The aim of this study was to evaluate the level of physical activity and cardiorespiratory fitness in teenagers with type 1 diabetes mellitus (T1D) in comparison with healthy scholar participants. Total of 154 teenagers (T1D=45 and CON=109). Height, weight, cardiorespiratory fitness (VO2max), and the level of physical activity by the Bouchard's Physical Activity Record were measured, and glycated hemoglobin (HbA1c)

Hypopituitarism is defined as the deficiency of one or more of the hormones secreted by the pituitary gland. Several developmental factors necessary for pituitary embryogenesis and hormone secretion have been described, and mutations of these genes in humans provide a molecular understanding of hypopituitarism. Genetic studies of affected patients and their families provide insights into possible mechanisms of abnormal pituitary development, however, mutations are rare. This review characterizes several of these developmental proteins and their role in the pathogenesis of hypopituitarism. Continuing research is required to better understand the complexities and interplay between these pituitary factors and to make improvements in genetic diagnosis that may lead to early detection and provide a future cure. HypopituitarismPituitary hormone deficiency is the partial or complete loss of single or multiple pituitary hormones from the anterior (AP) and/or posterior pituitary (PP). The etiology, often multifactorial and secondary to neurological insult, includes head injury, neurosurgical sequelae, infiltrative disorders and cranial radiotherapy. A subset of patients may present either at birth with congenital hormone deficiency or develop deficiency with no previous neurological injury or pathology. These patients are diagnosed with idiopathic hypopituitarism and often have multiple or combine pituitary hormone deficiency (CPHD). The incidence and prevalence of hypopituitarism is still unclear. One report, which summarizes data from separate European populations, cites an incidence of 11.9 to 42.1 per million inhabitants per year, while the prevalence is estimated from 300 to 455 per million inhabitants [1].Pituitary hormone deficiencies most commonly occur in the AP or adenohypophysis. The mature adenohypophysis contains five major pituitary cell types that produce six hormones; corticotrophs -adrenocorticotrophic hormone (ACTH), thyrotrophs-thyroid stimulating hormone (TSH), lactotrophs -prolactin (PRL), somatotrophs -growth hormone (GH), and gonadotrophs -lutenizing hormone (LH) and follicle stimulating hormone (FSH). A balanced and orchestrated sequence of events dependent on the temporal and spatial appearance developmental factors is necessary for normal pituitary development. Disruption of this cascade due to mutations in any of these gene products affects the ontogeny of one or several of the pituitary cell types and ultimately leads to hormone deficiency.

Our findings suggest that, in addition to thyroid hormonogenesis, the DUOX2 N-terminal domain may play a role in thyroid development.

The prevalence of CH was within the previously reported range of 1:3000-4000. Ectopy was the most common etiology. Clinical analysis revealed distinct hormonal patterns in TH subgroup when compared with other variants of TD, with genetic abnormalities identified only in few cases in the TSH-R, PAX8, and NKX2.5 genes.

Congenital hypothyroidism (CH) is the most common congenital endocrine disorder, with an incidence of 1:2,000 to 1:4,000 live births and it is a leading preventable mental retardation. Neonatal Screening Programs allow early identification of the disease and the adequate treatment of affected children can avoid the complications related to deprivation of the hormone. Most cases of primary congenital hypothyroidism (85%) are due to thyroid dysgenesis (ectopia, hypoplasia or agenesis) while the remaining result from defects in hormone synthesis. Affected children (> 95%) usually have no symptoms suggesting the disease at birth. The most frequent symptoms and signs are prolonged neonatal jaundice, hoarse cry, lethargy, slow movements, constipation, macroglossia, umbilical hernia, large fontanelle, hypotonia and dry skin. Around the world, various strategies are used for the screening of the CH. In Brazil, screening for CH is mandatory by law and usually done by serum TSH in dried blood collected from the heel. The recommended age for performing this test is after 48 hours of life until the 4 th day. Diagnostic confirmation is required dosing TSH and free T 4 or total T 4 in serum. Arq Bras Endocrinol Metab. 2013;57(3):184-92Keywords Congenital hypothyroidism; neonatal screening RESUMO O hipotireoidismo congênito (HC) é o distúrbio endócrino congênito mais frequente, com incidência variando de 1:2.000 a 1:4.000 crianças nascidas vivas e uma das principais causas de retardo mental que pode ser prevenida. Os Programas de Triagem Neonatal para a doença permitem a identificação precoce dos afetados e seu tratamento de modo a evitar as complicações da falta do hormônio. A maioria dos casos de hipotireoidismo congênito é decorrente de disgenesias tireoidianas (85%), entre elas a ectopia, hipoplasia ou agenesia tireoidianas, e os demais resultam de defeitos de síntese hormonal. As crianças afetadas (> 95%) geralmente não apresentam sintomas sugestivos da doença ao nascimento. Os sintomas e sinais mais comuns são: icterícia neonatal prolongada, choro rouco, letargia, movimentos lentos, constipação, macroglossia, hérnia umbilical, fontanelas amplas, hipotonia e pele seca. Várias estratégias são utilizadas para a triagem do HC. No Brasil, esta é obrigatória por lei e geralmente é feita com a dosagem de TSH em sangue seco coletado do calcanhar. A idade recomendada para sua realização é após as 48 horas de vida até o quarto dia. A confirmação diagnóstica é obrigatória com as dosagens de TSH e T 4 livre ou T 4 total. Arq Bras Endocrinol Metab. 2013;57(3):184-92 Descritores Hipotireoidismo congênito; triagem neonatal