Human chorionic gonadotropin (hCG) is produced primarily by differentiated syncytiotrophoblasts, and represents a key embryonic signal that is essential for the maintenance of pregnancy. hCG can activate various signaling cascades including mothers against decapentaplegic homolog 2 (Smad2), protein kinase C (PKC), and/or protein kinase A (PKA) in several cells types by binding to luteinizing hormone/chorionic gonadotropin receptor (LHCGR) or potentially by direct/indirect interaction with transforming growth factor beta receptor (TGFβR). The molecule displays specialized roles in promoting angiogenesis in the uterine endothelium, maintaining myometrial quiescence, as well as fostering immunomodulation at the maternal-fetal interface. It is a member of the glycoprotein hormone family that includes luteinizing hormone (LH), thyroid-stimulating hormone (TSH), and follicle-stimulating hormone (FSH). The α-subunit of hCG displays homologies with TSH, LH, and FSH, whereas the β subunit is 80–85% homologous to LH. The hCG molecule is produced by a variety of organs, exists in various forms, exerts vital biological functions, and has various clinical roles ranging from diagnosis and monitoring of pregnancy and pregnancy-related disorders to cancer surveillance. This review presents a detailed examination of hCG and its various clinical applications.

Objective: To compare the INTERGROWTH-21st Century growth standard to the Hadlock standard in predicting small for gestational age (SGA) and adverse neonatal outcomes. Method: This is a prospective cohort study on women with singleton gestations referred for fetal growth ultrasound between 26.0 and 36.6 weeks gestational age (GA). The primary outcome is prediction of neonatal SGA. Neonatal SGA was defined as birthweight <10th percentile for GA by Alexander chart. The discriminatory ability of the growth standards was compared using area under receiver operating characteristic curves (AUC). Results: Among 1054 patients who met inclusion criteria, 139 (13.2%) had neonatal SGA. The mean interval between estimated fetal weight and birthweight was 6.7 ± 3.1 weeks. Composite adverse neonatal outcome was seen in 300 (28.4%) patients. The sensitivity for identifying SGA neonates was higher for Hadlock compared with INTERGROWTH-21st standard (41.7 vs. 24.5%); AUC (95% CI) were 0.69 (0.65–0.73) and 0.62 (0.58–0.65), respectively. Both standards were comparable in predicting the composite adverse neonatal outcomes; AUC (95% CI) were 0.52 (0.50–0.53) and 0.52 (0.50–0.54), respectively; p = .28. Conclusions: The Hadlock standard had a moderate but higher discriminatory ability for predicting neonatal SGA compared to the INTERGROWTH-21st project standard. However, the two standards were poor predictors of early adverse neonatal outcomes. Rationale: The Intergrowth-21st project was recently introduced with the goal of providing a universal benchmark for comparing growth across different ethnicity. We performed a prospective cohort study to compare the Intergrowth-21st standard with the commonly used Hadlock standard for predicting pregnancies at risk for neonatal SGA and adverse outcomes. Hadlock fetal growth standard is moderately superior at predicting neonatal SGA compared to the Intergrowth-21st standard. Both standards are poor at predicting adverse neonatal outcomes. These findings, however, need further validation.

Sickle cell disease has been shown to demonstrate extensive variability in disease severity among and between individuals, the variability highlighted by differing genetic haplotypes. Despite the abundance of reports of functional significance due to polymorphisms of endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1) genes, the role of these polymorphisms in mediating sickle cell disease pathophysiology among African Americans is presently unclear. To deconvolute their potential significance among African Americans with sickle cell disease, we examined the genetic diversity and haplotype frequency of eNOS and ET-1 polymorphisms in disease (n = 331) and control (n = 379) groups, with a polymerase-chain reaction restriction fragment length polymorphism assay. We report that genotypic and allelic frequencies of eNOS variants are not significantly different between groups. eNOS homozygote mutants, which had been shown to have clinical significance elsewhere, showed no statistical significance in our study. On the other hand, and contrary to previous report among Africans with sickle cell disease, the endothelin-1 homozygous mutant variant showed significant difference in genotypic (p = 2.84E-12) and allelic frequencies (p = 2.20E-16) between groups. The most common haplotype is the combination of T786C homozygote wild-type variant with homozygote mutant variants of G5665T (ET-1) and Glu298Asp (eNOS). These results show that endothelin-1 (rs5370) polymorphism, rather than endothelial nitric oxide synthase polymorphism might play a significant role in disease severity or individual clinical outcomes among African Americans with sickle cell disease. This would have profound implications for designing and/or advancing personalized care for sickle cell patients and relieving disease complications.

We report a case of combined severe aortic stenosis and regurgitation in a pregnant patient with a history of congenital bicuspid aortic valve. The patient presented at 22 weeks of gestation with angina and pre-syncopal symptoms. During her admission, she experienced intermittent episodes of non-sustained ventricular tachycardia and hypotension. A multi-disciplinary healthcare team was assembled to decide on the appropriate medical and surgical treatment options. At 28 weeks of gestation, the patient underwent a caesarean delivery immediately followed by a mechanical aortic valve replacement.