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Thyroid Disorders Message Board

Thyroid Disorders Board Index

Given I have both Hashimoto's and Graves, and lived through this HADES... I will bite and give my 2 cents here.

By definition: Hashitoxicosis is an autoimmune thyroid disorder that is being recognized more and more. However some MDs refuse to acknowledge it at this time. This disorder I will label HTC is in which individuals with autoimmune hypothyroidism (Hashimoto's thyroiditis -HT ) experience intermittent or sporadic periods where they also have symptoms of hyperthyroidism. These sufferers can be described as having both HT and Graves' disease if the antibodies associated with both diseases are present.

How does HTC manifest? Well it can be complicated, but the disease process in focuses around the thyroid cell destruction and periodic thyroid tissue stimulation. Thyroid peroxidase and thyroglobulin antibodies cause thyroid cell inflammation and destruction. As thyroid cells die, their stored supplies of thyroid hormone (T4) are suddenly released into the blood circulation. These sudden bursts of thyroid hormone are responsible for the fleeting symptoms of hyperthyroidism. It makes medicating difficult, often a patient thinks that they need to have their medications adjusted and they suspect that their thyroid medication is too high. On other days, when they're dragging, depressed and experiencing weight gain, they suspect that their thyroid hormone replacement dose is too low. It is a sucky thyroid roller coaster.. but that is the Hashimoto's component to this issue.. what if you have the Graves antibodies as well? How do they play in the game?

Blocking TSH receptor antibodies, Thyroid binding inhibiting immunoglobulins (TBII) and thyroid stimulating immunoglobulins (TSI or stimulating TSH receptor antibodies) that are present as have one purpose. They trick, fool, and expect the thyroid to make more T4 and T3 for release and use in the body. Well how is this bad? How does this play well with Hashimoto's? It doesn't. Increasing the tissue TPO and TG activity to increase T4 production and shipment ticks Hashimoto's TPOAb and TGAb off big time. They increase and have to work harder to kill off that which they consider dangerous and foreign invaders. As a result your periods of hyperT due to reserve T4 release become more dramatic and violent.

All in all if you have TSI, TRAb, TBII and TPOAb and TGAb you are in for a long ride. Your thyroid is a battle ground and your body will have to hand the fall out. You will have to watch your Ft3 and Ft4 levels like a hawk and treat your resultant symptoms accordingly. This tends to mean managing each separately. I have to treat heart issues with a short lived beta-blocker. I also had a standing order of prednisone to take and suppress my immune system when the war between hyperT and hypoT got to difficult. It's not uncommon in one's lifetime to have HT, GD, primary myxedema and Hashitoxicosis manifest and be dominant at different times. My GD was dominant during my pregnancy.. then HTC took over, now I am pretty much HT. I did enjoy many a day with myxedema.. and that sucks as well. It is all controllable and treatable. You just have to stay up on your own care and not let an MD ignore your issues as they arise. In the end Hashimoto's will win because it will see all thyroid tissue destroyed.. no matter what. Graves antibodies and effects depend on having living functional thyroid tissue. If there is not thyroid the antibodies sit and twiddle their psuedothumbs.


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