Re: Hashi swings--please share your experience.

January 11, 2008

could be a million things. Anemia, sugar issues, gh issues, chronic fatigue syndrome, etc...

Hashi swings--please share your experience.

I have hashi's, but not on meds yet.I will have several days where I feel great--plenty of energy, getlots 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 againfor a few days, then I'm down again.Does this sound like Hashi's or something else?

January 11, 2008

Hi ,

Can't remember if you mentioned this before or not - it's hard to

keep track of my kids and my problems...

Anyway, have you ever had the Graves' ab's tested? If so, what were

the results? My Hashi/Graves' daughter does this sometimes all in

the same day. I don't have to worry about loosing my hair to low

thyroid as I'm pulling it out trying to find someone who can treat

her effectively. She'll be cold, tired, exhausted and then all of a

sudden can't sit still, nervous energy and talks so fast I don't

understand her -hyper. With diet changes it's a tad bit better, but

nothing to write home about.

Good luck,

Bj

>

> 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?

>

January 11, 2008

Hi BJ.

Yes I have TSI of 102. Do you think that is the cause?

Does you daughter have the terrible fatigue, aches and pains, when

she's in a downswing?

> >

> > 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?

> >

>

January 11, 2008

Hi ,

I thought TSI was universal like TSH, but it must not be. Her TSI is

not near that high if that is a percentage her lab results say 38%

(normal <30) and her TRAB is 27% (normal <16). She doesn't have

aches per say, she feels weak like her legs won't hold her up kind of

exhausted and sometimes grabs on to us to get her balance and it

makes her sick to eat. If she sits down she is out " asleep " . She

does sleep a lot and I am fearful of how this will affect her in a

couple of years since she's so exhausted now.

I think she needs to be on both thyroid replacement and anti-thyroid

meds to bring down the ab levels and hopefully stablize her condition

for both the hashi and Graves' but haven't found a doc who will even

listen much less consider it.

Bj

> > >

> > > 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?

> > >

> >

>

January 11, 2008

Hi, Sounds like it might be a combination of thyroid and adrenal, since I have experienced the same and the doctor concluded that it is both of those. The things I have found most helpful for supplements (which were recommended by the doctor) were bio-identical cortisol, 5-HTP - 500 mg 2x a day, and Inositol supplements (B vitamin family) (2-3x a day 1000 mg) and 1000 mg per hour when anxiety is coming on hard. Joanna

January 11, 2008

-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.

I just wish there was way to know for sure while it's happening.

-- In Thyroiditis , Joanna wrote:

>

> Hi,

>

> Sounds like it might be a combination of thyroid and adrenal,

since I have experienced the same and the doctor concluded that it is

both of those. The things I have found most helpful for supplements

(which were recommended by the doctor) were bio-identical cortisol,

5-HTP - 500 mg 2x a day, and Inositol supplements (B vitamin family)

(2-3x a day 1000 mg) and 1000 mg per hour when anxiety is coming on hard.

>

> Joanna

>

January 15, 2008

Hi ,

Those antibodies can really be tough to figure out.

The best way to think about them is like this;

In Graves disease, the antibodies are targetting the TSH receptors

that are found on the outside of the thyroid (external) and are

the 'gas pedals' for thyroid hormone production, and must be engaged

to be able to make hormone. These antibodies are called TSH Receptor

antibodies.

In Hashimotos, the antibodies are targetting substances found in the

follicular (internal) cells of the thyroid. These antibodies are

called " anti-thyroid " antibodies - aka TPOab and TGab.

So one type of antibody targets the INSIDE of the thyroid (and also

denotes damage) and the other antibody targets the OUTSIDE of the

thyroid and doesn't cause destructive damage, but controls the rate

of hormone production.

MORE ON TSH RECEPTOR ANTIBODIES:

There are several types of TSH Receptor antibodies: Some will

stimulate the receptor cells (TSI aka TSab, causing HypERthyroidism)

and others will cause a decrease in hormone by blocking TSH from

getting to the receptor cells (Blocking TRab) and these can cause

hyPOthyroid if there is too much " blocking " going on and not

enough " stimulating " . Blocking antibodies can block both TSI and

TSH. Enough of them can shut down the entire hormone production.

Both Blocking and Stimulating types of TRab will prevent TSH from

getting to the receptors on the gland.

One of assays (tests) used to measure TRab is called TBII. This test

measures what percent of the TSH will be blocked (inhibited) from

stimulating the TSH receptor (by the TRab antibodies). This test

won't be able to tell how much of these antibodies are blocking and

how much are stimulating types --- the test only measures how much

TSH is being kept from binding to the site. (Which gives a round-

about figure on how much TRab is attached there).

Hope that was a little easier understood??

Here are some more abbreviations:

Antibodies:

Tgab = Thyroglobulin antibody (Marker for autoimmune-caused

inflammation) One of the " anti-thyroid " antibodies

TRAb = TSH receptor antibodies (directed against the TSH receptor on

the thyroid & other locations)

TSI = Thyroid-stimulating immunoglobulin, aka TSH-Receptor

Stimulating antibody or TSab - this causes Graves hyperthyroidism

(One of the TRabs)

TBab = TSH-Receptor Blocking antibody, aka TSBab (One of the TRabs)

TBII = thyroid-binding inhibitory immunoglobulin (TBII) - detects

both classes of TRAb, including TSI and TBab.

TBII Dynotest Trak (human) = this is a newer TBII assay that is

reported to have a higher sensitivity to detecting all binding

TRabs, including TSI. This one uses human cells in lieu of porcine

cells.

TPOab or Anti-TPOab = antithyroid peroxidase antibody (Marker for

inflammation) One of the " anti-thyroid " antibodies

AMA = antimicrosomal antibody (outdated, replaced by TPOab)

Take care!

Val

>

> 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?

>

January 15, 2008

Hi Bj,

First, the TBII test isn't for binding antbodies, it's to note how

much TSH " binding inhibiting " is going on. (all TRab antibodies are

binding type). When TRab bind, they then deflect the TSH away (this

is the same location where TSH is supposed to bind). These antibodies

wrest control away from the TSH, and take over.

But the TBII test can't tell whether these are stimulating the

receptors or doing nothing to the receptors (blocking). If you have

enough TRab that are blocking (doing nothing) and they wont let any

TSH in either, then the thyroid will stop functioning.

TBII is " TSH-binding inhibiting immunoglobulin. They can also be

called " Thyrotropin-binding inhibiting immuno " because " thyrotropin "

is just the longer name for TSH.

> If I understand you correctly, TRab and/or

> TBII tests are not picking up the blocking receptor antibodies.<

The TBII tests WILL pick up Blocking receptor abs, but when you get

the range, it will be something like <17% normal. But blocking abs

can be less than that and still cause plenty of trouble --- that TBII

test range was built to measure how much TSH inhibiting by TSI will

cause hYPER. But even a small amount of TSH-inhibiting TRab *can*

cause hypO - especially if the TSI is low. And *MOST* especially if

TSH is already low too.

That's where I am now. I had low TSH (.30) and a TSI of 119%, with

hyPO T4 and T3 numbers, so I have to take 50mcg Synthroid with 2.5mg

MMI. I need to stay on the MMI to continue getting my TSI/TBII to

fall. But I need the Synthroid too, because I will go hypO without

any thyroid stimulation.

>

> What about the people who have positive TSI and positive TBII?

> Wouldn't these blocking abs affect them as well?<<<<

Yes ma'am. I think I was in that scenario too --- at diagnosis I had

a TSI of 223% and had VERY MILD hypERthyroidism (only my T3 was

elevated, but only a tiny bit. T4 was normal). Most people would have

been very hypER, but not me. My first thought was that I had a

damaged gland or something (I do have TPOabs). But after a year and

not getting my TSH back, that was a clue that there were a lot of

blocking TRabs involved.

>I read through all the links and I wonder if the `blocking' abs can

affect patients similarly who have all the abs for Hashi TPO/TG and

the Graves' abs TSI and TRab (TBII) who aren't being treated and

have never taken neither ATD nor a Thyroid replacement drug. Have

you ever come across any literature on that scenario? <<

I have seen oodles of people who claim to be " in remission " from

Graves in this exact scenario. They went on ATD long enough to see

their T4 and T3 come into normal range, TSI fell, but still have

plenty of TRab/TBII showing in their system -- still inhibiting the

TSH from binding. Having TBII is evidence that they still have some

very active autoimmune issues going on. But they can

remain " euthyroid " for years like that.

They sometimes even call this " Euthyroid Eye Disease " , because

sometimes the titres of antibodies can be EXTREMELY high, but enough

of a balance between blocking and stimulating to keep the thyroid

hormones looking just fine (Normal T4 and T3). But then the eyes get

really beat up in the process due to the high levels of TRab

antibodies. Sometimes the worse cases of Graves eye disease is during

these false " euthyroid " periods.

> Every doc we've seen says this is rare especially in a young girl.

>They refuse to give her ATD -it will make her HypO and Thyroid

>replacement will make her HyPer and giving both is just mad

medicine.<

For someone dx'd as " Hashi's " , it's probably going to be really hard

to convince a doc to do that. But if she has TRab and goes hypER at

times,that should get him to understand that the dx would be Graves

and that the best therapy is to get the thyroid under control with

ATD, and then supplement with Synthroid to " force " the levels to

remain stable, until the TRab go into remission. But I know how hard

that is...because I'm on doc #3 right now, trying to find one who'll

do just that!

>>>On her lab result sheets, her tests say `thyrotropin

> binding' at one lab and `TSH receptor bind' at the other. The

doctor who orders her labs writes " TSH receptor binding " and " TSH

receptor stimulating " for the TSI test. *So, evidently we need to

add the blocking test as well. Would it be called *TSH receptor

blocking* or *TSH receptor stimulating-blocking* or " TSBab* or

what?? <<<

It can be called any of those names (TBab, TSBab, TSH receptor

blocking ab) but as far as I know, that test is not commercially

available. (at least that's what the Univ of Chicago tell us, and

they are the ones using B & R on kids, so they'd probably be honest)

Good luck to you and your daughter! It isn't an easy task to find a

doc who will listen to what you want, and then pay attention to new

research you bring forth. We had to drive out of state to find our

Ped Endo, and he turned out to be one that is working in labs doing

research most of the time - only in the hospital clinic one day per

month. I think that's the only way these docs can stay up to date on

all this stuff -- it's really overwhelming -- and I only read about

ONE disease! Imagine trying to keep up with several at a time? wowza.

Take care!

Val

>

> >

> > Hi all,

> >

> > In the discussion on possible hyPER swingsÂ and back toÂ hypO and

> vice versa, the information I have posted below pertains to those

of

> yourÂ 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

> quiteÂ hypO even on tiny bits of ATD (but with low or veryÂ low-

> normalÂ TSH).Â

> >

> > IÂ was dx'd with mildÂ Graves in Nov 06Â (with overlapping

> thyroidÂ inflammation - TPOabs) and amÂ 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 thatÂ scientists are finding that

> the antibody that causes Graves disease (TSI) can also switch the

way

> it works, and start toÂ behave as a hyPO antibodies by blocking the

> glands receptorsÂ at certain times (without causing stimulation).

> This seems to occur the mostÂ shortly before the Graves disease

shows

> up, or some monthsÂ after a Graves person starts ATD medictions.Â

> >

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

> >

> > Sadly, some doctors wrongly assume the autoimmune

> glandÂ hasÂ atrophied anytime someone shows with hypO symptoms (due

> to seeing TPOabs/TGabs) and assumes the thyroid has stopped

> functioning due to damage,Â when it's actuallyÂ it is likely that

> itÂ now isÂ under the control ofÂ the TRab that are making it shut

> down (blocking stimulation) -- andÂ the antibody that is doing

> itÂ justÂ might be theÂ SAME antibody that caused the

> originalÂ stimulation in the first place; Â But is now attaching to

a

> differentÂ 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

> testsÂ as " high " - they can be seenÂ as low (or normal)

Â aroundÂ 45%

> and stillÂ causeÂ a lot ofÂ symptoms -Â so they may get missed

> completely if these aren'tÂ being picked up.Â Â

> >

> > I used to think that if the TRab test or TBII testÂ 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 negativeÂ ranges. I saw a study yesterday

> where a manÂ with GRaves disease and being treated with ATD,Â 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.

> >

> > OnlyÂ the actual " blockingÂ TRab " (TBab)Â test willÂ show for

> SUREÂ if you have theseÂ (a test which is nearly impossible to get

> through commercial channels, unless you live in Japan or work in a

> research lab).Â The man in the study above was lucky that his docs

> did run blocking TRab testsÂ 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 studyÂ 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

> >

> > Gravesâ€™ 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 Gravesâ€™ disease

> >

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

> >

> > reported that approximately one third of patients with

> >

> > Gravesâ€™ 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 antibodiesÂ and the

> biological activity of blocking type thyrotropin receptor antibody

> (TBab).Â

> >

> > 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)Â 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....