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Re: Betrayed and put into what type of condition? Phillipa

Posted by Larry Hoover on April 2, 2007, at 12:18:29

In reply to Re: Betrayed and put into what type of condition? Larry Hoover, posted by Phillipa on April 1, 2007, at 13:07:57

Okay, so your blood work was last done six weeks ago, you're going to get more done, and you're confused about having markers for both Hashimoto's thyroiditis, and Grave's disease.

Here's an excellent little summary review of autoimmune thyroiditis:

What you'll see there is that both diagnoses are one and the same thing. The only difference is functional, i.e. if your thyroid hormone is high and your TSH low, they call it Grave's, whereas the alternative is called Hashimoto's. The confusing aspect of this is the two names. Hashimoto's is a remitting-recurring disorder, often punctuated by episodes of hyperthyroid (i.e. Hashimoto's can look like one kind of Grave's disease.). Also, anxiety and depression are commonplace with autoimmune thyroiditis. There can even be some rather severe neurological difficulties arising from it. The idea is to get your antibody levels down. There have been some very noteworthy trials of selenium supplementation, which reduce antibody levels dramatically. It really can't hurt you to give that a try. Your dose should be 200 mcg/day of selenium. You can get it anywhere..... Walmart, for example.

Here's another good article. On the 2nd page, there is an excellent description of the symptoms from acute thyroiditis. I wonder if that's exactly what you're feeling....

There is no fast way to change thyroid function, as the blood serum contains proteins which absorb thyroid hormone like sponges. You've got to stick with the changes you make, to let them become noticeable. I'm sorry this is so hard for you, but your new pdoc is probably right about your psych problems arising with the thyroiditis. Even knowing that, though, doesn't mean we can predict how best to treat your symptoms. You still have to experiment.


Biofactors. 2003;19(3-4):165-70.
Selenium in the treatment of autoimmune thyroiditis.
Gartner R, Gasnier BC.
Department of Endocrinology, Medizinische Klinik Innenstadt, University of Munich, D-80336 Munich, Germany.

We recently conducted a prospective, placebo-controlled clinical study, where we could demonstrate, that a substitution of 200 microg sodium selenite for three months in patients with autoimmune thyroiditis reduced thyroid peroxidase antibody (TPO-Ab) concentrations significantly. Forty-seven patients from the initially 70 patients agreed to participate in a follow-up cross-over study for further six months. One group (n = 13), which initially received selenium continued to take 200 microg sodium selenite (Se-Se), one group stopped taking selenium (Se-0) ( n = 9), another group which received placebo started to take 200 microg selenium (n = 14) (Plac-Se) and the last group was without selenium substitution (Plac-0) (n = 11). TPO-Ab concentrations were measured at beginning and the end of the study. In the Se-Se group, the TPO-Ab concentrations further significantly p = 0.004) decreased from 625 +/- 470 U/ml to 354 +/- 321 U/ml, in the Se-0 group the TPO-Ab concentrations increased significantly p = 0.017) from 450 +/- 335 to 708 +/- 313 U/ml. In the placebo group, the TPO-Ab concentrations in those patients who were followed without selenium substitution were unchanged (1351 +/- 940 vs. 1724 +/- 1112 U/ml, p = 0.555). In contrast, the patients who received 200 microg sodium selenite after placebo, the TPO-Ab concentrations decreased significantly (p = 0.029) from 1182 +/- 723 to 643 +/- 477 U/ml.

J Endocrinol. 2006 Jul;190(1):151-6.
Selenium treatment in autoimmune thyroiditis: 9-month follow-up with variable doses.
Turker O, Kumanlioglu K, Karapolat I, Dogan I.
Thyroidology Unit, Department of Nuclear Medicine, GATA Haydarpasa, Istanbul, Turkey.

The aim of this study is to investigate the long-term (9 months) effects of variable doses (200/100 microg/day) of L-selenomethionine on autoimmune thyroiditis (AIT) and the parameters affecting the success rate of this therapy. The present study was designed in three steps: (1) 88 female patients with AIT (mean age = 40.1 +/- 13.3 years) were randomized into two groups according to their initial serum TSH, thyroid peroxidase antibody (TPOAb) concentrations, and age. All the patients were receiving L-thyroxine to keep serum TSH <or=2 mIU/l. Group S2 (n = 48, mean TPOAb = 803.9 +/- 483.8 IU/ml) received 200 microg L-selenomethionine per day, orally for 3 months, and group C (n = 40, mean TPOAb = 770.3 +/- 406.2 IU/ml) received placebo. (2) 40 volunteers of group S2 were randomized into two age- and TPOAb-matched groups. Group S22 (n = 20) went on taking L-selenomethionine 200 microg/day, while others (group S21) lowered the dose to 100 microg/day. (3) 12 patients of group S22 (group S222) went on taking L-selenomethionine 200 microg/day, while 12 patients of group S21 (S212) increased the dose to 200 microg/day. Serum titers of TPOAb decreased significantly in group S2 (26.2%, P < 0.001), group S22 (23.7%, P < 0.01) and group S212 (30.3%, P < 0.01). There were no significant changes in group C and group S222 (P > 0.05). TPOAb titers increased significantly in group S21 (38.1%, P < 0.01). A significant decrease in thyroglobulin antibody titers was only noted in group S2 (5.2%, P < 0.01). L-selenomethionine substitution suppresses serum concentrations of TPOAb in patients with AIT, but suppression requires doses higher than 100 microg/day which is sufficient to maximize glutathione peroxidase activities. The suppression rate decreases with time.




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