Graves after all.

Well, my TSI is through the roof so I have Graves after all, and maybe Hashimotos too, but I don't know how to tell for sure.

Here's an update from my Graves group about antibodies. Again, if you are about to die of boredom, you can always quit reading, but for me this was riveting!

>Your doc is right that some people with TPOab wont ever go hypO. Did you know that people who have been choked or hit in the throat can also have TPOabs? All it takes to create TPOabs is to have some thyroid cells break (from any reason). So TPOabs aren't what causes Hashi's - they are just the "markers" that you might have that disease. (which is caused by lymphocytic infiltration which breaks open the cells).

So its not really accurate to call TPOabs "Hashi's antibodies". They are antibodies that appear when a thyroid cell has been ruptured. So you could have a slight injury that doesn't affect function, but still have positive TPOabs (which can self perpetuate since they themselves can bring on more inflammation via complement immune cells).

When a person has lymphocytic infiltration, the TPOabs are usually the first sign this has occured. It's the quickest and easiest method we have to check for broken thyroid cells at this time. As far as Blocking TRab being a "Hashi's" antibody - there are still a LOT of docs/researchers who believe this. In the past, any antibody that cause "HYPER" was a "Graves" antibody and any antibody that caused "HYPO" was a Hashi antibody. They didn't fully understand how they caused these different issues.

But NEW research is showing that the Graves hyper-causing antibody (TSab, aka TSI) may actually be the SAME antibody that causes blocking TRab hyPO. The ONLY change is that the antibody is now binding to a different spot (epitope) on the TSH receptor (without doing any destruction themselves).

In fact, some researchers don't even call it "Graves disease" anymore - they call this disease "TSH Receptor Autoimmunity", which can shift from stimulation to blocking randomly; hyper to hypO etc. No thyroiditis involved at all. If the same antibody causes both hyPEr and hypO, then it must be one disease.

Hashimotos is "lymphocytic infiltration into follicular cells causing chronic thyroiditis". The TSH receptor doesn't play a part in this disease. The cells involved are thyroid follicular (inner) cells that are destroyed gradually.

Indeed, blocking TRab can make the hypO of Hashimotos *WORSE*, but the Blocking TRab are STILL part of TSH Receptor Antibodies. They aren't a direct component of the destructive Hashi's thyroiditis.

The theory that TSab and TBab are probably the same antibody is so new that it's going to take more research and more time before clinicians begin to understand that Hashi's is chronic destruction of cells -- something that blocking TRab don't cause (except perhaps via antibody complement).

Until scientists can actually test to distiguish more easily between the different hypO's; ~ between TSH receptors that have been blocked by TBab ~ or from a thyroid cell that has no function left (Hashis), Some docs will probably continue to label ANY autoimmune-hyPO as "Hashimotos thyroiditis".

But other docs are already calling this "Hypothyroid Graves" or "Euthyroid Graves" (stimulating and blocking TRab at the same time).

But the fact is - there are people with TBab that have NO thyroiditis at all. So these two diseases - Hashimotos Thyroiditis vs HypO- Graves - are completely distinct, BUT can be overlapping.

I agree with your doc that TPOabs are probably going to be around forever, just due to how they can perpetuate inflammation of the thyroid. TRab, on the other hand, CAN be brought under control and go into remission. And that's why it's SO COOL he's willing to let you try B&R to get rid of them! :D

Just make sure to keep the TSH receptors from being overstimulated into becoming an antigen again (ie Keep TSH low). <

Then here are my lab results (which took what seemed to me to take forever!)
antibody tests:
TSI is 564% (0-129%)
TPO 1607 (not the 4000+ needed to qualify for biolynk unfortunately)
thyroid function tests:
TSH less than .0004
FT4 2.48 (0.614-1.76)
TT3 341 (85-205)

>The TSI number is one of the TRabs - is the TRab that causes stimulation (thyroid stimulating immunoglobulins).

The number 564% is very high - and comes from the percentage of receptor stimulation when healthy,normal receptors are exposed to your blood. This test only picks up the stimulation caused by antibodies. It doesn't pick up any non-stimulating blocking they may be doing.

Total TRab (TBII) is the other test. This measures the FULL amount of TRab you have. When you have high TSI, it is useless to get this test because it will show high. (since TSI is high).

When TSI drops down to under 200, that's when you'll want to monitor the FULL amount of TRab antibodies - thats because you wouldn't want to stop therapy while these are highly active.

If Total TRab (TBII) is still showing high while your TSI is under 200, then this indicates that your disease is still highly active (despite probably having normal or low thyroid hormones) and those other TRab can switch back to stimulating any time after you stop therapy. This is when B&R comes into play and can keep you on track
for remission - it will just take longer than usual.<