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Background: Thrombocytopenia is a common problem during pregnancy and often inappropriately managed. This study aimed to assess the prevalence and causes of maternal thrombocytopenia at term with special attention to immune mechanisms of thrombocytopenia and the need for assessing fetal risks., Methods: We conducted a 1-year population-based surveillance study involving 4,382 fullterm (at least 37 weeks' gestation) women (83.8% of the study population) and their infants from the city of Helsinki. Maternal and cord platelet counts were performed at delivery. Immune studies were performed if maternal platelet counts were less than 100 x 10(9)/l; 95% confidence intervals (CIs) were calculated from the binomial distribution., Results: A total of 317 women (7.3%; 95% CI 6.5, 8.1) had platelet counts of less than 150 x 10(9)/l. Most cases (81%) of maternal thrombocytopenia at term were due to gestational thrombocytopenia, which had no impact on either the mother or the fetus unless associated with some other medical or obstetric disorder. Other causes of thrombocytopenia were preeclampsia (16%) and idiopathic thrombocytopenic purpura (ITP) (3%). There was no association between maternal and fetal platelet counts: of the infants born to thrombocytopenic mothers, 2.1%, had thrombocytopenia in the cord blood, which did not differ significantly from the 2.0% of thrombocytopenic infants born to non-thrombocytopenic mothers., Conclusion: Women with gestational thrombocytopenia do not require alteration of their treatment. Fetal blood sampling is not considered necessary when thrombocytopenia is discovered unexpectedly at term.

The primary problem in the measurement of reticulated platelets (RP) stained with thiazole orange (TO) by flow cytometry is the definition of a threshold limit for fluorescence positivity. We evaluated settings for the threshold gate for TO positivity based on two principles: a fluorescence histogram (median FL1, Relative FL1) or a plot of forward light scatter (FSC; reflecting the distribution of the platelet size) versus fluorescence intensity (% RP). These methods were applied prospectively in examination of 54 healthy blood donors (16 females) and a total of 50 blinded patient samples: pregnant women with thrombocytopenia (Group 1A, n = 11), thrombocytopenic women after delivery (Group 1B, n = 9) and healthy women with a thrombocytopenic newborn (Group 2, n = 30). Group 1A displayed higher median FL1 (mean 306, CI 279-332) as compared to that of Group 2 (mean 266, CI 255-277; p = 0.0038) or to that of the female controls (mean 249, CI 231-268; p < 0.001). Relative FL1 was also higher in the patients of Group 1A than those of Group 2 (p = 0.037). When analysing the % RP, the difference between these groups was not significant. In the patients (n = 50), the median FSC (mean 407, SD 40, CI 395-418) was also higher than that of the controls (n = 54; mean 383, SD 25, CI 376-390; Mann-Whitney U-test, p = 0.0015). In Group 1A, a significant correlation was observed between the Patient median FL1 and Patient median FSC (r = 0.62, p = 0.043). When developing methods for the measurement of RP, it seems to be useful to analyse the data with more than one principle to define the threshold limit for TO positivity.

Objective: To assess the prevalence and causes of thrombocytopenia among full-term infants., Methods: We conducted a 1-year, population-based surveillance study involving all full-term infants (at least 37 weeks' gestation) born to native Finnish women in Helsinki. In cases of thrombocytopenia (cord platelet count less than 150 x 10(9)/L) clinical risk factors were evaluated and immunologic studies were performed on both parents and on the infant; 95% confidence intervals (CIs) were calculated on the basis of binomial distribution., Results: Platelet counts were done in cord blood from 4,489 infants, 84.9% of the study population. Eighty-nine infants had platelet counts below 150 x 10(9)/L (2.0%; 95% CI 1.5, 2.3) in cord blood and 11 were less than 50 x 10(9)/L (0.24%; 95% CI 0.10, 0.38). All causes of clinically important thrombocytopenia, those presenting with bleeding and requiring treatment, were related to fetomaternal alloimmune thrombocytopenia. The incidence of severe alloimmune thrombocytopenia was one in 1500 live births and one in 900 of all thrombocytopenia. An immunologic mechanism was involved in ten of 65 (15.4%; 95% CI 6.6, 24.2) infants studied and in four of 15 (26.7%; 95% CI 4.3, 49.1) cases of severe thrombocytopenia., Conclusion: Immunologic studies should be considered in all cases of severe neonatal thrombocytopenia for careful monitoring and prevention of potentially severe complications in subsequent pregnancies.

Prenatal treatment of fetomaternal alloimmune thrombocytopenia (FMAIT) in previously affected families is of great clinical importance. We report here our experience in the prenatal treatment of 15 severely thrombocytopenic fetuses. Thrombocytopenia was in 13 cases due to immunization to HPA-1a, in one case to HPA-5b, and in one case to HPA-6b. Thirteen fetuses received altogether 34 intrauterine platelet transfusions, seven of them in combination with maternal-administered intravenous gammaglobulin (IVIG) and two in combination with IVIG and prednisone. Six of the 13 fetuses had only one transfusion just prior to delivery. In our experience, IVIG seemed to be less effective than reported; only two fetuses of eight treated initially with weekly maternal-administered IVIG responded, and these were the mildest affected cases in the study. On the other hand, owing to the short survival time, weekly platelet transfusions could only partly maintain a safe platelet count in the four fetuses treated with serial intrauterine platelet transfusions. The number of transfusions needed to be limited because of the high cumulative risk associated with repeated procedures. Three of 34 intrauterine platelet transfusions were associated with near-loss of three different fetuses due to prolonged fetal bradycardia after the transfusion. In conclusion, overall neonatal outcome was good, with no mortality; among the study group there was no intracranial haemorrhage (evaluated by postnatal ultrasonography) compared with one case in their untreated siblings. However, the problem of the optimal treatment of FMAIT remains to be solved. For the moment, the treatment of choice is a combination of maternal IVIG and platelet transfusions in severely affected cases. Serial fetal blood samplings (FBS) are needed in order to monitor the fetus with sufficient care.

Objective To study the clinical usefulness of maternal anti- HPA-1a antibody levels in predicting severe foetomaternal alloimmune thrombocytopenia ( FMAIT). Background Recent studies using an international anti- HPA-1a standard have shown a correlation between maternal antibody levels and neonatal thrombocytopenia. Cut-off values for identifying high-risk pregnancies have also been suggested. Materials In 1986-2010, HPA-1a alloimmunisation was confirmed in 84 women with 129 pregnancies. Maternal samples were obtained at delivery and during subsequent pregnancies. Anti- HPA-1a was quantified using a MAIPA assay with a detection limit of 0·8 IU mL-1 ( WHO reference serum 03/152). Antibody levels were compared with the severity of neonatal disease in the index and in the subsequent pregnancies. Results In the index cases, the correlation between an anti- HPA-1a level and neonatal platelet count did not reach statistical significance ( n = 77, P = 0·074). However, the platelet counts and antibody levels in cases with cutaneous ( n = 45) or intracranial haemorrhage ( n = 7) were significantly different from cases with no evidence of bleeding ( n = 20). In the subsequent pregnancies, there was a stronger association between the second trimester anti- HPA-1a level and the foetal platelet count ( n = 16, P = 0·046). The positive predictive value of the maternal antibody level for a foetal platelet count <20 × 109 L-1 was 90%, but the negative predictive value only 31%. Conclusion Although a higher anti- HPA-1a level correlated with a more severe neonatal disease, barely detectable antibody levels were also observed in severely affected pregnancies. Cut-off values with sufficient sensitivity and specificity to identify these foetuses could not be found. A previous obstetric history still remains the most useful predictive parameter for severe FMAIT in clinical practice. [ABSTRACT FROM AUTHOR]