Normal pregnancy relies on a careful balance between immune tolerance and suppression. It is known that strict regulation of maternal immune function, in addition to components of inflammation, is paramount to successful pregnancy, and any imbalance between proinflammatory and anti-inflammatory cytokines and chemokines can lead to aberrant inflammation, often seen in complicated pregnancies. Inflammation in complicated pregnancies is directly associated with increased mortality and morbidity of the mother and offspring. Aberrant inflammatory reactions in complicated pregnancies often lead to adverse outcomes, such as spontaneous abortion, preterm labor, intrauterine growth restriction, and fetal demise. The role of inflammation in different stages of normal pregnancy is reviewed, compared, and contrasted with aberrant inflammation in complicated pregnancies. The complications addressed are preterm labor, pregnancy loss, infection, preeclampsia, maternal obesity, gestational diabetes mellitus, autoimmune diseases, and inflammatory bowel disease. This article examines the role of various inflammatory factors contributing to aberrant inflammation in complicated pregnancies. By understanding the aberrant inflammatory process in complicated pregnancies, novel diagnostic tools and therapeutic interventions for modulating it appropriately can be identified.

Introduction Preeclampsia (preE) is pregnancy-induced hypertension affecting a significant proportion of pregnant women worldwide and can cause detrimental effects in the mother and newborn. Some of the effects in the newborn include neonatal thrombocytopenia. Pertaining specifically to neonatal thrombocytopenia, several questions remain unanswered. Discussion According to the current literature, neonatal thrombocytopenia due to maternal preE is highly prevalent in the general population and the incidence is reported to be around 30% worldwide. This review gives an insight into the syndrome and summarizes the possible pathological mechanisms, the diagnostic approach, complications, and therapeutic interventions of neonatal thrombocytopenia. It also identifies the involvement of other cell lines, apart from platelets in the newborns. Furthermore, we suggest a future prospective study to investigate the pathogenesis of preE and plan a study involving animal models to come up with a possible therapeutic intervention to prevent preE and its various consequences in neonates.

ObjectiveDespite growing knowledge of the pathophysiology leading to the development of preeclampsia (PreE) and diabetes mellitus (DM), the interaction between the two disease processes needs to be further examined. This study compared normal pregnancies to those complicated with preE, gestational diabetes mellitus (GDM), and/or pre-existing diabetes in order to assess the effects of elevated glucose on placental development and its potential role in the pathogenesis of preE.MethodsThe chart review was performed in an IRB approved retrospective cross-sectional study of live born singleton deliveries. A total 621 subjects were randomly selected from deliveries occurring between 2008 to 2011 at Baylor Scott & White Memorial hospital. Statistical analysis was performed using Duncan's post-hoc test and ANOVA.ResultsPatients who developed preE had higher systolic and diastolic blood pressures than those who did not develop preE (p<0.05). Patients with either pre-existing diabetes or GDM were older. There was no difference among groups for gravidity (p=0.21) with an average gravidity of 2.7 (1.8SD) for 621 subjects and a range of 1 to 14 pregnancies. Patients with preE delivered earlier in pregnancy than those without preE regardless of diabetes status. However, those with preE and pre-existing diabetes delivered significantly earlier at 35.0+/−0.4 than the other two preE groups (*p<0.05 for each), suggesting more severe condition. Additionally, patients with pre-existing diabetes who developed preE delivered smaller babies than those with pre-existing diabetes without preE (1.00±0.03, p<0.05 for each). However, the development of GDM did not result in smaller babies for those pregnancies with preE.ConclusionsThe development of preE in those with pre-existing diabetes led to growth restriction and more severe disease as evidenced by lower birth weights and earlier gestational ages at delivery. These differences were not seen in GDM pregnancies. This supports the concept that elevated glucose levels during placental development in the first trimester may alter the placenta and lead to restriction later in pregnancy when a second stimulus triggers preE.