Dealing with symptoms in the general population: lessons learned from the Danish Symptom Cohort

Background: Placental mesenchymal dysplasia (PMD) is a distinct syndrome of unknown aetiology that associated with significant fetal morbidity and mortality. Intrauterine growth restriction common, yet, paradoxically, many the fetuses/newborns have been diagnosed Beckwith-Wiedemann (BWS). Methods: We report two cases PMD high levels androgenetic (complete paternal uniparental isodisomy) cells in placenta document, one case, likely contribution to fetus as well. Results: The same haploid complement found was present coexisting biparental cells, suggesting origin from single fertilisation event. Conclusions: Preferential allocation normal into trophoblast explains absence overgrowth, key feature this syndrome. Interestingly, distribution appears differ reported for artificially created mouse chimeras. Androgenetic mosaicism first time provides an PMD, may be novel mechanism BWS unexplained intrauterine restriction.