“
“Context: Newborns with congenital hypothyroidism (CH) have an increased risk for congenital heart defects (CHD) due to a common embryonic developmental program between thyroid gland and heart and great vessels.\n\nObjective: Our objective was to investigate the prevalence and origin

of thyroid disorders in young patients with CHD.\n\nDesign and Setting: We conducted a prospective observational study between January 2007 and January 2009 in academic Pediatric Cardiosurgery and Endocrinology.\n\nPatients: Patients included 324 children (164 males, 160 females, aged 0.2-15.4 yrs) with CHD.\n\nIntervention: Subjects underwent hormonal and genetic screening.\n\nMain Outcome Measures: Serum TSH and thyroid hormone levels were assessed.\n\nResults: Two CHD patients were diagnosed with CH at the

Cilengitide solubility dmso neonatal VX-770 datasheet screening (1: 162). Mild hypothyroidism (serum TSH > 4.0 mu U/ml) was diagnosed and confirmed 6 months later [TSH = 5.4 +/- 1.5 mu U/ml; free T(4) = 1.3 +/- 0.2 ng/dl (normal values 0.8-1.9)] in 37 children (11.5%) who were negative at neonatal screening. Hypothyroidism was not related to type of CHD, whereas TSH levels positively correlated with serum N-terminal pro-type B natriuretic peptide levels. Biochemical and ultrasound findings consistent with thyroid autoimmunity were present in three of 37 hypothyroid children (8.1%). One

patient had hemiagenesis (2.7%). Variations in candidate genes were screened in CHD patients. NKX2.5 coding sequence was normal in all samples. A 3-Mb microdeletion in 22q11.2 was detected in three patients (8.3%), whereas only known polymorphisms were identified in TBX1 coding sequence.\n\nConclusions: CHD patients have an increased risk for both CH (10-fold higher) and acquired mild hypothyroidism (3-fold higher). Unrecognized mild hypothyroidism may negatively affect the outcome of CHD children, suggesting that thyroid function should be repeatedly checked. ALK inhibitor Thyroid autoimmunity and 22q11.2 microdeletions account for small percentages of these cases, and still unknown mechanisms underline such a strong association. (J Clin Endocrinol Metab 96: E1115-E1119, 2011)”
“The man in-the-street who frequently asks the question “Why am I here?” finds even more difficulty with the question “Why are parasites here?” The public’s distaste for parasites (and by implication, for parasitologists!) is therefore understandable, as maybe was the feeling of early 20th century biologists that parasites were a puzzle because they did not conform to the then widely held association between evolution and progress, let alone the reason why a benevolent Creator should have created them.