Perinatal outcome and later implications of intrauterine growth restriction.

This chapter reviews outcomes for children who have intrauterine growth retardation (IUGR) or small-for-gestation-age (SGA) status at birth. Such infants are at risk for increased perinatal mortality, birth adaptation complications, including perinatal acidosis, hypoglycemia, hypothermia, coagulation abnormalities, and selected immunologic deficiencies. IUGR infants also appear to be at great risk for complications of prematurity, including chronic lung disease and necrotizing enterocolitis. Childhood implications for IUGR include an increased risk for short stature, cognitive delays with decreased academic achievement, and a small but significant increased risk of neurologic disorders, including cerebral palsy. Low socioeconomic status is correlated with the occurrence of IUGR and is significantly related to long-term disabilities. Morbidities associated with preterm delivery appear to be additive to those associated with fetal growth restriction so IUGR, preterm infants may be at great risk for poor neurodevelopmental outcome.

Changes in amelogenesis in the rat incisor following short-term hypocalcaemia.

There is a relationship between hypocalcaemia and the enamel hypoplasia. Earlier studies in rats have reported a severe hypocalcaemia and enamel hypoplasia a month after thyro-parathyroidectomy (TPTX). The aims of this study were to look at earlier stages and to attempt to correlate morphological changes with alterations in the distribution of amelogenin. Twenty-five Wistar rats were, under anaesthesia, thyro-parathyroidectomized. Sham operated rats were included as controls. After 14, 30 or 57 days, the animals were reanesthatized and the tissues fixed by intracardiac perfusion of fixative. The lower incisors were processed for light microscopy and immunogold electron microscopy. After 14 days the thyro-parathyroidectomised rats were severely hypocalcaemic but amelogenesis was morphologically similar to controls. After 30 and 57 days, enamel defects were observed in the late secretory and early maturation stages in the thyro-parathyroidectomised rats. The immunocytochemical study revealed a concentration of stippled material immunolabelled for amelogenin at the secretory pole of the ameloblasts in the hypocalcaemic rats. The absence of enamel defects after 14 days suggests that this was an insufficient hypocalcaemic period to induce morphological alterations. The concentration of stippled material containing amelogenin suggests that alterations in matrix formation may be the basis of the morphological changes.

Perinatal calcium metabolism: physiology and pathophysiology.

Disturbances in mineral homeostasis are common in the neonatal period, especially in premature infants and infants who are hospitalised in an intensive care unit. In many cases these disturbances are thought to be exaggerated responses to the normal physiological transition from the intrauterine environment to neonatal independence. By contrast, some disturbances in calcium homeostasis are the result of genetic defects, which in many instances can now be identified at the molecular level. In other cases hypocalcaemia or hypercalcaemia may result from pathological intrauterine conditions, birth trauma or stress, or fetal immaturity. Diagnosis and management of hypocalcaemia and hypercalcaemia in the neonate and infant requires specific knowledge of perinatal mineral physiology and the unique clinical and biochemical features of newborn mineral metabolism. In this chapter we will provide a brief overview of calcium metabolism with an emphasis on the neonatal transition, followed by discussion of the common causes of hypercalcaemia and hypocalcaemia.

El hijo de madre diabética / Diabetic mother offspring

Dado que la diabetes mellitus puede estar presente a lo largo de todo el embarazo, la exposición prenatal a la misma puede resultar en diferentes patologías (transtornos del crecimiento, prematuridad, abortos, mortinatos, malformaciones y alteraciones de la homeostasis) que perduran en el periodo neonatal. El principal mecanismo patogenico de estas alteraciones es la hiperinsulinemia, producida por el incremento de glucosa y aminoácidos en la circulación fetal. Las manifestaciones clínicas más frecuentes son: macrosomía, hipoglucemia, hipocalcemia e hipomagnesemia e hipertrofia septal cardíaca. En nuestro país, la diabetes es la segunda causa de embriopatía con una tasa de 0,204 por cada 10000 recién nacidos, parece existir paralelismo entre el número de defectos congénitos y el grado de control metabólico. La relación entre la diabetes gestacional y las malformaciones congénitas no esta claramente establecida, incluso para algunos autores es incierta, en esta situación el mejor parámetro de predicción es la glucemia basal elevada.Las mejoras en el cuidado anteparto, la monitorización fetal, el control riguroso del metabolismo materno y la educación materna, disminuyen la morbi-mortalidad perinatal. Además un buen control del metabolismo materno durante el periodo periconcepcional resulta en un descenso de la incidencia de malformaciones congénitas.El mayor riesgo de diabetes mellitus en los hijos de madre diabética es independiente de los factores de riesgo para la morbilidad perinatal, sin embargo, presentan índice de masa corporal, tensión arterial y niveles de glucosa tras la curva de tolerancia a la glucosa elevados, cuando se evalúa a los 18 y 26 años. El índice de desarrollo mental no es significativamente diferente entre los hijos de madre diabética y los hijos de madres normales (AU)