Fetal hepatic calcifications can be caused by infections, chromosomal disorders, thrombotic events, ischemic hepatic necrosis and subcapsular hematomas among others events. Its features and clinical significance are still not well known. We performed an observational study to describe fetal hepatic calcifications and its association with main clinical and histopathological findings from the fetal autopsy database, between 2007 and 2014. Raw odds ratio analysis was performed. We reviewed 591 fetal autopsies: 14 cases with hepatic calcifications, 102 fetuses with chromosomal disorders; 13 with diagnosis of TORSCH (toxoplasma, rubella, syphilis, cytomegalovirus, herpes virus 1 and 2, and others) and 207 with any abnormality in the umbilical cord (UC). The relation between hepatic calcifications and chromosomal disorders in our series had significance. It is known that hepatic calcifications are common in chromosomal disorders, transplacental infections and UC abnormalities, those conditions are risk factor for hepatic calcifications formation; we suggest hepatic calcifications should alert the pathologists in order to consider these etiologies in first instance.

The increasing rates of preterm birth among twins implicate that solid data on associated risks and outcomes are required. Assessment of zygosity is often based on clinical criteria (evaluation of placenta; same gender, birth weight discordance as surrogate criteria for monochorionic/monozygotic twins). The aim of this study was to compare clinical versus genetic assessment of zygosity and to compare causes of preterm delivery as well as outcome data of very-low-birth-weight (VLBW; birth weight <1,500 g) twins stratified to zygosity. In a multicenter study, we selected n = 176 sets of same gender twins and determined zygosity genetically. In a subgroup of 123 sets of twins, the attending physicians at the study centers were asked to document the parameter ‘zygosity’ (monozygotic/dizygotic) on the basis of their clinical judgment. Concordance between genetic and clinical assessment was 62.7% for monozygotic twins and 88.9% for dizygotic twins, respectively. Outcome parameters (death, BPD, ROP, NEC, IVH) were comparable in both groups. Genetically dizygotic twins were significantly more often born due to intrauterine infection (33% vs. 20% in monozygotic twins, p < .01) and antenatal antibiotics were more frequently given to mothers of dizygotic twins (62% vs. 47% in monozygotic twins, p < .01). Obstetric complications such as twin-twin-transfusion-syndrome were only seen in monozygotic twins as expected. The unexpected increase of antenatal antibiotic treatment and birth due to intrauterine infection in dizygotic twins should be confirmed in additional VLBW twin-cohorts.