Question About Labs + Mmi Dose Change - Graves' Disease and Thyroid Discussion - Living with Graves Disease

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Question About Labs + Mmi Dose Change


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#1 FourT6and2

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Posted 27 April 2021 - 03:52 PM

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Hi everybody! It's been a long time since I was diagnosed and logged on here. My Graves' has been pretty much controlled since diagnosis 11/2017. I've been on 2.5mg/day of MMI for about a year or so and doing well. A few months ago my Dr. advised lowering the dose to 2.5mg 5x/week instead of every day. And after my most recent labs, she wants to again lower my dose to 2.5mg 4x/week.

 

My Dr. was looking for a rise in my TSH to signal a reduction in MMI. And that happened last round of labs. All my numbers look good still, but after dropping my dose from every day to 5x/week, my TSH has dropped. But still within normal range. And Dr. now wants to lower dose even more. But I'm concerned my TSH will drop even more, below the normal range. And then I'll have to raise the MMI dose again. Any thoughts?

 

Here are my current numbers and lab ref. ranges:

 

FT4: 13 pmol/L (10 - 18)

FT3: 4.3 pmol/L (2.6 - 5.7)

Albumin, serum/plasma: 4.2 g/dL (3.5 - 5.0)

Creatinine: 1.33 mg/dL (0.73 - 1.24)

eGFR: 68-79 (>59)

Vit. D: 35 ng/mL (20 - 50)

PTH: 61 ng/L (18 - 90)

Calcium, serum: 9.5 mg/dL (8.4 - 10.5)

Phosphorus: 2.7 mg/dL (2.3 - 4.7)

Calcium ionized: 1.24 mmol/L (1.14 - 1.34)

TSH: 1.23 mIU/L (0.45 - 4.12) DOWN FROM 2.0 BEFORE LOWERING MMI DOSE

TSI: <89% of baseline (<140%)




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#2 mmztcass

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Posted 27 April 2021 - 04:36 PM

Hi FourT6and2:

 

Your doctor is doing the right thing to lower the MMI dosage to allow the Free T4 to come up.  The goal for many people with Graves' in order to feel their best there at, is to allow the Free T4 to come up to the upper third range.

 

As for the TSH dropping when the MMI dosage was lowered, please do not worry.  As long as there are any positive TSI numbers, the TSH numbers will not be accurate.  Instead we must look at the Free Ts to go by how we feel to adjust our meds by and don't even ook at the TSH.

 

In my case, I have been in remission for about 15 months now with no meds.  My TSH levels is low because I still have positive TSI and TRAb antibodies numbers even though these are lowering down gradually.  Instead I look to see how my Free Ts are doing and go by how I feel with these numbers.

 

If your doctor is looking at the TSH and is not aware of how the TSI and TRAb antibodies for Graves' Disease can make the numbers wonky, then she may not be well informed about thyroid disease. 

 

The doctor I see is aware how the TSH can act with the positive thyroid antibodies and isn't concern and he looks at only the Free Ts.  

 

{{{hugs}}}



#3 FourT6and2

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Posted 27 April 2021 - 07:05 PM

Thanks for the info!

 

My Dr. isn't concerned with or really watching FT4. At least she hasn't mentioned trying to increase that. She is concerned with TSH. And waited for it to start rising before lowering my MMI. And now that it did rise, she lowered my dose, but TSH dropped after doing that. So my worry is that if she continues to lower my MMI, TSH will continue to drop and FT4/FT3 will increase and I'll start to experience symptoms again. My TSI result shows below the threshold for Graves' diagnosis as far as I'm aware?

 

When I was diagnosed, my TSI was in the 300% range. Now it's below 89% and the reference states normal is below 140%.



#4 mmztcass

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Posted 28 April 2021 - 03:56 PM

Hi FourT6and2:

 

If it were me I'd find another doctor that looks at the Free Ts and not at the TSH.  Any doctor who doesn't realize that for the Graves' Disease patient who will have positive thyroid antibodies which the TSH really can't be used to see how one is doing, doesn't understand the thyroid very well.  :rolleyes:   

 

There was a point in my life that I managed my own thyroid care for a great number of years (still do).  While I was on the MMI, I ordered labs on my own or used my doctor whom I currently see, for labs.  I watched the Free Ts to tweak my MMI to keep my FT4 at the upper third range and the FT3 at mid range.  When I have ordered labs on my own, I only ordered the FT3 and the FT4 tests.  I never bothered with ordering a TSH test.   :)

 

Getting the TSI to come down even lower such as in the 20s or less would be even better.  :)  B)

 

{{{hugs}}}



#5 Allies

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Posted 17 May 2021 - 05:28 PM

Thanks for the info!
 
My Dr. isn't concerned with or really watching FT4. At least she hasn't mentioned trying to increase that. She is concerned with TSH. And waited for it to start rising before lowering my MMI. And now that it did rise, she lowered my dose, but TSH dropped after doing that. So my worry is that if she continues to lower my MMI, TSH will continue to drop and FT4/FT3 will increase and I'll start to experience symptoms again. My TSI result shows below the threshold for Graves' diagnosis as far as I'm aware?
 
When I was diagnosed, my TSI was in the 300% range. Now it's below 89% and the reference states normal is below 140%.

Hi FourT6and2 :)

TSI is mostly useful as a measurement for 'active' or 'hyperthyroid' phases of Grave's disease (which doesn't look like a problem for you at the moment :) ). Most of the treatment guidelines recommend the TRAB (TSH receptor antibodies) test be used for diagnostic purposes, and even for indicating remission, as this test measures all of the functionally different types of Grave's antibodies (including TSI) together as one measurement. TSI is thyroid stimulating immunoglobulin and this has pretty definitively been singled out as the antibody that causes hyperthyroidism in Grave's disease - it acts a little like TSH on steroids by stimulating the thyroid gland to produce more (and more) thyroid hormones. TSI doesn't always exist by itself though; a person with Grave's can have a mix of the functionally different TRABs.

Thus far three distinct sub types of TRAB have been identified: TSI (which as stated above can cause hyperthyroid phases of Grave's), blocking/inhibiting TRAB (which can cause a hypothyroid phase by blocking hormone production) and 'neutral' - I find neutral TRAB quite worrying as there is some recent-ish research suggesting that rather than being functionally neutral these particular antibodies can cause thyroid cell death (apoptosis). All of these different types of TRAB bind to TSH receptors cells throughout our bodies. The stimulating and blocking types do so in a way that prevents TSH from binding there, and this is believed to be a possible mechanism behind low or suppressed TSH in Grave's disease (and subsequently why TSH levels should be viewed with a degree of caution).

The fact that we can have more than one type of TRAB present at any one time, and also that these are not necessarily increasing or decreasing at the same rate makes Grave's disease rather complex at a cellular level. It's thought for instance that having a mix of mostly stimulating or blocking antibodies together can result in these 'balancing' each other out resulting in somewhat stable (if not necessarily ideal) thyroid hormone levels. Even the proposed apoptotic action of 'neutral' TRAB is thought to be mitigated by either TSH or TSI - both of which stimulate thyroid gland growth (so not just increased hormone production) therefore potentially replacing any cells that have been destroyed. It's all very interesting!

Figuring out what all this might mean on a practical or personal level is rather challenging. Elevated TSI can indicate that TSH measurements are to be taken with a pinch of salt, and should not be the sole parameter for medication or hormone therapy adjustment. I think we also need to be aware that the blocking TRABs may also interfere with the hypothalmus/pituitary/thyroid axis and therefore if these are present TSH should not be relied on here either.

Basically this is a rather long-winded way of saying that mostly TSH is the worst parameter to use for judging thyroid status in the presence of Grave's disease, and that TSI is also only one marker for this - and one that cannot identify hypothyroid phases of Grave's.
TSH is also the cheapest test which probably goes a long way towards explaining why a fair bit of effort has gone into defining it as a gold standard test for thyroid function. This might be perfectly fine for someone without a wonky thyroid gland, but I stongly believe it is a mistake to rely on TSH once there is a problem identified.

Allies
:)

#6 FourT6and2

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Posted 03 June 2021 - 12:15 AM

Hi FourT6and2:

 

If it were me I'd find another doctor that looks at the Free Ts and not at the TSH.  Any doctor who doesn't realize that for the Graves' Disease patient who will have positive thyroid antibodies which the TSH really can't be used to see how one is doing, doesn't understand the thyroid very well.  :rolleyes:   

 

There was a point in my life that I managed my own thyroid care for a great number of years (still do).  While I was on the MMI, I ordered labs on my own or used my doctor whom I currently see, for labs.  I watched the Free Ts to tweak my MMI to keep my FT4 at the upper third range and the FT3 at mid range.  When I have ordered labs on my own, I only ordered the FT3 and the FT4 tests.  I never bothered with ordering a TSH test.   :)

 

Getting the TSI to come down even lower such as in the 20s or less would be even better.  :)  B)

 

{{{hugs}}}

 

I don't think the labs differentiate/list TSI if it's lower than 89. That is the threshold. It just says it's LOWER than 89%.



#7 FourT6and2

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Posted 03 June 2021 - 12:22 AM

Well what I feared would happen has happened. Dr. lowered dose to 2.5mg, 4x/week instead of every day (so I'm skipping mon/wed/fri). My TSH levels have dropped and my FT4 and FT3 have risen. And I'm starting to feel symptomatic and losing muscle mass.

 

But that's not the half of it.

 

Over the last 2-3 years, since diagnosis and starting methimazole, I've noticed declining results on my kidney function test eGFR. My endo has always said it's no big deal, I'm probably dehydrated, don't worry about it, blah blah blah. Nothing to do with your thyroid or methimazole. Fast forward a few years to last month and my endocrinologist finally said hey maybe you should see a nephrologist about that... Saw one today and he was like... uhhhh.... yeah you have chronic kidney damage, most likely from the methimazole. He wants to run a bunch of tests and then do a kidney biopsy to confirm drug-induced kidney nephron death.

 

I'm 37. Male. In great physical shape. No other medical conditions. No other medications. I don't drink. I don't smoke. No diabetes. No over the counter drugs. I work out and stay active. I've been bringing this up to my endocrinologist for 3 years and she has swept it under the rug the whole time. But now suddenly she's like yeah you should get it checked out. And lo and behold... a kidney doc is like dude... your Graves' treatment is damaging your kidneys. If it's confirmed, then I guess I'll have to either remove my thyroid or ablate it with radioactive iodine and then go on hormone pills for the rest of my life and hopefully my kidneys aren't screwed.

 

My eGFR went from 98 to 68 since beginning treatment in 2018. If it continues at this rate, I'll need dialysis or a kidney transplant in 5-6 years.



#8 mmztcass

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Posted 03 June 2021 - 02:03 PM

FourT6and2:

 

Wow, what a bummer!   :(   

 

If I had something like this happen to me I'd probably would want to go for the surgery rather than radiation.  

 

Please do update and let us know the outcome.   :wub:

 

{{{hugs}}}



#9 Allies

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Posted 03 June 2021 - 04:59 PM

Hi FourT6and2,

First off, after your experience with your endo (brushing your concerns away) don't be too quick to assume that a nephrologist is much better. Specialists tend to be quite myopic - which can be helpful up to a point, but they can sometimes lose sight of the bigger picture.

It could be that methimazole has played a part in the slowly increasing eGFR, but there is also a suggestion that low thyroid hormones themselves can contribute to kidney dysfunction, and antithyroid drugs can certainly get us to a point where our thyroid hormones are too low to enable our bodies to function properly - kidneys included. The paper linked below goes into some of the complexities at play between kidney and thyroid gland function

https://eje.bioscien...e/160/4/503.xml

I've only skim-read this, but you might find it a little enlightening - especially since it suggests that kidney function can sometimes be improved if thyroid hormone levels are sufficient but not too high (at least that's my interpretation after a quick read)

What are your current results for FT3 and FT4? I've been under the impression that the loss of muscle mass in hyperthyroidism primarily occurs at very high thyroid hormone levels - if that is right then maybe the muscle loss you are experiencing is due to something else effecting your protein synthesis (notably kidneys also seem to be involved in this process)

While it's possible you may have become hyperthyroid since April after lowering the methimazole, that would mean that your TSI has increased significantly since the relationship of thyroid stimulating immunoglobulin (TSI) to hyperthyroid phases of Grave's disease is well established.

...and just because I'm so facinated with TRABs (all of them, not just TSI), it may, or may not, be significant that TSH receptor cells are not confined to thyroid glands (this is also pretty well established) and they do exist in our kidneys as well. There have been one or two studies into how the different forms of TRAB may effect bone turn-over when they bind to the TSH receptors on our bones, by extension the stimulating or inhibitory effects of TRAB might also have an effect on things like kidney function - although I have not seen anything that specifically refers to this happening in the kidney

Table 1 in the below paper lists some of the extrathyroidal sites where TSH receptors are known to occur

https://www.ncbi.nlm...cles/PMC151075/

Sorry to bring up the Grave's antibodies again, but I can't help feeing that these are important in our efforts to get, and stay, well. Also note that I may be projecting my own experiences here: my TSI is not negative, but when last tested was well below the cut-off point for hyperthyroid Grave's disease (as yours was), but my overall TRAB is still quite elevated (albeit much lower than previously). To me this is sufficient to indicate that like many with Grave's disease, I have a mix of stimulating and inhibitory TRAB (this is also known about in research circles, but has not filtered down into general medical practice yet) When I factor in my 'low normal' thyroid hormones i can make an educated guess that at present blocking/inhibitory TRAB have a slight upper hand here :( ...and I don't like it, not one little bit. 'Low normal' is a total cop-out, basically amounting to saying that everybody is absolutely fine if their hormone levels fall anywhere within a rather large population reference interval. I beg to differ.

One last thought that occurs, and I'm even sorrier for venturing into this particular territory: Elaine Moore has suggested that coronavirus vaccines, in stimulating the immune system may cause an increase in TRAB - I think she concludes that this is a temporary blip; but maybe something to bear in mind if you have been vaccinated during this period? (As it might mean a temporary change in thyroid function)

Allies :)

#10 mmztcass

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Posted 03 June 2021 - 05:54 PM

FourT6and2:

 

As Allies said, what are your latest labs for the Free T3 and the Free T4?  You mentioned that these have risen from the every other day dosing.  

 

The thyroid likes daily dosing rather than an every other day dosing.  Dosing the MMI daily with 1.25 mg per day might be a better choice.

 

Are you still seeing the same doctor who looks only at the TSH rather than the Free Ts to dose the MMI?  If so, please find another doctor who will dose the MMI according to the Free T4.  Graves' Disease will have positive thyroid antibodies which will lower down the TSH and the numbers from that will not even be accurate.

 

If your doctor continues using the TSH as a guideline to raise or lower the MMI your Free Ts will suffer and cause the roller coaster effect of going up and down continuously.  Your doctor can benefit by reading some pubs and/or articles about the TSH and the thyroid antibodies and why the antithyroid meds cannot be used to dose to get the TSH to come up or to go down.

 

{{{hugs}}} 



#11 FourT6and2

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Posted 03 June 2021 - 07:20 PM

Thanks guys.

 

My endo doesn't *just* look at TSH. She looks at a whole bunch of labs, including FT3/FT4, TSI, TSH, creatinine, calcium, phosphorus, urine tests, etc. But she's been waiting for TSH to start climbing on its own with the same 2.5mg/day of MMI for the last year or two. Once it started going up she then started lowering methimazole dose. She still looks at FT3/FT4.

 

RE: muscle loss... I'm pretty well tuned into my body. I notice small changes, even from day to day, because I'm an athlete and performance is easily tracked. My thyroid hormone levels haven't skyrocketed or anything, but I think they're too high even though they're in the normal range. I definitely function better and pack on muscle mass easier when they are more in the middle of the range rather than the upper quadrant.

 

I'm still in the middle of a 24hr urine collection for my nephrologist. But my labs from the other day came back and my creatinine and eGFR have actually returned to levels I saw about two years ago. eGFR is up and creatinine is down. Now... this could be because I haven't worked out super hard in a few weeks and therefore have less creatinine in my blood? Or it could be because I've not been taking as much methimazole and that drug might have an effect on the kidneys. Or it could be my thyroid hormone levels are higher now as someone mentioned and that can maybe play some part in kidney function or at least test results? I don't know. It's just frustrating.

 

Also the relationship between thyroid hormone and renal function as described in that journal/article is interesting. I'm not hypothyroid. And I'm not currently hyperthyroid either based on lab results. But I wonder if changes in thyroid hormone, even within the normal ranges as outlined by the labs, still affect kidney function and lab results? Because as I'm decreasing methimazole and thyroid hormones are increasing, my kidney function seems to have bounced back a bit. But too early to tell. I wish I could sit my endocrinologist and nephrologist down in the same room together... Doctors just don't communicate with each other.

 

Latest labs:

 

screen_shot_2021_06_03_at_9_33_24_am_by_

screen_shot_2021_06_03_at_9_33_16_am_by_

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screen_shot_2021_06_03_at_9_32_58_am_by_

screen_shot_2021_06_03_at_9_33_55_am_by_

screen_shot_2021_06_03_at_9_33_45_am_by_

screen_shot_2021_06_03_at_9_32_28_am_by_

screen_shot_2021_06_03_at_9_33_36_am_by_

screen_shot_2021_06_03_at_9_32_51_am_by_

screen_shot_2021_06_03_at_9_32_38_am_by_



#12 Allies

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Posted 04 June 2021 - 06:51 PM

Hi FourT6and2 :)

That' rather a relief that the eGFR is looking better :) Annoying as it is not knowing exactly why it is better, let's take a moment to do a little happy dance :D

Our bodies are incredibly complicated and very individual, and the individual range for hormones, where a person feels best is not hard and fast. There were a couple of studies several years ago that found that an individual's optimal range for thyroid hormones is around half the size of the population reference interval - these individual ranges did not always completely fit within the population intervals, sometimes they extended a little above and sometimes they sat in the bottom half of the range. So it could be that your particular body does not feel comfortable in the high end of the range, or it could be you are undergoing an adjustment period - I remember being very uncomfortable early on when my antithyroid meds were adjusted and the hormone levels were shifting. A little patience might be needed while you wait to see what happens next. Your TSH is also within the population reference interval, so even if that were a reliable metric in monitoring Grave's disease it's not yet suggesting a dose increase is needed :)

Dividing the dose as Mmztcass suggests would provide more even coverage, from memory methimazole is metabolised reasonably quickly (PTU is metabolized much quicker and I think carbimazole is a little slower since the body first has to change it into methimazole). Dividing the dose is an easy tweak that works well for some people :)

Another factor to consider is cellular health, if the thyroid hormone cannot enter the cells, or is unable to be used properly in the cells then more hormone is not necessarily better. I imagine that this also means that if one's cells are healthy and really efficient, then less thyroid hormone may be needed to get the job done. You are very fit, so this could apply to you :D - but this is a little on the speculative side

You certainly want to avoid kidney disease. I guess at some point coming off the methimazole would be good, and perhaps your endo is working towards this. TSH isn't totally useless, but it does need interpreting with some caution - your TSI could be low enough not to cause outright TSH suppression or low TSH; however there may be undetected blocking antibodies (the TSI test only measures the stimmulating type). The blocking TRAB can effect TSH levels and interfere with thyroid hormone production. The saftest course of action is to look first at thyroid hormone levels and clinical symptoms, then TSH. Putting the TSH in pole position doesn't really recognise that it can take some time for the hypothalmus/pituitary/thyroid axis to recover.

#13 FourT6and2

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Posted 04 June 2021 - 07:32 PM

Hi FourT6and2 :)

That' rather a relief that the eGFR is looking better :) Annoying as it is not knowing exactly why it is better, let's take a moment to do a little happy dance :D

Our bodies are incredibly complicated and very individual, and the individual range for hormones, where a person feels best is not hard and fast. There were a couple of studies several years ago that found that an individual's optimal range for thyroid hormones is around half the size of the population reference interval - these individual ranges did not always completely fit within the population intervals, sometimes they extended a little above and sometimes they sat in the bottom half of the range. So it could be that your particular body does not feel comfortable in the high end of the range, or it could be you are undergoing an adjustment period - I remember being very uncomfortable early on when my antithyroid meds were adjusted and the hormone levels were shifting. A little patience might be needed while you wait to see what happens next. Your TSH is also within the population reference interval, so even if that were a reliable metric in monitoring Grave's disease it's not yet suggesting a dose increase is needed :)

Dividing the dose as Mmztcass suggests would provide more even coverage, from memory methimazole is metabolised reasonably quickly (PTU is metabolized much quicker and I think carbimazole is a little slower since the body first has to change it into methimazole). Dividing the dose is an easy tweak that works well for some people :)

Another factor to consider is cellular health, if the thyroid hormone cannot enter the cells, or is unable to be used properly in the cells then more hormone is not necessarily better. I imagine that this also means that if one's cells are healthy and really efficient, then less thyroid hormone may be needed to get the job done. You are very fit, so this could apply to you :D - but this is a little on the speculative side

You certainly want to avoid kidney disease. I guess at some point coming off the methimazole would be good, and perhaps your endo is working towards this. TSH isn't totally useless, but it does need interpreting with some caution - your TSI could be low enough not to cause outright TSH suppression or low TSH; however there may be undetected blocking antibodies (the TSI test only measures the stimmulating type). The blocking TRAB can effect TSH levels and interfere with thyroid hormone production. The saftest course of action is to look first at thyroid hormone levels and clinical symptoms, then TSH. Putting the TSH in pole position doesn't really recognise that it can take some time for the hypothalmus/pituitary/thyroid axis to recover.

 

Makes sense, thanks. Well my TSH was much higher before... 2-point-something. Now it's dropped down to 0.86 since reducing methimazole. Ideally, we'd want to see TSH maintain a higher level while methimazole is reduced. Otherwise it signals that I'm still hyperthyroid, no?

 

As far as eGFR goes, that's not the only data we are looking at. Creatinine clearance results just came back but I'm not sure how to interpret them and my nephrologist appointment isn't until mid July but I'm going to try to move it up.

 

My 24hr creatinine clearance came back high. But my eGFR and serum creatinine and spot/sample urine creatinine from one day ago came back normal. So no idea what's happening.



#14 Allies

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Posted 05 June 2021 - 12:57 AM

Makes sense, thanks. Well my TSH was much higher before... 2-point-something. Now it's dropped down to 0.86 since reducing methimazole. Ideally, we'd want to see TSH maintain a higher level while methimazole is reduced. Otherwise it signals that I'm still hyperthyroid, no?
 

Hi again :)

Suppressed (or below range) TSH indicates overt hyperthyroidism only if either, or both, FT3 and FT4 are high (particularly above the top of the population reference intervals).. I believe its actually impossible to be hyperthyroid if the actual thyroid hormones are not elevated, although it is possible to be subclinically hyperthyroid.

From:
2016 American Thyroid Association Guidelines for Diagnosis and Management of Hyperthyroidism and Other Causes of Thyrotoxicosis
https://www.liebertp...9/thy.2016.0229

"Overt hyperthyroidism is defined as a subnormal (usually undetectable) serum thyrotropin (TSH) with elevated serum levels of triiodothyronine (T3) and/or free thyroxine estimates (free T4). Subclinical hyperthyroidism is defined as a low or undetectable serum TSH with values within the normal reference range for both T3 and free T4. Both overt and subclinical disease may lead to characteristic signs and symptoms, although subclinical hyperthyroidism is usually considered milder"

So no, a TSH of 0.86 (0.45 - 4.12) with within range thyroid hormones is not considered hyperthyroid. Even if the TSH were to keep falling, as long as the FT3 and FT4 do not increase too much it would not indicate overt hyperthyroidism. This is why it is best to treat according to thyroid hormones rather than TSH.

2018 European Thyroid Association Guideline for the Management of Graves' Hyperthyroidism
https://www.ncbi.nlm...les/PMC6140607/

"The starting dose of ATD can be gradually reduced (titration regimen) as thyrotoxicosis improves. Thyroid function tests are reviewed 3 - 4 weeks after starting treatment, and the dose is titrated based on free T4 and free T3 levels. A substantial proportion of patients reach euthyroidism within 3 - 4 weeks of treatment. TSH levels often remain suppressed for several months and therefore do not provide a sensitive index of early treatment response" (p. 11)

George Kahaly, the lead author of the 2018 Europen guidelines has been heavily involved in research into TRAB, and having read quite of few of his research papers (and others in this area), it's apparent that low or suppressed TSH can be present in Graves patients for much longer than a few months - infact some of the research is carried out specifically to try and figure out why this occurs for some patients. It could be that this is not particulary common, but until it is known for certain why it happens and how to correctly identify when it is happening, treating Graves patients according to TSH levels at any point is a questionable practice.

...and yet this is often what we have to deal with :) This is partly due to cost - if you've ever paid for private test you'll know that they are not particularly cheap (and if the cost is multiplied by the number of patients with Grave's disease the cost can be huge) Somewhat related to cost is the idea that a low or suppressed TSH, in itself, can lead to things like osteoporosis. It's very unclear if this is true, and osteoporosis itself is rather complicated. It's true that bones have TSH receptors, but it's also true that TSH is not the only thing that binds to these - and that's a can of worms that's not yet understood. It sadly also seems true that people with Grave's, especially post-menopausal women are more likely to suffer from osteoporosis - but it may have more to do with high thyroid hormone levels (high FT4 is often implicated), autoantibodies (TRAB and rheumatoid factor have both been implicated), or something else.

 
As far as eGFR goes, that's not the only data we are looking at. Creatinine clearance results just came back but I'm not sure how to interpret them and my nephrologist appointment isn't until mid July but I'm going to try to move it up.
 
My 24hr creatinine clearance came back high. But my eGFR and serum creatinine and spot/sample urine creatinine from one day ago came back normal. So no idea what's happening.

I don't really know anything about the relationships between these things :( Too busy reading about the TRABs :) You could try a search in PubMed (a great resource when researching) If you do that, let us know if you find anything interesting!

Mid July is rather a long wait, perhaps this means the results you have had are not thought to require urgent attention - which would be a good thing, right :)

#15 mmztcass

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Posted 05 June 2021 - 03:12 PM

Hi FourT6and2:

 

You could print out the above pubs from Allies to give to your doctor to read about the TSH and why it can't be used at all for Graves' Disease as long there are any positive thyroid antibodies coming from the TSI and the TRAb.  We need to go by how we are doing from the Free T3 and the Free T4.

 

Keep in mind that how we are feeling - either hypER or hypO are coming from the Free T3 and the Free T4 numbers.  The TSH, whether it goes high or low, doesn't tell us how we are feeling.  Only the FT3 and the FT4 as these are the actual thyroid hormones that one feels from.   

 

When I go for labs as a self-pay I never really order the TSH test only the two tests of the FT3 and the FT4 as I know I am likely to have positive antibodies coming from the TSI and TRAb.  When I can afford it, I will order the TSI.  Otherwise I wait until I see my doctor to order all these tests and have my insurance cover these.   

 

{{{hugs}}}



#16 FourT6and2

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Posted 07 June 2021 - 11:33 AM

So my endo says I don't have any positive antibodies from TSI at least. The labs show I'm well below detection range (<89% baseline). She says this means the lab can't detect TSI, it's that low (which is good!). But they didn't test TRAB. My endo wants to now raise my methimazole dose back up to 2.5mg every day lol. I don't know why they've been lowering it the last few months! They were trying to ease me off of it to see how I would respond I guess. But TSH has dropped and I told her I've been feeling a bit jittery/hyper so she decided to raise it up again... PENDING more info RE: kidney function.

 

She also was very adamant that she's never heard of methimazole-related kidney dysfunction. Nor any kidney-related disease associated with Graves'... Whereas my nephrologist says otherwise. My endo recommended I seek out a second opinion from another nephrologist.

 

She says there is a risk with the liver and methimazole, but not the kidneys. And that if I have a kidney problem it might be another auto-immune disorder since where there's one, there can be others.

 

Really... the issue here is high creatinine. Don't know why that is. Maybe too much meat in my diet. Maybe I workout too much. Maybe I have some other health issue. Next step is more serum creatinine test, urine collection, and kidney ultrasound. Then quite possibly a kidney biopsy.

 

In the meantime, I have to decide whether to raise my methimazole back up to my previous dose. I feel pretty good all thins considered. 



#17 mmztcass

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Posted 07 June 2021 - 01:55 PM

Hello FourT6and2:

 

Neither of your Free T3 nor your Free T4 are elevated and your doctor wants you to now go back to taking 2.5 mg of MMI daily rather than every other day dosing.  I would be considering dosing daily at 1.25 mg per day rather than daily at 2.5 mg.   

 

The main issue, I feel for you, is that your MMI dosing has been yo yo'd into difference amounts and that has been putting you into the rollercoaster of hypO and hypER in short amount of time causing stress on your system including the Kidney issue.  

 

Please find another doctor who will not go all over the board with different dosing for you.  Slow and steady wins the race here and definitely a lot easier on your system.  

 

{{{hugs}}}



#18 Allies

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Posted 08 June 2021 - 02:33 PM

Hi FourT6and2,

While we can be jittery when hyper, it's not the only possible cause - of course it's the explanation we leap towards when we have Grave's disease, because it's logical and tremors are one of the recognised hyper symptoms. I get jittery at times and I'm not hyper. I've come to believe it could be stress related, so could point more at adrenal gland function than thyroid. Our adrenal glands sit on top of the kidneys, so I wonder if there may be some particular cross-talk there? (Probably more cross-talk than there is between endocrinologists and nephrologists lol).

It's all very well for your endo to point out that an autoimmune disorder sometimes makes us prone to further autoimmune issues (a really good argument for trying to figure out if there are any dietary or environmental triggers that we might be able to address:) ), but what is she planning to do about this? Is she running tests? Or is she working on the assumption that if there is something else going on it's not endocrine related? I think you've pretty much ruled out type 2 diabetes, which falls under the purview of endocrinologists, but adrenal function is also an endocrine issue and could possibly be explored. I think mostly endos are concerned with the extremes of adrenal function (Addisons or Cushings diseases - both reasonably uncommon and quite extreme) but it would be useful to rule these out (and most likely they would be), and of course get the results and reference intervals so that you can ascertain for yourself if your adrenals are performing well (because like with many things it might be best to try and optimise function before function is irreversibly lost)

The nephrologist can probably check for autoimmune kidney problems.

I'm intrigued by the high creatinine. It does look like levels may be higher shortly after eating red meat, and since muscle damage might also influence results, testing shortly after a workout could also contribute to this. Did you have a pretty good workout and then a nice big steak before the high creatinine test? :D If you workout regularly and eat a lot of meat, you could try not doing those things for a while and then test - if the results are lower that would give you an indication of what might be going on, at least in the immediate aftermath. If you are on a carnivore diet this might be a challenge





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