Guest guest Posted May 4, 2009 Report Share Posted May 4, 2009 Angel, You wrote: > ... some patients have binding > > by auto-antibodies to the T4 stopping it from being turned into T3. > this is why they need to > > take Armour or T3 , as the T4 is not being used properly. I think you are conflating two different issues. Binding is a serum storage function of the enzymes thyroid binging globulin, prealbumin, and albumin. These all bind about equally with T4 and T3, but the bound form is protective, effectively holding T4 and T3 in reserve in the blood. Binding slows deiodization to T2 and T1, so both are available longer. Without binding, the half lives of both would be much shorter. The bound forms are effectively in equilibrium with the frees. As FT3 and FT4 are converted and used, the binding function releases and more free forms are made available to the cells. That is why binding is called a storage function. In contrast, the antibodies attack either thyroid peroxidase (TPO) or thyroglobulin (Tg, not the same as thyroid binding globulin), which are both precursors of T4 production and binding. Thus, anti-TPO prevents the gland from producing T4. TPO is also involved in conversion, so antibodies to this enzyme do interfere a bit with conversion, but this is by attacking the TPO and not by binding to T4. This is similar to the action of the drugs propylthiouracil and methimazole, which are used to treat Grave's. Conversion problems are most often associated with a lack of the 5'-deiodinase or to production of excess RT3. Chuck Quote Link to comment Share on other sites More sharing options...
Guest guest Posted May 4, 2009 Report Share Posted May 4, 2009 Thanks for putting that in Chuck I was just asked how Hashis intefered with conversion, thanks for explaining luv Dawnx Quote Link to comment Share on other sites More sharing options...
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