No abstract

There are previous indications that transplacental transmission of cytomegalovirus (CMV), parvovirus B19 (PB19) and herpes simplex virus types 1 and 2 (HSV-1/2) cause fetal infections, which may lead to fetal death. In a prospective case-control study we examined the incidence of these viruses in intrauterine fetal death and their association with fetal and placenta pathological findings. Molecular assays were performed on placenta tissue extracts of 62 fetal deaths and 35 controls for the detection of CMV, PB19 and HSV-1/2 genomes. Formalin-fixed, paraffin-embedded liver, spleen and placenta tissues of fetal death cases were evaluated histologically. Thirty-four percent of placental specimens taken from intrauterine fetal deaths were positive for any of the three viruses (16%, 13%, and 5% positive for CMV, PB19, and HSV-1/2, respectively), whereas only 6% of those taken from full term newborns were positive (P = 0.0017). No dual infection was observed. This difference was also observed when fetal deaths with a gestational age <20 weeks or a gestational age >20 weeks were compared with the controls (P = 0.025 and P = 0.0012, respectively). Intrauterine death and the control groups differed in the detection rate of CMV DNA (16% and 3%, respectively; P = 0.047), which was more pronounced in a gestational age >20 weeks (P = 0.03). Examination of the pathological findings among the PCR-positive and PCR-negative fetal deaths revealed that hydrops fetalis and chronic villitis were more common among the former group (P = 0.0003 and P = 0.0005, respectively). In conclusion, an association was detected between viral infection and fetal death, which was more pronounced in the advanced gestational age. Fetal hydrops and chronic villitis were evidently associated with viral DNA detection in cases of intrauterine death.

The early (intrauterine and neonatal) life environment plays an important role in programming the susceptibility in later life to chronic degenerative diseases, such as obesity, cardiovascular diseases, diabetes mellitus, cancer and osteoporosis.Among other hormones, leptin plays a major role in the regulation of the overall metabolism and has multiple neuroendocrine (adeno-and neuro-hypophysis axes and the hypothalamus-pituitary-adrenal axis) and immune functions.The hormone exerts its actions beginning in the early life time period, regulating the intrauterine and early extrauterine life growth and development, as well as the adaptation to extrauterine life, neonatal thermogenesis and response to stress. Recent findings also support a role of leptin in the process of fetal bone remodeling and brain development.Therefore, it is of interest to explore the physiology of leptin in early life, as well as those factors that may perturb the balance of the hormone with pathological consequences in terms of confining an increased risk for disease in later life.This review aims to summarize reported findings concerning the role of leptin in early life, as well as the association of fetal, maternal and placental factors with leptin levels, while attempting to speculate mechanisms through which these factors may influence the risk for developing chronic diseases in later life.

The IL12RB1 locus is Alu-enriched and therefore prone to rearrangements at various positions. CNVs should be considered in the genetic diagnosis of IL-12Rβ1 deficiency.