Thethyroidhormone,thyroxine(T4)isproducedbythethyroidgland.Animportantcomponentinthesynthesisisiodine.Themajorformofthyroidhormoneinthebloodisthyroxine(T4).ThyroxineisconvertedtotheactiveT3(threetofourtimesmorepotentthanT4)withincellsbydeiodinases(5"-iodinase).Thyroxine-bindingglobulin(TGB)isthemajorcarrierproteinforcirculatingthyroidhormone.Onlyaverysmallfractionofthecirculatinghormoneisfree(unbound)-T40.03%.Whenthyroidhormoneisbound,itisnotactive,sotheamountofFT3/FT4iswhatisimportant.Forthisreason,measuringtotalthyroxineinthebloodcanbemisleADIng.TheconcentrationoffreethyroidhormonesinthebloodisregulatedbyanegativefeedbackmechanisminvolvingTSH.ThebindingofT4byTBGplaysakeyroleinthisfeedbackmechanismandthemostsignificantchangesthatoccurinT4bindingcapacityaretheresultofalterationsinTBG.ChangesinthecirculatinglevelsofTBGwillresultinaproportionalincreaseordecreaseintheconcentrationoftotalT4.However,measurementofserumFT4isunaffectedbychangesinT4proteinbindinglevelsandthereforecorrelateswellwiththefunctionalthyroidstateinmostindividuals.FactorsresponsIBLefordiscrepanciesbetweenserumtotalT4levelsandtruethyroidstatesincludeTBGconcentration,estrogenichormones(pregnancy,oralcontraceptivesandestrogen)anddrugsthatbindtoTBGpreventingitsbindingtoFT4Thethyroninesactonthebodytoincreasethebasalmetabolicrate,affectproteinsynthesisandincreasethebody"ssensitivitytocatecholamines(suchasadrenaline)bypermissiveness.Thethyroidhormonesareessentialtoproperdevelopmentanddifferentiationofallcellsofthehumanbody.Thesehormonesalsoregulateprotein,fat,andcarbohydratemetabolism,affectinghowhumancellsuseenergeticcompounds.Numerousphysiologicalandpathologicalstimuliinfluencethyroidhormonesynthesis.Thyrotoxicosisorhyperthyroidismistheclinicalsyndromecausedbyanexcessofcirculatingfreethyroxine,freetriiodothyronine,orboth.BothT3andT4areusedtotreatthyroidhormonedeficiency(hypothyroidism).