# Thyroglobulin antibodies doubled in 3 months and endo says I shouldn't be worried?



## paperbag

Hi,

This is only my 2nd post here. I just had my thyroid tested for the first time in a long time in September. My TSH and T4 were in the normal range, but I had elevated anti-thyroglobulin. My thyroglobulin antibody was 36 IU/ml, and the range was 0-23.

I was retested yesterday, and now the thyroglobulin antibody is up to 66 IU/ml. So the anti-Tg has doubled in only three months.

The endocrinologist says I shouldn't be worried, because I don't have any antibodies to thyroid peroxidase (TPO). She said the Tg antibody was a very non-specific marker.

This doesn't make sense to me. Why do they even test anti-Tg if it doesn't matter? If it's so non-specific? What's the point?

I asked her yesterday when I saw her, what would be a high level of anti-Tg that I should worry about, and she said over 100. She said an anti-Tg level of 36 IU/ml was very mild, and some people wouldn't even consider that elevated.

That also confuses me. Why does their own lab flag it as elevated and show you the "High value" and show you that yours is higher than that, if it's not a problem? Are they just trying to freak you out needlessly? And then they tell you not to worry?

I am seriously concerned that my Anti-TG doubled in 3 months. That seems ridiculously fast. If that keeps up...well...it's not good.

But the endocrinologist just thinks all I need to do is come back every 6 months to re-check the antibody levels. Just wait, while you get sicker, until your thyroid is dead, and then they can start treating you for Hashimoto's. This seems insane to me. Whatever happened to prevention being more cost effective than treatment?

I feel like I'm just sitting here doing nothing while my body eats up my thyroid.


----------



## Andros

paperbag said:


> Hi,
> 
> This is only my 2nd post here. I just had my thyroid tested for the first time in a long time in September. My TSH and T4 were in the normal range, but I had elevated anti-thyroglobulin. My thyroglobulin antibody was 36 IU/ml, and the range was 0-23.
> 
> I was retested yesterday, and now the thyroglobulin antibody is up to 66 IU/ml. So the anti-Tg has doubled in only three months.
> 
> The endocrinologist says I shouldn't be worried, because I don't have any antibodies to thyroid peroxidase (TPO). She said the Tg antibody was a very non-specific marker.
> 
> This doesn't make sense to me. Why do they even test anti-Tg if it doesn't matter? If it's so non-specific? What's the point?
> 
> I asked her yesterday when I saw her, what would be a high level of anti-Tg that I should worry about, and she said over 100. She said an anti-Tg level of 36 IU/ml was very mild, and some people wouldn't even consider that elevated.
> 
> That also confuses me. Why does their own lab flag it as elevated and show you the "High value" and show you that yours is higher than that, if it's not a problem? Are they just trying to freak you out needlessly? And then they tell you not to worry?
> 
> I am seriously concerned that my Anti-TG doubled in 3 months. That seems ridiculously fast. If that keeps up...well...it's not good.
> 
> But the endocrinologist just thinks all I need to do is come back every 6 months to re-check the antibody levels. Just wait, while you get sicker, until your thyroid is dead, and then they can start treating you for Hashimoto's. This seems insane to me. Whatever happened to prevention being more cost effective than treatment?
> 
> I feel like I'm just sitting here doing nothing while my body eats up my thyroid.


Please read this....... http://www.drlowe.com/emailnewslette...0/11.20.10.htm
If you are not pleased with this doc and I don't think you are, please seek out another.

I am on your side 100% re all of this. Let us know;please!


----------



## lainey

Thyroglobin IS non specific--it is made by the thyroid, and some people naturally have antibodies to it. The presence of these particular antibodies are only useful as a marker in people who are being TREATED for thyroid cancer--specifically, these interfere with the measurement of thyroglobin, which in that case could indicate the regrowth of the thyroid after it has been removed.

*High* levels of these antibodies number in the thousands.

Seek a second opinion if you like, but I agree with this endo. You can't treat the antibodies, and you can't give thyroid medication to someone if their levels don't warrant it. All you probably need at this point is monitoring to see if your levels are falling out of the normal range, at which time treatment can begin.


----------



## paperbag

I am not sure you are correct on this. I admit I am new to thyroid problems, but I have some training in biochemistry.

I don't think thyroglobulin antibodies are only useful as a marker for people being treated for thyroid cancer. I believe this to be true, because when the doctor orders a "thyroid antibody" test, the lab automatically does both a TPO antibody test and a Tg antibody test. At least, that's how the hospital I go to does it. There is no separate box to check for the individual antibody tests. They always check both auto-antibodies.

While it is true that Anti-Tg interferes with measuring Tg, and that Tg needs to be measured in people with thyroid cancer, Anti-Tg interferes with measurement of Tg simply because the lab measures Tg using antibodies, and your body is already making anti-Tg antibodies. These auto-antibodies your body is making hide the Tg from the antibodies that the lab test uses. That's why they interfere with lab tests for Tg level in people with thyroid cancer.

High levels of Anti-Tg are...well...whatever they flag as high on the lab report. Mine are flagged as high, three times over the high reference value. It makes no sense to flag something as high, if it's not high. That just makes the patient nervous for no reason.

I can cite you a study in which L-thyroxine was used to lower antibody levels in people with normal thyroid function.

The first author is Duygu Yazgan Aksoy. The article is called "Effects of Prophylactic Thyroid Hormone Replacement in Euthyroid Hashiomto's Thyroiditis". Endocrine Journal, Volume 52, number 3, 2005


----------



## lainey

>>High levels of Anti-Tg are...well...whatever they flag as high on the lab report. Mine are flagged as high, three times over the high reference value. It makes no sense to flag something as high, if it's not high. That just makes the patient nervous for no reason.<<

Lab ranges can vary from place to place, and some labs give reference ranges, and some merely indicate if you are positive or negative.

Lab ranges are not always black and white. Liver function tests, for example, are not really "high" until they are several times above the range. Ditto for blood cell counts. Your antibodies are not really "high" by that standard, from my own anecdotal experience on these forums and seeing the results that people post. High, by those standards can run into the thousands. Perhaps thats why the endo gave you the brush off, because she sees a lot of these and has a different frame of reference on what "high" is.

Elevated antibodies can be found in the normal population--they are an indicator of ...... what? Possible disease process, yes. However, their mere presence doesn't indicate a need for treatment unless they significantly disrupt thyroid function.

You don't appear to have that happening yet, because your thyroid levels are normal. The presence of antibodies is not a guarantee that you will or won't have a problem. If your TSH levels are normal, the antibodies are significant only in the sense that you should monitor thyroid function to see if a problem develops.

As for your study, here is a link to the full text (and it would be nice if you included the link yourself): http://www.jstage.jst.go.jp/article/endocrj/52/3/337/_pdf

Did you notice that in the treatment group, their antibodies numbered in the thousands? Also, they were medicated to the point of being nearly clinically hyper--a state that is generally not considered healthy, or sustainable. Did you notice that in the untreated group, only one person became clinically hypothyroid during the study period? In the end, the conclusions point out that a healthy control was not used, so they could not be sure if their "effect" was due to the medication or a natural wane in the disease process, so they were not able to clearly demonstrate the effect of T4 medication. How can they presume that early treatment will forestall the development of thyroid disease, if they don't follow the patients in the treatment group afterward to see if they actually become clinically hypothyroid after the medication is withdrawn?

Who would want to start taking a medication before they need it, to slow the process of a disease that is going to cause them to need the medication in the end? How are you really preventing anything at all at that point? Could this result in people being treated unnecessarily, if not all of them go on to develop thyroid disease?

As I said, get a second opinion. At the moment, however, those ranges on the lab results are making "the patient nervous for no reason".


----------



## paperbag

The hospital I go to gives a reference range for everything. My anti-Tg was 3x over this. I'm sure values vary from place to place and at different times, but we can't dismiss every result with this reasoning that "it's all relative", since otherwise, what would be the point of ever testing your thyroid function?
All I know is, according to their specific tests, which have their own specific reference ranges, my antibodies are too high. Because lab tests to vary by lab, this would argue in favor of me getting a second opinion and a second test at a second hospital, not against getting a second opinion.

The central idea of my point, and the paper I cited, was that elevated anti-bodies do need to be treated. I could understand if the auto-antibodies are stable, and the thyroid function is stable, then just monitoring the patient seems reasonable.
But if the auto-antibodies are going up quickly, I don't think it makes sense to wait for things to get worse, to lose an organ entirely, before deciding it's time to do something about it.

The point is, the thyroid may be malfunctioning before you "see" it on the TSH or T4 values. Disease is progressive. It has to start and get worse. So the auto-antibodies increasing is a reasonable sign of this. There are people with confirmed Hashimoto's that have normal levels of T4 and TSH. That was the main concept of the paper I cited. The patients were "euthyroid".

I'm sorry I did not include the link to the paper, but I didn't remember where I found it, and I thought providing all the info I did would help.

In the treated and non-treated groups, both had anti-TPO antibodies in the thousands. But I'm was never referring to anti-TPO. I am referring to anti-Tg. The anti-Tg levels were between 0 and 2.3 AU. I have no idea what AU stands for though, so I'm having a hard time interpreting this part of the study. But it clearly shows that the anti-Tg antibodies decreased to 0 in the treated group, whereas they got worse in the non-treated group.

As for the patients being hyper-thyroid, the authors clearly state that "serum TSH levels were checked one month after treatment and maintenance dose was adjusted so that serum TSH levels were kept as low-normal (0.35 - 1.125 uIU/ml). All patient were re-evaluated at 3rd, 6th, and 9th months and serum TSH, FT4, FT3, Tg-AB and TPO-Ab were measured."

Yes I did notice that 1 person become hypothyroid. Isn't it interesting this only happened in the un-treated group? (And of course, by the way, the only way they could have known a patient was hypothyroid is because, as stated, they were monitoring everyone's thyroid levels to make sure they were euthyroid.)

I don't know if you are deliberately trying to confuse the findings or just don't understand. Their reference to not having a healthy control was specifically about the increases in CD8+ cells in both groups. They were looking at possible cellular mechanisms of the decreased levels of auto-antibodies, and the CD8+ cells were not it. That was it. It wasn't at all about the effect of the entire treatment. In their own words "LT4 treatment at doses keeping TSH at low-normal levels appears to be effective not only in decreasing the autoantibody levels but also in the goiter size. Although this immunomodulating effect cannot be explained through any alterations in lymphocyte sub-populations (though CD8+ levels increased it was independent of LT4 treatment), there appears to be an inhibitory effect of LT4 treatment on the ongoing disease process in Hashimoto's thyroiditis patients."

I'm not sure what you mean by how can they presume that early treatment will stall the disease. All patients already were confirmed to have Hashimoto's at the start of the study. That was one of the main points. They only treated patients with Hashimoto's.

Your question of who would want to take a medication before they need it, is begging the question. You are assuming they don't need it. This study showed that taking LT4 can decrease auto-antibodies, which presumably would prevent Hashimoto's in people in the first place. The patients had high antibody levels and confirmed Hashimoto's. If someone has high antibody levels that are going up, but doesn't have Hashimoto's yet, why wait to develop Hashimoto's? That was one of the central ideas. That you do need it to prevent the antibodies levels from getting so high that you get Hashimoto's.

The idea is prevention. Why wait to get the disease if you can prevent it. Why wait until you lose your thyroid until you start treating it? How many years do you have to suffer until your TSH levels and T4 levels are off and then someone starts helping you? The patients in this study clearly already had Hashimoto's but were euthyroid, so you could wait a lifetime.

To avoid treating patients unnecessarily, only treat patients whose antibody levels are going up rapidly, and who also have signs of the beginnings of Hashimoto's, such as increasing thyroid volumes as determined by ultrasonography.


----------



## lainey

>>All of the patients were positive for TP0-AB, where as 24.1% were negative for the Tg-Ab. No significant correlation was detected between antibody titer, thyroid volume and lymphocyte populations.<<

Do you mean to imply, that in a reliable study, they would be measuring the effect on the Tg-Ab when almost one quarter of the test subjects didn't have it in the first place? They actually say, that while other studies implicate Tg-Ab in the pathogenesis, this wouldn't be at work here because some of their subjects don't have it.

I checked the conclusions again and, it seems that, because of the cytological findings, they feel that the immune process may be independent of LT4 therapy, because there were no cytological changes in either of the subject groups. In the medicated study group, their antibodies went down, their goiters were reduced. They did not attribute the reduction of the antibodies to the LT4 therapy directly, and in this case it's my opinion that they were referring to the TPO antibodies primarily, as that is what was common to all subjects.

Are you sure you are not confusing the results of the study and how they apply to your results?

Unless you follow the patients afterward, to determine how many more actually become hypothyroid on their own after the medication from the study period is withdrawn, you can't say if anything has been accomplished other than lowering the antibodies and reducing the size of the goiter in the study subjects while the study took place. You are using it to justify prophylactic treatment in the name of prevention, when the authors themselves conclude that the selection of such patients for treatment, duration and dose are still subjects to be determined. Have you found the further studies then that support this in practice? In my mind, this is a single study has limited utility as it stands. You set patients up for management with repeated blood tests, medication and the expenses and side effects thereof. There is no prevention of anything here, it is merely starting the patient on what would possibly become their course of treatment earlier than necessary. In doing so, you suppress the working thyroid of a patient. Why would you want to do that?

Antibodies alone do not indicate disease. They perhaps are a harbinger of disease process, but not all patients that have antibodies develop full blown disease. People who don't have antibodies at all also go on to develop thyroid disease. This is why antibodies generally are not treated in an of themselves--because by doing so, it would potentially lead to over treatment. "Do no harm"

You have mildly elevated levels of one set of thyroid autoantibodies, and none of the other. You want me to agree with you that you have a problem that deserves more than the monitoring that your doctor suggested, and quite frankly I don't. Your present endo suggested a reasonable course of action based on the current information in your results, and common standards of practice.

For the third time, of course run your results past another doctor, or several more. It might take a while to find one that will treat you, if that is what you believe that you need.


----------



## Andros

paperbag said:


> Hi,
> 
> This is only my 2nd post here. I just had my thyroid tested for the first time in a long time in September. My TSH and T4 were in the normal range, but I had elevated anti-thyroglobulin. My thyroglobulin antibody was 36 IU/ml, and the range was 0-23.
> 
> I was retested yesterday, and now the thyroglobulin antibody is up to 66 IU/ml. So the anti-Tg has doubled in only three months.
> 
> The endocrinologist says I shouldn't be worried, because I don't have any antibodies to thyroid peroxidase (TPO). She said the Tg antibody was a very non-specific marker.
> 
> This doesn't make sense to me. Why do they even test anti-Tg if it doesn't matter? If it's so non-specific? What's the point?
> 
> I asked her yesterday when I saw her, what would be a high level of anti-Tg that I should worry about, and she said over 100. She said an anti-Tg level of 36 IU/ml was very mild, and some people wouldn't even consider that elevated.
> 
> That also confuses me. Why does their own lab flag it as elevated and show you the "High value" and show you that yours is higher than that, if it's not a problem? Are they just trying to freak you out needlessly? And then they tell you not to worry?
> 
> I am seriously concerned that my Anti-TG doubled in 3 months. That seems ridiculously fast. If that keeps up...well...it's not good.
> 
> But the endocrinologist just thinks all I need to do is come back every 6 months to re-check the antibody levels. Just wait, while you get sicker, until your thyroid is dead, and then they can start treating you for Hashimoto's. This seems insane to me. Whatever happened to prevention being more cost effective than treatment?
> 
> I feel like I'm just sitting here doing nothing while my body eats up my thyroid.


We won't let that happen.

Here is info.

Thyroglobulin Ab and cancer
http://qjmed.oxfordjournals.org/content/59/2/429.full.pdf

http://www.mdlinx.com/endocrinology...963/?news_id=811&newsdt=092010&subspec_id=419

You may need another doctor if this one doesn't "get it!"

66 is not awfully high but when you factor in that you probably should not have any and the fact that it has doubled in a short period of time..............???

I'm with you; I could not agree more.


----------



## Andros

paperbag said:


> I am not sure you are correct on this. I admit I am new to thyroid problems, but I have some training in biochemistry.
> 
> I don't think thyroglobulin antibodies are only useful as a marker for people being treated for thyroid cancer. I believe this to be true, because when the doctor orders a "thyroid antibody" test, the lab automatically does both a TPO antibody test and a Tg antibody test. At least, that's how the hospital I go to does it. There is no separate box to check for the individual antibody tests. They always check both auto-antibodies.
> 
> While it is true that Anti-Tg interferes with measuring Tg, and that Tg needs to be measured in people with thyroid cancer, Anti-Tg interferes with measurement of Tg simply because the lab measures Tg using antibodies, and your body is already making anti-Tg antibodies. These auto-antibodies your body is making hide the Tg from the antibodies that the lab test uses. That's why they interfere with lab tests for Tg level in people with thyroid cancer.
> 
> High levels of Anti-Tg are...well...whatever they flag as high on the lab report. Mine are flagged as high, three times over the high reference value. It makes no sense to flag something as high, if it's not high. That just makes the patient nervous for no reason.
> 
> I can cite you a study in which L-thyroxine was used to lower antibody levels in people with normal thyroid function.
> 
> The first author is Duygu Yazgan Aksoy. The article is called "Effects of Prophylactic Thyroid Hormone Replacement in Euthyroid Hashiomto's Thyroiditis". Endocrine Journal, Volume 52, number 3, 2005


I would like to add that my doctor keeps my TSH suppressed because that in fact keeps my Lupus Anti-DNA waaaaaaaaaaaaaaaaaaaaaaaaaay under control. And the same was true when I had infiltration to the eyes from Graves'. While the eyes have to be treated independently, keeping that TSH down helped a lot and I do mean a lot. My eye surgeon once told me that he could not effectively treat the eyes until we could find a doctor to get the thyroid issue under control and it was "he" who found me the doctor to do that.

Thanks for the citation link.


----------



## paperbag

I don't understand your suspicion on the point of testing anti-Tg antibodies just because not all patients had them. As you said, not all patients with Hashimoto's are positive for anti-Tg. But for those who are, then of course they would test the effect of their treatment on anti-Tg.

I'm sorry but I think your interpretations of the conclusion are not accurate again. They are stating that, yes, in fact the auto-antibodies are directly effected by their LT4 treatment. Auto-antibodies are an "immune process" What is independent of LT4 treatment are the CD8+ cell levels. I think you are missing this distinction. They were looking for an explanation at the cellular level for this decrease in auto-antibodies by looking at different types of lymphocytes. Since the CD8+ lymphocytes went up in both groups, their LT4 treatment could not be decreasing auto-antibodies via an effect on CD8+ cells. 
And not because, as you stated, there were no cytological changes. Rather, because the cytological changes (CD8+ levels) went up in both the control and the treatment group. This is a good example of how it was well controlled, because they used a group of patients who did not receive treatment and monitored them as well. I will quote the passage again:

"LT4 treatment at doses keeping TSH at low-normal levels appears to be effective not only in decreasing the autoantibody levels but also in the goiter size. Although this immunomodulating effect cannot be explained through any in alterations lymphocyte sub-populations (though CD8+ levels increased it was independent of LT4 treatment), there appears to be an inhibitory effect of LT4 treatment on the ongoing disease process in Hashimoto's thyroiditis patients."

I'm not sure why you think they were referring to TPO antibodies primarily. They never say that. Also, they devote an entire figure just to Anti-Tg (figure 3).

No I don't think I am confusing the results of this study with how they reply to me. I found this study very interesting to my situation. The authors state: "Early treatment of euthyroid Hashimoto's thyroiditis patients with L-thyroxine may slow down not only the disease process itself but through its immune modulating events it may also affect the course of other auto-immune disease which accompany."

Since I may be a future Hashimoto's patient with normal thyroid hormone levels, this may be good information for me to have in the future. I want to be prepared and educate myself on what I can do to help slow the illness.

You said that the authors would have to follow the patients afterward to see how many became hypothyroid. I don't think this is the point. Remember, the definition of these patients are those with confirmed Hashimoto's but who are euthyroid. They may never become hypothyroid. Yet they still have Hashimoto's. So following the patients for hypothyroidism misses the point. They already have Hashimoto's.

I am really surprised when you say that the only thing that was accomplished was "lowering the antibodies and reducing the size of the goiter". You don't think that's a major benefit to Hashimoto patients?

Yes I agree the authors say that there are still things that remain to be determined, such as what type of patient should be treated, the duration of treatment, and the dose. No I have not found further studies. I haven't looked. I am new to this. I have been reading this paper first. I agree this is a single study and you can't make firm conclusions from one study, it has to be confirmed. I am just saying this study is interesting, applies to me, and I have disagreed with a lot of your interpretations of this one study.

When you say "there is no prevention of anything here", I just don't see how you can say that, given the results of the paper. What a sweeping statement to make.

I am not setting anybody up. If you have Hashimoto's, you're going to need blood tests and medication and have to pay for it and have side effects. If you are developing Hashimoto's, why not try to prevent it if you can? This study suggests it's possible, though there is still more to be determined. From this one paper you definitely can't say there is a standard regimen to do in order to prevent Hashimoto's But it raises the possibility of prevention, instead of just waiting around to get sick.

If it is clear you are developing Hashimoto's, for example, your anti-Tg is high, your anti-TPO is high, you have increased thyroid volume, then you make an informed decision based on all the factors unique to the patient on whether to try to head the disease off, or wait for it to develop. I think this option should be available to the patient. I don't think you should only be handed one option to just wait and get sicker. I think the patient and the doctor together, based on the trends in the patient's lab tests, should make an informed decision on whether to wait for the disease to get worse, or to try to slow it or prevent it. I suppose you do suppress the working thyroid, but it won't be working for much longer if you are developing Hashimoto's.

Antibodies alone do no indicate disease, this is true, but they are a major test for Hashimoto's. This is clearly known. I don't know why you left this part out. I agree there are other tests, such as ultrasonography, but because there are other tests does not imply that antibody tests are not useful.

Well, at this point I don't mind if you don't agree with me. I don't understand why you say, on the one hand, of course run my results past another doctor, yet on the other hand say you don't agree that I should, and that I should just stick to my doctor's "reasonable course of action".

You don't need to keep repeating to run my results past another doctor. It's what I plan to do. And no, I'm not looking for one that will treat me. I think I might need preventative treatment, given the trend in my antibodies. However, I'm looking to verify my current doctor's recommendation.
Think of it this way. You think this paper I cited cannot be interpreted in isolation. I agree with you. It needs to be verified. Well, I think the same is true for my thyroid tests. I think they should be verified by another doctor and lab. I think it's better to get multiple opinions. If they all say, "you're fine", then I will be very relieved.


----------



## lainey

If you don't have TPO antibodies, Hurthle cell changes as per an FNA of your thyroid, I fail to see why you are obsessing over the need to prevent something that hasn't been diagnosed yet.

You could have your thyroid removed and you would still have the Tg-Ab. You could cut to the chase and prevent the disease right there, if they were guaranteed to be the cause, end the suffering and take replacement hormone to avoid future problems.

Ridiculous, right?

I didn't leave anything out. The part that you are missing is that presence of Tg-Ab doesn't necessarily mean that you have a thyroid problem, nor does it guarantee that one will develop. Putting a patient on thyroid replacement hormone merely because they have antibodies is not a form of prevention, it is treating something before it starts. To prevent the disease, you would have to stop the autoimmune response to the antibodies--merely lowering their number doesn't necessarily do that--because they are there, you need to find the trigger to the response--behavior, environment, genetics--which factor of many do you think replacement hormone is going to modulate? Why does it happen in some people and not in others? In my mind, then the risks of over treatment with thyroid hormone--heart damage, osteoporosis--far outweigh any benefits that could be derived from "preventing" the traditional, and fairly benign, symptoms of hypothyroidism.

Some reliable reading, if you haven't found it:
http://www.thyroidmanager.org/Chapter8/8-frame.htm

Explore the whole book. It's peer reviewed, written and kept up to date by endocrinologists.


----------



## paperbag

Well, I don't think I'm "obsessing". I don't think educating myself by reading journal articles, and getting a second opinion, is obsessing. And I don't particularly like being pathologized by people who hardly know me, so I would appreciate it if you didn't.

I don't understand the attitude of ignoring potential warning signals until the disaster happens. You could have high cholesterol and never have a heart attack either. But it makes sense to take cholesterol lowering drugs because the benefits outweigh the risk.

My point is, diseases don't just one day appear out of no where. They develop over time. There are markers. There are trends. If you start to see a disease developing, it makes sense to me to try to prevent it, if you can. This is how all other diseases are that I know of are handled. My mom had a suspicious lump in her breast. They didn't just let it develop into cancer and then treat the cancer.

I must say you make some weird arguments. I could have my thyroid removed? Ok...I guess. But then I would basically have self induced Hashimoto's, which is what I'm trying to prevent. And yes, that is ridiculous.

When I said you were leaving things out, I was referring to your statement about antibodies alone do not indicate a disease. Of course they don't, I don't think I said they did. That is why I mentioned ultrasonography several times.

I do understand that the presence of Tg-Ab doesn't necessarily mean that I have a thyroid problem. It is not 100% certain. However, it is certainly a risk factor. It deserves further investigation. Especially since my Tg-Ab doubled in 3 months. To me, it is the speed with which the Tg-Ab is increasing that is most worrisome.

The point I'm making is that my current doctor would not do anything, even if I had verified Hashimoto's by ultrasonography or biopsy or fine needle aspiration. My doctor would just wait until my TSH or T4 were affected. In essence, just letting the antibodies destroy the thyroid until the TSH or T4 levels changed. Literally, they don't do anything until your thyroid is so destroyed that it changes the TSH and T4. It's like letting your arteries clog, and the doctor does nothing until you actually have a heart attack.

I never said to put someone on thyroid meds just because they have Anti-Tg antibodies. I said:

"If it is clear you are developing Hashimoto's, for example, your anti-Tg is high, your anti-TPO is high, you have increased thyroid volume, then you make an informed decision based on all the factors unique to the patient on whether to try to head the disease off, or wait for it to develop."

This should be an informed decision with the patient and doctor about the risks and benefits. In your mind it may not be worth the risk. In someone else's mind, it might be. I think people should be able to make this decision with their doctor. An informed decision, knowing the risks.

Also, I would guess (I may be wrong) many people on this board would disagree with your characterization of the symptoms of Hashimoto's as 'fairly benign'. Honestly, to me that sounds very dismissive, and invalidating, of how painful Hashimoto's can be, and how much it can change your life. 
It makes me wonder how seriously you take this illness.

Maybe we should stop discussing this?


----------



## lainey

>>My point is, diseases don't just one day appear out of no where. They develop over time. There are markers. There are trends. If you start to see a disease developing, it makes sense to me to try to prevent it, if you can. This is how all other diseases are that I know of are handled. My mom had a suspicious lump in her breast. They didn't just let it develop into cancer and then treat the cancer.<<

Exactly. That's what monitoring is for, that's what your endo suggested, yet that's what you are dissatisfied with.

I CAN'T give you the validation you want.

As for characterization, I live with hypothyroidism, and find it annoying but generally not deadly, and have no problem being sympathetic to people who are suffering. However, I see people every day who live well with worse conditions, and everyone's goal should be to learn, gain some perspective, and do the same.


----------



## paperbag

Exactly...what?

I do not disagree with monitoring at all. In fact I was the one who went back early (at 3 months instead of 6 months) for more monitoring. My endo had written on my test results "Return in 6 months or sooner if symptoms indicate". Since I was having increased symptoms, I went back at 3 months. The doctor acted confused as to why I was even there, as if she had forgotten her own notes. (that's another story)

Anyway, my issue is that my endo would never do any preventative treatment at all.

Let's say I had high anti-TPO, high anti-Tg, and increased thyroid volume. The doctor still wouldn't do anything at all until the TSH or T4 levels changed. The endo told me this specifically.

It's not the monitoring I disagree with, it's their approach to the problem once it is clearly in the early stages of Hashimoto's that scares me. Even if I had clearly diagnosed Hashimoto's, they wouldn't do anything until the thyroid was damaged to the point that the TSH or T4 levels were affected.

It's this "wait and get sicker" philosophy that I disagree with.


----------



## McKenna

> If someone has high antibody levels that are going up, but doesn't have Hashimoto's yet, why wait to develop Hashimoto's? That was one of the central ideas. That you do need it to prevent the antibodies levels from getting so high that you get Hashimoto's.


My understanding from my endo was that when a person has Hashi's, using thyroid meds can help "put the thyroid to sleep", thus preventing further attacks and damage. The way it was explained to me was for people who already had the disease, was experiencing gland destruction and symptoms. We tried thyroid meds in my case, but I was already having high TPO, and hypo labs and symptoms. It didn't work in my case because I had hyper stuff going on too.

I have Hashi's, had hashitoxicosis, and had a TT a few months ago. My antithryoglobulin levels were never raised and my TPO is higher now, two months after surgery, than it was back in the summer. Antibodies wax and wane and I don't even have a thyroid for them to attack, but I still have antibodies. I don't know what that means, and hopefully they will go down. I'm getting another TPO in two months to follow up.

I think you should definitely follow it, but I don't think thryoid replacement may be the best solution if you are not hypo thyroid yet. When I was having hypo labs, but hyper stuff going on (high TSI antibodies, high uptake, hyper symptoms), the thryoid meds was like adding fuel to the fire and I felt it made me worse.



> It's this "wait and get sicker" philosophy that I disagree with.


 Yes, that's frustrating. I remember feeling the same way. It seems like everything to do with diagnosing thryoid issues takes a long time. Years and years for most people. What are your current labs? Showing anything near hypo?



> it's their approach to the problem once it is clearly in the early stages of Hashimoto's that scares me.


 Do you believe yourself to be in the early stages of Hashimoto's?


----------



## lainey

If your TSH and T4 levels are not affected, you are technically not "sick" yet in the clinical sense that most doctors work from.

So now we're cycling back around to all of the reasons why doctors don't prescribe thyroid hormone to people before they need it.

>>Anyway, my issue is that my endo would never do any preventative treatment at all.<<

There are soooo many other potential reasons for thyroid symptoms. This is why you see them described often as "benign" or "non-specific"--such as low iron, low vitamin D or B--the list goes on and all should be ruled out.

Umm, we're back to, you're going to need to find a good body of evidence that says that there is "preventative" treatment, including the elimination of all other possible sources of your symptoms, and then a doctor to execute it. Given that most endos are conservative in this regard, you might want to look for a naturopath or other holistic doctor that's willing to trial you on medication based on your symptoms rather than your labs.


----------



## lavender

The "normal" range of any labwork is just a reference point. Many people feel at their best at a particular point in the range. If your T3 and T4 are at the lower end of the reference range and your TSH is at the higher end, you may feel better with thyroid replacement. However, if T3 and t4 are at the higher end, you run the risk of causing yourself to become hyper thyroid which is not pleasant at all.

I know that I had irregular thyroid blood work 4 years before my doctors decided that I had anything serious enough to follow up or treat, even though I had thyroid symptoms the whole time. I couldn't even convince my doc to run thyroid test on a yearly basis. My doc waited until I needed to be hospitalized to treat me, and I was so sick that I lost 6 months of my life, my job, my health insurance.

Needless to say, I feel pretty passionately about following up and preventing things from getting worse in the early stages of an illness. I may have saved myself a whole lot of unnecessary suffering if I had done the research you are doing now 4 years ago and not simply accepted my doctor's dismissal. I was dismissed by a holistic practitioner, a family doctor and a rheumatologist.

If I've learned anything about this, it has been to listen to my body, my own inner sense of knowing, research things for myself, and to keep looking for answers when I know something is wrong!


----------

