My mother's hypothyroid symptoms improved along with improved TSH and free T4 levels (she isn't on thyroid medication). TgAb are back to normal. TPOAb has dropped down from 1200 U to 250 U.
The doctor ordered a thyroid ultrasound and her results shows old thyroiditis; nodules have all disappeared on the right thyroid lobe (largest nodule was 1.2 cm) and 50% reduction in the left thyroid lobe (largest nodule was 1.6 cm); thyroid gland reduced in size with no goiter.
Dr Mark Hyman has an interesting article: "Glutathione: The Mother of All Antioxidants" to explain more about oxidative stress as well. Here is a study on oxidative stress and Hashi's...
Enhanced oxidative stress in Hashimoto's thyroiditis: inter-relationships to biomarkers of thyroid function. Clin Biochem. 2013 Mar;46(4-5):308-12...
Oxidative stress has been implicated in the pathogenesis of several inflammatory and immune-mediated disorders including Hashimoto's thyroiditis (HT). The objectives of the present cross-sectional investigation were to estimate serum glutathione (GSH) status and the activities of its recycling enzymes in HT and to explore their interrelationships with biomarkers of autoimmunity and thyroid function.
DESIGN AND METHODS:
Newly diagnosed females with HT (n=44) and 58 matched control subjects were recruited. Thyroid hormone profile, anti-thyroperoxidase anti-body (TPO-AB), anti-thyroglublin antibody (Tg-AB), thyroid volume (Tvol), urinary iodine excretion (UIE), GSH and the activities of glutathione peroxidase (GPx), glutathione reductase and gamma-glutamyltransferase were assessed.
Median UIE in HT was slightly but not significantly higher than that of controls. HT group exhibited higher levels of TSH, TPO-AB, Tg-AB and larger Tvol when compared with controls (P<0.001). The means of GSH and GPx in HT patients were significantly different from those of controls (P<0.001). In HT subjects, significant associations were seen between Tvol on TSH, GSH on TPO-AB, GSH on TSH and TPO-AB titers on TSH, respectively.
This is the first study to demonstrate a substantial reduction in GSH status in HT subjects. Secondly, the interrelationship between the GSH contents and TPO-AB titers in HT provides a preliminary data to support the notion that GSH diminution is a hallmark of in the events leading to oxidative stress activation and the development of immunological intolerance in HT. Further studies are required to elucidate the role of GSH in the etiology of down-regulation of thyroid function."
I was interested by your comments about oxidative stress, so I read through info about it and its relationship to hypothyroidism. I did not see anything that seemed to relate to Hashi's. How did you determine that your mother's Hashi' had gone into remission?
We have had some members who had their thyroid removed simply because they have Hashimoto's, however, they have ended up not doing much, if any, better following the TT than they did prior. Aside from that, it's quite rare for a doctor to be willing to remove a thyroid that might still be working, unless there's cancer present or the person has Graves or some other problem. Hashimoto's does not "turn into" cancer. Thyroid cancer is present in less than 5% of those with nodules and you don't even have nodules.
I don't know what you mean about the ENT refusing to operate because your TSH was too high and he feared you might go into thyroid storm on the table. One doesn't go into thyroid storm because of high TSH; one goes into thyroid storm because of high thyroid hormones.
All of that said, let's get down to business and figure out why your treatment isn't working. Most of the long standing members of this forum have Hashimoto's (including nodules), are on some form of thyroid replacement and are doing just fine.
First off, if you're on Synthroid, you should be getting tested periodically, for the thyroid hormones, Free T3, Free T4 and the pituitary hormone, TSH. If you have test results for those, please post them, along with reference ranges, which vary lab to lab and have to come from your own lab report.
If you aren't getting tested for these hormones, you need to find a doctor who will test them, because these are what determines the type of treatment you should be getting. You can't just be put on a medication, then never monitored and if that's what's happened, that's why you're not doing well. I can't imagine any doctor simply continuing to prescribe a given dosage of synthroid without monitoring the hormone levels in the patient, but if yours did, you need a new doctor, asap.
As far as other autoimmune diseases go, removing your thyroid will not prevent you from getting another one (or more) autoimmune. Autoimmunes run in families, though not every member of the family will get the same autoimmune(s). For instance, I have Hashimoto's and Pernicious Anemia, my son has Type I Diabetes and my daughter has SLE.
The first order of business is to post your most recent lab results and we can go from there.
The problem isn't the thyroid gland but the immune system. My mother did a lifestyle overhaul which reduced her oxidative stress and her Hashimoto's thyroiditis has gone into remission. You might be interested in this article: "What thyroid patients should know about Oxidative Stress."
When I'm stressed I have hyperthyroid flare ups. I've had both types of Hashitoxicosis but the Graves antibodies caused very hyperthyroid symptoms.
The Medical Journal Of European Endocrinology - Hashitoxicosis – Three Cases and a Review of the Literature...
"It should be pointed out that, especially in the US literature, the term ‘hashitoxicosis’ is sometimes used to describe an autoimmune thyroid disease overlap syndrome of Graves’ and Hashimoto’s disease. In this article the term is strictly limited to the ‘leakage’ symptoms of active Hashimoto’s disease."