LUS may be used to predict the need for surfactant replacement in extremely preterm neonates with RDS.

Background: The question of whether children with subclinical hypothyroidism (SH) should be treated or not is controversial due to the lack of studies on outcomes of SH children treated with L-thyroxine (L-T₄) versus those receiving no therapy. Objectives: (a) To evaluate thyroid tests under L-T₄ and after therapy withdrawal in 69 SH children (group A) and (b) to compare our results with those recorded in 92 untreated children (group B). Design: Group A children were treated for 24 months and TSH and FT₄ levels 3 months after therapy withdrawal were compared with those measured in group B at the end of follow-up in order to investigate treatment effects. Results: The prevalence of children who had normalized TSH at the end of follow-up was higher in group A, but the prevalence of those who had normalized or maintained unchanged TSH was similar in the two groups, as was the prevalence of children who exhibited a TSH increase >10 mU/l. In group A, TSH values at 27 months were associated with baseline values. Conclusions: (a) Two-year treatment in SH children is unable to modify posttherapy outcome of hyperthyrotropinemia; (b) therapy is unable to prevent the risk of further TSH increase after treatment withdrawal, and (c) posttherapy TSH outcome is conditioned by baseline TSH.

Background Women with polycystic ovarian syndrome have a high prevalence of metabolic syndrome and type 2 diabetes mellitus. Blacks and Hispanics have a high morbidity and mortality due to cardiovascular disease and diabetes mellitus in the general population. Since metabolic syndrome is a risk factor for development of type 2 diabetes and cardiovascular disease, understanding any racial and ethnic differences in metabolic syndrome amongst women with polycystic ovarian syndrome is important for prevention strategies. However, data regarding racial/ethnic differences in metabolic phenotype amongst women with polycystic ovary syndrome is inconsistent. Objective To determine if there are racial/ethnic differences in insulin resistance, metabolic syndrome and hyperandrogenemia in women with polycystic ovarian syndrome. Study Design Secondary data analysis of a prospective multicenter, double blind controlled clinical trial, the Pregnancy in Polycystic Ovary Syndrome II study, conducted in 11 academic health centers. Data on 702 women with polycystic ovarian syndrome aged 18-40 years who met modified Rotterdam criteria for the syndrome and wished to conceive were included in the study. Women were grouped into racial/ethnic categories Non-Hispanic Whites, non-Hispanic Blacks and Hispanic. The main outcomes were the prevalence of insulin resistance, metabolic syndrome and hyperandrogenemia in the different racial/ethnic groups. Results BMI (35.1 ± 9.8 vs. 35.7 ± 7.9 vs. 36.4 ± 7.9 kg/m2) and waist circumference (106.5 ± 21.6 vs. 104.9 ± 16.4 vs. 108.7 ± 7.3 cm) did not differ significantly between non-Hispanic White, non-Hispanic Black and Hispanic women. Hispanic women with PCOS had a significantly higher prevalence of hirsutism (93.8 vs. 86.8%), abnormal free androgen index (FAI) (75.8 vs. 56.5%), abnormal homeostasis model assessment (HOMA) (52.3 vs. 38.4%) and hyperglycemia (14.8 vs. 6.5%), as well as lower sex hormone binding globulin compared to non-Hispanic Whites. Non-Hispanic Black women had a significantly lower prevalence of metabolic syndrome (24.5 vs. 42.2%) compared with Hispanic women, and lower serum triglyceride levels compared to both Hispanics and non-Hispanic Whites (85.7 ± 37.3 vs. 130.2 ± 57.0 vs. 120.1 ± 60.5 vs. mg/dL, p<0.01), with a markedly lower prevalence of hypertriglyceridemia (5.1 vs. 28.3 vs. 30.5%, p<0.01) compared to the other two groups. Comment Hispanic women with PCOS have the most severe phenotype, both in terms of hyperandrogenism and metabolic criteria. Non-Hispanic Black women have an overall milder polycystic ovarian syndrome phenotype than Hispanics and in some respects, than Non-Hispanic White women.

Autoimmune polyendocrinopathy candidiasis ectodermal dystrophy (APECED) is a rare autosomal recessive disease, caused by mutations of a single gene named autoimmune regulator gene (AIRE) which results in a failure of T cell tolerance within the thymus. Chronic mucocutaneous candidiasis, chronic hypoparathyroidism, and Addison's disease are the hallmarks of the syndrome. APECED is also characterized by several autoimmune endocrine and nonendocrine manifestations, and the phenotype is often complex. Moreover, even though APECED is a monogenic disease, its clinical picture is generally dominated by a wide heterogeneity both in the severity and in the number of components even among siblings with the same AIRE genotype. The variability of its clinical expression implies that diagnosis can be challenging, and a considerable delay often occurs between the appearance of symptoms and the diagnosis. Since a prompt diagnosis is essential to prevent severe complications, clinicians should be aware of all symptoms and signs of suspicion. The aim of this paper is to give an overview on the clinical presentation and diagnostic criteria of APECED and to focus on current knowledge on genotype-phenotype correlation.