Thyroid UK
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A child with rash told to start Synthroid.hashimoto?lyme?

Hello. An 8 years old with a red rash was asked by her dr. to do some blood tests because, he couldn't tell why she has the rash. With no prior history in thyroid issues, blood tests results showed the following:

FreeT4 0.89 ( range0.8-2.3)

Free T3 4.55 (1.8-4.6)

TSH 36.72 ( 0.3-5)

Antithyroglobulin Ab. 7 ( <15.0)

Antiperoxidase Ab. 55.3 ( <10)

What do you think ? Is she hypo ? Hashimoto?

The dr. prescribed 25 mcg Synthroid already. Any help is appreciated please.

23 Replies

I'm not sure we can comment much on children's health. In general the blood tests suggests she has a failing thyroid gland. As the gland starts to fail and fT4 falls the TSH rises so as to stimulate the thyroid more. The lowish fT4, highish fT3 are typical as T4 to T3 conversion increases in an attempt to maintain active (T3) thyriod hormone levels.

It is important that children get expert support initially for thyroid problems because left untreated they can lead to developmental problems, although this really applies to infants and babies. Also, the reference intervals for children are different to adults, the doctor needs to note this when titrating treatment.

It was correct to start the child on Synthyroid, she should have another blood test in a month or so. It might be an idea to ask for a referral to a paediatric endocrinologist for her initial care. Once she is sorted the family doctor can take over ongoing care. She will most likely need to take thyroid hormone for life, which is not a problem as you are replacing a natural hormone and not taking a drug.

You should make a list of any questions and put these to your doctor. Hypothyroidism could lead to a rash, usually in the shins. If the rash disappears with thyroid hormone treatment then it might well have been due to the thyroid. If the rash remains the doctor will need to find another cause but of course continue to treat her thyroid.


Thank you for your reply. Don't you think she might have got a tick, which caused her antibodies to rise? I am suspecting a lyme disease. I am thinking about asking her doctor to test her for lyme disease. would it be a good idea?

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I don't know anything about lyme disease but it sounds a bit extreme. I'm guessing it would depend upon where the rash is and how quick it came on. I'm sure there will be other signs of lyme disease but I've no idea what they are! There can be so many causes of a rash, it could be stress or a seasonal allergy or it may just go away.


jimh111 has made suggestions I'd agree with. I relied on my daughter's GP who didn't get her referred to a Specialist and was so angry with me for 'putting ideas into her head' when I mentioned my sister had been diagnosed with Rheumatoid and I rue the day I didn't look further as she is now severely disabled. I cannot look back and say 'I wish'.......

This is one link and if you 'google' there's more than one in the same subject:


I live in the U.S. and my husband has had Lyme disease twice. The first signs of Lyme are usually not a rash like measles or hives, but a red welt where the tick bit him and then a bull's eye group of circles leading out from the central welt. You can look up pictures online. They did a blood test on him and then he was prescribed 42 Doxycycline tablets. The blood tests often do not come back positive, but if there is the bull's eye markings then they can pretty much know its Lyme. There are about 4 other tick born diseases, so as a precautionary measure I would ask your child's doctor to do a tick panel. Has your child been in the woods or weeds? It can't hurt to run it by the doctor. My husband also ran fever and have flu-like symptoms.


I would just like to add that Synthroid is not natural, not as far as the body is concerned anyway, it is synthesized. If the pharmaceutical industry was able to create a thyroid drug truly identical to the natural hormone it is designed to replace it would not be able to lay claim to a patentable proprietary, profitable product. NDT is the only natural thyroid replacement product.

Like all drugs Synthroid is not risk free and can interfere with calcium causing it to be lost in the urine and has a negative impact on insulin.

I wouldn't want to comment on a child's health, but I would want to thoroughly investigate everything that may be causing/contributing to her symptoms, anything from skin contact, air pollutants, food allergies and infections.


Just for clarification. Levothyroxine (Synthroid) is synthesized levothyroxine. The thyroid produces a number of thyroid hormones including levo and dextro thyroxine (denoted 'T4'). The dextro form is a mirror image isomer of levo, levo is much more potent, detro has very little effect and to be honest has not been studied.

Levothyroxine is converted by the body to triiodothyronine ('T3') which is the active form of the hormone. For most patients, especially those who present with high TSH, low fT4 the patient is able to convert T4 to T3. Levothyroxine has the advantage that it has a long half life (7 days) and so the patient receives a stable dose. Liothyronine (T3 tablets) has a short half life of 1 to 2 days) which means that blood levels of T3 vary. This isn't so important but it makes it very difficult to interpret blood hormone levels. Although it is more important to pay attention to signs and symptoms a young child may not be able to relate subtle variations in their condition.

Natural dessicated thyroid (NDT) is dried extract of pigs thyroid. The major prescription only brands such as 'Armour' are quality products, I wouldn't trust other forms of NDT for a child. NDT has a much higher proportion of T3 and so gives the wrong balance of hormone. However, some patients need NDT, they don't recover with levothyroxine. It's true that levothyroxine also gives the wrong balance (it doesn't contain T3) but usually the patient can make sufficient T3 from levothyroxine (L-T4).

Sorry if this is too detailed. Levothyroxine is the same molecule as naturally produced by the thyroid but it doesn't contain all the thyroid products. It usually works for most patients and is much cheaper than prescribed NDT. Levothyroxine came off patient many years ago and has very small profit margins due to its low price. Many doctors are (rather unreasonably) unwilling to prescribe NDT.

I recommend using levothyroxine unless you find it just isn't working. Once she has been stabilised on a dose make sure your pharmacist gives you the same brand each time as the potency can vary between brands.

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No, its not too detailed at all, but I am aware of the various forms of Synthroid/Levothyroxine/NDT although I am sure it is information that is useful for everyone. However, the only point I was trying to make was that Levothyroxine is not natural - being an isomer/mirror image doesn't make it natural. Admittedly it does have the same chemical structure but it takes on a different shape - that's all I was trying to say really.



As far as I know synthetic levothyroxine is identical to human levothyroxine with the same shape (apart from initially having sodium bonded to it). It is of course not identical to the other hormones T3, T2, and T1 (not sure if the latter two are strictly hormones). And levothyroxine is different to dextrothyroxine which is the mirror image of levothyroxine. The essential point that levothyroxine sodium is not natural is correct but once in the blood levothyroxine is exactly the same molecule as the levothyroxine produced by the thyroid.

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Completely agree about levothyroxine.

Dextrothyroxine has been used - but it has some oddities and was generally abandoned due to the effects it has on the heart.

Still has niche applications:

Have to wonder how much is costs?


Jimh111, I am not trying to be argumentative or awkward, just someone who has had a long battle with an UAT and a struggle to get to the bottom of the myriad of information/misinformation I found myself faced with. I have no desire to prove myself right about anything, in fact I would much prefer to be proved wrong - its the only way I can learn. This is a link, which I hope you will have the time and patience to plough through:-


I've read this advertorial! The author is rather confused because although the T4 in 'Thiroyd' is bound up differently it is the same T4, specifically levothyroxine. (I'm surprised they were not aware of it being bound right from the outset). Once the levothyroxine gets into the bloodstream it binds to human TBG, TTR and albumin. Regardless of all the dubious detail in this blog about absorption the actual amount of total T4 and free T4 can be measured by an assay. These assays are highly specific and accurate to within a few percent. So, all the hypothesised issues around absorption and binding to TBG are not relevant, the blood tests will tell you how much is free or bound.

However, many people seem to need NDT for whatever reason, the presence of T3 or possibly some other hormone. On the specific point about levothyroxine it is exactly the same in both L-T4 and NDT. My point being that someone taking levothyroxine is taking a hormone their thyroid makes and not a drug.

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Well, they say attack is the best form of defence. It is not technically an advertorial, its not an advert and its not an editorial. It is an independent bio-analytical chemist from a closed facebook forum challenging a manufacture about the efficacy of their product - it is not being used for publication. If you think the poster is dubious or lacking in knowledge, I can't really comment. However I have no doubt that when levo-T arrives in the blood stream it follows the same pathway as the thyroxine produced naturally in our own gland.

But Levo-T4 is not the same as either our own thyroxine or NDT. It is similar but not identical, it has the same chemical composition but it acts like putting your left-hand glove on your right hand - its not identical. I assume that Levo-T4 eventually deiodinates to T2 and T1 (not sure) but unlike NDT it doesn't contain calcitonin which is needed to regulate calcium. How much calcitonin can/or is produced by a damaged thyroid I do not know - depends on the extent of the damage I assume.

We have no doubt reached an impasse, but my mind is always open (goodness knows I have changed it many times) but for now thanks for your time - I appreciate your input.


Trouble with calcitonin is that a) we know that porcine calcitonin is not identical to human calcitonin; b) we have little, if any, evidence that it can actually reach the bloodstream; c) we have no idea much much, how consistent or almost anything else about the calcitonin content of desiccated thyroid; d) we know little of the impact of porcine calcitonin on humans.

We might do well to remember that salmon calcitonin was withdrawn as it seemed possibly implicated in causing cancer.


Thank you for your reply. Pig hormones resemble human hormones most closely, only humans can make human thyroxine, so unless they extract thyroxine from human cadavers nothing else is going to be exactly the same. However, it does seem counterintuitive that if the thyroxine in NDT is effective (which is the closest we can get to the natural thyroxine produced by our own glands) that the calcitonin contained within it wouldn't be just as effective.

Salmon calcitonin is not derived directly from salmon, it is synthetic, made in a lab, its structure is just modelled on the calcitonin found in salmon.

At the end of the day I don't think there is much (if any) reliable independent research to be had on pig calcitonin (although if you find any I would be very interested) and its role in the human body. As most funding for medical research comes from pharmaceutical companies, I don't see that changing any time soon.

Thanks again


Thyroxine is a pretty simple molecule by biological standards. Manufacture of thyroxine is a process that has been conserved in animals, especially those with backbones, for an extremely long time. I do not believe that there is any difference between porcine, human, and synthetic thryoxines except the acknowledged sodium salt. That there may be significant differences in delivery is certainly true - as also impurities whether from manufacture or as breakdown products.

Calcitonin is a complex protein.

I cannot see any reason at all to assume that porcine calcitonin is any more similar than other porcine proteins - that is, they vary in similarity but many differ at least a little.

I certainly agree there is little evidence about porcine calcitonin. There is some:

In human gastric fluid, the larger peptides including somatostatin, calcitonin, secretin, glucagon, and insulin were metabolized rapidly...

Of course, we do not have good evidence for the effect of the rest of desiccated thyroid (thyroglobulin, etc.) on the metabolism of peptides such as calcitonon.


I am not entirely sure that I understand your second sentence "Manufacture of thyroxine is a process........." so don't feel able to comment. I agree porcine and human thyroxine molecules are the same but neither of them are the same as LT4 which is chemically the same but it has a different shape. Shape is important - the body knows the difference. Delivery of replacement thyroxine (from whatever source) I think is always destined to have a variety of difficulties, we are not designed to swallow thyroxine - not that there seems to be much choice, its better than the alternative.

Regarding calcitonin, I wasn't trying to say porcine calcitonin had more similarities with human calcitonin - just that if the whole porcine molecule works adequately in the human body the calcitonin contained within it must be equally adequate, although how good a job it does will no doubt depend on the health of the gut it arrives in.

I read your link, it was very interesting and probably goes some way to highlighting what happens to calcitonin when it arrives in the gut. is not a direct study of porcine calcitonin in the human gut. It is a study of pharmaceutical calcitonin et al in the gut.


Shape is important - the body knows the difference.

What is the difference in the shape? (That is, once it has been absorbed.)


Thats a very good question - not sure I can give you a satisfactory answer.

Thyroxine has two isomers - Levo-T and Dextro-T which are stereoisomers. I think the body has a preference for L-isomers and this is what is contained in Levothyroxine (not sure if any D isomers get left in - not deliberately anyway). Isomers of the same molecule have the potential to have different physical or chemical properties. An extreme example of an unwanted side effect of an isomer was the drug used for morning sickness which caused deformities in the fetus - thalidomide - but it did the job it was designed for in preventing morning sickness.

I think the pharmaceutical industry has tightened up its procedures since back then to ensure that unwanted isomers are tested more thoroughly and/or removed. Using single isomers (LT4) these days is more popular in the pharmaceutical industry because it reduces adverse drug reactions and lessens the metabolic, renal, hepatic load of the drug.

LT4 does the job it was designed to do - provide T4 only, which then (I assume) goes on to convert into T3 using the body's own natural mechanisms.

If isomers are known to have adverse reactions and interfere with other processes in the body I don't see why LT4 should be excluded from that (unless you know differently). There are plenty of natural isomers in the body which have well established functions and cause no adverse reactions - why is it then that the adverse reactions to isomers only seem to occur when they are made in a lab. Do you think the body might have just figured it out?


Meant to say, I found the study quite reassuring in the sense that they chose the pig and human model as comparisons for the study. They are at least acknowledging that the physiology of the pig is near enough to our own as to provide similar results.


With a TSH of 36 the child is hypothyroid. With positive antibodies she has autoimmune thyroid disease and her thyroid is going to get more and more damaged as time goes on.

In the UK, doctors don't treat the thyroid on the basis of just one test showing problems. There are viruses that can raise TSH temporarily, or affect thyroid output temporarily. So they wait until a second test is done three months later. If thyroid function tests are still abnormal then they treat. (That is in an ideal world. There are many doctors who get it wrong and make the patient wait a lot longer or ignore poor results completely for as long as possible. And I would agree that waiting three months when you feel awful is torture.)

If there is a suspicion that the child has Lyme Disease then waiting to test for that and treat it is NOT a good idea - tests and treatment (if necessary) should be done as soon as possible. And Lyme Disease can, apparently, trigger Hashimoto's Thyroiditis (autoimmune hypothyroidism).

Some reading for you :

Quote from the above link :

Specifically, some research has shown that the Borrelia bacteria that causes Lyme Disease can trigger Hashimoto's thyroiditis in some people. So there are some patients who had undiagnosed or untreated Lyme Disease, only to go on to develop an underactive thyroid later.

To find the above links I searched for

"can lyme disease cause thyroid issues"

There are lots more links to look at.

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Just to add to my previous response ...

I'm assuming that you live in the US, because you mentioned Synthroid.

I just wanted to point out that Synthroid has a massive advertising budget, and on the strength of that many Americans assume it must be the best product. But underneath all the hype it is just Levothyroxine, like all the other brands of Levo tablets that are available in the US, and they all have to have the same strength of product and life span of product as Synthroid does. If the child taking the Synthroid doesn't get well on it then it is well worth trying the others.


Thank you everyone for your informative replies. Really appreciate it. Bless you all.


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