Re: Hashi swings--please share your experience.

[Guest guest]

Hi ,

I forget whether you have had a complete saliva panel done? That would

tell you your adrenal/cortisol status.

I wouldn't start HC without testing, as its hard enough to get it right

even with a proper baseline. You need to be off all adrenal

meds/licorice/HC etc for two weeks before testing. So consider testing

before trying anything for adrenals.

I'm sure you know all this, but thought I'd mention anyway.

sol

b53cjf wrote:

> -Joanna,

> Yes I was thinking it there could be an adrenal component to this.

>

> I do have those supplements but I probably need to increase the

> inositol. I do have HC so I need to see if that will help too.

>

>

[Guest guest]

yeah i agree, definitely do the 24hr cortisol saliva test before

starting a supplement like cortisol.

i have High cortisol and trying even something like ACE (adrenal

cortex extract) gave me big problems

huge anger, and a buffalo hump/

and i had all the same symtpoms as folks with LOW cortisol.

-Carol

-- In Thyroiditis , sol wrote:

>

> Hi ,

> I forget whether you have had a complete saliva panel done? That

would

> tell you your adrenal/cortisol status.

> I wouldn't start HC without testing, as its hard enough to get it

right

> even with a proper baseline. You need to be off all adrenal

> meds/licorice/HC etc for two weeks before testing. So consider

testing

> before trying anything for adrenals.

> I'm sure you know all this, but thought I'd mention anyway.

> sol

>

> b53cjf wrote:

> > -Joanna,

> > Yes I was thinking it there could be an adrenal component to

this.

> >

> > I do have those supplements but I probably need to increase the

> > inositol. I do have HC so I need to see if that will help too.

> >

> >

>

[Guest guest]

Sol,

So are you saying you think these symptoms are more adrenal than thyroid?

I did a saliva test several months ago, I suppose I should do another.

I'm not currently taking any adrenal support because these days I'm

afraid anything will put me into a hyper phase again.

> > -Joanna,

> > Yes I was thinking it there could be an adrenal component to this.

> >

> > I do have those supplements but I probably need to increase the

> > inositol. I do have HC so I need to see if that will help too.

> >

> >

>

[Guest guest]

Hi Carol,

Wow, that's terrible that the ACE was pushing you into Cushing's.

What are you doing for your high cortisol?

>

> yeah i agree, definitely do the 24hr cortisol saliva test before

> starting a supplement like cortisol.

>

> i have High cortisol and trying even something like ACE (adrenal

> cortex extract) gave me big problems

> huge anger, and a buffalo hump/

> and i had all the same symtpoms as folks with LOW cortisol.

>

> -Carol

>

>

[Guest guest]

Don't know why I let her email go by, but it just occurred to me that

phosphatadyl serine (sp?) is used for that very purpose. Don't know whether

I'd ever add to the problem by using adrenal supplements because they all

have the same thing in them that is way too high for her. Why would she be

using them, if she has HIGH cortisol? That's for LOW cortisol! The above

mentioned supplement, though, is specifically for high cortisol.

Re: Hashi swings--please share your experience.

> Hi Carol,

> Wow, that's terrible that the ACE was pushing you into Cushing's.

>

> What are you doing for your high cortisol?

>

>

>

>

>

>>

>> yeah i agree, definitely do the 24hr cortisol saliva test before

>> starting a supplement like cortisol.

>>

>> i have High cortisol and trying even something like ACE (adrenal

>> cortex extract) gave me big problems

>> huge anger, and a buffalo hump/

>> and i had all the same symtpoms as folks with LOW cortisol.

>>

>> -Carol

[Guest guest]

I've actually lost track of what you said your symptoms were, sorry, I

was just responding to your post about an " adrenal component " . But as

Carol said low cortisol and high cortisol symptoms can be similar.

People have reported thinking they were high cortisol and taking

supplements to reduce it, but later found out they were actually low

cortisol. And vice versa. Even more confusing is that according to the

stages of adrenal fatigue at

http://www.chronicfatigue.org/ASI%201%20.html the early stages are high

cortisol.

If it has been several months since your last salive panel and you are

thinking about treating adrenals, definitely would be good to do another

test. I did the complete panel at Canary Club (Diagnos-Techs).

Were you doing any adrenal support at all when you went hyper on thyroid?

I can't say I really understand all this, but I know everything has to

work together, if your cortisol is very low you won't be able to

tolerate armour, etc. If RT3 is high, ditto. If ferritin is low ditto as

well. This is what I read on the adrenals list.

I'm also sure Hashi's complicates too, because of the reported swings

from hyper to hypo.

sol

b53cjf wrote:

> Sol,

> So are you saying you think these symptoms are more adrenal than thyroid?

>

> I did a saliva test several months ago, I suppose I should do another.

>

> I'm not currently taking any adrenal support because these days I'm

> afraid anything will put me into a hyper phase again.

>

[Guest guest]

Hi all,

In the discussion on possible hyPER swings and back to hypO and vice versa, the information I have posted below pertains to those of your who have any detectable levels of TSI and/or TRab. I've been recently researching this area because my TSI quickly went down after starting ATD therapy, my TBII went from above normal to well into "normal" range (8% - normal <17%) in just a few months, but instead of coming into euthyriod range like I thought I would, I went quite hypO even on tiny bits of ATD (but with low or very low-normal TSH).

I was dx'd with mild Graves in Nov 06 (with overlapping thyroid inflammation - TPOabs) and am taking 50mcg Synthroid with 2.5mg MMI and know that my Synthroid needs to be increased since this dose only keeps me barely in normal range.

I've read quite a bit recently that scientists are finding that the antibody that causes Graves disease (TSI) can also switch the way it works, and start to behave as a hyPO antibodies by blocking the glands receptors at certain times (without causing stimulation). This seems to occur the most shortly before the Graves disease shows up, or some months after a Graves person starts ATD medictions.

So I'm pretty sure that's where I"m at now.

Sadly, some doctors wrongly assume the autoimmune gland has atrophied anytime someone shows with hypO symptoms (due to seeing TPOabs/TGabs) and assumes the thyroid has stopped functioning due to damage, when it's actually it is likely that it now is under the control of the TRab that are making it shut down (blocking stimulation) -- and the antibody that is doing it just might be the SAME antibody that caused the original stimulation in the first place; But is now attaching to a different location on the receptor - but still blocking TSH.

The part that really makes this hard to detect is that these blocking TSI antibodies often don't show up in TBII/TRab tests as "high" - they can be seen as low (or normal) around 45% and still cause a lot of symptoms - so they may get missed completely if these aren't being picked up.

I used to think that if the TRab test or TBII test was within the normal range (<17%), that meant you couldn't have Blocking TRab, but now I know that isn't true and the blocking TRab seem to be highly potent - even very small numbers can especially cause hypO effects when the TSI is in low or negative ranges. I saw a study yesterday where a man with GRaves disease and being treated with ATD, later ended up needing 75mcg Synthroid to maintain euthyroid, had only small amount of TBII, no TSI, and was highly positive for Blocking TRab antibodies.

In other words --- his TSI shifted and became blocking TRab.

Only the actual "blocking TRab" (TBab) test will show for SURE if you have these (a test which is nearly impossible to get through commercial channels, unless you live in Japan or work in a research lab). The man in the study above was lucky that his docs did run blocking TRab tests and he was positive. Otherwise, they would have just assumed his thyroid had died (due to TBII being negative).

I don't have all those studies saved (the one above), but here are a couple others explaining the same thing:

Note the the Graves disease subjects in the study below all had positive TPOabs (which is typical), and these different types of TRab may play a part in that destruction.

http://jcem.endojournals.org/cgi/reprint/76/2/504.pdf

Thyrotropin Receptor Antibodies in Hypothyroid

Graves’ Disease*

KANJI KASAGI, AKINARI HIDAKA,

"...In all patients except one, thyroid function was changeable, with

euthyroid and even subclinical hyperthyroid episodes occurring during

the course of the illness.....

The possibility that TSH-blocking antibodies are a significant

cause of hypothyroidism in hypothyroid Graves’ disease

has been discussed (10, 18, 20). Tamai et al. (13) recently

reported that approximately one third of patients with

Graves’ disease who developed hypothyroidism after antithyroid

drug treatment had a blocking-type TRAb.

TSBAb activities were weakly and transiently positive in two of our

cases. However, the assay was performed using samples with

high TSAb activities that may have affected to some extent

the accuracy of the measurement. The results of the present

experiments measuring TSBAb activities in TSAb-positive

samples indicate that the normal range widens as TSAb

activity increases...

And........

Negative correlation between the conversion of thyrotropin receptor-bound blocking type thyrotropin receptor antibody (TBab) to the stimulating type (TSI) by anti-human IgG antibodies and the biological activity of blocking type thyrotropin receptor antibody (TBab).

Cho BY, Shong MH, Chung JH, Lee HK, Koh CS, Min HK.

Department of Internal Medicine, Seoul National University College of Medicine, Korea.

It has been reported that receptor-bound blocking type TSH receptor antibody (TBAb) can be converted to the stimulating type by anti-human IgG antibodies. To evaluate the relationship between the conversion of receptor-bound blocking type TRAb to the stimulating type and the biological activity of blocking type TRAb, we compared converting activities of blocking type TRAb from 10 patients with primary nongoitrous hypothyroidism with both the doses of blocking type TRAb which show 50% inhibition of 125I-bTSH binding to the TSH receptor and those which show 50% inhibition of TSH-stimulated cAMP production in cultured rat thyroid cells (FRTL-5).

The additions of anti-human IgG antibody to FRTL-5 cell-bound blocking IgGs resulted in the increase in cAMP (antibody stimulated thyroid hormone) production in a dose-dependent manner and the converting activities (percent increase of cAMP production) also depended on the doses of blocking IgGs. The converting activities were significantly correlated with the doses of blocking IgGs which showed 50% inhibition of 125I-bTSH binding to the TSH receptor (r = 0.71, p = 0.011). And these converting activities were also significantly correlated with the doses of blocking IgGs which showed 50% inhibition of TSH-stimulated cAMP increase (r = 0.81, p = 0.002), and were negatively correlated with thyroid stimulation blocking antibody activities (r = 0.58, p = 0.02).

We have demonstrated that all cell-bound blocking type TRAb were converted to the stimulating type by anti-human IgG antibody and the degree of conversion was negatively correlated with the biological activity of blocking type TRAb.(ABSTRACT TRUNCATED AT 250 WORDS)

http://www.koreamed.org/SearchBasic.php?DT=1 & RID=89601

and....

Serum Thyrotropin Receptor Antibodies (TRab) Concentrations in Patients with Graves' Disease Before, at the End of Methimazole Treatment, and After Drug Withdrawal: Evidence That the Activity of Thyrotropin Receptor Antibody (TRab) and/or Thyroid Response, Modify During the Observation Period

C. Carella, G. Mazziotti, F. Sorvillo, M. Piscopo, M. Cioffi, P. Pilla, R. Nersita, S. Iorio, G. Amato, L.E. Braverman, E. Roti

Thyroid. Mar 2006, Vol. 16, No. 3: 295-302

http://www.liebertonline.com/doi/abs/10.1089/thy.2006.16.295

And.......

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1808638

Elevated ANA levels were associated with the atrophic variant of autoimmune thyroid disease and may affect the volume of the thyroid gland, and there was no statistically significant association to the HLA system.

More new features than ever. Check out the new AOL Mail!

[Guest guest]



See if those two tests for Grave's are run by www.healthcheckusa.com. I believe it is the same two antibodies, with the blocking one included in the testing. TRab, right? Well, that one is run along WITH the TSI one. Is this the same antibody you are talking about that is hard to find anyone to get to run, or is it another one? I've never tried testing for these, but I know I should, as I have way too many confusing symptoms. Five yrs ago, I did test very high for the TPOab and the TGab, both in the thousands, but it had never occurred to me at that time that I MAY have both Grave's and Hashi's. I know I have Hashi's, but the symtomology is just too confusing, and I feel like I am so hard to regulate, despite trying every single combo of thyroid hormone spectrums that there are. Feeling very well for runs of a couple of wks, then feeling "hyper" (or something like it) for a week or two or even for a couple of months, then feeling grossly sickly hypo for some time. I'm testing twice a yr now, but I just can't run and test every single 6 wk period of time, too expensive for me. It's only been withing the last yr or 6 months or so that I've been considering that I may have all of the above antibodies and THEN some! My symptoms change way too often for "nothing" new happening to me. I know, I haven't tested for adrenal fatigue, but, other than maybe an adrenal "dump", I just can't see me improving that rapidly, only to go back to feeling grossly ill, when I have modified my lifestyle, diet, etc......I ALWAYS (for the last past 4 yrs or so) have a nonexistent or very low TSH, which is fine for Hashi's people, BUT there are also other variables there, like a pituitary problem or a couple of pituitary problems), and it's also strange that it would be low, still, after my thyroid hormones went down to midrange this last testing, for the first time in a very long time. It is so confusing, and I feel like I've had to become a scientist to even keep a level head on my shoulders about all of this! Holy cow, sometimes ya just feel like you are drowning! God, what IS it!!!!!!!!!!!!!!! No way will I ever have the money to find out what ALL is going on in there, even with insurance, plus the cost of airplane tickets and hotel rooms to go to a DECENT doctor who knows to run all these tests!!!!!!!!!!! The last few days, then on and off for a few months now, I have felt like I had a bad case of the flu, minus the fever. In fact, my body temps (taking them about 4 times a day) have been ranging anywhere from 97.0 all the way up to a 99 or so, and you never know what time of day these temps are going to appear, as they have absolutely no particular pattern to them. I can be feeling extremely ill at 97 or extremely ill at 99, so there is no rhyme or reason to it all, I can't figure out any of it with my own self. Three yrs ago, when being on Armour for a yr and a half, and on a 2 grain dose for more than 4 months, I suddenly developed a 160 heart rate that wouldn't calm down til I'd been off ALL thyroid meds for two to three days. When I reimplemented it, I started taking 125 to 150 of T4, along with the 30 mgs of Armour for most of the time since then, but having to drop the Armour at intervals of several days, in order to "feel right", when just days before I "felt right" on the above mixture, even for months at a time. It's ridiculous. This is why I'm thinking that I've got every single thyroid antibody known to mankind, and I'm thinking that this one daughter of mine does also, as hers can never seem to be regulated either. The other Hashi's daughter ALWAYS feels well, even though she's older than the other one (37), except for one tiny little hitch last yr.

Re: Hashi swings--please share your experience.

Hi all, In the discussion on possible hyPER swings and back to hypO and vice versa, the information I have posted below pertains to those of your who have any detectable levels of TSI and/or TRab. I've been recently researching this area because my TSI quickly went down after starting ATD therapy, my TBII went from above normal to well into "normal" range (8% - normal <17%) in just a few months, but instead of coming into euthyriod range like I thought I would, I went quite hypO even on tiny bits of ATD (but with low or very low-normal TSH). I was dx'd with mild Graves in Nov 06 (with overlapping thyroid inflammation - TPOabs) and am taking 50mcg Synthroid with 2.5mg MMI and know that my Synthroid needs to be increased since this dose only keeps me barely in normal range.I've read quite a bit recently that scientists are finding that the antibody that causes Graves disease (TSI) can also switch the way it works, and start to behave as a hyPO antibodies by blocking the glands receptors at certain times (without causing stimulation). This seems to occur the most shortly before the Graves disease shows up, or some months after a Graves person starts ATD medictions. So I'm pretty sure that's where I"m at now.Sadly, some doctors wrongly assume the autoimmune gland has atrophied anytime someone shows with hypO symptoms (due to seeing TPOabs/TGabs) and assumes the thyroid has stopped functioning due to damage, when it's actually it is likely that it now is under the control of the TRab that are making it shut down (blocking stimulation) -- and the antibody that is doing it just might be the SAME antibody that caused the original stimulation in the first place; But is now attaching to a different location on the receptor - but still blocking TSH.The part that really makes this hard to detect is that these blocking TSI antibodies often don't show up in TBII/TRab tests as "high" - they can be seen as low (or normal) around 45% and still cause a lot of symptoms - so they may get missed completely if these aren't being picked up. I used to think that if the TRab test or TBII test was within the normal range (<17%), that meant you couldn't have Blocking TRab, but now I know that isn't true and the blocking TRab seem to be highly potent - even very small numbers can especially cause hypO effects when the TSI is in low or negative ranges. I saw a study yesterday where a man with GRaves disease and being treated with ATD, later ended up needing 75mcg Synthroid to maintain euthyroid, had only small amount of TBII, no TSI, and was highly positive for Blocking TRab antibodies.In other words --- his TSI shifted and became blocking TRab.Only the actual "blocking TRab" (TBab) test will show for SURE if you have these (a test which is nearly impossible to get through commercial channels, unless you live in Japan or work in a research lab). The man in the study above was lucky that his docs did run blocking TRab tests and he was positive. Otherwise, they would have just assumed his thyroid had died (due to TBII being negative).I don't have all those studies saved (the one above), but here are a couple others explaining the same thing:Note the the Graves disease subjects in the study below all had positive TPOabs (which is typical), and these different types of TRab may play a part in that destruction.http://jcem.endojournals.org/cgi/reprint/76/2/504.pdf

Thyrotropin Receptor Antibodies in Hypothyroid

Graves’ Disease*

KANJI KASAGI, AKINARI HIDAKA,

"...In all patients except one, thyroid function was changeable, with

euthyroid and even subclinical hyperthyroid episodes occurring during

the course of the illness.....

The possibility that TSH-blocking antibodies are a significant

cause of hypothyroidism in hypothyroid Graves’ disease

has been discussed (10, 18, 20). Tamai et al. (13) recently

reported that approximately one third of patients with

Graves’ disease who developed hypothyroidism after antithyroid

drug treatment had a blocking-type TRAb.

TSBAb activities were weakly and transiently positive in two of our cases. However, the assay was performed using samples with

high TSAb activities that may have affected to some extent

the accuracy of the measurement. The results of the present

experiments measuring TSBAb activities in TSAb-positive

samples indicate that the normal range widens as TSAb

activity increases...

And........

Negative correlation between the conversion of thyrotropin receptor-bound blocking type thyrotropin receptor antibody (TBab) to the stimulating type (TSI) by anti-human IgG antibodies and the biological activity of blocking type thyrotropin receptor antibody (TBab). Cho BY, Shong MH, Chung JH, Lee HK, Koh CS, Min HK.Department of Internal Medicine, Seoul National University College of Medicine, Korea.It has been reported that receptor-bound blocking type TSH receptor antibody (TBAb) can be converted to the stimulating type by anti-human IgG antibodies. To evaluate the relationship between the conversion of receptor-bound blocking type TRAb to the stimulating type and the biological activity of blocking type TRAb, we compared converting activities of blocking type TRAb from 10 patients with primary nongoitrous hypothyroidism with both the doses of blocking type TRAb which show 50% inhibition of 125I-bTSH binding to the TSH receptor and those which show 50% inhibition of TSH-stimulated cAMP production in cultured rat thyroid cells (FRTL-5). The additions of anti-human IgG antibody to FRTL-5 cell-bound blocking IgGs resulted in the increase in cAMP (antibody stimulated thyroid hormone) production in a dose-dependent manner and the converting activities (percent increase of cAMP production) also depended on the doses of blocking IgGs. The converting activities were significantly correlated with the doses of blocking IgGs which showed 50% inhibition of 125I-bTSH binding to the TSH receptor (r = 0.71, p = 0.011). And these converting activities were also significantly correlated with the doses of blocking IgGs which showed 50% inhibition of TSH-stimulated cAMP increase (r = 0.81, p = 0.002), and were negatively correlated with thyroid stimulation blocking antibody activities (r = 0.58, p = 0.02). We have demonstrated that all cell-bound blocking type TRAb were converted to the stimulating type by anti-human IgG antibody and the degree of conversion was negatively correlated with the biological activity of blocking type TRAb.(ABSTRACT TRUNCATED AT 250 WORDS)http://www.koreamed.org/SearchBasic.php?DT=1 & RID=89601and....

Serum Thyrotropin Receptor Antibodies (TRab) Concentrations in Patients with Graves' Disease Before, at the End of Methimazole Treatment, and After Drug Withdrawal: Evidence That the Activity of Thyrotropin Receptor Antibody (TRab) and/or Thyroid Response, Modify During the Observation Period

C. Carella, G. Mazziotti, F. Sorvillo, M. Piscopo, M. Cioffi, P. Pilla, R. Nersita, S. Iorio, G. Amato, L.E. Braverman, E. Roti

Thyroid. Mar 2006, Vol. 16, No. 3: 295-302http://www.liebertonline.com/doi/abs/10.1089/thy.2006.16.295And.......http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1808638Elevated ANA levels were associated with the atrophic variant of autoimmune thyroid disease and may affect the volume of the thyroid gland, and there was no statistically significant association to the HLA system.

[Guest guest]

Hi

i was testing as High cortisol before taking the ACe, so think that

is why i had the bad side effects to it.. i didn't need

anymore you can search for my old posts " high cortisol " and see

the few other supplements i tried

btw, i just - for the 1st time- got my cortisol tested via the

conventional Blood test

my FRee Cortisol (at 8AM) = .80 (NOrmal .07-.93)

Total Cortisol (8am) = 17 (Normal = 5-21)

so both are on the higher end of their normal ranges

and i believe i would still test *slightly high on a saliva test,,

just haven't tested saliva for 6 months ($

for my previous high cortisol (and low ferritin = 36)

i have changed /overhauled my diet/nutrition to be low glycemic and

NO caffeine (nor chocolate. to bad , i LOVED it all.

-and cheated a lot due to cravings (and too much t4??)

i am also going gluten free again on Thyroid DRs orders (based on

the fact i have autoimmune hashis. She doesn't think its a good

idea.

i *always had food sensitivities and food CRavings, so i think my

diet impacts my adrenals in a huge way!

then just added the armour SLowly to the longterm t4; took a long

time, but i was very " adrenally sick " due to a lot of life-stress

the last 3 years..

sad ; if only they knew about AF when i was diagnosed hashis and put

on (too little) armour as a kid,, i could have had good health the

last decades . ironic.

-Carol

> >

> > yeah i agree, definitely do the 24hr cortisol saliva test before

> > starting a supplement like cortisol.

> >

> > i have High cortisol and trying even something like ACE (adrenal

> > cortex extract) gave me big problems

> > huge anger, and a buffalo hump/

> > and i had all the same symtpoms as folks with LOW cortisol.

> >

> > -Carol

> >

> >

>

[Guest guest]

HI

my **ALternative DR MD actually suggested i try ACE even tho he knew

i had High cortisol !!

it just affirms to me , that even the ALternative DRs don't know

much about our plight.

ironically , he is also the dr who suggested i do the 24hr cortisol

saliva test (and i was only 5 pts high TOtal)

this is the same dr who said,, I can't believe you are SO sensitive

to armour, when your cortisol is only 5 pts too high....

HELLO??? :)oh well.

***basically DRs do NOT know what they are doing with us

Hypot/autoimmune/Adrenal Fatiguie patients..

he has been in business for over 15 years and admitted he had never

met a patient like me (IE so sensitive to armour)

he started out as MD/ allergist and does chelation also..

AND he is on some of the armour and top docs lists!!!

-btw, my ferritin was low (38ish) but he never suggested doing

anything for that..

he did charge me a lot of money for accupuncture,, and it -or the

ashwaganda type supplements --

did help my TInnitus much more than it is now!!!

but basically, it took Time (and lifestyle/diet efforts) to heal my

adrenals (and raise ferritin?)

enough so that i am Now less sensitive to armour.

-Carol

> >>

> >> yeah i agree, definitely do the 24hr cortisol saliva test before

> >> starting a supplement like cortisol.

> >>

> >> i have High cortisol and trying even something like ACE (adrenal

> >> cortex extract) gave me big problems

> >> huge anger, and a buffalo hump/

> >> and i had all the same symtpoms as folks with LOW cortisol.

> >>

> >> -Carol

>

[Guest guest]

Hi! I have been diagnosed for about 3 years now. I have only had TSH

and a few other tests run. I have not felt like I had much energy and

am hoping to find a good doctor soon!

I felt better when taking Armour but my endo and PCP did not want me on

that. I am scheduled for a visit with another doctor and have many good

things about that. I also started taking an Adrenal complex and a

women's multivitamin and have felt much better. I think that I am going

to stop for the week prior to my appointment with my new doctor in

order to get a good reading on my labs as to what is really going on.

>

> I have hashi's, but not on meds yet.

>

> I will have several days where I feel great--plenty of energy, get

> lots done, sleep well, positive mood.

>

> Then I'll wake up one morning and feel dreadful--terrible fatigue,

> heart pounding, migrating aches and pains, difficulty sleeping.

>

> This will last a couple of days, them I'm back to feeling great again

> for a few days, then I'm down again.

>

> Does this sound like Hashi's or something else?

>

>

>

[Guest guest]

Val,

As always, you are a wealth of great info.

I really feel like I could have understood this whole antibody thing

by now, what with reading your stuff here and on Grave's group, and

the links you provide.

But the thing keeping me from grasping is the multiple names for

several antibodies. It is confusing the heck out of me.

I thought I remembered a chart or something you posted on Grave's that

listed the all the common names used for each antibody, but I didn't

save it and couldn't find it after that.

Could you re-post that here?

>

>

> Hi ,

>

> Several comments you made in your post are signs that you may well

have Graves and Hasih's both. In fact, 95% of people with Graves have

Hashi's too, since Hashi's means simply, inflammation of the thyroid

gland targetted by immune cells. Some even think that ALL Graves

people have Hashi's -- since they know (through biopsy) that

sometimes TPOab antibodies can stay within the realm of the thyroid

and don't get picked up in blood tests.

>

> But back to the TBII/TRab testing. The blocking TRabs that cause

hyPO in Graves people are called TBab or sometimes TSBab.

(TSH-Receptor blocking antibodies). The test for these is nearly

impossible to find in the USA.

>

> However, there are " TOTAL " TSH-Receptor antibody tests you can get,

but these will pick up all types of TSH-Receptor antibodies

(stimulating and blocking). This test is also known as TBII, which

measures how much TSH will be deflected (inhibited)Â away from binding

to the thyroid's TSH-receptor cells (by the TRab that have already

attached themselves there).

>

> These TRab/TBII can also confuse the pituitary gland in the same

way it causes the thyroid to be confused. This often causes

the pituitary to cut down production of TSH. (but not in every case).

>

> HOWEVER --- Blocking TRab are now known to cause much more hypO

effect than first thought. It doesn't take much at all. So a TBII

test that shows less than 17% (what they consider normal)Â doesn't

mean there are no blocking TRab in that result. You can sometimes have

Blocking TRab that is only half as much as the TSI to cause a hyPO

effect. So the TBII might show 8% (<17% normal) and yet you can

still be affected by Blocking TRab.

>

> But remember that TBII (TRab) test will pick up the TOTAL of all

of the TRab -- so you will need a TSI test to measure against that too.

>

> Yes, you can get the TBII/TRab test from Healthcheck, but you

cannot get the test that only measures just the blocking TRab from

Healthcheck. You can also get the test for only the stimulating

(hyPER-causing) type of TRab -- that one is called TSI.

>

> Since TBII/TRab affect the TSH-Receptor cells of both the pituitary

and the thyroid (and eyes, skin, brain, thymus and even yet

undiscovered places where we might have TSH-Receptor cells)  if you

have a consistently low TSH, then it's highly likely you have TRab

that is messing with both the thyroid and the pituitary.

>

> Hope that helps!

>

> Here's some info about that...from the Journal of Clinical

Endocrinology & Metabolism

>

> http://jcem.endojournals.org/cgi/content/full/86/10/4814

>

> " .....we recently showed that the pituitary contains a TSH receptor

through which TSH secretion may be down-regulated via a paracrine

feedback loop. In Graves’ disease, TSH receptor autoantibodies may

also bind this pituitary receptor, thus causing continued TSH

suppression. "

>

> Take care!

> Val

>