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1.
Pediatr Diabetes ; 21(1): 48-52, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31628775

RESUMO

Type 1 diabetes mellitus (T1D) incidence in children varies across regions and countries, showing a continuous rise globally. Chile has mandatory T1D notification and guaranteed access to diagnosis and treatment since 2005, providing a strong model to evaluate T1D epidemiology. OBJECTIVE: To determine T1D incidence in Chilean population under 20 years between 2006 and 2014. METHODS: We reviewed mandatory notifications of T1D in Chile's public health system. RESULTS: A total of 4153 T1D cases in population under 20 years were notified from 2006 to 2014. Median age was 14 years and 51% were male. The average annual T1D incidence was 12 per 100 000 population, with an increase from 10.2 in 2006 to 13.8 in 2014 (ß 0.5 95% confidence interval [CI] 0.4-0.7, P < .001). A significantly increasing linear trend of T1D incidence was observed in groups of 0 to 4 years (ß 0.33, 95% CI 0.06-0.59, P = .02), 5 to 9 years (ß 0.68 95% CI 0.27-1.10, P = .006), and 10 to 14 (ß 0.94, 95% CI 0.67-1.20, P < .001), but increase was less pronounced in the oldest children aged between 15 and 19 years (ß 0.22, 95% CI -0.03 to 0.44, P = .052). The lowest regional T1D incidence was observed in the Araucanía region, which has the highest rate of indigenous population. CONCLUSION: Incidence rates of T1D in Chile, evaluated through a mandatory notification program, are rapidly increasing in children and adolescents. If increasing trends persist, Chile will reach T1D incidence rates of Western developed countries in the next decade.


Assuntos
Diabetes Mellitus Tipo 1/epidemiologia , Adolescente , Distribuição por Idade , Criança , Pré-Escolar , Chile/epidemiologia , Diabetes Mellitus Tipo 1/diagnóstico , Feminino , Humanos , Incidência , Lactente , Recém-Nascido , Masculino , Programas Obrigatórios , Estudos Retrospectivos , Distribuição por Sexo , Adulto Jovem
2.
Clin Kidney J ; 7(5): 457-63, 2014 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-25878777

RESUMO

BACKGROUND: Fibroblast Growth Factor-23 (FGF23) and cofactor Klotho are key regulators of mineral metabolism in chronic kidney disease (CKD), but little is known about the mechanisms that regulate their production. This study evaluates longitudinal changes of FGF23 and Klotho levels and their regulatory factors in children on chronic peritoneal dialysis (PD). METHODS: FGF23, Klotho, 25(OH) vitamin D, 1,25-dihydroxyvitamin D and parathyroid hormone (PTH) plasma concentrations were measured during 1 year of follow-up in PD children. Anthropometric and dialytical parameters were evaluated in addition to mineral metabolism variables. RESULTS: Thirty-one patients under chronic PD were followed for 12 months. FGF23 mean plasma levels at Month 1 were significantly increased compared with controls, 215.1 ± 303.6 versus 9.4 ± 5.7 pg/mL, respectively (P < 0.001). Baseline Klotho levels were 41% lower in patients compared with controls, 132.1 ± 58 versus 320 ± 119.4 pg/mL, respectively (P < 0.001), and did not correlate with FGF23 and phosphorus levels. At Month 12, FGF23 (195 ± 300 pg/mL) and Klotho levels (130 ± 34 pg/mL) remained similar to baseline values. Log-FGF23 correlated significantly with height/age Z score (r= -0.38) and residual renal function (r = -0.44), but no correlation was found with serum phosphorus, phosphate intake, PTH and vitamin D levels. The log-FGF23 strongly correlated with calcium levels at Months 1, 6 and 12, however, this relationship was blunted if serum phosphorus was >6 mg/dL. By multiple regression analysis, calcium was the strongest variable determining FGF23 levels. CONCLUSIONS: In this longitudinal study, FGF23 levels are markedly increased, and Klotho levels are reduced in PD children compared with controls. FGF23 levels appeared to be regulated primarily by serum calcium, showing a significant correlation at each time of measurement. This relationship was lost in patients with phosphorus >6 mg/dL. These observations may have important consequences to the therapeutic management of phosphate homeostasis in CKD patients.

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