Association of leptin receptor expression in placenta and peripheral blood mononuclear cell with maternal weight in birth outcomes.

INTRODUCTION: The pregnancy period represents the most intense period of growth and development. Pre-pregnancy weight influences weight gain during pregnancy. Leptin is a hormone mainly derived from white adipose tissue, during pregnancy leptin is also produced by the placenta. It has been suggested that the effects of placental leptin on the mother may contribute to endocrine-mediated alterations in energy balance; a dysregulation in leptin levels or its receptors may lead to poor birth outcomes. Therefore, the main goal of the present study was to analyze the differences in birth outcomes by maternal weight with the expression level of leptin receptor in maternal peripheral blood mononuclear cell (PBMC) and placental tissue. METHODS: Women with full-term gestation and its offspring were enrolled. Total RNA from maternal PBMC and placenta was obtained to perform the analysis of expression of the leptin receptor (LEPR) gene trough real-time PCR technique. Data were analyzed using one-way ANOVA or Mann-Whitney u test when applicable. Pearson correlation coefficient was used to determine the relationship between continuous variables (Stata v.13); p ≤ 0.05 was considered statistically significant. RESULTS: No statistically significant differences were found between LEPR expression level and the BMI studied groups in maternal PBMC and placental tissue. Interaction between gestational weight gain (GWG) and LEPR in maternal PBMC explain in a 32% the variability of the newborn weight. CONCLUSIONS: LEPR expression level in maternal PBMC correlates with newborn measurements independent from sex. GWG can affect fetal development by increasing fetal birth weight.

Hipomagnesemia en el embarazo: ¿factor de riesgo de preeclampsia severa? / Hypomagnesemia during pregnancy: Risk factor for severe preeclampsia?

Resumen Objetivo: Demostrar que la hipomagnesemia es un factor de riesgo de preeclampsia severa. Materiales y métodos: Estudio de casos y controles efectuado en pacientes atendidas en el Hospital de la Mujer entre los meses de enero de 2015 a enero de 2016. Grupo de estudio: pacientes con preeclampsia severa y controles embarazadas sanas, con determinación de las concentraciones de magnesio sérico. Resultados: Se estudiaron 200 pacientes; la edad media de las embarazadas hipertensas fue de 24.6 años, y 23.5 años de las normotensas. La diferencia entre ambas fue de 1.1 años (p > 0.05). La mediana en semanas de gestación de las mujeres hipertensas fue de 37 y de 39 para las sanas, respectivamente; la diferencia fue de 2 (p = 0.0001). La mediana del magnesio de las mujeres hipertensas fue de 1.7 mg/dL, y en las no hipertensas 1.8 mg/dL, (p = 0.0053); RM: 1.72 IC95%: 1.0- 3.13; p = 0.005. Conclusiones: Se demuestra que la hipomagnesemia es un factor de riesgo de preeclampsia severa.

Abstract Objective: To demonstrate that hypomagnesemia is a risk factor for severe preeclampsia. Materials and methods: A case-control study conducted in patients treated at the Hospital de la Mujer between the months of January 2015 and January 2016. The study group included patients with severe preeclampsia and healthy pregnant controls with determination of concentrations of magnesium serum. Results: 200 patients were studied; the average age of the hypertensive pregnant women was 24.6 years, and 23.5 years of the normotensive women. The difference between the two was 1.1 years (p > 0.05). The median in weeks of gestation of hypertensive women was 37 and 39 for healthy women, respectively; the difference was 2 (p = 0.0001). The median magnesium of the hypertensive women was 1.7 mg/dL, and in the non-hypertensive 1.8 mg/dL, (p = 0.0053); RM: 1.72 IC95%: 1.0- 3.13; p = 0.005. Conclusions: in this study group, it was shown that hypomagnesemia is a risk factor for severe preeclampsia.

Budd-Chiari Syndrome in a Patient with JAK-2 V617F and Factor V G1691A Mutations.

Myeloproliferative neoplasms (MPN) are considered a risk factor for Budd-Chiari syndrome (BCS). The current classification of MPN by the World Health Organization is based on the presence of JAK-2 V617F somatic mutation, which is present in 40 to 60% of patients with BCS. Factor V Leiden mutation is found in around 53% of patients with BCS, representing the most common prothrombotic disease associated with the disorder. We describe a 48-year old woman with a past medical history of deep venous thrombosis in the left upper extremity and one episode in both lower extremities, one episode of transient ischaemic attack and essential thrombocythemia, who presented with jaundice, ascites and hepatomegaly. Budd-Chiari syndrome was diagnosed based on findings on Doppler ultrasound and liver biopsy. Doppler ultrasound showed narrowness of hepatic veins and inferior vena cava in its hepatic portion, diffuse echotexture and portal hypertension. Liver biopsy showed congestion of sinusoids and portal fibrosis. The patient was found to be a heterozygous carrier of Factor V and homozygous wild type G20210A prothrombin mutations. The JAK-2 V617F mutation was detected by allele-specific polymerase chain reaction (AS-PCR). The association of these mutations is rare, with only a few cases reported in the literature. The patient was treated with oral anticoagulation and antiplatelets with good results and proper follow-up. In conclusion, due to the possible coexistence of multiple prothrombotic factors in patients with Budd-Chiari syndrome, the approach to these patients must be focussed on searching for multiple factors and should include the JAK-2 V617F mutation.