Dear Medical Community =)
I was diagnosed with Hashimoto's several years ago. My TPOab was near 6,000.
TSH was in the range that would be considered normal for normal people. I have been taking medication since 2003. My labs have not come back normal once yet.
I still feel like absolute garbage. I hurt all the time. I'm tired all the time. My bones ache and I can't hold information in my head long enough to do basic calculations. Finally, my hair is falling out and my skin has erupted with a vengence, amongst a variety of other symptoms that I don't have the energy to repeat here.
I have attempted to examine these problems from just about every possible medical perspective. I have seen professionals in each of the following fields: general medicine, infectious disease, endocrinology, neurology, rheumatology, gynecology, and dermatology. So far, the only answer they have really offered is that I have Hashimoto's (and an
ovarian cyst). Needless to say, that really doesn't help much...
When I ask about why my thryoid antibodies are SO high, I am told, "We don't treat for antibodies, we treat for
TSH." While I understand that this is a skillful, but not incorrect evasion of the question =), and while I understand that this is what a large majority of the literature states, I have an absolute need to throw my question out there in the hope of finding SOMEONE who may have, in the course of his or her career, run across SOME obscure study addressing this question definitively or otherwise.
Antibodies are typically made by the body in response to invasive pathogens or in response to inflammatory disease processes, correct? If antibody titres are diagnostically useful in identifying and measuring immune responses to pathogens and inflammatory conditions, (
rheumatoid arthritis, for example) then why is it not considered clinically significant in Hashimoto's thryoiditis? Is there a specific reason why A is true in situation 1 and not true in situation 2?
I understand that we can't assume that what is true in one situation can be generalized to suit all situations; yet, it seems this is a question which, in comparison to the more visibly disabling diseases, hasn't been very well studied. Is there ANYONE out there who can tell me:
(1) Why my antibodies are SO high compared to the average Hashi patient.
(2) Why the levels haven't fallen in response to the medication.
(3) Why antibodies are considered the cornerstone of diagnosis for this disease, but then are not considered clinically significant in evaluating the progression of this disease.
(4) What I should do the next time a doctor tells me that the bone
pain is a result of
depression =)
Any information you might have (or might have heard of) would be very helpful in directing my efforts to find a treatment that actually makes me feel better. If anyone is up for a research project, or if you know of anyone who is looking for research subjects, I would truly appreciate the reference!
