RESUMEN
OBJECTIVE: To assess hematologic and biochemical blood variables in growth-restricted fetuses and relate them to biophysical measurements. METHODS: Blood was sampled from 22 growth-restricted fetuses. All had normal karyotypes and no congenital infections. Venous pH, partial pressure of oxygen, hematocrit, glucose, uric acid, urea, creatinine, total protein, total and direct bilirubin, aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltransferase, alkaline phosphatase, lactic dehydrogenase, amylase, pseudocholinesterase, creatinine kinase, triglycerides, and cholesterol were measured and compared with our reference range. RESULTS: Ultrasound measurements of abdominal circumference correlated with fetal pH (r = 0.64), partial pressure of oxygen (r = 0.52), glucose (r = 0.67), total bilirubin (r = -0.54), lactic dehydrogenase (r = -0.48), and triglyceride levels (r = -0.65). Compared with fetuses with present end-diastolic velocities in the umbilical artery, the eight with absent end-diastolic velocities had lower pH (median z score -4.31), partial pressure of oxygen (median z score = -2.39), glucose (median z score = -2.01), and cholesterol (median z score = -2.34), and higher gamma-glutamyltransferase (median z score = 2.43), lactic dehydrogenase (median z score = 3.75), urea (median z score = 1.33), creatinine (median z score = 1.23), and triglyceride levels (median z score = 1.71). Only triglycerides correlated with abdominal circumference, independent of Doppler results. CONCLUSION: Growth-restricted fetuses with absent end-diastolic velocities in the umbilical artery had more marked acidemia, hypoxemia, hypoglycemia, and abnormal liver function than those with end-diastolic velocities. Triglyceride levels were inversely related to fetal size independent of Doppler results. High triglyceride levels might reset fetal homeostatic mechanisms, leading to disturbances of lipid metabolism in later life.
Asunto(s)
Retardo del Crecimiento Fetal/metabolismo , Glucosa/metabolismo , Metabolismo de los Lípidos , Hígado/metabolismo , Equilibrio Ácido-Base , Sangre Fetal/química , HumanosRESUMEN
We previously reported that trisomy 21 (T21) fetuses have an intrinsic lipid metabolism abnormality resulting in higher serum cholesterol levels than their matched controls. In an attempt to clarify the biochemical basis of this derangement we analyzed the liver cholesterol levels and activation of the sterol regulatory element binding proteins SREBP-1 and SREBP-2. We report here for the first time that SREBP-1 and SREBP-2 are present in human fetal liver and their activation follows a different regulatory pattern. Moreover T21 fetuses show a peculiar pattern of SREBP activation which, at variance from control fetuses, involves sterol-independent maturation of SREBP-1. Multiple defects accompanied the lipid derangement in T21, resulting in high circulating and tissue cholesterol. This may serve as an early biochemical marker of an unknown, possibly genetically determined mechanism, whose consequence on lipid homeostasis during postnatal and adult life is still not understood.
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Proteínas Potenciadoras de Unión a CCAAT , Proteínas de Unión al ADN/metabolismo , Síndrome de Down , Hígado/metabolismo , Proteínas Nucleares/metabolismo , Factores de Transcripción/metabolismo , Western Blotting , Colesterol/sangre , Colesterol/metabolismo , Homeostasis , Humanos , Hígado/embriología , Proteína 1 de Unión a los Elementos Reguladores de Esteroles , Proteína 2 de Unión a Elementos Reguladores de EsterolesRESUMEN
Two women without a specific risk had fetuses with multiple malformations diagnosed by ultrasound; extensive biochemical investigations on fetal blood revealed clues which would have allowed the correct diagnosis of a genetic condition: Pallister-Killian syndrome in one with increased fetal LDH, and Smith-Lemli-Opitz type II syndrome in the other with low fetal cholesterolaemia. When compared with chorionic villus sampling and amniocentesis, rapid karyotyping in women with multiple fetal malformations by fetal blood sampling allows the collection of additional data which may lead to the diagnosis of specific genetic syndromes.
Asunto(s)
Sangre Fetal/química , Enfermedades Genéticas Congénitas/diagnóstico , Diagnóstico Prenatal , Anomalías Múltiples/sangre , Anomalías Múltiples/diagnóstico por imagen , Adulto , Amniocentesis , Colesterol/sangre , Muestra de la Vellosidad Coriónica , Aberraciones Cromosómicas , Cromosomas Humanos Par 12 , Femenino , Humanos , Cariotipificación , L-Lactato Deshidrogenasa/sangre , Masculino , Embarazo , Síndrome de Smith-Lemli-Opitz/diagnóstico , Síndrome , Ultrasonografía PrenatalRESUMEN
Nitric oxide (NO) plays a key role in the pathophysiology of inflammation and sepsis. The regulation of the peripheral inducible NO synthase (iNOS-responsible for the massive NO synthesis in inflammation) has been extensively studied in sepsis, but little is known about the actual NO production and its dependence on the location of the primary stimulus (endotoxin, LPS). We measured the activation of the NO pathway after a central (intracerebroventricular) or systemic (intravenous) low dose of LPS (2.5 micrograms/mouse) in three ways: the accumulation of its stable end products (nitrites/nitrates) in the circulation, the induction of iNOS mRNA and the decrease in sodium nitroprusside-dependent ADP ribosylation of proteins in the liver and brain. Plasma nitrites/nitrates increased after LPS by either route. iNOS mRNA was induced in the liver after intravenous and, to a lower extent, in the brain after intracerebroventricular LPS. Ex vivo ADP ribosylation was decreased in both organs after both administration routes, although to different degrees (higher in the liver after intravenous and in the brain after intracerebroventricular administration), suggesting that NO had been produced in the periphery and in the brain after both routes of LPS administration, despite the fact that no LPS is expected to reach the brain after peripheral low-dose injection. Our data thus demonstrate a cross-talk between periphery and brain in the regulation of NO by LPS. Additionally, the possibility of iNOS-independent NO synthesis stimulated by LPS is implied by the discrepancy between the amount of local NO production suggested by ADP ribosylation and the iNOS mRNA levels.