[Severe vitamin D deficiency in children from Punta Arenas, Chile: Influence of nutritional status on the response to supplementation]. / Deficiencia severa de vitamina D en niños de Punta Arenas, Chile: influencia de estado nutricional en la respuesta a suplementación.

UNLABELLED: There is a high risk of vitamin D (VD) deficiency in the population of southern Chile that can be treated with VD supplements. Weight excess (WE) can influence the response to supplements. OBJECTIVES: To study the prevalence of VD deficiency and the effect of cholecalciferol (VD3) supplements in healthy children from Punta Arenas, Chile, and evaluate a possible association with nutritional status. METHODOLOGY: Demographic and anthropometric data, as well as laboratory assessment of serum 25-hidroxyvitamin D (25OHD) and other bone metabolism parameters were evaluated. After baseline evaluation, children were supplemented with VD3 1600 IU/day for one month, after which 25OHD was retested. RESULTS: Of the 108 children studied, 50% were boys, and had a mean age of 9.6±0.5 years. Nutritional assessment showed that 39% had normal weight, 46% were overweight, and 15% were obese. Median 25OHD was 10.9ng/ml: 96.3% had deficiency (<20ng/ml) and 3.7% insufficiency (20-29ng/ml). Severe deficiency was found in 62% (<12ng/ml). Baseline 25OHD was not affected by nutritional status. After supplementation, median 25OHD was 17.5ng/ml: 62% had deficiency, 36% insufficiency, and 2% sufficiency (>30ng/ml). Children with WE had a significantly lower increase in 25OHD than children with normal weight (5±5.5 vs. 7.7±4.9, p=03). Children with WE may require 32% higher VD dose than normal weight children to attain the same 25OHD concentration. CONCLUSIONS: Chilean schoolchildren from Punta Arenas have high prevalence of WE and VD deficiency, with a majority in the range of severe VD deficiency. WE interferes in the response to VD supplementation, leading to a lower increase in 25OHD.

Deficiencia severa de vitamina D en niños de Punta Arenas, Chile: influencia de estado nutricional en la respuesta a suplementación / Severe vitamin D deficiency in children from Punta Arenas, Chile: Influence of nutritional status on the response to supplementation

En población austral existe un alto riesgo de deficiencia de vitamina D (VD) que puede tratarse mediante suplementación nutricional. El exceso de peso (EP) podría afectar la respuesta a su suplementación. Objetivos: Estudiar la prevalencia de deficiencia de VD y el efecto de la suplementación con colecalciferol (VD3) en niños sanos de Punta Arenas, Chile, y evaluar la posible asociación con el estado nutricional. Metodología: Se obtuvieron datos demográficos, antropométricos y medición sérica de 25-hidroxivitamina-D (25OHD) y parámetros de metabolismo óseo. Luego se suplementó a los niños con VD3 1.600 UI/día por un mes y se reevaluó 25OHD sérica. Resultados: Se estudiaron 108 niños, 50% hombres, edad promedio 9,6 ± 0,5 años. Un 39% eran eutróficos, 46% con sobrepeso y 15% obesos. La mediana de 25OHD fue 10,9 ng/ml: 96,3% tenían deficiencia (< 20 ng/ml) y 3,7% insuficiencia (20 a 29 ng/ml). Se pesquisó deficiencia severa (< 12 ng/ml) en 62%. La concentración basal de 25OHD no varió según estado nutricional. Luego de la suplementación, la mediana de 25OHD fue 17,5 ng/ml: 62% con deficiencia, 36% insuficiencia y 2% suficiencia (> 30 ng/ml). Los niños con EP tuvieron un alza de 25OHD significativamente menor que niños eutróficos (5 ± 5,5 vs. 7,7 ± 4,9, p = 0,03). Niños con EP requerirían dosis de VD 32% mayores que niños eutróficos para lograr la misma concentración de 25OHD. Conclusiones: Niños escolares de Punta Arenas presentan alta prevalencia de EP, deficiencia de VD y la mayoría en rango de deficiencia severa. El EP interfiere en la respuesta a suplementación farmacológica, logrando menor alza de 25OHD.

There is a high risk of vitamin D (VD) deficiency in the population of southern Chile that can be treated with VD supplements. Weight excess (WE) can influence the response to supplements. Objectives: To study the prevalence of VD deficiency and the effect of cholecalciferol (VD3) supplements in healthy children from Punta Arenas, Chile, and evaluate a possible association with nutritional status. Methodology: Demographic and anthropometric data, as well as laboratory assessment of serum 25-hidroxyvitamin D (25OHD) and other bone metabolism parameters were evaluated. After baseline evaluation, children were supplemented with VD3 1600 IU/day for one month, after which 25OHD was retested. Results: Of the 108 children studied, 50% were boys, and had a mean age of 9.6 ± 0.5 years. Nutritional assessment showed that 39% had normal weight, 46% were overweight, and 15% were obese. Median 25OHD was 10.9 ng/ml: 96.3% had deficiency (< 20 ng/ml) and 3.7% insufficiency (20-29 ng/ml). Severe deficiency was found in 62% (< 12 ng/ml). Baseline 25OHD was not affected by nutritional status. After supplementation, median 25OHD was 17.5 ng/ml: 62% had deficiency, 36% insufficiency, and 2% sufficiency (>30 ng/ml). Children with WE had a significantly lower increase in 25OHD than children with normal weight (5 ± 5.5 vs. 7.7 ± 4.9, p = 03). Children with WE may require 32% higher VD dose than normal weight children to attain the same 25OHD concentration. Conclusions: Chilean schoolchildren from Punta Arenas have high prevalence of WE and VD deficiency, with a majority in the range of severe VD deficiency. WE interferes in the response to VD supplementation, leading to a lower increase in 25OHD.

Frequency of familial hyperaldosteronism type 1 in a hypertensive pediatric population: clinical and biochemical presentation.

Familial hyperaldosteronism type 1 is an autosomal dominant disorder attributed to a chimeric CYP11B1/CYP11B2 gene (CG). Its prevalence and manifestation in the pediatric population has not been established. We aimed to investigate the prevalence of familial hyperaldosteronism type 1 in Chilean hypertensive children and to describe their clinical and biochemical characteristics. We studied 130 untreated hypertensive children (4 to 16 years old). Blood samples for measuring plasma potassium, serum aldosterone, plasma renin activity, aldosterone/renin ratio, and DNA were collected. The detection of CG was performed using long-extension PCR. We found 4 (3.08%) of 130 children with CG who belonged to 4 unrelated families. The 4 patients with CG had very high aldosterone/renin ratio (49 to 242). In addition, we found 4 children and 5 adults who were affected among 21 first-degree relatives. Of the 8 affected children, 6 presented severe hypertension, 1 presented prehypertension, and 1 presented normotension. High serum aldosterone levels (>17.7 ng/dL) were detected in 6 of 8 subjects (range: 18.6 to 48.4 ng/dL) and suppressed plasma renin activity (≤0.5 ng/mL per hour) and high aldosterone/renin ratio (>10) in 8 of 8 children (range: 49 to 242). Hypokalemia was observed in only 1 of 8 children. We demonstrated that the prevalence of familial hyperaldosteronism type 1 in a pediatric hypertensive pediatric population was surprisingly high. We found a high variability in the clinical and biochemical characteristics of the affected patients, which suggests that familial hyperaldosteronism type 1 is a heterogeneous disease with a wide spectrum of presentations even within the same family group.