Searchable abstracts of presentations at key conferences in endocrinology

ea0010p89 | Thyroid | SFE2005

The effect of high calcium on activity of thyroid gland in rat

Ebrahimian F , Zahedi Asl S

The effects of goitrogens on the thyroid gland have been much studied and calcium is considered as a goitrogen in some cases. Since the level of calcium is high in drinking water of some cities of Khuzestan province, the effects of high calcium intake on the function of thyroid gland is investigated in this study. For this purpose the concentration of thyroid hormones is measured in rats.The study was carried out on73 male and female rats. The animals we...

ea0007p235 | Thyroid | BES2004

Evaluation of thyroid function in patients with chronic active HCV and HBV hepatitis treated with interferon-alpha

Esfahanian F , Alavian M , Ziaee A

Aims: To evaluate thyroid gland dysfunction during interferon alfa (INF-alpha)therapy in patients with the hepatitis B virus (HBV) and hepatitis C virus (HCV)Methods: 58 patients with HCV and 18 patients with HBV were studied prospectively before and with 2 months intervals during INF-alpha therapy. Measurements of serum thyroxine,triiodothyronine, thyrotropine, triiodothyronine resin uptake, thyroid peroxidase antibodies (TPOAbs), and thyroglobulin anti...

ea0005p257 | Thyroid | BES2003

Does iodide modulate the biological outcome of activating thyrotropin receptor mutations?

Al-Khafaji F , Ludgate M

Does Iodide Modulate The Biological Outcome of Activating Thyrotropin Receptor Mutations?Dr. F. Al-Khafaji and Dr. M. LudgateHyperthyroidism is caused by pathogenic activation of the thyrotropin receptor (TSHR) either by the thyroid stimulating antibodies of Graves' disease (GD) or activating TSHR mutations. These produce nodular goitre or familial hyperthyroidism. The pathogenic mechanism predominating varies according to the iodide intake, with nodular goitre account...

ea0004s10 | Ageing and cellular senescence | SFE2002

Extending Lifespan

Bartke A , Dominici F , Turyn D

Complex interactions between aging and the endocrine system include an important role of hormones in mediating effects of genotype on longevity. In Caenorhabditis elegans and Drosophila melanogaster, striking extension of life span can be produced by targeted disruption (knock out, KO) of genes that control signaling pathways homologous to insulin/insulin-like growth factor signaling in mammals. In the mouse, Mus musculus, longevity is greatly increased by spontaneous and expe...

ea0004p52 | Endocrine tumours and neoplasia | SFE2002

No evidence of a role for mutations in the cAMP-dependant Protein Kinase A regulatory subunit in hyperfunctioning adrenocortical adenomas

Swords F , Arola J , Clark A

The molecular mechanisms underlying adrenal adenomas have not yet been elucidated. Many groups have sought mutations within the ACTH receptor as well as its downstream signalling pathway, although none have yet been identified. However, mutations in the alpha regulatory subunit of the cAMP dependant Protein Kinase A (PRKAR1A) have recently been described in more than 50% of patients with Carney complex. This syndrome is characterised by nodular adrenocortical hyperplasia as we...

ea0004p87 | Steroids | SFE2002

CONCORDANCE OF RESULTS FOR TWO METHODS OF CALCULATING FREE TESTOSTERONE CONCENTRATION. ARE THE RESULTS VALID?

Ivison F , Robinson A , Diver M

Many laboratories offer a simple ratio of total testosterone (T):SHBG as an index (FAI) of free androgens. Methods for measuring free T (fT) are time consuming (equilibrium dialysis, ED) or reveal concentrations at odds with accepted values (RIA). The validity of FAI has been questioned and an alternative assessment by computation of fT recommended (1). We use a simpler calculation (2) producing results comparable to established literature. We have compared results obtained by...

ea0004dp6 | Diabetes, metabolism and cardiovascular | SFE2002

No evidence of a role for mutations in the cAMP-dependant Protein Kinase A regulatory subunit in hyperfunctioning adrenocortical adenomas

Swords F , Arola J , Clark A

The molecular mechanisms underlying adrenal adenomas have not yet been elucidated. Many groups have sought mutations within the ACTH receptor as well as its downstream signalling pathway, although none have yet been identified. However, mutations in the alpha regulatory subunit of the cAMP dependant Protein Kinase A (PRKAR1A) have recently been described in more than 50% of patients with Carney complex. This syndrome is characterised by nodular adrenocortical hyperplasia as we...

ea0002p51 | Growth and development | SFE2001

Effects of fetal adrenalectomy on the binucleate cell population in ovine placenta near term

Ward J , Wooding F , Fowden A

In ovine placenta, binucleate cells (BNCs) are formed from trophectodermal uninucleate cells and produce placental lactogen (PL) and pregnancy associated glycoproteins (PAGs). BNC numbers cells are stable throughout most of pregnancy, yet fall abruptly just before term (Wooding et al., 1994), at a time when endogenous fetal cortisol levels are rising. This study looked at the effect of abolishing the normal prepartum cortisol rise by fetal adrenalectomy on the BNC population i...

ea0029p1572 | Thyroid (non-cancer) | ICEECE2012

Gestational hyperthyroidism in women from mild to moderate iodine deficiency (ID) areas

Presti S. , Moleti M. , Di Bella B. , Sturniolo G. , Di Mauro F. , Trimarchi F. , Vermiglio F.

Graves’ disease (GD) and gestational transient thyrotoxicosis (GTT) are the main causes of hyperthyroidism in pregnancy, their prevalence ranging between 0.1–0.4% and 0.3–11%, respectively.Aim of the study: To evaluate both prevalence and outcome of gestational hyperthyroidism in mild to moderate ID areas.Subjects and methods: 482 consecutive pregnant women who had never undergone thyroid function evaluation before a...

ea0011p897 | Thyroid | ECE2006

The GH response to ghrelin in humans is reduced in conditions of hyper- and hypothyroidism

Broglio F , Prodam F , Riganti F , Gramaglia E , Rossetto R , Maccario M , Ghigo E

Both hyper- and hypothyroidism show reduced spontaneous and GHRH-stimulated GH secretion. Although impaired GHRH secretion and activity as well as reduced GH pituitary synthesis have been reported in these pathological conditions, a definitive description of the underlying pathophysiological mechanisms have not been provided yet. Ghrelin elicits a potent GH-releasing effect partially mediated by a functional somatostatin antagonism and a synergic interaction with GHRH. Moreove...