RESUMO
The burden of type 2 diabetes mellitus (T2DM) among Indigenous children and adolescents is much greater than in non-Indigenous young people and appears to be rising, although data on epidemiology and complications are limited. Young Indigenous people living in remote areas appear to be at excess risk of T2DM. Most young Indigenous people with T2DM are asymptomatic at diagnosis and typically have a family history of T2DM, are overweight or obese and may have signs of hyperinsulinism such as acanthosis nigricans. Onset is usually during early adolescence. Barriers to addressing T2DM in young Indigenous people living in rural and remote settings relate to health service access, demographics, socioeconomic factors, cultural factors, and limited resources at individual and health service levels. We recommend screening for T2DM for any Aboriginal or Torres Strait Islander person aged > 10 years (or past the onset of puberty) who is overweight or obese, has a positive family history of diabetes, has signs of insulin resistance, has dyslipidaemia, has received psychotropic therapy, or has been exposed to diabetes in utero. Individualised management plans should include identification of risk factors, complications, behavioural factors and treatment targets, and should take into account psychosocial factors which may influence health care interaction, treatment success and clinical outcomes. Preventive strategies, including lifestyle modification, need to play a dominant role in tackling T2DM in young Indigenous people.
Assuntos
Diabetes Mellitus Tipo 2/etnologia , Havaiano Nativo ou Outro Ilhéu do Pacífico , Saúde da População Rural , Adolescente , Austrália , Criança , Diabetes Mellitus Tipo 2/diagnóstico , Diabetes Mellitus Tipo 2/prevenção & controle , Diabetes Mellitus Tipo 2/terapia , Serviços de Saúde do Indígena , Disparidades nos Níveis de Saúde , Humanos , Hipoglicemiantes/uso terapêutico , Programas de Rastreamento , Comportamento de Redução do Risco , Serviços de Saúde RuralRESUMO
Familial hypocalciuric hypercalcemia (FHH) is known to be caused by heterozygous inactivating mutations of the calcium sensing receptor (CaSR) gene. We report an infant with transient neonatal hypercalcemia who was found to be homozygous for a polymorphism at A986S of the CaSR.
Assuntos
Hipercalcemia/genética , Doenças do Recém-Nascido/genética , Polimorfismo Genético , Receptores de Detecção de Cálcio/genética , Cálcio/sangue , Análise Mutacional de DNA , Humanos , Hipercalcemia/sangue , Recém-Nascido , Doenças do Recém-Nascido/sangue , Masculino , Valores de ReferênciaRESUMO
OBJECTIVE: To evaluate the effect of rosiglitazone, an insulin sensitizer, on glycaemic control and insulin resistance in adolescents with type 1 diabetes mellitus (T1DM) RESEARCH DESIGN AND METHODS: Randomized, double-blind, placebo-controlled crossover trial of rosiglitazone (4 mg twice daily) vs. placebo (24 wk each, with a 4 wk washout period). Entry criteria were diabetes duration >1 yr, age 10-18 yr, puberty (>or=Tanner breast stage 2 or testicular volume >4 mL), insulin dose >or=1.1 units/kg/day, and haemoglobin A1c (HbA1c) >8%. Responses to rosiglitazone were compared with placebo using paired t-tests. RESULTS: Of 36 adolescents recruited (17 males), 28 completed the trial. At baseline, age was 13.6 +/- 1.8 yr, HbA1c 8.9 +/- 0.96%, body mass index standard deviation scores (BMI-SDS) 0.94 +/- 0.74 and insulin dose 1.5 +/- 0.3 units/kg/day. Compared with placebo, rosiglitazone resulted in decreased insulin dose (5.8% decrease vs. 9.4% increase, p = 0.02), increased serum adiponectin (84.8% increase vs. 26.0% decrease, p < 0.01), increased cholesterol (+0.5 mmol/L vs. no change, p = 0.02), but no significant change in HbA1c (-0.3 vs. -0.1, p = 0.57) or BMI-SDS (0.08 vs. 0.04, p = 0.31). Insulin sensitivity was highly variable in the seven subjects who consented to euglycaemic hyperinsulinaemic clamps. There were no major adverse effects attributable to rosiglitazone. CONCLUSION: The addition of rosiglitazone to insulin did not improve HbA1c in this group of normal weight adolescents with T1DM.
Assuntos
Glicemia/metabolismo , Diabetes Mellitus Tipo 1/tratamento farmacológico , Hipoglicemiantes/administração & dosagem , Insulina/administração & dosagem , Tiazolidinedionas/administração & dosagem , Adiponectina/sangue , Adolescente , Método Duplo-Cego , Quimioterapia Combinada , Feminino , Hemoglobinas Glicadas , Humanos , Resistência à Insulina , Masculino , Rosiglitazona , Resultado do TratamentoRESUMO
OBJECTIVE: To describe the natural history and risk factors for persistent microalbuminuria in children and adolescents with type 1 diabetes followed for up to 15 years. RESEARCH DESIGN AND METHODS: This study contained a longitudinal cohort of 972 patients; analysis of baseline risk factors was performed using logistic regression and predictors over time using survival analysis. Albumin excretion rate was measured on three consecutive timed overnight urine collections on at least two occasions. Normoalbuminuria was defined as a median albumin excretion rate < 7.5 microg/min, borderline microalbuminuria as 7.5-20 microg/min, and microalbuminuria as 20-200 microg/min. Microalbuminuria was further classified as persistent if its duration was >12 months. Median age was 12.7 years (interquartile range 11.5-14.4) and diabetes duration 6.5 years (4.1-9.3) at first assessment, and median follow-up was 6.2 years (range 1-15.3). RESULTS: The incidence of persistent microalbuminuria was 4.6 (95% CI 3.3-6.1) per 1,000 patient-years. Predictors of persistent microalbuminuria from the first assessment using multiple logistic regression were high cholesterol (odds ratio 2.2 [95% CI 1.2-4.0]) and borderline microalbuminuria (2.5 [1.2-5.2]). Predictors using Cox regression were HbA(1c) (hazard ratio 1.4 [95% CI 1.1-1.7]), age at diagnosis (1.2 [1.1-1.3]), obesity (3.6 [0.8-15.5]), and insulin dose (2.7 [1.0-7.5]). CONCLUSIONS: Children and adolescents with type 1 diabetes who have borderline microalbuminuria are more than twice as likely to develop persistent microalbuminuria. In addition to poor glycemic control, clinical markers of insulin resistance were associated with an increased risk of microalbuminuria.
Assuntos
Albuminúria/urina , Diabetes Mellitus Tipo 1/complicações , Adolescente , Albuminúria/complicações , Albuminúria/patologia , Criança , Progressão da Doença , Humanos , Resistência à Insulina/fisiologia , Modelos Logísticos , Estudos Longitudinais , Fatores de Risco , Análise de SobrevidaRESUMO
BACKGROUND: To describe the presenting clinical features of coeliac disease in a single paediatric centre, and to determine if the presenting features vary with age. METHODS: A review was conducted of children who had been referred with clinical suspicion of coeliac disease to the paediatric gastroenterology department of a tertiary paediatric hospital in Sydney, Australia. Coeliac disease was defined using standard histological criteria. Medical records were reviewed retrospectively. RESULTS: Clinical data were available for 74 cases of proven coeliac disease. Only 9% of patients were less than 2 years of age at diagnosis. Pre-school children (age < 5 years) presented with different symptoms to school children (age > or = 5 years). The most common presenting features in younger children were diarrhoea, irritability and weight loss. However, in older children, abdominal pain was the most common presenting feature. CONCLUSION: We found a significant difference in the clinical features of coeliac disease in pre-school compared to school age children.