
authors.initials: A
authors.lastname: Olsson
authors.forename: P O
authors.initials: PO
authors.lastname: Andersson
authors.forename: Lilian
authors.initials: L
authors.lastname: Tengborn
authors.forename: Hans
authors.initials: H
authors.lastname: Wadenvik
mesh_terms: D000244:Adenosine Diphosphate / Q000494:pharmacology; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001323:Autoantibodies / Q000097:blood; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D010974:Platelet Aggregation / Q000187:drug effects / Q000276:immunology; D010976:Platelet Count; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000276:immunology; D019038:Platelet Glycoprotein GPIb-IX Complex / Q000276:immunology; D010980:Platelet Membrane Glycoproteins; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000097:blood*
chemical_list: D001323:Autoantibodies; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019038:Platelet Glycoprotein GPIb-IX Complex; D010980:Platelet Membrane Glycoproteins; C032193:glycoprotein receptor GPIb-IX; D000244:Adenosine Diphosphate