Affiliation:
1. Weill Cornell Medicine
2. Cornell University
3. University of Washington Department of Pediatrics
4. Hurley Medical Center
5. Natibabiesorg
6. The Rockefeller University
7. Amsterdam Universitair Medische Centra
8. Versiti Blood Research Institute
Abstract
Objective: This study tests the clinical hypothesis that FNAIT
secondary to anti-HPA-1a results in smaller newborns, and the corollary
hypothesis that antenatal management of FNAIT in HPA-1a-incompatible
pregnancies increases birthweight by reducing the effects of
anti-HPA-1a. Design: FNAIT-affected siblings, one untreated and
one treated for FNAIT, were paired for the purpose of comparing their
birthweights. Birthweights of FNAIT-affected and -unaffected pups in a
mouse model of HPA-1a-specific-FNAIT were also analyzed.
Setting: New York Presbyterian-Weill Cornell Medical Center,
New York, NY; Versiti Blood Research Institute, Milwaukee, WI.
Population: 270 FNAIT-affected newborns from a randomized
clinical trial; responders to a NAITbabies.org; and pups in a mouse
model of HPA-1a-specific-FNAIT were evaluated. Methods:
Birthweight percentiles of untreated FNAIT-affected neonates were
compared to those of published controls and treated FNAIT-affected
siblings using one-sample, two-tailed t-tests. Body weights of
FNAIT-affected and -unaffected pups in a mouse model of
HPA-1a-specific-FNAIT were analyzed similarly. Main Outcome
Measures: The difference in birthweight percentile between untreated
and treated FNAIT-affected siblings was analyzed. Results:
Untreated siblings were not small compared to normal controls. However,
treated siblings in both cohorts had significantly higher birthweight
percentiles compared to their untreated, affected sibling.
FNAIT-affected neonatal pups had lower body weights than
FNAIT-unaffected pups. Conclusions: The effect of treatment,
especially high dose IVIG believed to “block” FcRn and lower maternal
anti-HPA-1a levels, to increase birthweights suggests maternal
anti-HPA-1a reduces birthweights. We believe this is mediated by
anti-HPA-1a binding to placental syncytiotrophoblasts, resulting in
placental inflammation.
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