Help with Thyroid Test Results Please

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These are my test results

Thyroid Panel With TSH TSH 2.950 (Reference Range: uIU/mL 0.450 - 4.500)

Thyroxine (T4) 9.7 ug/dL (Reference Range: 4.5 - 12.0)

T3 Uptake 33 % (Reference Range: 24 - 39)

Free Thyroxine Index 3.2 (Reference Range: 1.2 - 4.9)

Thyroxine (T4) Free, Direct, S T4, Free(Direct) 1.68 ng/dL (Reference Range 0.82 - 1.77)

Antithyroglobulin Ab Thyroglobulin, Antibody 3.0 High IU/mL (Reference Range: 0.0 - 0.9)
Please Note: Low positive Thyroglobulin antibodies are seen in a portion of the asymptomatic populations. Antithyroglobulin antibodies measured by Beckman Coulter Methodology

Reverse T3, Serum 20.5 ng/dL (Reference Range: 9.2 - 24.1)

Thyroid Peroxidase (TPO) Ab 13 IU/mL (Reference Range: 0 - 34)

Triiodothyronine,Free,Serum 2.4 pg/mL (Reference Range: 2.0 - 4.4)

I've been taking l-selenomethionine and my TPO Antibodies went down from around 500 to 13! Wow. It really works! I'm confused about the TSH. It went from almost 0 to 2.9. Not sure what is going on there. I am not doing anything different or taking a different dose of synthroid so I assume another part of my thyroid was destroyed by my immune system in some way.

My question is the high amount on the antithyroglobulin antibodies. I don't even know what that is. I got the test through an online lab and it was included with the TPO antibody test. I can't really get a clear description on this type of antibody through the internet. Does anyone know if it is something to worry about? All I get is it is some autoimmune reaction to a protein in the thyroid. The "please note" message under the results seems to indicate my positive results are on the low end. I think that is what they are implying. Does anyone else here have these antibodies? Do you know what it means?
 

drob31

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Antibodies Are The Definitive Test for Hashimoto’s
TPO and TgAb antibodies, however, are considered the definitive test for whether or not you have Hashimoto’s. Basically, if either one or both of these are found to be above the lab range values, then you are positive for the disease.
https://www.hashimotoshealing.com/understanding-hashimotos-antibodies/


I'm not sure how 3.0 compares to a higher value based on the range.
 

Ema

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The testing methodology for TgAb changed a couple of years ago so you have to be careful that you are comparing apples to apples. For the Beckman Coulter methodology, that is the correct range.

So you have some Tg antibodies. The pathological significance of this is unknown though it can indicate Hashi's (which you already know you have). Some healthy people also have Tg Abs. I don't know of any way to lower it at this time so I would not worry about it. The people who need to worry about it are those who don't have a thyroid due to cancer and are using it and thyroglobulin together to monitor for a recurrence of cancer.

Thyroid Panel With TSH TSH 2.950 (Reference Range: uIU/mL 0.450 - 4.500)
Thyroxine (T4) Free, Direct, S T4, Free(Direct) 1.68 ng/dL (Reference Range 0.82 - 1.77)
Reverse T3, Serum 20.5 ng/dL (Reference Range: 9.2 - 24.1)
Triiodothyronine,Free,Serum 2.4 pg/mL (Reference Range: 2.0 - 4.4)
This is my non-medical opinion based on my own experiences with thyroid treatment.

Most non-medicated people feel best with their TSH between 1-2. On thyroid meds, the TSH often falls much lower, sometimes even below the reference range. This does not equate to hyperthyroidism or signify increased risks to bones or heart health. Many doctors don't even bother with the TSH once a patient is medicated because it is of limited use in monitoring thyroid levels. Symptoms and free thyroid hormone levels are much more important in determining if a patient is properly medicated.

So, your FT4 is at the top of the range, your FT3 is at the bottom of the range, and your RT3 is high in range. This says to me that you are converting T4 poorly. Instead of getting FT3, the active thyroid hormone, you are getting an abundance of RT3 which does nothing to relieve hypothyroid symptoms.

Raising a T4 only med like Synthroid is unlikely to help improve this situation. The last thing you would want is for your FT4 to go up any higher...your RT3 would likely just go up and you are still left functionally hypothyroid.

If it were me, I would ask my doctor about switching to a T4/T3 containing med like Armour or Naturethroid or adding Cytomel (T3) to your current regime. You will probably need to lower your T4 as you add in the T3.

I would also consider working on your liver health since a lot of thyroid conversion is dependent on solid liver function.

Hope this is helpful.
 

Gondwanaland

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Someone share with me some useful links about atoimmune thyroiditis and thyroid physiology which I didn't have the time to study yet, so perhaps we could study them together:

http://www.nature.com/nrendo/journal/v9/n4/fig_tab/nrendo.2013.29_F2.html

I− is actively transported into the thyrocyte through a NIS. This element enters into the follicular lumen from the cytoplasm via the transporter pendrin. In the colloid, I− is oxidized by the TPO H2O2 system and is then used to iodinate tyrosyl residues in Tg, forming MIT and DIT. H2O2 is generated by the NADPH-dependent oxidase/peroxidase (DUOX). T4 and T3 are produced by coupling of iodinated tyrosyl intermediates (MIT and DIT), which are then endocytosed, hydrolysed in lysosomes and secreted into the bloodstream. Thyrocytes might accumulate oxidative damage as a result of constant exposure to H2O2 and/or an impairment of the antioxidant system during ageing. This phenomenon might induce morphological and functional damage, such as alterations in structure and antigenicity of Tg and TPO (ROS-modified molecules are shown in orange), responsible for several thyroid diseases, including those of an autoimmune or neoplastic nature. Abbreviations: DIT, diiodotyrosine; H2O2, hydrogen peroxide; I−, iodine; MIT, monoiodotyrosine; NIS, sodium-iodide symporter; Tg, thyroglobulin; TPO, thyroid peroxidase.
http://www.hindawi.com/journals/jtr/2013/182472/

Figure 1: Thyroglobulin and thyroid peroxidase in thyroid hormone biosynthesis. The essentiality of thyroglobulin and thyroid peroxidase is shown in this simplified diagram of thyroid hormone biosynthesis. Thyroglobulin acts as the skeleton in thyroid hormone synthesis. It is synthesized and glycosylated in the rough endoplasmic reticulum, and is exocytosed through the apical membrane. Thyroid peroxidase acts in three parts (a) it oxidizes iodine, (b) organifies iodide to the tyrosine residues to the thyroglobulin forming monoiodotyrosine and di-iodotyrosine (c) Couples monoiodotyrosine and di-iodotyrosine to either T4 or T3 (TPO: thyroid peroxidase, Tg: thyroglobulin, MIT: monoiodotyrosine, DIT: di-iodotyrosine, T4: thyroxine, and T3: triiodothyronine).
http://www.glowm.com/section_view/h...nd%20Tests%20of%20Thyroid%20Function/item/306

Fig. 1. Diagram of the major steps involved in thyroid hormone synthesis and secretion. Tg, thyroglobulin; DIT, diiodotyrosine; MIT, monoiodotyrosine; ECF, extracellular fluid; 5´D type I, 5´-iodothyronine deiodinase; TPO, thyroid peroxidase; TSH, thyroid-stimulating hormone. (Brent GA: Thyroid Hormones (T4, T3). In Conn PM, Melmed S [eds]: Endocrinology: Basic and Clinical Principles, p 291. Totowa, NJ, Humana Press, 1996.)
@picante
 

picante

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So, your FT4 is at the top of the range, your FT3 is at the bottom of the range, and your RT3 is high in range. This says to me that you are converting T4 poorly. Instead of getting FT3, the active thyroid hormone, you are getting an abundance of RT3 which does nothing to relieve hypothyroid symptoms.

Raising a T4 only med like Synthroid is unlikely to help improve this situation. The last thing you would want is for your FT4 to go up any higher...your RT3 would likely just go up and you are still left functionally hypothyroid.
This is how I understand it, too. The function of reverse T3 is to downregulate the metabolism in times of illness and starvation.
http://blog.zrtlab.com/clearing-up-...iodinases-and-thyroid-hormone-bioavailability
Reverse T3 (3,3’,5’-triiodothyronine, rT3) is a biologically inactive metabolite of thyroxine (T4) formed by selective deiodination; the active thyroid hormone T3 is formed by removal of an iodine atom in the outer ring of T4, while rT3 is formed by removal of an iodine atom in the inner ring of T4.
A normal ratio of T3/RT3 would be like a gentle brake so you don't speed up out of control; your ratio is more like skid marks on the pavement.

Triiodothyronine,Free,Serum 2.4 pg/mL (Reference Range: 2.0 - 4.4)
Reverse T3, Serum 20.5 ng/dL (Reference Range: 9.2 - 24.1)
When I was on dessicated pig thyroid about 8 years ago, I had my RT3 tested for the first time: my result was 207 pg/mL, almost exactly what yours is if you convert ng/dL to pg/mL.

At that time, the Yahoo T3 forum had a formula for calculating the ratio (which involved moving some decimal points around, since different labs were using different units). A minimum healthy ratio was said to be 20:1. Mine was 14.9 by that method.

My FT3 was higher than yours. By the same method, your ratio is 11.7. Dr. Wilson, Dr. Lowe, and several others have said that this is the best method we have of gauging cellular thyroid metabolism.

Nobody feels very good with their FT3 at the low end of the range, btw.
 

picante

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I think they're saying that the critical thing happening when antibodies start appearing is too much hydrogen peroxide exposure:
From Izzy's first diagram:
Thyrocytes might accumulate oxidative damage as a result of constant exposure to H2O2 and/or an impairment of the antioxidant system during ageing. This phenomenon might induce morphological and functional damage, such as alterations in structure and antigenicity of Tg and TPO
I know high H2O2 has been a concern of yours for quite a while, @Gondwanaland. (And I can't remember which antioxidant process is involved, at the moment.) This doesn't really explain why you have high Tg antibodies, while I have high TPO antibodies. Or why @Mya Symons had high TPO antibodies, and now has high Tg antibodies. (That's a real mystery! Have you had the Tg antibodies measured before now?)

I'm not sure selenomethionine had much to do with reducing my TPO antibodies. They came down from 500-something when I started taking T3-only, and were consistently 85-95 for years. Recently they've actually come down to 59! It may be from stopping vitamin D supplementation, which I did at my ND's suggestion because my calcitriol was high.
 

Gondwanaland

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Or why @Mya Symons had high TPO antibodies, and now has high Tg antibodies.
One year ago ( @ahmo ) and I listened to a webinar where a pharmacist mentioned this switch in antibodies and that he uses to treat his patients alternating the medication T3 - T4 (is that right @ahmo ?)

As I said I didn't have the time to study this myself yet, but apparently if you make too much thyroglobulin, the body will send antibodies against it. Then you treat it with _ _ _ _ (?) and the body will start making too much TPO (?), then you have to treat it by using _ _ _ _ (?)
 

picante

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One year ago ( @ahmo ) and I listened to a webinar where a pharmacist mentioned this switch in antibodies and that he uses to treat his patients alternating the medication T3 - T4 (is that right @ahmo ?)

As I said I didn't have the time to study this myself yet, but apparently if you make too much thyroglobulin, the body will send antibodies against it. Then you treat it with _ _ _ _ (?) and the body will start making too much TPO (?), then you have to treat it by using _ _ _ _ (?)
Very intriguing! The plot thickens.
 
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I think they're saying that the critical thing happening when antibodies start appearing is too much hydrogen peroxide exposure:
From Izzy's first diagram:


I know high H2O2 has been a concern of yours for quite a while, @Gondwanaland. (And I can't remember which antioxidant process is involved, at the moment.) This doesn't really explain why you have high Tg antibodies, while I have high TPO antibodies. Or why @Mya Symons had high TPO antibodies, and now has high Tg antibodies. (That's a real mystery! Have you had the Tg antibodies measured before now?)

I'm not sure selenomethionine had much to do with reducing my TPO antibodies. They came down from 500-something when I started taking T3-only, and were consistently 85-95 for years. Recently they've actually come down to 59! It may be from stopping vitamin D supplementation, which I did at my ND's suggestion because my calcitriol was high.

No, I never had an antithyroglobulin test. I didn't even know it existed and only got it because it was free with the TPO test. I have taken synthroid for years and always had high TPO antibodies. I really do think the l-selenomethionine did work for taking down the TPO antibodies. Nevertheless, it is just a number reduction. I'm still feeling the same.

Selenium and TPO antibody reduction: http://online.liebertpub.com/doi/abs/10.1089/thy.2007.0040
 
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One year ago ( @ahmo ) and I listened to a webinar where a pharmacist mentioned this switch in antibodies and that he uses to treat his patients alternating the medication T3 - T4 (is that right @ahmo ?)

As I said I didn't have the time to study this myself yet, but apparently if you make too much thyroglobulin, the body will send antibodies against it. Then you treat it with _ _ _ _ (?) and the body will start making too much TPO (?), then you have to treat it by using _ _ _ _ (?)
Wow. This sounds like a never ending cycle. I really need to spend some time looking for a naturopath or D.O. who knows about Hashimoto's. I'm moving back to Seattle soon. It will help to be in a big city instead of a small town -- more options.