[Neonatal alloimmune thrombopenia in anti-HPA-3a (Baka) immunization]. / Thrombopénie néonatale allo-immune par immunisation anti-HPA-3a (Baka).

BACKGROUND: Neonatal alloimmune thrombocytopenia (NAIT) in the HPA-3a system is responsible for less than 5% of all cases of NAIT. CASE REPORT: Thomas, a male infant, was born at 39 weeks of gestation after an uncomplicated pregnancy. Delivery was normal. The Apgar score was 9 at 1 minute, and 10 at 5 and 10 minutes. At 1 hour of age, he displayed extensive petechiae and purpura over the back. The platelet count was 8,000/mm3. Hematesis and extensive petechiae were noted, leading to an exchange transfusion followed by a transfusion of 0.5 U/kg of random donor platelets, 0.4 g/kg/d of intravenous immunoglobulin (IVIg) and 10 mg/kg/d of corticosteroids. IVIg were discontinued on d5 and corticosteroids on d10. There was no relapse of thrombocytopenia. A neonatal alloimmune thrombocytopenia with an HPA-3a (Baka) incompatibility was confirmed. CONCLUSION: HPA-3a incompatibility is certainly more frequent than the rare cases reported and must be searched for in all cases of neonatal thrombocytopenia.

Measurement of tPA and tPA-PAI-1 complexes by ELISA, using monoclonal antibodies: clinical relevance.

Two ELISA methods using monoclonal antibodies, are described for the measurement of tPA:Ag and tPA-PAI-1 complexes. On normal population tPA:Ag was found with a mean value of 5 ng/ml. Furthermore, despite that tPA activity was very low, only 50% (mean value) was measured as stable complexes with PAI-1. Important increase of tPA:Ag was observed in various pathologies (cardiac infarction, septicemia, respiratory distress syndrome). In liver disease, tPA:Ag reached high levels up to 100 ng/ml. Impaired liver clearance can potentiate the increased concentration which results from endothelial release. In all patients with elevated tPA:Ag level, 70 to 100% of tPA was complexed to PAI-1. Excess release of PAI-1 accompanys the increased release of tPA as it is proved by presence of high residual PAI-1 activity. Addition of exogeneous tPA to these pathological plasmas induced a high increase in tPA-PAI-1 complexes. Venous stasis in normal population resulted in a parallel increase of tPA:Ag and tPA-PAI-1 complexes. Although about a two fold increase was obtained for both parameters, post venous stasis plasma presented a much higher fibrinolytic activity while PAI-1 activity was moderately elevated. tPA:Ag and tPA-PAI-1 complexes have diagnosis and prognosis value in various pathologies as indicators of stimulated release of fibrinolysis activator and inhibitor.