Caracterización de recién nacidos a término con deshidratación hipernatrémica / Characterization of full term newborns with hypernatremic dehydration

INTRODUCCIÓN: La deshidratación hipernatrémica neonatal es una condición grave y su incidencia se ha incre mentado en los últimos años, repercutiendo en complicaciones que llevan a la hospitalización del recién nacido. OBJETIVO: Describir las características clínicas y de laboratorio de recién nacidos a término con diagnóstico de deshidratación hipernatremica. PACIENTES Y MÉTODO: Estudio observacional descriptivo de recién nacidos a término que se hospitalizaron por deshidratación hiperna trémica entre los años 2014 y 2016. Se incluyeron recién nacidos a término mayores de 37 semanas con signos clínicos de deshidratación (mucosas secas, fontanela deprimida, llanto sin lágrimas, signos de pliegue cutáneo) y/o pérdida excesiva de peso mayor de 7% y sodio sérico mayor a 145 mEq/L. Se registraron variables sociodemográficas y bioquímicas para su análisis. RESULTADOS: Se incluyeron 43 neonatos. El 60,5% de sus madres fueron primigestantes, el 90% de los neonatos recibieron lactancia materna exclusiva, las madres reportaron problemas en la lactancia materna en el 76,7%. La pérdida de peso al ingreso con respecto al peso de nacimiento fue de 15,3% en promedio. El 83,3% contaba con seguro de salud público. 65,1% presentó signos clínicos de deshidra tación al ingreso y 83,5% signos neurológicos transitorios. El promedio de sodio fue de 155 mEq/L al ingreso. El descenso de sodio en las primeras 24 horas de manejo fue 7,74 mEq/L (0,32mEq/L por hora). La corrección de la hipernatremia fue en el 55,8% por vía oral y la estancia hospitalaria de 4 días en promedio. CONCLUSIONES: Los problemas de alimentación se presentaron en un (76%) madres primigestantes en un (88,4%). El 90,6% de esta población administraban lactancia materna exclusiva, resultados que pueden contribuir para alertar al profesional de la salud a identificar de forma oportuna, signos de alarma y un control precoz posterior al alta del puerperio y a la toma de medidas preventivas.

INTRODUCTION: The hypernatremic neonatal dehydration is a severe condition whose incidence has increased in recent years resulting in complications leading to the hospitalization of the newborn. OBJECTIVE: Describe the clinical and laboratory characteristics of term-newborns with Hypernatremic Dehy dration diagnosis. PATIENTS AND METHOD: Descriptive observational study of hospitalized term- newborns due to hypernatremic dehydration between a period from 2014 to 2016. Term newborns over 37 weeks with clinical signs of dehydration (dry mucous membranes, depressed fontanel, tear less crying, signs of the cutaneous pleat), and/or excessive weight loss greater than 7% and serum sodium greater than 145 mEq/L were included. Sociodemographic and biochemical variables were recorded for analysis. RESULTS: 43 neonates were included. 60.5 percent of their mothers were pri- miparous, 90 percent of neonates received exclusive breastfeeding, mothers reported breastfeeding problems in 76.7 percent. Incoming neonates reported weight loss compared to birth weight at 15.3% on average. 83.3% had public health insurance. 65.1% had dehydration clinical signs at entry and 83.5% transient neurological signs. The average sodium was 155 mEq/L at revenue. The sodium decrease in the first 24 hours of handling was 7.74 mEq/L (0.32mEq/L per hour). The correction of the hypernatremia was 55.8% by oral intake and 4 days hospital stay on average. CONCLUSIONS: The feeding's problems came up in a (76%), primiparous mothers in an (88.4%). 90.6 percent of this population administered exclusive breastfeeding, results that can help to alert the health professional to timely identification, warning signs, and early post-discharge control and preventive measures.

[Characterization of full term newborns with hypernatremic dehydration]. / Caracterización de recién nacidos a término con deshidratación hipernatrémica.

INTRODUCTION: The hypernatremic neonatal dehydration is a severe condition whose incidence has increased in recent years resulting in complications leading to the hospitalization of the newborn. OBJECTIVE: Describe the clinical and laboratory characteristics of term-newborns with Hypernatremic Dehy dration diagnosis. PATIENTS AND METHOD: Descriptive observational study of hospitalized term- newborns due to hypernatremic dehydration between a period from 2014 to 2016. Term newborns over 37 weeks with clinical signs of dehydration (dry mucous membranes, depressed fontanel, tear less crying, signs of the cutaneous pleat), and/or excessive weight loss greater than 7% and serum sodium greater than 145 mEq/L were included. Sociodemographic and biochemical variables were recorded for analysis. RESULTS: 43 neonates were included. 60.5 percent of their mothers were pri- miparous, 90 percent of neonates received exclusive breastfeeding, mothers reported breastfeeding problems in 76.7 percent. Incoming neonates reported weight loss compared to birth weight at 15.3% on average. 83.3% had public health insurance. 65.1% had dehydration clinical signs at entry and 83.5% transient neurological signs. The average sodium was 155 mEq/L at revenue. The sodium decrease in the first 24 hours of handling was 7.74 mEq/L (0.32mEq/L per hour). The correction of the hypernatremia was 55.8% by oral intake and 4 days hospital stay on average. CONCLUSIONS: The feeding's problems came up in a (76%), primiparous mothers in an (88.4%). 90.6 percent of this population administered exclusive breastfeeding, results that can help to alert the health professional to timely identification, warning signs, and early post-discharge control and preventive measures.

Antiproliferative effects of Bortezomib in endothelial cells transformed by viral G protein-coupled receptor associated to Kaposi's sarcoma.

The Kaposi's Sarcoma-associated Herpes virus G Protein-Coupled Receptor (vGPCR) is a key molecule in the pathogenesis of Kaposi Sarcoma. We have previously demonstrated that the proteasome inhibitor Bortezomib inhibits NF-κB pathway, which is required for tumor maintenance in endothelial cells that express vGPCR (vGPCR cells). In this work, we further investigated Bortezomib anti-proliferative mechanism of action. We demonstrated that Bortezomib decreases vGPCR cell number in a dose-dependent manner and induces cell morphology changes. Bortezomib decreases ERK1/2 phosphorylation whereas induces the accumulation of MKP-3 - a specific ERK1/2 MAP kinase phosphatase - in time and concentration dependent manner (1.5-32h; 0.25-1nM). The transcription factor FOXO1 is activated by dephosphorylation and regulates p21 expression. Here, we demonstrated that Bortezomib increases FOXO1 protein and decreases its phosphorylation in a concentration dependent manner (0.25-1nM). Bortezomib (0.5nM, 24h) also increase nuclear FOXO1 protein, in line with FOXO1 dephosphorylation induced by the drug. Consistent with FOXO1 dephosphorylation/activation, p21 mRNA expression is increased by Bortezomib in a MKP-3-dependent way. Bortezomib (0.5nM, 24h) also decreases VEGF, an ERK1/2 -dependent effect. It is concluded that in vGPCR cells, Bortezomib decreases ERK1/2 and FOXO1 phosphorylation through MKP-3 accumulation, leading ERK1/2 deactivation and FOXO1 activation respectively and, consequently, to cell proliferation inhibition, p21 induction and VEGF repression. Taken together, all these events contribute to the anti-tumoral effect of Bortezomib.