Maternal serum cortisol levels during pregnancy differ by fetal sex.

BACKGROUND: Males and females have different patterns of fetal growth, resulting in different sizes at birth. Increased maternal cortisol levels in pregnancy negatively impact fetal growth. However, it is unknown whether sexual dimorphism displays differences in maternal cortisol levels already during early pregnancy and to what extent it explains sex differences in intra-uterine growth. The present cross-sectional study investigated whether fetal sex was associated with the level of maternal serum total cortisol in first half of pregnancy and its contribution to sex differences in fetal growth. METHOD: The study population comprised 3049 pregnant women from the Amsterdam Born Children and their Development (ABCD)-cohort). Total serum cortisol levels were determined during pregnancy. Multivariable linear regression was used to determine fetal sex differences in maternal cortisol levels and its association with sex differences in fetal growth measured as birth weight standardized for gestational age, parity and sex. RESULTS: Maternal serum total cortisol increased during pregnancy from on average 390 ± 22 nmol/L (at 5th week) to 589 ± 15 nmol/L (at 20th week). Women carrying a female fetus had higher maternal total cortisol levels. This sex difference was not significant before the 11th week; at the 12th week the difference was 15 ± 7 nmol/L which increased to 45 ± 22 nmol/L at the 20th week (p-for-interaction=0.05). Maternal total cortisol levels were associated with birth weight (ß:-0.22;P < 0.001). However, sex differences in birth weight were not explained by related maternal total cortisol levels. CONCLUSION: The sexual dimorphic maternal serum total cortisol levels are apparent after the first trimester but do not explain the different patterns of fetal growth.

Pancreatitis, pregestational diabetes and hyperchylomicronia in a pregnant woman with COVID-19.

A 37-year-old pregnant woman, was diagnosed with acute pancreatitis whilst being infected with COVID-19. Additionally, she had a hyperchylomicronemia and an uncontrolled (most probably, pre-gestational) type 2 diabetes. The coronavirus is able to enter the pancreatic cells through ACE-2 receptors. On the pancreatic level, ACE- 2 receptor expression is present but not as abundant as on pulmonary level. However, with inflammation (due to hyperchylomicronemia), the ACE-2 receptor expression may change and hypothetically make the pancreas more susceptible for a Covid-19 surinfection. Here it is difficult to conclude whether the COVID-19 infection contributed substantially to the development of pancreatitis. Late term pregnancy, uncontrolled glycaemia and the heterozygote mutation in the GPIHBP1 gene (c.523G>C p; Gly175Arg), all contribute to increased TG levels, a principal factor in the development of pancreatitis. This case shows a rare but serious clinical presentation late in pregnancy that could have interesting consequences postpartum.

Remnant lipoproteins and atherosclerosis.

A recently developed assay for quantification of remnant-like particle cholesterol has provided considerable evidence that reinforces the concept that elevated levels of plasma remnants are associated with increased cardiovascular disease in different populations and distinct patient groups. In this review, we provide a brief summary of the most recently published studies, emphasizing the clinical relevance of remnant analysis. We discuss recent evidence that sheds light on the mechanisms that may underlie the atherogenicity of remnant lipoproteins. Taken together, these data provide new insight into the significance of remnant lipoproteins in the onset and development of premature atherosclerosis.