David Böhm (Gießen/ DE), Dr. Sandra Wienzek-Lischka (Gießen/ DE), Dr. Nina Cooper (Gießen/ DE), Heike Berghöfer (Gießen/ DE), Katja Müller (Gießen/ DE), Dr. Behnaz Bayat (Gießen/ DE), Prof. Dr. Gregor Bein (Gießen/ DE), Prof. Dr. Ulrich Sachs (Gießen/ DE)
Background
In fetal/neonatal alloimmune thrombocytopenia (FNAIT), maternal alloantibodies against paternal human platelet antigens (HPA) cross the placenta and lead to platelet destruction. The extent of thrombocytopenia varies among neonates, and inflammation may constitute an important trigger
Methods
A set of stable inflammatory markers was measured in serum samples from 100 neonates with low platelet counts, of which n=50 were diagnosed with FNAIT due to anti-HPA-1a antibodies and n=50 were thrombocytopenic without detectable maternal HPA antibodies.
Results
Concentrations of C-reactive protein, soluble CD14, procalcitonin, and sFlt-1 did not differ between the two cohorts. There was no correlation between C-reactive protein or soluble CD14 and the platelet count, but a negative correlation was observed between procalcitonin concentrations and the neonatal platelet count in both cohorts. sFlt-1 concentration and the platelet count were correlated in FNAIT cases exclusively. None of the inflammatory markers was statistically different between cases with and without ICH.
Conclusion
We were unable to identify systemic inflammation as a relevant factor for thrombocytopenia in FNAIT. The antiangiogenic enzyme sFlt-1 did correlate with the platelet count in the FNAIT cohort. Our findings may give rise to the hypothesis that placental inflammation rather than systemic inflammation modulates disease severity in FNAIT.
Offenlegung Interessenkonflikt:
n/a