TBAb hypothyroidism diagnosed in a mother and baby

In this post, I’d like to share with you a real-life story, suitable for the holiday season, that might warm your hearts as much as it warmed mine. And by the end, it might even motivate you to learn more or take action.

Newsflash from 2016: A newborn baby’s hypothyroidism with a TSH of 117 mcIU/mL was properly diagnosed and was successfully treated.

But it only happened because of a series of fortunate events!

This type of hypothyroidism affecting both mother and baby was caused by thyroid antibodies.

But it was not caused by the well-known antibodies that cause Hashimoto’s and Graves’ disease.

Instead, the baby’s case was caused by TSH-receptor blocking antibodies (abbreviated TBAb or TSBAb). The mother’s TBAb antibodies had crossed the placenta and blocked TSH hormone from stimulating the baby’s thyroid gland.

This type of congenital hypothyroidism is easy to misdiagnose.

Fortunately, Korean pediatricians understood this condition, and Konkuk University Medical Center in Seoul, Korea, is equipped with the special antibody tests required to diagnose this rare disorder.

It is extremely urgent to detect and treat gestational, congenital, and early childhood hypothyroidism because early development depends on thyroid hormone sufficiency.

Fortunately for the baby, the hypothyroidism was temporary, lasting fewer than 10 months, during which time, treatment with synthetic T4 thyroid hormone was well-monitored to minimize potential underdose or overdose.

Fortunately for the mother, her undiagnosed cause of adult-onset hypothyroidism was finally understood, after having being treated on LT4 for 2.5 years already.

I’ll tell the story in this post, and then I’ll provide further context about the TSH receptor-blocking antibody (TBAb) and congenital hypothyroidism.

I’ll conclude as Kim and colleagues did, by articulating the current challenges of diagnosing the innocent TBAb mothers and other human beings, not just the innocent TBAb babies.

Source

In 2016, three Korean endocrinologists published this case study:

• Kim, M. R., Park, H. W., & Chung, S. (2016). A baby with congenital hypothyroidism born to a hypothyroid mother who expressed undiagnosed thyroid stimulation blocking antibody. Annals of Pediatric Endocrinology & Metabolism, 21(3), 161–163. https://doi.org/10.6065/apem.2016.21.3.161

Summary

Here is the short story in 11 acts.

Imagine that you are the baby in this tale.

1. Two and a half years ago, your mother was diagnosed with hypothyroidism and treated with standard levothyroxine (LT4) therapy. However, doctors did not investigate the cause of her hypothyroidism.
2. Now here you are, about to be born. Your mother’s rarely-detected thyroid antibodies have blocked circulating TSH hormone from stimulating your own thyroid gland in the womb.
3. Fortunately, your mother is being treated with enough thyroid hormones before she became pregnant with you, and all during pregnancy. Your body and hers have been bathed in enough thyroid hormone supply from a pharmaceutical source. Because of this, you didn’t suffer gestational hypothyroidism or brain damage.
4. And again, fortunately, your mother’s antibodies don’t seem to cause your thyroid gland to shrivel up and become permanently atrophied. Thyroid gland atrophy occasionally happens when a person makes their own TSH-receptor blocking antibodies and they attack a person’s own thyroid, after birth. But you’ve got her borrowed antibodies, and perhaps the attack doesn’t last long enough to cause damage.
5. And again, fortunately, when you are born, your country has a screening program for congenital hypothyroidism, and you receive a heel-prick test for TSH and Free T4 only three days after birth.
6. Oh wow! Doctors are surprised to see your TSH is very high and your Free T4 is low! Your thyroid hormones have crashed because your mom’s LT4 doses are no longer coming to you through the placenta, but your mom’s TBAb antibodies are still blocking TSH from stimulating your thyroid. Your doctors must feel so excited that they can save you from harm! The routine screening is worthwhile! They found a rare case of congenital hypothyroidism! They whisk you and mom off to the university hospital.
7. You say hello to your pediatricians at the different hospital. They say you need to be treated with thyroid hormone right away, despite the fact that no other signs of hypothyroidism are present, like no goiter (thyroid swelling). Fortunately, you haven’t been hypothyroid long enough to cause harm yet, because your Total T3 level is still just barely above the bottom of the neonatal reference range, and that’s the most vital, active thyroid hormone.
8. Fortunately, your pediatricians have access to some pretty fancy tests that can measure both types of TSH-receptor antibodies together and separately. They find the antibodies they were looking for in both you and your mother. In fact, they find almost every known thyroid antibody under the sun is active — TPOab, TGab, TBAb, TSAb. You’ve both got stimulating and blocking antibodies floating in your blood potentially contradicting each other, but the blocking antibodies predominate and block almost 100% of your body’s TSH receptors. The Tc99m thyroid scan shows zero uptake.
9. Fortunately, your thyroid gland is healthy according to ultrasound, so you have a chance of recovery after your mother’s confusing chorus of antibodies clear out of your body. But the pediatricians have to monitor your therapy carefully over 10 months to make sure you don’t become grossly overdosed or underdosed on LT4 hormone. It isn’t easy. Your thyroid hormones get too high at one point. Good thing they’re watching.
10. At 10 months, your mother is also tested again. She continues to have high TBAbs and needs to continue her LT4 treatment. But fortunately, you can both continue your lives in good thyroid health as long as LT4 serves her well. Let’s hope momma does not flip back and forth between her TBAb and TSAb antibodies while a fragment of functional thyroid tissue yanks her thyroid hormone status hither and thither while on LT4.
11. The pediatricians aren’t sure when you can be safely weaned off LT4, but they plan to do so after they write an article about you, to share your story with other scientists and physicians. Fortunately, your parents give consent to share your story.

Notice how many times I’ve had to say “fortunately.”

When things work out fortunately at every turn of events, it’s a beautiful story. A screening program, medical knowledge, and appropriate testing prevented harm.

Even better, the physicians cared about future babies and mothers in other countries, so they wrote the article.

This is the way things need to work so that thyroid patients with TBAb hypothyroidism don’t fall through the cracks.

And here I am, amplifying what they wrote by reviewing and summarizing it 5 years later.

I have personal reasons to share this story.

I can identify with the mother, although my story’s series of events is very different.

I’m a person with indirect evidence of both TSAb and TBAb in my lab history, who was treated with LT4 after a TSH over 150, without any sign of a goiter, and without being tested for any antibodies.

My doctors didn’t care to fully diagnose my rare form of hypothyroidism because they were taught the common mantra that antibodies make no difference to LT4 therapy. Well here’s the news. TSAb and TBAb can destabilize the body’s response to thyroid therapy. I didn’t get antibody tests or a thyroid ultrasound until 13 years later, when I was very sick with very low T3 during a TBAb antibody flare, when I learned that my thyroid gland was completely atrophied at 0.5mL and my TPOab was normal.

Fortunately for others, my blind LT4 treatment began shortly after my childbearing years, so my antibody fluctuations and my chronic low T3 could not harm a future baby’s life. Women past childbearing age apparently don’t deserve autoimmune diagnoses when they become hypothyroid.

But I did have a miscarriage in my teens. I can’t help but wonder if undetected, untreated thyroid autoimmunity was a reason. I look back and see many symptoms that make it likely.

So, that’s why I had to write about this article.

Without amplification, precious gems like this Korean pediatricians’ case study article can get buried in thyroid science history. They lay there waiting to be rediscovered, hidden under sciencey titles like “A baby with congenital hypothyroidism born to a hypothyroid mother who expressed undiagnosed thyroid stimulation blocking antibody.”

It is a clear and accurate title, but only if you already know what those words mean. And as of 2021, both my body and my mind know what those words can mean.

So now I’d like to share with you more about what this story means to babies and adults with TSH receptor blocking autoimmunity.

What is the role of antibodies in congenital hypothyroidism?

Congenital hypothyroidism (CH) means that a person is born with hypothyroidism.

CH has an incidence rate of approximately 1:2,000 to 1:4,000 newborns (Rastogi & LaFranchi, 2010). Scientists speculate its low incidence may be partly due to gaps in screening.

Hashimoto’s thyroiditis does not cause congenital hypothyroidism.

Hashimoto’s in children “rarely occurs before 4 years of age, with peak age of incidence around adolescence (10-12 years)” (Ramesh et al, 2015). The antibody that causes Hashimoto’s is the thyroid peroxidase antibody (TPOab), and it is often found in conjunction with the thyroglobulin antibody (TgAb).

However, regardless of the presence of TPO and TG antibodies in neonates, “TPOAb and TgAb have no effect on fetal thyroid function” (Wang et al, 2021). It can take many years for TPOab and inflammatory cytokines to cause enough thyroid damage (lymphocytic infiltration and fibrosis) to reduce FT4 levels and elevate TSH.

In contrast, both types of TSH receptor antibodies (TRAb) can have immediate effects on thyroid function in mother and fetus.

• It is commonly known that fetal and neonatal hyperthyroidism are caused by the TSH receptor stimulating antibody (TSAb) crossing the placenta.
• However, it is less commonly known that even if a hypothyroid mother is not biochemically hypothyroid while she is treated with thyroid hormones, transient congenital hypothyroidism can be caused by her maternal TSH-receptor blocking antibodies (TBAb) crossing the placenta.

Kim and colleagues can be praised for their diagnostic skills because they found the needle in the haystack.

The incidence rate of transient congenital hypothyroidism caused by TBAb is low. It only occurs in 2 of every 100 babies diagnosed with CH (Brown et al, 1996). By contrast, the incidence of congenital hyperthyroidism caused by the opposing antibody, TSAb, is “4 times higher than that for transient neonatal hypothyroidism due to maternal TSH receptor blocking antibodies” (Alexander et al, 2017)

It is also confusing when transient CH does not present itself until after screening.

The baby in Kim’s article was fortunate. It is easier to detect TBAb congenital hypothyroidism when TSH is clearly high in the first week. But

a diagnosis “may be delayed in babies born to mothers with a mixture of stimulating and blocking antibodies. Thus, results on newborn screening may be paradoxically normal.”

(Alexander et al, 2017)

Therefore, knowing whether the mother may transmit TBAb is valuable because of the potential for ignorance or misdiagnosis of TBAb in the neonate who is NOT so fortunate.

Without careful testing, TBAb-caused transient CH may be misdiagnosed as another type of CH in which a baby is born without a thyroid gland.

This other condition is called “thyroid agenesis.” If a newborn baby is given a TSH test, FT4 test, and then treated without further investigation, or if they get a TSH plus thyroid uptake scan but not a thyroid ultrasound or a TBAb test, the lack of uptake on the scan may be mistaken for a case of permanent thyroid agenesis instead of transient autoimmune CH.

The consequence of non-diagnosis is far worse, but the consequence of misdiagnosis could be years of unnecessary LT4 hormone treatment and monitoring, and potential under- and overdose during critical, formative years.

Indeed, in thyroid science history, it required TBAb testing to disentangle these two types of CH. Before 1990, it was suspected that congenital thyroid agenesis was caused by maternal TBAb. It seemed like a logical hypothesis because it was known that the TBAb antibody was strongly associated with thyroid gland atrophy (atrophic thyroiditis, which used to be called “primary myxedema”). However, this hypothesis was tested by a 1990 study that analyzed TRAb levels in the population of mothers with other types of “sporadic” CH. They compared those mothers’ TRAb results with two mothers with primary myxedema whose newborns had transient CH and high TRAb titres. The study found the “sporadic” CH mothers negative for TRAb in all but one case, who was found to have undiagnosed TRAb hypothyroidism (Brown et al, 1990).

Therefore, they learned that thyroid agenesis does not require maternal TSH receptor blocking antibodies.

And so, 30 years later, many people don’t know that TBAb antibodies still matter, and their diagnosis may be rare only because it’s rare to have the skills and equipment to diagnose.

What is the TSH receptor blocking antibody? (TBAb)

The TSH receptor blocking antibody is one of three types of TSH-receptor antibodies (TRAb). It is #2 in this list arranged by the most commonly understood to the least understood by thyroid scientists and physicians:

1. TSH receptor stimulating antibody (TSAb). This is well known to cause Graves’ disease, autoimmune hyperthyroidism. This antibody stimulates the receptor and prevents apoptosis (cell death).
2. TSH receptor blocking antibody (TBAb or TSBAb). This blocks the receptor and causes hypothyroidism. It is highly associated with cases of permanent Atrophic Thyroiditis, but it does not always cause thyroid atrophy.
3. TSH receptor cleavage (neutral) antibody. This antibody does not cause hypo- or hyperthyroidism, but it is implicated in thyroid damage in Graves’ and may also play a role in thyroid atrophy. It sends a signal of apoptosis into the cell when unopposed by the TSAb. (Morshed & Davies, 2015)

Most people with TRAb antibodies are either #1. TSAb hyperthyroid or #2. TBAb hyperthyroid.

Although it is impossible for a person to be hypothyroid and hyperthyroid at the same time, some individuals alternate between two or three thyroid states:

• phases of TSAb-induced hyperthyroidism,
• phases of TBAb-induced hypothyroidism, and
• phases of balanced euthyroidism.

Those phases can occur in any order. Fluctuations between extremes can happen in a matter of a few weeks.

• See our review “Remissions and fluctuations in autoimmune thyroid disease: TRAb” — especially the case studies of “flip flops between hyper and hypo” on Page 2 of the article.

However, If a severe TBAb antibody flare happens to cause severe atrophic thyroiditis, the hypothyroidism is permanent even if the TSAb returns, because there is no longer enough functional thyroid tissue to stimulate.

• See “The THIRD type of autoimmune thyroid disease: Atrophic Thyroiditis“

The blocking and stimulating antibodies can also coexist in a body at the same time. When they do, they enact a “tug of war” and the antibody that dominates determines the thyroid hormone status (hypo, hyper or euthyroid) and influences the gland’s health over time.

Contrary to common belief, the existence of these antibodies cannot be predicted by the thyroid peroxidase antibody (TPOab) that causes Hashimoto’s Thyroiditis. The TPO antibody is regulated independently from these TSH receptor antibodies.

• Some people with TSH-blocking hypothyroidism, Atrophic Thyroiditis, or Graves’ have normal or unmeasurable TPOab.
• A person with Hashimoto’s and high TPOab can suffer from a TSAb or TBAb antibody flare.

Confused by all the antibodies? So are many physicians.

Unfortunately, simplistic either-or thinking about Hashimoto’s “versus” Graves’ antibodies, and utter ignorance of the TBAb antibody, can lead to misdiagnosis and harm.

To bring order to the complexity, it can be helpful to visualize these antibodies as overlapping areas of a spectrum of thyroid autoimmunity:

• See “The Spectrum of Thyroid Autoimmunity.”

Diagnosing TBAb in hypothyroid mothers

I’d like to amplify Kim and colleagues’ call for diagnosis of TSH receptor antibodies in hypothyroidism by quoting other scientists and physicians on this issue.

There are many good reasons to diagnose TBAb besides pregnancy and potential harm to a child, but let’s look at the reasons they give.

Brown and colleagues provide a persuasive argument for the detection of women of childbearing age who are subject to these antibodies:

“Although the underlying immunological mechanisms remain unclear, the persistence of these blocking antibodies in some patients for many years explains the tendency for a mother to have multiple affected offspring.

The tendency for others to switch from secreting a preponderance of stimulatory to blocking antibodies complicated in some cases by decreased thyroid gland responsivity is the basis for the change from hyperthyroidism to hypothyroidism (11, 12).

Hypothyroidism can also precede hyperthyroidism (13).

In rare instances, a more complicated neonatal
picture can result due to the coexistence of blocking antibodies and stimulatory ones.

In this case, a delayed onset of neonatal Graves’ disease occurs because of the progressive dilution of the more potent inhibitory effect over time (14).

In the present study, two mothers had more than one affected infant, and one patient has had successively a normal, a hyperthyroid, and a hypothyroid baby.

For these reasons, genetic counselling is of utmost importance to alert mothers of the high risk of recurrence and to ensure prompt evaluation (and treatment) of all subsequent offspring.“

(Brown et al, 1996)

In 1997, Pasquier and colleagues called for suspicion of congenital TBAb based on the mother’s autoimmune thyroid status:

The TBAb antibody is not truly “rare” in patients diagnosed with thyroid disease. One study found TBAb in 15% of hypothyroid patients (Nordmeyer et al, 1988) and a more recent review found TBAb in up to 10% of Hashimoto’s patients with elevated TPOab.

“Transient neonatal hypothyroidism should be suspected in infants with a history of maternal autoimmune thyroid disease. …

“early recognition is pertinent in order to avoid unnecessary treatment and parental anxiety.”

(Pasquier et al, 1997)

Pasquier’s case study was of a mother who had two children with TBAb, and she had been treated for “idiopathic primary nongoitrous hypothyroidism since adolescence” — a synonym for atrophic thyroiditis (AT).

Indeed, the activity of TBAb is even more prevalent in patients with atrophic thyroiditis (AT). Various studies have found them to be between 10 and 75% TRAb positive (Fröhlich & Wahl, 2017), making the antibody even more of a priority for testing during pregnancy if the mother has an atrophied thyroid gland.

As I’ve mentioned, severe permanent thyroid gland atrophy is believed by many scientists to be caused by TBAb, so we can begin by looking for clear signs of either thyroid atrophy or blocking antibodies, like a high TSH with no goiter.

The medical myth that thyroid atrophy is “end-stage Hashimoto’s” is a red herring. It gives a false excuse to stop looking for and understanding the TBAbs that can cause blocking hypothyroidism and/or thyroid atrophy. It is an “end-stage” myth born of scientific ignorance and ethnocentrism (many of the best articles were written by Japanese scientists), made possible by sneaky fluctuating antibodies that can disappear and flip-flop, and motivated by a medical desire to simplify thyroid autoimmunity, cut costs, and dumb down thyroid therapy. There is no evidence that TPOab can cause thyroid atrophy and a lot of evidence that TBAb can:

• See “BIBLIO: Atrophic Thyroiditis.”

But this very strong evidence of past TBAb activity, thyroid gland atrophy (usually 5mL or lower thyroid volume), is rarely discovered in hypothyroid women because thyroid ultrasounds are rarely considered beyond cases of goiter or nodules.

Unfortunately, even Kim’s case study of this mother and infant failed to comment on the mother’s thyroid gland volume. I looked to see if they published a follow-up case study article about her case, but nope, they didn’t (not yet).

The call for TBAb testing was echoed by Parks et al, in 2010, with the addition of thyroid scan and ultrasound:

“TRBAb testing should be considered for all newborns with a maternal history of hypothyroidism.

Because of the blocking antibodies, the thyroid gland cannot be visualized by ¹²³I or ⁹⁹Tc scans, but the gland should be demonstrable in the normal anatomic location by ultrasonography.

(Parks et al, 2010)

Indeed, if you read it again carefully for its logic, the passage above suggests that in the absence of a TBAb test,

1. an empty iodine uptake thyroid scan in the presence of
2. a normal thyroid ultrasound

can confirm the diagnosis of TBAb by visualizing the effects of the antibody on a normal thyroid.

Another class of patients with high TBAb activity has very recently come to light: Graves’ disease after radioiodine (RAI) ablation of the thyroid. Although titres of the blocking antibody were considered positive if more than 17%, the incidence of TBAb positivity increased tremendously:

• Before RAI, only 4.5% had TBAb
• 1-6 months after RAI, 55% had TBAb, and 10% had both TBAb and TSAb.
• 7-12 months after RAI, 58% had TBAb, and 32% had both.
• 13-60 months after RAI, 65% had TBAb, and 7% had both.
• 60+ months after RAI, 56% had TBAb. (Fang, et al, 2021)

However, at the end of 2021, medical ignorance of TBAb in hypothyroid mothers may still be a barrier to the detection of neonatal TBAb. The antibody is rarely diagnosed as a contributing cause of a mother’s hypothyroidism before pregnancy.

For every diagnosis there needs to be a test.

Testing challenges

In North America and Britain, it is difficult to find a blood test that can accurately measure titres of the TSH receptor blocking antibody (TBAb). False negatives may occur more often than one suspects, as described by Diana and colleagues:

“The co-presence of TBAb and TSAb in the serum of a patient has been speculated to have a counteracting effect, similar to a tug-of-war [6].

In TSAb bioassays, the co-presence of TBAb and TSAb created a net sum, possibly evening out and remaining non-detectable.

• TSAb [assay] detects net TSAb, but cannot detect TBAb.

• TBAb [assay] detects either net TBAb (positive inhibition) or net TSAb (negative inhibition).

• Neither assay detects them ‘independently’ [12].”

(Diana et al, 2017)

But don’t give up. There are ways to get around this current problem.

This antibody makes footprints in the sand.

• Look for signs like the one mentioned above, the thyroid scan may contradict the thyroid ultrasound.
• Where there’s a medical will, there’s a way to diagnose. Be creative. Think about the role of recombinant human TSH (rhTSH, Thyrogen brand) injections in the diagnosis of TSH receptor blocking antibodies. If injected TSH does not raise T4 and T3 levels consistent with the gland’s health status in ultrasound (where even Hashimoto’s damage can be seen), something is blocking that signaling pathway.
• I’ve written a guide with memes: “Infographics for Antibody testing.”
• I’ve also written about how inappropriate TSH secretion during LT4 treatment is a sign: “The TSAb stimulating antibody can lower TSH despite euthyroid status.” This same mechanism can inflate TSH via the blocking antibody, as I’ll show in my own case study and others to come.
• Read stuff to learn more than most specialists know. Many endocrinologists do not read their own science that explains how TRAb antibodies can manipulate the TSH via pituitary TSH receptors: “How TSH ultrashort feedback works, and antibody interference.”

Let’s move forward to better diagnosis.

What does Kim’s article say about the challenges of diagnosis? (I’ve corrected a few minor errors in English translation)

We described a baby with transient congenital hypothyroidism born to a mother who was not [aware of] the cause of her hypothyroidism. …

In adult hypothyroid patients with autoimmune thyroiditis, hypothyroidism attributable to TSB Ab is uncommon (15%
of patients).

As measurement of TSH receptor Ab levels is considered appropriate only in patients with Graves’ disease, such tests are recommended only if a pregnant woman has a history of Graves’ disease, not hypothyroidism.

For this reason, it is difficult to define the cause of hypothyroidism caused by TSB Ab. In this situation, transplacental passage of TSB Ab can cause neonatal hypothyroidism in a pregnant patient.

Although several cases [of] TSB Ab-associated congenital hypothyroidism have been reported, screening [for] TSH receptor Ab is still seldom [done] in adults.

And almost all clinicians have focused on only treatment of hypothyroidism or hyperthyroidism regardless of the presence of TSH receptor Ab in [a] baby [or] adult.

However, it should be borne in mind that a hypothyroid baby born to a mother with hypothyroidism attributable to TSB Ab may have severe neonatal hypothyroidism.

Therefore a testing for TSB Ab in adults with hypothyroidism with TSH receptor Ab is required.

Especially in pregnant mothers, TSB Ab should be assayed; this is important in terms of both maternal and child health.

(Kim et al, 2016)

Let’s ponder what they’ve just said.

Unfortunately, in most health care systems today, upon diagnosis of acquired hypothyroidism AFTER the neonatal phase, the bias is to blindly presume absence of TRAb of any type — stimulating, blocking, or cleavage. Almost no one bothers to use the TRAb antibody test because it is incorrectly presumed only to be active in cases of florid Graves’ hyperthyroidism.

Unfortunately, most acquired hypothyroidism cases are presumed to be caused by Hashimoto’s thyroiditis alone if the TPO antibody level is elevated. If the TPO antibody is not elevated or not tested at all, the cause may be left undetermined and treatment goes on its merry way, blind to both etiology and prognosis.

However, Kim’s case study and others confirm that the presence or absence of the TPO antibody and/or TSAb antibody does not rule in or out the presence or absence of the TBAb antibody.

Why should one have to rely on a series of fortunate events to find TBAb in a child before it causes more harm to a mother and her children?

Why are people so hung up about the TPO antibody, when it’s not a “gateway” antibody? It’s one of many antibodies that can harm. It’s not a proxy for all forms of autoimmune thyroid disease. It’s not the only cause of autoimmune hypothyroidism.

As bad as TPOabs can be when it joins hands with those nasty inflammatory cytokines, a person thought to have Hashimoto’s can suffer from more than just TPOab. This mother and baby sure did, with almost every thyroid antibody out of the ball park at the same time, TRAb, TPOab, TGab, TBAb and even the presence of TSAb!

Some patients may have fluctuating or concurrent TBAb and TSAb that makes “net blocking” activity difficult to assess without specific test for TBAb.

Overall, Kim’s study shows one reason why it helps to have a TBAb hypothyroidism diagnosis.

It matters in cases of transient congenital hypothyroidism which may be misdiagnosed as permanent CH, or left untreated if the TSH does not rise at the right time for screening.

TBAb diagnosis also matters before pregnancy and after childbearing years, and also in MEN.

Let’s not be ageist or sexist. That baby may be a boy or a girl. Someday they may become hypothyroid from a TBAb attack like their mother’s.

It matters to people with atrophied thyroids and to people with blocking antibodies before their thyroid becomes atrophied. Does anyone care about preventing thyroid atrophy?

It matters in people with Graves’ disease after RAI ablation or thyroidectomy, when TSH wobbles illogically due to TBAb/TSAb antibody interference, when doctors mistakenly trust the TSH and blame the patient for noncompliance.

It matters because TSH receptors are located in many tissues beyond the thyroid gland, and therefore TSH-receptor autoimmunity is a multisystem disorder.

It matters because there is no such thing as an antibody-ectomy, and LT4 therapy does not always treat people with these fluctuating antibodies very well.

Want to support action?

We are hoping to launch a capacity-building campaign in 2022 so we can launch a Canadian provincial petition and a federal petition, better than the petition we began with in 2018.

Our campaign theme will be “falling through the cracks.” It will focus on finding and fixing cases of undiagnosed or mistreated thyroid disease that have fallen through the cracks of our medical system.

See our Donate and Support page in our main menu.

– Tania S. Smith, PhD,

Thyroid patient, thyroid science analyst, and President, Thyroid Patients Canada.

References