Longitudinal study of the newborn small for gestational age. Growth recovery and conditioning factors / Estudio longitudinal del recién nacido pequeño para la edad gestacional. Crecimiento recuperador y factores condicionantes

Background: small-for-gestational-age (SGA) newborns present a higher morbidity and mortality rate when compared to infants born appropriate for gestational age (AGA), as well as insufficient growth, with height far from their target and in some cases a low final height (< -2 SDs). Objective: the aim of this study was to determine when catch-up growth (CUG) in height occurs in these children, and which factors are associated with lack of CUG. Material and methods: this is a retrospective study of SGAs born between 2011 and 2015 in a secondary hospital. Anthropometric measurements were taken consecutively until CUG was reached, and fetal, placental, parental, newborn, and postnatal variables were studied. Results: a total of 358 SGAs were included from a total of 5,585 live newborns. At 6 and 48 months of life, 93.6 % and 96.4 % of SGAs achieved CUG, respectively. By subgroups, symmetric SGAs performed worse than asymmetric SGAs with CUG in 84 % and 92 % at 6 and 48 months of life, respectively. The same occurred in the subgroup of preterm SGAs with respect to term SGAs, with worse CUGs of 88.2 % and 91.2 % at 6 and 48 months of life, respectively. Prematurity, symmetrical SGA, intrauterine growth retardation (IUGR), preeclampsia, previous child SGA, perinatal morbidity, and comorbidity during follow-up were associated with absence of CUG. Conclusions: the majority of SGAs had CUG in the first months of life. The worst outcomes were for preterm and symmetric SGAs (AU)

Antecedentes: el recién nacido pequeño para la edad gestacional (PEG) presenta mayor morbimortalidad que el recién nacido con peso adecuado (PAEG), así como un crecimiento insuficiente con talla alejada de la talla diana y, en algunos casos, talla final baja (< -2 DE). Objetivo: el objetivo de este estudio fue determinar en qué momento se produce el crecimiento compensador (CUG) de la talla en estos niños y conocer qué factores se asocian a la falta de dicho crecimiento compensador. Material y métodos: estudio retrospectivo de los recién nacidos PEG entre los años 2011 y 2015 en un hospital secundario. Se tomaron medidas antropométricas de forma consecutiva hasta alcanzar el CUG y se estudiaron las variables fetales, placentarias, parentales, neonatales y posnatales. Resultados: se incluyeron 358 PEG de un total de 5585 recién nacidos vivos. A los 6 y 48 meses de vida alcanzaron el CUG el 93,6 % y 96,4 % de los PEG, respectivamente. Por subgrupos, los PEG simétricos obtuvieron peores resultados que los PEG asimétricos, con CUG del 84 % y 92 % a los 6 y 48 meses de vida, respectivamente. Lo mismo ocurrió en el subgrupo de PEG prematuros respecto de los PEG a término, con CUG peores del 88,2 % y 91,2 % a los 6 y 48 meses de vida, respectivamente. La prematuridad, el PEG simétrico, la restricción del crecimiento intrauterino, la preeclampsia, tener un hijo previo PEG, la morbilidad perinatal y la comorbilidad durante el seguimiento se asociaron a la ausencia de CUG. Conclusiones: la mayoría de los PEG alcanzaron el CUG en los primeros meses de vida. Los peores resultados fueron para los PEG prematuros y simétricos (AU)

Déficit de GH tipo II: de la clínica al diagnóstico genético / GH deficiency type II: From the clinical to the genetic diagnosis

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Parada cardíaca: presentación mortal de una miocarditis viral / Cardiac arrest: Fatal presentation of viral myocarditis

La miocarditis es un trastorno inflamatorio del miocardio que cursa con la necrosis de los miocitos. La principal causa son las infecciones virales. La presentación clínica es muy variada: desde formas leves hasta formas fulminantes que cursan con la muerte y que se inician frecuentemente con síntomas banales. Presentamos el caso de un niño de 18 meses que acude a urgencias por astenia y anorexia de 24h de evolución, con antecedente de fiebre en el contexto de infección respiratoria de vías altas la semana anterior. A su llegada a urgencias y durante las primeras horas de observación la exploración física fue rigurosamente normal. Posteriormente presentó empeoramiento progresivo del estado general (palidez y mala perfusión periférica) con alteraciones analíticas (acidosis metabólica, insuficiencia renal e hiperglucemia) y de forma brusca parada cardiorrespiratoria sin respuesta a maniobras de reanimación cardiopulmonar (AU)

Myocarditis is an inflammatory disease of the myocardium accompanied by necrosis of myocytes. The main causes are viral infections. The clinical presentation varies from mild forms to devastating ones which usually begin with trivial symptoms with progression, in some cases, to death. We report the case of an 18 month-old male toddler consulting for asthenia and anorexia for the last 24h and a previous history of respiratory tract infection with high fever in the last week. Upon arrival at the emergency room and during the first hours of admission, physical examination was perfectly normal. Later, his general state gradually deteriorated, with biochemical disturbances (metabolic acidosis, renal failure and hyperglycaemia) and, eventually, a sudden cardiac arrest, with no response to cardiopulmonary resuscitation manoeuvres (AU)

[Cardiac arrest: fatal presentation of viral myocarditis]. / Parada cardíaca: presentación mortal de una miocarditis viral.

Myocarditis is an inflammatory disease of the myocardium accompanied by necrosis of myocytes. The main causes are viral infections. The clinical presentation varies from mild forms to devastating ones which usually begin with trivial symptoms with progression, in some cases, to death. We report the case of an 18 month-old male toddler consulting for asthenia and anorexia for the last 24h and a previous history of respiratory tract infection with high fever in the last week. Upon arrival at the emergency room and during the first hours of admission, physical examination was perfectly normal. Later, his general state gradually deteriorated,with biochemical disturbances (metabolic acidosis, renal failure and hyperglycaemia) and, eventually, a sudden cardiac arrest, with no response to cardiopulmonary resuscitation manoeuvres.

Tumoración hipofisaria secundaria a hipotiroidismo primario: un caso de hiperplasia tirotropa que simula un adenoma hipofisario / Hypophyseal tumour growth secondary to primary hypothyroidism: a case of a hypophyseal adenoma induced by thyrotropic hyperplasia

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[11beta-hydroxylase deficiency: improvement of final height with growth hormone and gonadotropin-releasing hormone analog]. / Déficit de 11beta-hidroxilasa: mejoría de talla final con hormona de crecimiento y análogos de LHRH Déficit de 11beta-hidroxilasa: mejoría de talla final con hormona de crecimiento y análogos de LHRH.

Steroid 11beta-hydroxylase deficiency is the second most common cause of congenital adrenal hyperplasia. 11beta-hydroxylase intervenes in cortisol synthesis and its deficiency leads to accumulation of adrenal androgens--producing prenatal virilization and, subsequently, hyperandrogenism--as well as 11-deoxycorticosterone, leading to the development of hypertension. We describe a 7-year-old girl who was referred for pubarche and accelerated skeletal maturation due to 11beta-hydroxylase deficiency. Because the patient's predicted height was below her target height, the combination of gonadotropin-releasing hormone analog and growth hormone was added to oral glucocorticoid therapy. With this therapeutic strategy, the patient's predicted height improved significantly and the girl reached a final height in agreement with her target height at the age of 13 years and 6 months.

Déficit de 11Beta -hidroxilasa: mejoría de talla final con hormona de crecimiento y análogos de LHRH Déficit de 11Beta -hidroxilasa: mejoría de talla final con hormona de crecimiento y análogos de LHRH / 11Beta-hydroxylase deficiency: improvement of final height with growthhormone and gonadotropin-releasing hormone analog

El déficit de 11Beta-hidroxilasa es la segunda causa más frecuente de hiperplasia suprarrenal congénita. La 11Beta-hidroxilasa interviene en la síntesis de cortisol y su déficit conlleva acumulación de andrógenos, produciendo virilización prenatal e hiperandrogenismo posterior, y 11-desoxicorticosterona, causante de hipertensión arterial. Se presenta una paciente de 7 años remitida por pubarquia y maduración ósea acelerada, debidas a déficit de 11Beta-hidroxilasa. Debido a que su pronóstico de talla final era muy inferior a su talla genética, se asoció la combinación de análogos de la hormona liberadora de hormona luteinizante (LHRH) y hormona de crecimiento al tratamiento con corticoides orales. Con dicha combinación terapéutica, su pronóstico de talla final mejoró significativamente, alcanzando a los 13 años y 6 meses una talla acorde a su talla

Steroid 11Beta-hydroxylase deficiency is the second most common cause of congenital adrenal hyperplasia. 11Beta-hydroxylase intervenes in cortisol synthesis and its deficiency leads to accumulation of adrenal androgens producing prenatal virilization and, subsequently, hyperandrogenism as well as 11-deoxycorticosterone, leading to the development of hypertension. We describe a 7-year-old girl who was referred for pubarche and accelerated skeletal maturation due to 11Beta-hydroxylase deficiency. Because the patient's predicted height was below her target height, the combination of gonadotropin-releasing hormone analog and growth hormone was added to oral glucocorticoid therapy. With this therapeutic strategy, the patient's predicted height improved significantly and the girl reached a final height in agreement with her target height at the age of 13 years and 6 months