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18 Thyroid International 2 2008Selected CommunicationsLewis Braverman and his colleagues, Boston MA,Albuquerque, NM, and Cary, NY, studied plasma, cordblood, and amniotic fluid iodide, and concluded that thehuman placenta, unlike that of the rabbit, was unableto concentrate iodide for the fetus.Angela Leung and colleagues, Boston, MA, reported thatcolostrum contained iodine in the range 27–385 μg/L(median 65 μg/L) but was not significantly associatedwith maternal UI. They postulated that dietary iodinewas available to nursing infants immediately at birth.Aranda N and colleagues, Queretaro, Mexico, applied toprostate cells lessons learned from treatment of breastcancer cell lines with molecular I 2 . They observed thatI 2 inhibited proliferation on prostate cell lines, whichwas reversible when I 2 was removed.Tran NQ and colleagues, Los Angeles, CA and Suwanee,GA, reported that TSH actively promoted perchloratetransport into thyroid cells in a dose dependent mannerand was nontoxic to cells as determined in an MTS cellproliferation assay.Marie Hansson and colleagues, Goteborg, Sweden,described sample variation for in vitro studies of iodinein thyroid tissues using X-ray fluorescence analysis.They found that tissues frozen at –20 °C gave resultscomparable with those obtained from fresh tissue,allowing the possibility of measuring iodine in smallsamples of benign or malignant tissues collected atsurgery and then stored.Steven Lamm and colleagues, Washington DC andKansas City, KS, described how the negative associationof serum thyroxine and urine perchlorate found forwomen of child bearing age with low iodine defined byUI was not found for those with low iodine defined bythe Urinary Iodine:Creatinine ratio (UICr).Takahiko Kogai and colleagues, Los Angeles, CA, reportedthat phosphoinositide-3-kinase (P13K) inhibitorsenhanced both iodide uptake and NIS mRNA expressionin FRTL5 cells treated with TSH. Radioiodide uptake butnot NIS mRNA expression was enhanced in papillarycancer BHP2-7 cells. The inhibitors alone, even in theabsence of TSH, promoted increased radioiodide uptake.They concluded that the inhibition of PI3K signalinghas a potential to increase the radioiodide accumulationin some differentiated thyroid cancer tissue.Okrojek R, Mainz, Germany, described proteome analysisof tear fluid in Graves’ orbitopathy (GO). Tear proteinswere analyzed by mass spectrometry (MS) usingSELDI-TOF MS arrays. The authors were able to identifyproteins which could serve as biomarkers for thediagnosis and follow-up parameters during treatmentfor GOJoanne Rovet and colleagues, Toronto, ON, studied subjectswith defined hypothyroidism in early pregnancyincluding contrast sensitivity (CS) conditions that tapregions of the visual neuroanatomic pathway. Theyfound that children with high TSH and low FT 4 hadlower CS compared to normal controls, whereas thegroups did not differ in visual acuity.Sanziana Roman, New Haven, CT, reported on calcitoninscreening in the US. The cost per test was $40compared to $ 23 for TSH. The prevalence of medullarythyroid carcinoma (MTC) was 0.78 % of thyroid nodules.Thus it cost approximately $ 5000 to detect onecase of MTC. They concluded that calcitonin screeningis feasible, with reduced mortality and a 13 % increasein cost, but that cost-effectiveness decision analysisstudies of routine calcitonin screening in patients withthyroid nodules are needed.Cristina Romei and colleagues, Pisa and Siena, Italy,demonstrated in a 10 year follow-up study that somaticRET mutation in MTC correlates with the presence oflymph node metastases at diagnosis, with a worse outcomein terms of persistence of disease and a significantlylower survival rate.
American Thyroid Association – Highlights of the 78 th Annual Meeting19Valter Boldarine and colleagues, Sao Paulo, Brazil,reported on an enhanced quantitative RT-PCR assay forblood thyroglobulin (Tg mRNA) using modified primersprepared from a region covering exons 40–41. Thisnew method for Tg mRNA quantification was reliable,allowed separation of patients free of disease from thosewith metastases, and could be an appropriate molecularmarker in the follow up of patients with DTC, especiallythose with positive TgAb.decreased growth plates, and elevated T 4 and TSH.Finally, the TSH receptor knockout animals have veryhigh levels of TSH with very low levels of T 4 . Theseanimals later develop severe osteoporosis that is notreversed with treatment with T 4 .On the same subject, Claudia Nakabashi, Sao Paulo,Brazil, reported that using a sensitive immunoassay forTg had comparable sensitivity in follow-up of patientswith DTC on T 4 suppression to measuring serum Tglevels after stimulation by inducing hypothyroidism.Raffaele Napoli, Naples, Italy, postulated that TSH itselfmay have an effect on vascular function independentfrom its role in stimulating thyroid hormone productionand release. They found that infusing high levels of TSHinto the brachial artery for 4 hours acutely and directlyaffects forearm blood flow and potentiates the vasodilatoryresponse to acetylcholine and the vasoconstrictoryresponse to norepinephrine.Stephen James and colleagues, Birmingham, UK, proposeda role for the monocarboxylate transporter MCT8independent of its T 3 transporting function. They foundthat repression of MCT8 by siRNA resulted in a significantincrease in proliferation in fetal embryonal NT2and placental JEG-3 cells in vitro, similar to that seenwith mutations of MCT8 reported in males with severepsychomotor defects. These results further extend theevidence of a potential role for MCT8 in the modulationof cell proliferation, independent of T 3 transport.The possibility that some of the effects of hypothyroidismon bone could be due to the high levels of TSH,rather than the low level of thyroid hormone, wasaddressed by Wendy Van der Deure and colleagues,Rotterdam, NL. They studied mice with total knockoutof the TRα gene, the TRβ gene or TSH receptor gene.Homozygous TRα1 knockout mice appear euthyroid,but have delayed ossification. In contrast, homozygousTRβ knockout mice have advanced ossification,
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