Publications
227 results found
Vaidya B, Williams GR, Abraham P, et al., 2008, Radioiodine treatment for benign thyroid disorders: results of a nationwide survey of UK endocrinologists., Clin Endocrinol (Oxf), Vol: 68, Pages: 814-820
BACKGROUND: A survey of physicians' practice relating to radioiodine administration for hyperthyroidism was carried out in the UK over 15 years ago and showed wide variations in patient management. This led to the development of national guidelines for the use of radioiodine in hyperthyroidism. As there have been significant advances in the field since that survey, we carried out another survey to study the prevalent practices relating to radioiodine therapy for benign thyroid disorders across the UK. SUBJECTS AND METHODS: We mailed 698 UK consultant endocrinologists a questionnaire on radioiodine treatment based on three patient scenarios: hyperthyroid Graves' disease, subclinical hyperthyroidism and nontoxic goitre. RESULTS: The response rate was 40%. For the scenario of an initial presentation of Graves' disease, 80%, 19% and 0.4% of respondents preferred thionamide, radioiodine or thyroidectomy, respectively. There were inconsistencies in respondents' recommendations on radioiodine dose, the use of pre- and post-radioiodine supplementary treatments, timing of a repeat dose, and the use of radioiodine in thyroid eye disease. For the case of subclinical hyperthyroidism, one-third of respondents would generally initiate treatment. The majority were more likely to treat subclinical hyperthyroidism in the presence of paroxysmal atrial fibrillation or osteoporosis. If a decision were made to treat subclinical hyperthyroidism, 63%, 35%, 1% and 0.4% would recommend radioiodine, thionamide, beta-blocker and thyroidectomy, respectively. For the scenario of nontoxic goitre, 62%, 21%, 13% and 5% favoured observation, thyroidectomy, radioiodine and thyroxine, respectively. CONCLUSIONS: There remain significant differences in several aspects of clinical practice relating to the use of radioiodine treatment for benign thyroid disorders in the UK.
Vaidya B, Williams GR, Abraham P, et al., 2008, Radioiodine treatment for benign thyroid disorders: results of a nationwide survey of UK endocrinologists, CLINICAL ENDOCRINOLOGY, Vol: 68, Pages: 814-820, ISSN: 0300-0664
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- Citations: 54
Guillot PV, Abass O, Bassett JHD, et al., 2008, Intrauterine transplantation of human fetal mesenchymal stem cells from first-trimester blood repairs bone and reduces fractures in osteogenesis impertecta mice, BLOOD, Vol: 111, Pages: 1717-1725, ISSN: 0006-4971
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- Citations: 130
Bassett JHD, Williams AJ, Murphy E, et al., 2008, A lack of thyroid hormones rather than excess thyrotropin causes abnormal skeletal development in hypothyroidism, MOLECULAR ENDOCRINOLOGY, Vol: 22, Pages: 501-512, ISSN: 0888-8809
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- Citations: 89
Cegla J, Williams GR, 2008, The short synacthen test: a short survival guide, Foundation Years Journal, Vol: 2, Pages: 306-308
Bassett JHD, Lu Y, Bernstein ND, et al., 2008, Biological Effects of Thyroid Hormone on Bone, 13th International Congress of Endocrinology, Publisher: MEDIMOND S R L, Pages: 175-+
Ghaffar A, Bassett JHD, Williams GR, 2008, Normocalcemic primary hyperparathyroidism, Reviews in Endocrinology, Vol: 2, Pages: 38-40
Murphy E, Glueer C, Reid DM, et al., 2008, Effect of thyroid status on the skeleton in post-menopausal women: The OPUS study, CALCIFIED TISSUE INTERNATIONAL, Vol: 82, Pages: S46-S46, ISSN: 0171-967X
O'Shea PJ, Guigon CJ, Williams GR, et al., 2007, Regulation of fibroblast growth factor receptor-1 (Fgfr1) by thyroid hormone: Identification of a thyroid hormone response element in the murine fgfr1 promoter, ENDOCRINOLOGY, Vol: 148, Pages: 5966-5976, ISSN: 0013-7227
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- Citations: 11
Williams AJ, O'Shea PJ, Williams GR, 2007, Complex interactions between thyroid hormone and fibroblast growth factor signalling., Curr Opin Endocrinol Diabetes Obes, Vol: 14, Pages: 410-415
PURPOSE OF REVIEW: Thyroid hormone and fibroblast growth factors are critically important for normal development. Recent evidence points to complex interactions between thyroid hormone and fibroblast growth factors that regulate cell proliferation and differentiation. We discuss mechanisms of thyroid hormone and fibroblast growth factor action, and identify downstream signalling responses that offer opportunities for regulatory crosstalk. RECENT FINDINGS: Thyroid hormone action is mediated by nuclear receptors that regulate gene expression in response to thyroid hormone. Recent studies have shown thyroid hormone also acts at the cell membrane via the alpha(V)beta(3) integrin receptor and these actions also communicate with nuclear responses to thyroid hormone. Fibroblast growth factors act via receptor tyrosine kinases to stimulate second messenger pathways that also communicate with nuclear events. Several common pathways, including mitogen-activated protein kinase, phosphatidylinositol 3-kinase, and signal transducer and activator of transcription signalling, are activated by thyroid hormone and fibroblast growth factor, and may act as points of convergence for interaction in tissues, such as bone, central nervous system and heart, as well as in the extra-cellular matrix and during angiogenesis. SUMMARY: Although there is convincing evidence that thyroid hormone and fibroblast growth factors interact widely, little is known about molecular mechanisms that determine this interplay. Future research in this expanding field may result in identification of new pharmacological targets for manipulation of cell proliferation and differentiation.
Perz JB, Marin D, Szydlo RM, et al., 2007, Incidence of hyperthyroidism after unrelated donor allogeneic stem cell transplantation, LEUKEMIA RESEARCH, Vol: 31, Pages: 1433-1436, ISSN: 0145-2126
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- Citations: 6
Bassett JHD, Nordstrom K, Boyde A, et al., 2007, Thyroid status during skeletal development determines adult bone structure and mineralization, MOLECULAR ENDOCRINOLOGY, Vol: 21, Pages: 1893-1904, ISSN: 0888-8809
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- Citations: 92
Williams GR, 2007, Hypogonadal bone loss: Sex steroids or gonadotropins?, ENDOCRINOLOGY, Vol: 148, Pages: 2610-2612, ISSN: 0013-7227
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- Citations: 12
Bassett JHD, O'Shea PJ, Sriskantharajah S, et al., 2007, Thyroid hormone excess rather than thyrotropin deficiency induces osteoporosis in hyperthyroidism, MOLECULAR ENDOCRINOLOGY, Vol: 21, Pages: 1095-1107, ISSN: 0888-8809
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- Citations: 127
Harvey CB, Bassett JHD, Maruvada P, et al., 2007, The rat thyroid hormone receptor (TR) Δβ3 displays cell-, TR isoform-, and thyroid hormone response element-specific actions, ENDOCRINOLOGY, Vol: 148, Pages: 1764-1773, ISSN: 0013-7227
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- Citations: 33
Galliford TM, Bernstein ND, Bassett JHD, et al., 2007, Contrasting roles for thyroid hormone in the developing and adult skeleton, Hot Thyroidology, Vol: www.hotthyroidology.com/editorial_172.html
Bassett JHD, O'Shea PJ, Chassande O, et al., 2006, Analysis of skeletal phenotypes in thyroid hormone receptor mutant mice, SCANNING, Vol: 28, Pages: 91-93, ISSN: 0161-0457
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- Citations: 5
Rabier B, Williams AJ, Mallein-Gerin F, et al., 2006, Thyroid hormone-stimulated differentiation of primary rib chondrocytes <i>in vitro</i> requires thyroid hormone receptor β, JOURNAL OF ENDOCRINOLOGY, Vol: 191, Pages: 221-228, ISSN: 0022-0795
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- Citations: 15
Foo JYA, Wilson SJ, Williams GR, et al., 2006, Measurement of pulse transit time using AT90S8535 microcontroller, MEASUREMENT, Vol: 39, Pages: 505-511, ISSN: 0263-2241
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- Citations: 5
Keenan N, Dhillo WS, Williams GR, et al., 2006, Unexpected shortness of breath in a patient with Cushing's syndrome, LANCET, Vol: 367, Pages: 446-446, ISSN: 0140-6736
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- Citations: 10
Bassett JHD, Swinhoe R, Chassande O, et al., 2006, Thyroid hormone regulates heparan sulfate proteoglycan expression in the growth plate, ENDOCRINOLOGY, Vol: 147, Pages: 295-305, ISSN: 0013-7227
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- Citations: 34
O'Shea PJ, Bassett JHD, Cheng S-Y, et al., 2006, Characterization of skeletal phenotypes of TRalpha1 and TRbeta mutant mice: implications for tissue thyroid status and T3 target gene expression., Nucl Recept Signal, Vol: 4
Bone development is extremely sensitive to alterations in thyroid status. Recently, we analyzed the skeletal phenotypes of mice with the dominant negative resistance to thyroid hormone (RTH) mutation PV targeted to either the thyroid hormone receptor (TR) alpha1 or beta gene. This perspective summarizes our findings to date and explores the wider implications for thyroid status and T3 target gene expression in individual tissues.
Murphy E, Bassett JHD, Williams GR, 2006, Disorders of calcium metabolism, The Practitioner, Vol: 250, Pages: 4-8
Barnard JC, Williams AJ, Rabier B, et al., 2005, Thyroid hormones regulate fibroblast growth factor receptor signaling during chondrogenesis, ENDOCRINOLOGY, Vol: 146, Pages: 5568-5580, ISSN: 0013-7227
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- Citations: 59
Martin N, Williams GR, 2005, Vitamin D deficiency, Horizons in Medicine, Editors: COR, Pages: 193-201, ISBN: 9781860162534
O'Shea PJ, Bassett JHD, Sriskantharajah S, et al., 2005, Contrasting skeletal phenotypes in mice with an identical mutation targeted to thyroid hormone receptor α1 or β, MOLECULAR ENDOCRINOLOGY, Vol: 19, Pages: 3045-3059, ISSN: 0888-8809
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- Citations: 102
Galliford TM, Murphy E, Williams AJ, et al., 2005, Effects of thyroid status on bone metabolism: a primary role for thyroid stimulating hormone or thyroid hormone?, Minerva Endocrinol, Vol: 30, Pages: 237-246, ISSN: 0391-1977
Thyroid hormones are essential for normal skeletal growth and the maintenance of bone mass in adulthood, although their mechanism of action in bone is poorly understood. Hypothyroidism causes impaired bone formation and growth retardation whereas thyrotoxicosis results in accelerated growth, advanced bone age and decreased bone mass. Adults with thyrotoxicosis or a suppressed thyroid stimulating hormone (TSH) from any cause have an increased risk of osteoporotic fracture. Conventionally, bone loss in thyrotoxicosis has been regarded as a direct consequence of thyroid hormone excess acting locally on bone. Recently, however, it has been proposed that TSH may be a direct negative regulator of bone turnover acting via the TSH receptor on both osteoblasts and osteoclasts. Thus, TSH deficiency could be partly responsible for the skeletal loss seen in thyrotoxicosis. Here we provide an overview of the molecular actions of thyroid hormone in bone and discuss in detail the current evidence relating to a possible role for TSH in bone metabolism.
Williams GR, 2005, Thyroid and bone, 2nd Joint Meeting of the European-Calcified-Tissue-Society/International-Bone-and-Mineral-Society, Publisher: ELSEVIER SCIENCE INC, Pages: S111-S111, ISSN: 8756-3282
Bassett JHD, O'Shea PJ, Nordstrom K, et al., 2005, Disruption of intramembranous and endochondral bone development in TR alpha 2 null mice, 2nd Joint Meeting of the European-Calcified-Tissue-Society/International-Bone-and-Mineral-Society, Publisher: ELSEVIER SCIENCE INC, Pages: S225-S225, ISSN: 8756-3282
Freitas FRS, Capelo LP, O'Shea PJ, et al., 2005, The thyroid hormone receptor β-specific agonist GC-1 selectively affects the bone development of hypothyroid rats, JOURNAL OF BONE AND MINERAL RESEARCH, Vol: 20, Pages: 294-304, ISSN: 0884-0431
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- Citations: 43
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