Energy Dense Salty Food Consumption Frequency Is Associated with Diastolic Hypertension in Spanish Children.

High blood pressure (BP) is a risk factor for cardiovascular disease and sodium consumption is related to high BP. Moreover, sugar-sweetened beverages (SSB) and the Dietary Approach to Stop Hypertension (DASH) influence BP. For this reason, we investigated whether: 1) children with risk of elevated BP had a higher consumption frequency (CF) of energy-dense salty foods (EDSF), high-sugary foods (HSF) and SSB or a low DASH score; and 2) children with a higher CF of EDSF showed a worse anthropometric and metabolic profile. Anthropometry, BP and general biochemical parameters were measured in 687 Spanish children (5-16 years) with normal or excess weight. A food frequency questionnaire was used to calculate EDSF, HSF and SSB consumption, and modified DASH score. Results showed that sex and pubertal stage influenced modified DASH score. Diastolic hypertension was associated to higher CF of EDSF in the whole sample and to higher CF of SSB in pubertal children, both independently of nutritional status. In addition, CF of EDSF was positively associated with CF of HSF and SSB and inversely associated with modified DASH score. Targeted policies and intervention programs, specific for different age ranges, should be established that aim to reduce salt consumption from snacks and processed foods, which could reduce HSF and SSB consumption as well.

Un caso inusual de síndrome de enterocolitis inducida por proteínas alimentarias / Unusual case of food protein-induced enterocolitis syndrome

El síndrome de enterocolitis inducido por proteínas alimentarias es un síndrome de hipersensibilidad gastrointestinal a alimentos no mediado por inmunoglobulina E, que, en su forma aguda, se manifiesta con vómitos repetitivos, palidez e hipotonía, que puede acompañarse o no de diarrea y producir un cuadro grave de deshidratación y letargia. Una prueba de provocación oral controlada es, en ocasiones, realizada para confirmar el diagnóstico y el tratamiento consiste en la eliminación del alimento causante. Se presenta el caso de un lactante de 3 meses con varios episodios de síndrome de enterocolitis tras la toma de biberón de leche de fórmula de inicio con tolerancia de otra marca comercial. Se encontraron diferencias en los ingredientes de su composición que podrían ser el origen de la sensibilización.

Food protein-induced enterocolitis syndrome is a nonimmunoglobulin E mediated gastrointestinal food hypersensitivity that manifests as profuse, repetitive vomiting, pallor and hypotonia, often with diarrhea leading to severe dehydration and lethargy (sepsis-like symptoms) in the acute setting. An oral food challenge is sometimes performed to confirm the diagnosis and treatment consists of elimination of the food trigger(s) from the diet. We report a case of a 3-months-old infant with several episodes of food protein-induced enterocolitis syndrome after taking infant formula milk with tolerance of another trademark. Differences in the composition of its ingredients could be the cause of the sensitization.

[Unusual case of food protein-induced enterocolitis syndrome]. / Un caso inusual de síndrome de enterocolitis inducida por proteínas alimentarias.

Food protein-induced enterocolitis syndrome is a nonimmunoglobulin E mediated gastrointestinal food hypersensitivity that manifests as profuse, repetitive vomiting, pallor and hypotonia, often with diarrhea leading to severe dehydration and lethargy (sepsis-like symptoms) in the acute setting. An oral food challenge is sometimes performed to confirm the diagnosis and treatment consists of elimination of the food trigger(s) from the diet. We report a case of a 3-monthsold infant with several episodes of food protein-induced enterocolitis syndrome after taking infant formula milk with tolerance of another trademark. Differences in the composition of its ingredients could be the cause of the sensitization.

El síndrome de enterocolitis inducido por proteínas alimentarias es un síndrome de hipersensibilidad gastrointestinal a alimentos no mediado por inmunoglobulina E, que, en su forma aguda, se manifiesta con vómitos repetitivos, palidez e hipotonía, que puede acompañarse o no de diarrea y producir un cuadro grave de deshidratación y letargia. Una prueba de provocación oral controlada es, en ocasiones, realizada para confirmar el diagnóstico y el tratamiento consiste en la eliminación del alimento causante. Se presenta el caso de un lactante de 3 meses con varios episodios de síndrome de enterocolitis tras la toma de biberón de leche de fórmula de inicio con tolerancia de otra marca comercial. Se encontraron diferencias en los ingredientes de su composición que podrían ser el origen de la sensibilización.

Abordaje del tabaquismo activo y pasivo desde la consulta de Pediatría / The approach to active and passive smoking in the Paediatric Clinic

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Déficit de ornitina transcarbamilasa: Caso clínico / Ornithine carbamoyltransferase deficiency: A clinical case

Los trastornos del ciclo de la urea suponen hasta el 60% de las hiperamoniernias graves neonatales. La base de los trastornos de este ciclo deriva en el déficit de una de sus enzimas. El déficit de la enzima ornitina transcarbamilasa es el más frecuente. Su pronóstico dependerá del grado de deficiencia enzimàtica, la edad, la precocidad del diagnóstico e inicio del tratamiento. Presentamos el caso de un adolescente que, a partir de un cuadro de parálisis facial periférica tratado con prednisona, presentó agravamiento de su estado general y falleció a los pocos días. Las cifras elevadas de amoniaco en sangre hicieron sospechar tardíamente de una alteración congénita del ciclo de la urea, que fue confirmada por su estudio genético post mortem. Se estudiaron los familiares y se asesoró a los afectos y portadores. Reflexionamos sobre la importancia de los programas de cribado neonatal y la posibilidad de aplicarlos en la detección de los errores congénitos del metabolismo.

Disorders of urea cycle account for up to 60% of severe neonatal hyperamoniemias. The base of this cycle disorders results in a deficit of its enzymes. Deficiency of the enzyme ornithine transcarbamylase is the most frequently detected. The prognosis depends on the degree of enzyme deficiency, age, early diagnosis and initiation of treatment. We report the case of a teenager who was treated with prednisone because of a peripheral facial palsy. He showed a progressive worsening and died a few days later. The high levels of ammonia made suspect a congenital disorder of urea cycle. The postmortem genetic study confirmed it. We studied the family and advised carriers. We reflect about the importance of the neonatal screening programs and their applicability for detection of inborn errors of metabolism.

Déficit de ornitina transcarbamilasa: Caso clínico / Ornithine carbamoyltransferase deficiency: A clinical case

Los trastornos del ciclo de la urea suponen hasta el 60% de las hiperamoniernias graves neonatales. La base de los trastornos de este ciclo deriva en el déficit de una de sus enzimas. El déficit de la enzima ornitina transcarbamilasa es el más frecuente. Su pronóstico dependerá del grado de deficiencia enzimOtica, la edad, la precocidad del diagnóstico e inicio del tratamiento. Presentamos el caso de un adolescente que, a partir de un cuadro de parálisis facial periférica tratado con prednisona, presentó agravamiento de su estado general y falleció a los pocos días. Las cifras elevadas de amoniaco en sangre hicieron sospechar tardíamente de una alteración congénita del ciclo de la urea, que fue confirmada por su estudio genético post mortem. Se estudiaron los familiares y se asesoró a los afectos y portadores. Reflexionamos sobre la importancia de los programas de cribado neonatal y la posibilidad de aplicarlos en la detección de los errores congénitos del metabolismo.(AU)

Disorders of urea cycle account for up to 60% of severe neonatal hyperamoniemias. The base of this cycle disorders results in a deficit of its enzymes. Deficiency of the enzyme ornithine transcarbamylase is the most frequently detected. The prognosis depends on the degree of enzyme deficiency, age, early diagnosis and initiation of treatment. We report the case of a teenager who was treated with prednisone because of a peripheral facial palsy. He showed a progressive worsening and died a few days later. The high levels of ammonia made suspect a congenital disorder of urea cycle. The postmortem genetic study confirmed it. We studied the family and advised carriers. We reflect about the importance of the neonatal screening programs and their applicability for detection of inborn errors of metabolism.(AU)

[Ornithine carbamoyltransferase deficiency. A clinical case]. / Déficit de ornitina transcarbamilasa. Caso clínico.

Disorders of urea cycle account for up to 60% of severe neonatal hyperamoniemias. The base of this cycle disorders results in a deficit of its enzymes. Deficiency of the enzyme ornithine transcarbamylase is the most frequently detected. The prognosis depends on the degree of enzyme deficiency, age, early diagnosis and initiation of treatment. We report the case of a teenager who was treated with prednisone because of a peripheral facial palsy. He showed a progressive worsening and died a few days later. The high levels of ammonia made suspect a congenital disorder of urea cycle. The postmortem genetic study confirmed it. We studied the family and advised carriers. We reflect about the importance of the neonatal screening programs and their applicability for detection of inborn errors of metabolism.

Déficit de ornitina transcarbamilasa: Caso clínico. / [Ornithine carbamoyltransferase deficiency: A clinical case].

Disorders of urea cycle account for up to 60

of severe neonatal hyperamoniemias. The base of this cycle disorders results in a deficit of its enzymes. Deficiency of the enzyme ornithine transcarbamylase is the most frequently detected. The prognosis depends on the degree of enzyme deficiency, age, early diagnosis and initiation of treatment. We report the case of a teenager who was treated with prednisone because of a peripheral facial palsy. He showed a progressive worsening and died a few days later. The high levels of ammonia made suspect a congenital disorder of urea cycle. The postmortem genetic study confirmed it. We studied the family and advised carriers. We reflect about the importance of the neonatal screening programs and their applicability for detection of inborn errors of metabolism.