Initial fetal platelet counts predict the response to intravenous gammaglobulin therapy in fetuses that are affected by PLA1 incompatibility

OBJECTIVE: Fetal alloimmune thrombocytopenia is the result of maternal feta l platelet antigen incompatibility; intracranial hemorrhage is its most ser ious complication. Our previous studies have demonstrated an inability to a ccurately predict fetal platelet counts in this disorder, The goal of the p resent investigation was to identify factors that would predict the respons e of the fetal platelet count to therapy so that use of fetal blood samplin g could be minimized. STUDY DESIGN: Patients who were eligible for the study were all those who ( 1) had alloimmune thrombocytopenia secondary to pl(A1) (HPA-1a, ZW(A)) plat elet antigen incompatibility, (2) were treated with maternally administered intravenous immunoglobulin at 1 g/kg of body weight per week, with or with out low dose steroids, and (3) had percutaneous fetal blood sampling before the initiation of therapy (first fetal blood sampling) and again 3 to 7 we eks afterwards (second fetal blood sampling), RESULTS: In this retrospective review, 74 patients who were affected by all oimmune thrombocytopenia had a median platelet count of 21,000 per microlit er at the first fetal blood sampling and 47,000 per microliter at the secon d fetal blood sampling, with a median increase in platelet count of 24,000 per microliter, Response to treatment was defined as either (1) an improvem ent in platelet count (the second fetal blood sampling greater than the fir st fetal blood sampling, and second fetal blood sampling > 20,000 per micro liter) or (2) a minimal decline in platelet count (the first fetal blood sa mpling greater than or equal to 40,000 per microliter and the difference be tween the first and second fetal blood sampling less than or equal to 10,00 0 per microliter). The first fetal blood sampling had prognostic value for the second fetal blood sampling (P =.0001), although the previous sibling b irth platelet count and history of sibling intracranial hemorrhage did not predict the platelet count at the first or second fetal blood sampling or t he change in platelet count between the samplings. When the patients were s egregated to first fetal blood sampling of > 20,000 per microliter versus l ess than or equal to 20,000 per microliter, the response rates for the 2 gr oups were 89% (33/37 patients) versus 51% (19/37 patients; P =.001). CONCLUSION: In fetal alloimmune thrombocytopenia secondary to Pl(A1) platel et antigen incompatibility, fetuses with platelet counts > 20,000 per micro liter at the initiation of therapy were predicted to maintain their platele t count at the second fetal blood sampling at > 20,000 per microliter. The characteristics of the previous sibling, as previously reported, did not pr edict the initial fetal blood sampling, the second fetal blood sampling, or the response to treatment.