Genetic polymorphism H131R of Fcgamma receptor type IIA (FcgammaRIIA) in a healthy Finnish population and in patients with or without platelet-associated IgG.

Patients (n=113) with histories of thrombocytopenia and with different profiles for platelet-associated IgG (PA-IgG) were subdivided according to the genetic polymorphism H131R in the Fcgamma receptor type IIA (FcgammaRIIA). PA-IgG was measured by the direct platelet immunofluorescence test (PIFT), and GP IIbIIIa and/or GP Ib-specific PA-IgG was investigated by a modified version of the direct monoclonal antibody-specific immobilization of platelet antigens (MAIPA) assay. As a control, the distribution of FcgammaRIIA polymorphism H131R was determined among 93 healthy Finnish blood donors. The frequencies for H131 and R131 were 0.56 and 0.44 (CI: 0.37-0.51), respectively, which did not differ significantly from those in other Caucasian populations. The distribution of the genotypes HH131, HR131 and RR131 in the patients and controls did not differ significantly. In the HH131 group, the PA-IgG was higher than in the RR131 group (p=0.082). Female patients with the genotype RR131 seemed to be younger than those with HH131 (p=0.065). Among the female patients, a significantly greater number were under 40 yr old in the RR131 group than in the HH131 group (p=0.0060). Within the RR131 group, the female patients were far younger than the male patients (median 29 vs. 61 yr; p=0.0021). The results point to the heterogeneity of immune thrombocytopenia, which may partly explain the poor predictive value of PA-IgG studies.

Idiopathic thrombocytopenic purpura in pregnancy.

OBJECTIVE: The aim of this study was to evaluate retrospectively our strategies in monitoring and treating pregnant women with idiopathic thrombocytopenic purpura (ITP). METHODS: Medical records were reviewed for diagnosis, clinical course, treatment, and neonatal outcome in 35 Finnish women with ITP giving birth to 55 neonates during 53 pregnancies. The outcome of the first (i.e. index) pregnancy was used in the statistical analyses. The platelet immunofluorescence test (PIFT) was used for detection of platelet autoantibodies. The correlation between neonatal platelet counts and results of PIFT was calculated with the Pearson's correlation coefficient and the Fisher's exact test. RESULTS: There were no serious bleeding complications although five of 35 women had platelet counts of less than 50 x 10(9)/l in the third trimester of the index pregnancy. Prophylactic platelet transfusions were given to six of 15 women delivered by cesarean section. Five of 35 (14.3%; 95% confidence interval, 2.6 to 25.8%) neonates had platelet counts of less than 50 x 10(9)/l median 3 days after delivery versus only one of 28 (3.6%; 95% confidence interval, 0.1 to 10.5%) at birth. No infant showed any clinical signs of intracranial hemorrhage. No significant correlation was encountered between neonatal thrombocytopenia and maternal platelet autoantibodies. The history of a previous infant with thrombocytopenia was the only important information in estimating the risk of fetal thrombocytopenia. CONCLUSIONS: To avoid unnecessary and possibly harmful monitoring and treatment, we need further tests for predicting the perinatal risks in pregnant women with ITP.

Comparison of the direct platelet immunofluorescence test (direct PIFT) with a modified direct monoclonal antibody-specific immobilization of platelet antigens (direct MAIPA) in detection of platelet-associated IgG.

Glycoprotein (GP)-specific platelet-associated IgG (PA-IgG) may be demonstrable in autoimmune-mediated thrombocytopenia. We studied 159 consecutive patients with histories of thrombocytopenia by a modified direct monoclonal antibody-specific immobilization of platelet antigens (direct MAIPA) assay, which immobilizes GP IIb/ IIIa, GP Ib/IX and GP Ia/IIa simultaneously. This modification requires smaller quantities of platelets than standard measurements performed separately. PA-IgG was present in 84/159 (53%) patients, as shown by the direct platelet immunofluorescence test (PIFT) with flow cytometry as a reference. PA-IgG against GP IIb/IIIa and/or GP Ib/IX and/or GP Ia/IIa was noted in 46 patients (29%), of whom 93% (43/46)-were also PA-IgG positive. The amount of PA-IgG detected by PIFT correlated directly with that detected by direct MAIPA (r = 0.71; P < 0.001). Only three patients 12548 with negative direct PIFT had GP-specific PA-IgG. GPV-specific PA-IgG was detected in 13 (10%) of the 125 patients, in whom further studies could be performed. In the subgroup of patients with GP-specific PA-IgG, the median fluorescence intensities of direct PIFT were higher than in patients with no GP-specific PA-IgG (P < 0.001). Direct PIFT and direct MAIPA divided the patients into asymmetric subgroups. However, the relative roles of these tests in the diagnosis of autoimmune-mediated thrombocytopenia await further studies.