Searchable abstracts of presentations at key conferences in endocrinology
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23rd Joint Meeting of the British Endocrine Societies with the European Federation of Endocrine Societies

ea0007oc17 | Thyroid | BES2004

Thyroid hormone (T3) activates fibroblast growth factor (FGF) receptor signalling in bone

Barnard J , Williams A , Harvey C , Williams G

FGFs and T3 are required for skeletal development. Activating mutations of FGF receptor-1 (FGFR-1) and FGFR-2 cause craniosynostosis, whilst FGFR-3 is a negative regulator of chondrocyte proliferation and activating mutations cause achondroplasia. Childhood hypothyroidism causes delayed ossification and growth retardation, whereas thyrotoxicosis accelerates bone development, induces premature growth plate and skull suture closure and causes short stature and craniosynostosis. ...

ea0007oc18 | Thyroid | BES2004

Biological consequences of gain-of-function thyrotropin receptor (TSHR) mutant expression in adipose tissue

Baker G , Gregory J , Bakhsh A , Betts P , Hughes I , Ludgate M

Neonates harbouring germline gain-of-function TSHR mutations (M453T, L629F) have been reported with transient proptosis. This resolves once euthyroidism is achieved. In contrast children expressing TSHR mutations (V597L, I486T) fail to thrive, with weight gain and height between the 0.4th and 2nd centiles. We have previously demonstrated TSHR expression in preadipocytes undergoing adipogenesis. We now investigate the consequences of constitutively active TSHR mutation expressi...

ea0007oc19 | Thyroid | BES2004

PBF predicts recurrence in thyroid cancer and potentiates the actions of PTTG in vitro

Stratford A , Boelaert K , Franklyn J , McCabe C

We have previously shown Pituitary Tumor Transforming Gene (PTTG) and basic Fibroblast Growth Factor (FGF-2) to be upregulated in thyroid cancer. PTTG requires interaction with the protein PBF (PTTG Binding Factor) to stimulate FGF-2 secretion, and hence promote tumour angiogenesis and growth. We now report that PBF is also upregulated in hyperplastic and neoplastic thyroid tissues compared with normal thyroid (N=11) (2.6-fold in multinodular goitre (N=25, P=0.002), and 3.3-fo...

ea0007oc20 | Thyroid | BES2004

Steroid modulation of peripheral cytokine expression: increased resistance to dexamethasone and progesterone inhibition of type 1 CD4+ response in autoimmune thyroiditis

Okosieme O , Premawardhana L , Parkes A , Lazarus J

Glucocorticoids may regulate the autoimmune response by influencing the shift in balance between type-1 and type-2 cytokine responses. To investigate the effect of steroids on peripheral cytokine expression in autoimmune thyroiditis we measured dexamethasone (Dex) and progesterone (Prg) inhibition of peripheral CD4+ T lymphocyte expressions of Interferon-gamma (IFN-g) (type-1 response) and Interleukin-4 (IL-4) (type 2 response) in both patients and healthy subjects.<p clas...

ea0007oc21 | Thyroid | BES2004

Gender, age, goitre type and serum TSH level predict thyroid neoplasia in 1500 patients with thyroid enlargement investigated by FNAC

Boelaert K , Horacek Y , Daykin J , Sheppard M , Franklyn J

1500 euthyroid patients (1302 females and 198 males, mean age 47.8) presenting with thyroid enlargement were evaluated by fine needle aspiration (FNAC) of the thyroid as the first line investigation. The final cytological or histological diagnosis was determined after surgery (n=556) or clinical follow-up for a minimum period of 2 years (mean 9.5 yrs, range 2-19 years). Goitre type was assessed clinically and classified as diffuse in 184, multinodular in 457 or solitary nodule...

ea0007oc22 | Thyroid | BES2004

Defining genetic predictors for the development of Graves' disease in young females

Collins J , Heward J , Cordell H , Franklyn J , Gough S

The HLA and CTLA-4 gene regions, on chromosomes 6p21 and 2q33 respectively, have been consistently associated with Graves' disease (GD). Recent data indicate that both DRB1 (in the HLA class II region) and the 3' untranslated region of the CTLA-4 gene are the most likely regions harbouring the aetiological variants for susceptibility to GD. It is not known, however, whether these variants lead to expression of specific sub-phenotypes in subjects with GD, or contribute to disea...