The etiology of cardiac hypertrophy in infants

This study aimed to describe the variety of etiologies currently identified in infants with cardiac hypertrophy (CH) and investigate whether there is a relation with hyperinsulinism, echocardiographic characteristics and prognosis. This retrospective cohort study included infants born between 2005 and 2018 with CH measured by echocardiography [interventricular septum (IVS) and/or left ventricular posterior wall (LVPW) thickness with Z-score ≥ 2.0]. Children with congenital heart disease or hypertension were excluded. Underlying diagnosis, echocardiographic and follow-up data were extracted from patient files. Seventy-one infants with CH were included. An underlying cause of CH was identified in two-thirds (n = 47). Most common etiologies of CH were malformation syndromes (n = 23, including Noonan n = 12) and maternal diabetes mellitus (n = 13). Less common causes were congenital hyperinsulinism (n = 3), metabolic- (n = 5), sarcomeric- (n = 2) and neuromuscular disease (n = 1). In half of the identified causes (n = 22) an association with hyperinsulinism was described, including maternal diabetes mellitus (n = 13), malformation syndromes with insulin resistance (n = 6) and congenital hyperinsulinism (n = 3). CH associated with hyperinsulinism was echocardiographically characterized by lower LVPW thickness, higher IVS:LVPW ratio and more frequent sole involvement of the IVS (all, p ≤ 0.02). CH associated with hyperinsulinism normalized more often (41 vs. 0%) with lower mortality rates (14 vs. 44%) compared to CH not associated with hyperinsulinism (all, p ≤ 0.03). Nowadays, an etiology of CH can be identified in the majority of infants. The development of CH is often associated with hyperinsulinism which is mainly characterized by focal hypertrophy of the IVS on echocardiography. Prognosis depends on the underlying cause and is more favorable in CH associated with hyperinsulinism.

Outcomes of Early-onset Preeclampsia With Severe Features at the University Hospital in Southern Thailand: a 15-year Experience

Purpose: To evaluate outcomes and factors associated with adverse outcomes among patients with early-onset preeclampsia with severe features at Songklanagarind Hospital. Methods: A retrospective study of 326 singleton women with early-onset preeclampsia with severe features treated at Songklanagarind Hospital between 2004-2019 was conducted. Baseline characteristics, management and outcomes were reviewed. Multivariate logistic regression was used to evaluate predictors of adverse outcomes. Statistical significance was set at p < 0.05.Results: There were no maternal mortalities, with 3.1% stillbirths and 6.7% neonatal deaths. High maternal serum creatinine (OR 3.26, 95% CI 1.27-8.36, p = 0.01) was significantly associated with adverse maternal outcomes. Early gestational age at delivery [< 28 weeks (OR 16.63, 95% CI 6.95-39.80, p <0.01), 28-32 weeks (OR 3.24, 95% CI 1.54-6.85, p <0.01)], maternal diabetes mellitus (OR 5.62, 95% CI 1.43-22.06, p = 0.01), high maternal serum creatinine (OR 2.66, 95%CI 1.20-5.93, p = 0.02) and elevated serum aminotransferases (OR 2.26, 95% CI 1.19-4.29, p = 0.01) were associated with serious adverse perinatal outcomes.Conclusions: Early-onset preeclampsia with severe features had favorable outcomes. Maternal diabetes mellitus, high serum creatinine, elevated serum aminotransferases and early gestational age at delivery were factors associated with poor outcomes.

N-3 polyunsaturated fatty acids effectively protect against neural tube defects in diabetic mice induced by streptozotocin

Folate cannot prevent all neural tube defects (NTD), indicating other pathogenesis still exists except for folate deficiency. Maternal diabetes mellitus during pregnancy can increase the risk of offspring NTD. Our...

Embryonic fatty acid metabolism in diabetic pregnancy: the difference between embryoblasts and trophoblasts

During the first days of development the preimplantation embryo is supplied with nutrients from the surrounding milieu. Maternal diabetes mellitus affects the uterine microenvironment, leading to a metabolic adaptation processes in the embryo. We analysed embryonic fatty acid (FA) profiles and expression of processing genes in rabbit blastocysts, separately in embryoblasts (EBs) and trophoblasts (TBs), to determine the potential consequences of maternal diabetes mellitus on intracellular FA metabolism. Insulin-dependent diabetes was induced by alloxan in female rabbits. On Day 6 post coitum, FA profiles in blastocysts (EB, TB and blastocoel fluid) and maternal blood were analysed by gas chromatography. The expression levels of molecules involved in FA elongation (fatty acid elongases, ELOVLs) and desaturation (fatty acid desaturases, FADSs) were measured in EB and TB. Maternal diabetes mellitus influenced the FA profile in maternal plasma and blastocysts. Independent from metabolic changes, rabbit blastocysts contained a higher level of saturated fatty acids (SFAs) and a lower level of polyunsaturated fatty acids (PUFAs) compared to the FA profile of the maternal plasma. Furthermore, the FA profile was altered in the EB and TB, differently. While SFAs (palmitic and stearic acid) were elevated in EB of diabetic rabbits, PUFAs, such as docosahexaenoic acid, were decreased. In contrast, in the TB, lower levels of SFAs and higher levels of oleic acid were observed. EB and TB specific alterations in gene expression were found for ELOVLs and FADSs, key enzymes for FA elongation and desaturation. In conclusion, maternal diabetes mellitus alters embryonic FA metabolism differently in EB and TB, indicating a lineage-specific metabolic adaptive response.