I wondered if anyone could answer a question for me?
In 2012 I was tested for Thyroid Peroxidase antibodies which came back positive, and Hashimoto's equates to the presence of antibodies to thyroid peroxidase. Previously I seem to remember that the enzyme Thyroid Peroxidase is involved in the conversion of T4 to T3, though can't quite remember where I read it.
Recently I read that there are 3 enzymes / genes involved in the conversion of T4 to T3, which are the Deiodinases (D1, D2 and D3). However, they then go on to say that deiodinase is a peroxidase enzyme which is involved in the activation or inactivation of thyroid hormones.
So I was wondering if the TPO antibodies tested for are the deiodinase enzymes that are being referred to as D1, D2 and D3?
And if it is whether it varies between them, such that they are specific to D1, D2 or D3?
Why I'm wondering is that I also read that some of the enzymes just convert T4 to T3 whilst others may convert to rT3 (inactive) so I was wondering if the presence of the antibodies / or poor functioning to one conversion path leaves you over reliant to a another less reliable pathway (as can get T3 or rT3)?
The other idea is that rT3 is like a Scottish £10 note (from cash converters) that you can't spend and £10 (T3) you can (from the bank), so it might look like you've withdrawn £20, your balance (T4) has decreased by that much but in some cases you can't use it. I was wondering if one of the pathway's is like cash converters (might be able to use but might not) and one is like the bank?
Are my hypothyroid symptoms because my metabolic currency in circulation is low (T3) or based on an unreliable pathway, such that I have a large number of Scottish £10 notes in circulation (rT3) that I can't use?
Many thanks, reading raises thousands of questions and apologies for my weird way of thinking
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Elizabeth14
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Thyroid Peroxidase is an enzyme used within the thyroid as part of the process of creating thyroid hormone. No point me trying to say any more than Wiki does for this:
Thyroid peroxidase, also called thyroperoxidase (TPO) or iodide peroxidase, is an enzyme expressed mainly in the thyroid where it is secreted into colloid. Thyroid peroxidase oxidizes iodide ions to form iodine atoms for addition onto tyrosine residues on thyroglobulin for the production of thyroxine (T4) or triiodothyronine (T3), the thyroid hormones.[1] In humans, thyroperoxidase is encoded by the TPO gene.[2]
One of the reasons that Thyroid Peroxidase antibodies are regarded pretty much as diagnostic is that in a healthy person, all the Thyroid Peroxidase enzyme is within the thyroid. It is only when the thyroid is damaged that some of the content spills out - carrying some Thyroid Peroxidase into the bloodstream. The immune system then tries to mop up that Thyroid Peroxidase by releasing Thyroid Peroxidase antibodies. Those antibodies attach to molecules of Thyroid Peroxidase marking them to be destroyed/removed from our systems by macrophages.
It is possible for physical damage (e.g. could be a car seatbelt or surgery) to damage the thyroid such that some Thyroid Peroxidase is released. This would be expected to be transient whereas with an autoimmune disorder slowly destroying the thyroid, there will be some Thyroid Peroxidase for long periods - many years.
Although the thyroid, in a healthy person, both creates and manages T3, a large proportion of the conversion of T4 to T3 takes place in the liver, kidneys, skeletal muscle, brain, etc. As well as within individual cells of the body.
I know little about how the developing body of someone without a thyroid manages thyroid hormone levels and conversion but your friend is simply not the same as someone who has a thyroid and is healthy. Their whole development will have tried to cope with the situation.
Yes but if you have hypothyroid symptoms you are not healthy. If you have an autoimmune reaction whereby antibodies mistakenly target the thyroid the result will be the same and there will be no functioning thyroid to convert T4 to T3, ultimately you will be in the same position.
There are genetic conditions which prevent a gene functioning (Deiodinase 2) correctly either completely or less effectively (only 10% function).
Deiodinase 2 (thyroid) seems to do just outer ring deiodination T4 to T3
If an autoimmune reaction destroys the thyroid you will be dependent on peripheral conversion.
Deiodinase 1 in the liver seems to result in outer ring deiodination or inner ring deiodination (T3 or rT3) of Thyroxine
Propranolol reduces peripheral conversion of thyroid hormones, and did not agree with me and I think because of antibodies / genetic I am more dependent on peripheral conversion.
When propranolol given (had 2 tablets), ultimately there was loss of consciousness as it impaired a system that I was more reliant on.
If you have an autoimmune reaction whereby antibodies mistakenly target the thyroid the result will be the same and there will be no functioning thyroid to convert T4 to T3
But, TPO antibodies do not target the thyroid. They target the TPO leaked into the blood during an immune system attack on the thyroid. They clean up the blood, they do not destroy the thyroid either by mistake or by design.
And, as helvella said, most conversion is done in the tissues, not in the thyroid. The thyroid makes T4, and it makes T3. And it is responsible for a little conversion of T4 to T3, but not the bulk of the conversion. That is done outside the thyroid. So, if you have no thyroid, it won't make a lot of difference as far as conversion is concerned. The difference is that you will lack the T3 made directly by the thyroid and be entirely dependant on conversion.
Hi but this says that in Hashimotos thyroiditis the granulocytes, neutrophils and eosinophils do target the thyroid, whereby there is granulocytic infiltration of the thyroid as part of the autoimmune reaction and is thought to be a chronic inflammatory reaction, (antigen presenting cells etc)
This is an extract:
The antibody profile was available in 22% of patients. Of these, anti-thyroid peroxidase antibodies were raised in 81.81% of patients and anti-thyroglobulin antibodies were raised in 63.63% of patients.
In the present study, high lymphoid to epithelial cell ratio was seen in 78% of cases, and 74% of cases showed Hurthle cell change. Follicular atypia was seen in 36% of cases. Lymphoid follicle formation was seen in seen in 54% of cases.
Follicular cell infiltration by lymphocytes, eosinophils and neutrophils was seen in 72%, 48% and 26% of cases, respectively. Plasma cells were seen in 18% of cases.
Now I was TPO antibody positive in 2012, TSH 6.2 at the time, I have hypothyroid symptoms but one of the most consistent findings has usually been a raised white cell count (over years the GP even did a little graph of it at the time), nothing ever prescribed. There is an inflammatory reaction which is antibody mediated and targeted on the thyroid.
Exactly but it depends which deiodinase is being used the thyroid Deiodinase 2 T4 to T3, liver Deiodinase 1 T4 to T3, or T4 to rT3
It will make a difference depending on the rate of conversion, and the quantity of the product.
The Deiodinases, D1, D2 and D3 differ and they vary in functionality and product whether T3 or rT3
I did not say TPO was a deiodinase, what the article is saying is that there is an association between the presence of TPO antibodies and Hashimotos thyroiditis which results in a chronic inflammatory reaction in the thyroid.
There is an infiltration of thyroid follicles by neutrophils, eosinophils and granulocytes the percentages are shown in the article.
Granulocytes and neutrophils can act as antigen presenting cells to lymphocytes.
Neutrophils are the most abundant circulating leukocytes and are critical effector cells of the innate immune system. ... Both at the site of inflammation as well as in LNs, neutrophils have been shown to interact with lymphocytes and antigen-presenting cells (APCs) or may act as APCs themselves (from article below).
Neutrophils acquire the capacity for antigen presentation to memory ...
There is presumably the release of inflammatory cytokines, resulting in chemotaxis which results in the infiltration by the neutrophils, and granulocytes in the thyroid
Previously I seem to remember that the enzyme Thyroid Peroxidase is involved in the conversion of T4 to T3, though can't quite remember where I read it.
Recently I read that there are 3 enzymes / genes involved in the conversion of T4 to T3, which are the Deiodinases (D1, D2 and D3). However, they then go on to say that deiodinase is a peroxidase enzyme which is involved in the activation or inactivation of thyroid hormones.
So I was wondering if the TPO antibodies tested for are the deiodinase enzymes that are being referred to as D1, D2 and D3?
Which is extremely confusing, but I interpreted it as best I could.
what the article is saying is that there is an association between the presence of TPO antibodies and Hashimotos thyroiditis which results in a chronic inflammatory reaction in the thyroid.
Yes, that's right. But, you don't have to have high TPO antibodies to have Hashi's. The antibodies are not the disease. It is not the TPO antibodies which attack the thyroid, and some Hashi's people never develop high antibodies, but the thyroid is slowly destroyed, anyway.
Enzymes are proteins and every protein has a code, which is specified by a gene.
So D1, D2 and D3 are deiodinases which are 3 different enzymes, whose code is specified by 3 different genes DIO1, DIO2 and DIO3 but have the same function.
De (removal of) / iodino (iodine) / ase (enzyme)
Each has the same function the removal of the iodine, which may result in conversion of T4 to T3 (removal from outer phenolic ring) or rT3 if it is from inner phenolic ring
From: Essentials of Medical Biochemistry (Second Edition), 2015
The below is what I've been trying to find out TPO catalyzes both iodination and coupling of iodotyrosine residues in Thyroglobulin (that was the original question and what I've been trying to find out)
Now I could do with a picture so I can look at the structure, and the reaction etc, a picture paints a 1000 words and all that
Thyroid peroxidase (TPO) is a key enzyme in thyroid hormone biosynthesis. It catalyzes both iodination and coupling of iodotyrosine residues in TG. Human TPO is located on chromosome 2p25, with 17 exons.
The thyroid peroxidase, is an enzyme expressed mainly in the thyroid where it is secreted into colloid. (Wikipedia)
If your immune system has been activated such that there are antibodies to TPO your body will recognize TPO as foreign and will try and destroy it. The TPO is secreted into colloid.
Any cell capable of acting as an antigen presenting cell (neutrophils) will bind to the particular epitope on the TPO enzyme which was responsible for activating the immune system in the first place and which it recognizes as foreign.
Antibody to TPO is present, the immune system has been activated, cells of the immune system capable of recognizing the epitope on TPO which activated the immune system will bind to TPO and that is secreted mainly in the thyroid into colloid.
So that is where the cells of the immune system will go, some immune cells may be found in plasma but others can move into tissue. Neutrophils (or any other APC) have an antigen binding site which has been activated (if you have TPO antibodies) and which recognizes TPO as foreign. That is why they are infiltrating the thyroid it is heading for the TPO in the colloid, it regards TPO as foreign and as such the immune system will attempt to remove it, the thyroid would be collateral damage
Having raised TPO antibodies means you have Hashi's, yes. But, the TPO antibodies themselves, do not enter the thyroid. The do not target the thyroid, and they do not attack the thyroid. It is the TPO in the blood that they are interested in. That's all.
Not really sure what you're asking, but seems to me you're confusing Thyroid Peroxidase with Thyroid Peroxidase antibodies. They're not the same thing.
Thyroid Peroxidase, TPO, is found in the thyroid. During an immune system attack on the thyroid - as happens with Hashi's - some TPO leaks out into the blood, where it shouldn't be. The TPO antibodies then come along to clear it away and destroy it. And, it's the TPO antibodies that is tested for when Hashi's is suspected, not the TPO itself.
rT3 is a sort of safety valve for the protection of the body. There is always some rT3 in the system, but it can rise to excess levels under certain circumstances. One of the circumstances is when a person has a conversion problem, and T4 builds up to a certain level and converts to more rT3 than T3. This is so that the person does not become 'hyper', with excess T3. rT3 stays in the body for a couple of hours, and is then converted to T2, the T2 to T1, and the component parts are then recycled. That way, the T4 is not entirely lost.
But, there can be other causes of high rT3, like and infection or starvation, when the body needs to conserve energy. The T4 is then converted to more rT3 than T3 so that the body is less able to exert itself, thereby conserving life.
I'm not sure high rT3 has anything to do with TPO, which, as you say, is involved in conversion, but conversion inside the thyroid itself - not peripheral conversion. The thyroid does produce a little rT3, but not very much, as far as I know. But, I'm not an expert, by any means!
No a friend has no thyroid (congenital hypothyroidism) and is on T4 only, as such he would be unable to convert at all hence it has to be done peripherally.
The reason for congenital hypothyroidism may result fro dyshormogenesis or as a result of specific genetic abnormalities (TSHR, MAP8, FOXE1) which can prevent the thyroid developing at all (agenesis, hemiagenes, etc)
Propanolol decreases peripheral conversion of t4 to t3
T3 and rT3 are structurally the only difference is that the iodine is remove from the outer phenolic ring to produce T3 whilst if removed from the inner phenolic ring it produces rT3 whilst similar structurally they are vastly different in functionality
There are genetic differences which may effect the production of thyroid hormones the insertion of an inappropriate stop codon can prevent the conversion totally which is the basis of the genetic test Dio2
I'm sorry, what has your friend's congenital hypothyroidism got to do with TPO antibodies and rT3? That doesn't make any sense.
I know what congenital hypothyroidism is, and I know what rT3 is, how it is converted. So, why are you quoting all that at me? As far as I understood your original question, your quotes have nothing to do with anything.
Hi what I was thinking if you have antibody attached to thyroid peroxidase as with TPO antibody, and the latter functions in deiodination, then there will be fewer binding sites available at which deiodination can occur.
Deiodination will be reduced as there are fewer empty sites at which this could occur especially if Dio2 not functioning effectively.
If there are 3 types of deiodinase enzymes are they tissue specific as in the thyroid, so that deiodination of T4 to T3 is via Deiodinase 2 (1 iodine atom removed from Thyroxine and always forms T3)
Or like the liver so that deiodination of T4 to T3 is via Deiodinase 1 (1 iodine atom removed from Thyroxine and can form either T3 or rT3)
I've attached a reference below (which if reading correctly liver uses Deiodinase 1 can do T3 or rT3:
What I'm thinking is that if in the situation of my friend you have no thyroid, or there is a genetic problem Dio2 (gene that can be checked) which stops it converting T4 to T3, you are then reliant on alternative paths the first alternative being the liver but here it is deiodinase 1
From what this says though rT3 is the preferred substrate and the conclusion was:
These results suggest that in human liver microsomes a single enzyme catalyzes the deiodination of the outer as well as the inner ring of iodothyronines by the same catalytic mechanism and with the same substrate specificity as the type I deiodinase of rat liver.
ORD (Outer Ring Deiodination) - T3
IRD (Inner Ring Deiodination) - rT3
I'm wondering if deiodinase 2 is predominantly in the auditory system and is the same in the thyroid hence congenital (genetic Dio2) problem would then cause congenital hypothyroidism and deafness in some cases
Why is there a link between tinnitus and hypothyroidism?
I was thinking if you have antibody attached to thyroid peroxidase as with TPO antibody, and the latter functions in deiodination, then there will be fewer binding sites available at which deiodination can occur.
The antibody isn't attached to thyroid peroxidase in the thyroid, where the thyroid peroxidase carries out its functions. It's when the thyroid peroxidase leaks into the blood, where it doesn't belong, that the antibody comes along to remove it. So, that theory doesn't hold water, I'm afraid.
Also, as it says, thyroid peroxidase is involved in the production of thyroid hormone, not the conversion. I made a mistake there. So, nothing to do with deiodination.
a genetic problem Dio2 (gene that can be checked) which stops it converting T4 to T3
A DIO2 defect doesn't mean that the T4 won't be converted to T3, it means there is a potential conversion problem.
Conversion doesn't just happen in the liver, it can happen in most tissues.
I gather from the above that you are now linking rT3 with deafness. But, I don't think there's any connection. rT3 is inert. But, I'm afraid I don't know the link between tinnitus and hypothyroidism, except that every cell in your body need T3 to function correctly. Presumably that means the auditory system, too. Although, tinnitus can be linked to nutritional deficiencies, so there could be an indirect link there.
Firstly, a Scottish £10 is perfectly valid tender anywhere in the UK and so can be used as payment in England. But apart from that, your metaphor doesn't work. Having T4 in your system isn't like money in a bank account whereby after say, your salary has gone in, you then make withdrawals throughout the following month until next pay day; and your bank statement will identify where the withdrawals have gone, such as to T3 or FT3, whilst the balance diminishes with each withdrawal. When well, or optimally medicated, there is a continuing replenishment of thyroid hormones available to the body, because to put it simply, the hormone system is minutely managed by a set of feedback/monitoring mechanisms. RT3 is not a redundant artefact, or the body getting something wrong. It has a significant and important purpose, and at "normal" level is indicative of "normal" functioning, and at elevated levels is indicative of something else being wrong, but it isn't the elevated level of RT3 which is itself wrong.
Yes but one of the arguments that was put forward against TSH is that under certain conditions (stress) one system is upregulated (thyroid) but another level it is down regulated (tissue level)
Isn't that the point I was making, that there is constant monitoring and re-regulation; and regarding RT3, if for instance, someone is in a state of say, severe nutritional deficit as a result of extreme dieting, more RT3:less T3 is produced as an inhibitor of energy expenditure. So whilst to be well we need optimum levels of the active T3, in that circumstance the greater need is to preserve energy.
Yes but that is the point that I'm making that whilst it is something that your body may be doing, it is not something that the medical profession is doing.
They only are recognising the system via TSH and thyroid that has been upregulated whilst ignoring that everything else has been downregulated.
Which is why you are left with hypothyroid symptoms and without treatment.
Now I don't know why my body responds as it does, but what I know is that it reacts a certain way. According to the medical profession it doesn't but being well acquainted with it for the last 52 years I know that it does.
What I don't know is why?
I want to know the what, why, when and how, it is only then I can change it, because nobody else will.
If deiodinase 2 cannot work due to an inappropriate stop codon, or there is a transposition such that the T4 to T3 conversion produced is reduced in quantity (10%) what other systems are in play and how effective are they and where are they.
If there are genetic links which result in both congenital hypothyroidism and deafness is it because there is a defect in the deiodinase enzyme Dio2 (ie inappropriate stop codon) and is it this enzyme which dominates in the auditory processing system. What is the link between hypothyroidism and tinnitus??
I don't know the answers, but I have plenty of questions and I NEED the answers
I seem to have got your back up initially and so I will compare rT3 to the Euro then if that is more acceptable, if you're in a store which cannot process it for a transaction, you cannot obtain what it is that you want (heat) and will remain cold.
My friend is on T4 only and has been since a baby (no thyroid), people have stated that the T4 is converted to T3 in the thyroid. Well since he has no thyroid and has always been given just T4, he's converting it somehow, then where (he's not dead)?
If it's in the liver mostly, is it causing the raised liver enzymes (struggling to convert T4) or is it an effect? Thyroid is it normally more efficient?
No you haven't got my back up at all, I simply wanted to address the erroneous statement. Some thing can be written in fora such as this, and within a single heartbeat, it has become something that the world and his dog knows to be absolute fact
In your other post about your friend, you raised the issue of T4 to T3 conversion, and I replied to you there, that in that regard, not having a thyroid isn't really the scale of problem you believe it to be since the majority of that conversion happens in the liver, and in other peripheral tissues. I think others have also explained that to you, so you need to accept that as fact otherwise it will continue to confuse you. That a relatively small amount of T3 is also produced in the thyroid means that that won't be the case where the thyroid is congenitally absent, or has been surgically removed, or chemically destroyed, or has simply given up the ghost and become atrophied over time for who knows what reason. But neither will there be any T4 production either, (presumably, although rarely there can be tumours containing thyroid tissue found in ovarian tumours, and there can be evidence of a thyroid mass secondary to the original site of the thyroid) so the direct concern arising from all those scenarios (at least since a thoughtful Dr came up with the first thyroid replacement/supplement in the 1890s) is to make up the dearth of thyroid hormones with an exogenous source. As the UK gold standard is that that is provided in the form of mono T4, if resulting levels of T3 are low, it is poor peripheral, and not thyroid conversion, which is then the concern. That poor conversion can sometimes arise from a genetic cause as in the variation sometimes found in the DIO2 gene for instance, which can be identified by the relevant genetic testing (see Regenerus laboratory); or may have a number of other exogenous or endogenous causes. I'm not sure that knowing the detail of genetic factors such as the impact of inappropriate stop codons, will benefit you in practise because the bottom line is that any poor conversion issue will be evident in the T4:T3 ratio of your blood results, and as there's no cure, it can be addressed by the addition of synthetic or bovine/porcine T3 supplementation. If I understand what you are contending is that there will be a ying to the yang of that effect, but if there is, I can't say, and it may be that you simply have to treat the problem you know about. Re deafness, I can't comment, because I'm not familiar with any evidence of congenital hypothyroidism in particular, directly causing deafness; rather than the fact of the hypothyroidism remaining un- or inadequately treated post-natally, being the cause ie. is the deafness also present at birth because the foetus has no thyroid, or does it develop post-natally where the hypothyroidism is not (well-)treated for a period of time? The same question is also true of all thyroid-associated disorders - is it the autoimmune or ideopathic conditions themselves, or the untreated nature of the resultant hypothyroidism, that is the cause of other disorders developing, whether directly or indirectly. ie. if we optimally replace missing thyroid hormones for instance, or make lifestyle changes that address antibody levels etc, as soon as the impairment of thyroid functionality is evident or threatened, can we avoid or resolve other conditions? So with regard to tinnitis, animal studies show that zinc deficiency is associated with decreased serum T3 levels; that zinc may play a role in thyroid hormone metabolism in patients with low T3, and may contribute to conversion of T4 to T3 in humans. Also, that individuals low in zinc also have an increased chance of tinnitus. So is it hypothyroidism/Hashimoto's that causes low zinc, because of say, the associated low stomach acid and poor GI tract condition, resulting in poor absorption and low levels of all vitamins and minerals, or is there some error of chemical mechanism, whereby the fact of being hypothyroid, untreated or otherwise, directly prevents the uptake of zinc from food for instance? I admit I don't know, but my assumption has always been that "hypothyroidism causes ......" generally, if not always, should more accurately be "un-medicated or less than optimally-medicated hypothyroidism causes .....". But I have no scientific evidence of that, only that to look at it very basically, there are hypothyroid people who are happy and healthy, and well-medicated with levothyroxine.
They do not test the T3, FT3 or rT3 they test only the TSH and FT4
With no thyroid there is definitely only peripheral conversion
Whether liver or anywhere else, that apparently uses DIO1, deiodinase, at present the liver enzymes are raised possibly inflammation but who knows
If only T4 (as now) is being given, it has to be converted somewhere then the raised liver enzymes suggest possibly fatty liver, inflammation or whatever suggests you are asking it to do something when it is already struggling. It has to convert the T4 to T3 when already in difficulties
There is supposedly a bit of an overlap postnatally with congenital hypothyroidism as the development is in stages
What is happening is that doctors are going by TSH and if lucky FT4, and in this area if less than 6 it is fine
Hi what I was thinking if you have antibody attached to thyroid peroxidase as with TPO antibody, and the latter functions in deiodination, then there will be fewer binding sites available at which deiodination can occur.
Deiodination will be reduced as there are fewer empty sites at which this could occur especially if Dio2 not functioning effectively.
If there are 3 types of deiodinase enzymes are they tissue specific as in the thyroid, so that deiodination of T4 to T3 is via Deiodinase 2 (1 iodine atom removed from Thyroxine and always forms T3)
Or like the liver so that deiodination of T4 to T3 is via Deiodinase 1 (1 iodine atom removed from Thyroxine and can form either T3 or rT3)
I've attached a reference below (which if reading correctly liver uses Deiodinase 1 can do T3 or rT3:
ncbi.nlm.nih.gov/pubmed/337...
What I'm thinking is that if in the situation of my friend you have no thyroid, or there is a genetic problem Dio2 (gene that can be checked) which stops it converting T4 to T3, you are then reliant on alternative paths the first alternative being the liver but here it is deiodinase 1
From what this says though rT3 is the preferred substrate and the conclusion was:
These results suggest that in human liver microsomes a single enzyme catalyzes the deiodination of the outer as well as the inner ring of iodothyronines by the same catalytic mechanism and with the same substrate specificity as the type I deiodinase of rat liver.
ORD (Outer Ring Deiodination) - T3
IRD (Inner Ring Deiodination) - rT3
I'm wondering if deiodinase 2 is predominantly in the auditory system and is the same in the thyroid hence congenital (genetic Dio2) problem would then cause congenital hypothyroidism and deafness in some cases
Why is there a link between tinnitus and hypothyroidism?
Hi what I was thinking if you have antibody attached to thyroid peroxidase as with TPO antibody, and the latter functions in deiodination, then there will be fewer binding sites available at which deiodination can occur.
But it doesn't! As I posted earlier, Thyroid Peroxidase does one thing only:
Thyroid peroxidase oxidizes iodide ions to form iodine atoms
The substrate for an enzyme is what it operates ON - not what it acts to produce. If an enzyme uses rT3 or T3 as its substrate, preferred or not, and its action is deiodination, it will produce T2.
Your link above does not work - I think you have copied a link as displayed rather than what it targets. The paper you referenced earlier is dated 1988 and, whilst it surely contains some good information, that is a long time ago in a field in which many thousands of papers are published every year.
Remembering what helvella wrote: "It is only when the thyroid is damaged that some of the content spills out - carrying some Thyroid Peroxidase into the bloodstream. The immune system then tries to mop up that Thyroid Peroxidase by releasing Thyroid Peroxidase antibodies. Those antibodies attach to molecules of Thyroid Peroxidase marking them to be destroyed/removed from our systems by macrophages." then I can't follow your thinking in your first two sentences.
The link you provided doesn't work I'm afraid, it seems to be missing its tale end.
There is a chronic inflammatory autoimmune reaction according to the National Institute of Health whereby there is a follicular cell infiltration by granulocytes, eosinophils and neutrophils of the thyroid
Cytomorphological Aspects of Hashimoto’s Thyroiditis: Our Experience at a Tertiary Center
As I mentioned in reply I had TPO antibodies in 2012, TSH 6.2 but there has been a raised white cell count, to the extent the GP did a little graph of it (consistent finding for years) which is consistent with the above report
The antibody profile was available in 22% of patients. Of these, anti-thyroid peroxidase antibodies were raised in 81.81% of patients and anti-thyroglobulin antibodies were raised in 63.63% of patients.
Follicular cell infiltration by lymphocytes, eosinophils and neutrophils was seen in 72%, 48% and 26% of cases, respectively. Plasma cells were seen in 18% of cases.
Cytomorphological Aspects of Hashimoto’s Thyroiditis: Our Experience at a Tertiary Center
TPO antibodies do not infiltrate the thyroid it is the cells which are capable of presenting antigen that do, as in follicular cell infiltration by lymphocytes (72%), eosinophils (48%), and neutrophils 26%
TPO can be found in thyroid follicles, which is why there is follicular cell infiltration by cells capable of presenting antigen as above that are capable of moving into tissues (and there is a binding site for the epitope which is specific on the APC for TPO and it has been activated)
The antibody profile was available in 22% of patients. Of these anti-thyroid peroxidase antibodies were raised in 81.81% of patients
Please inform the publisher of clinical medical insights of pathology there reasoning is way off in that case!
The information that I have previously stated can be found at Lab Tests Online under Hashimotos autoimmune thyroiditis otherwise knows as chronic lymphocytic thyroiditis
Hashimoto's disease is the most common form of autoimmune thyroiditis and the leading cause of hypothyroidism in the United States. Although currently thought to be due to chronic autoimmune-mediated lymphocytic inflammation of the thyroid tissue, the exact pathophysiology remains unclear. Patients are initially asymptomatic or hyperthyroid, progressing to hypothyroidism as the organ parenchyma is destroyed. Diagnosis is based on a combination of specific antibodies, thyroid function tests, and sonography of the thyroid. Treatment involves lifelong hormone replacement therapy with levothyroxine (L-thyroxine).
Epidemiology
Prevalence: 5% in the US; Hashimoto's disease is the most common form of thyroiditis and the most frequent cause of hypothyroidism in the US.
Sex: ♀ > ♂ (7:1)
Age of onset: occurs in all age groups, particularly in women aged 30–50 years
References:[1][2][3]
Epidemiological data refers to the US, unless otherwise specified.
Pathophysiology
Unknown etiology: Genetic and environmental factors likely play a role.
Immunological mechanisms
Associations with HLA-DR3, DR4, and DR5 have been proposed
Cellular (especially T cells) and humoral immune responses are activated. → active B lymphocytes produce antibodies towards thyroid peroxidase (TPO) and thyroglobulin (Tg) → destruction of thyroid tissue
Associations: often associated with Non-Hodgkin's lymphoma or autoimmune diseases
References:[1][4][5]
Clinical features
Early-stage
Primarily asymptomatic
Goiter: non-tender or painless, rubbery thyroid with moderate and symmetrical enlargement
Transient hyperthyroidism (e.g., irritability, heat intolerance, diarrhea) is possible (hashitoxicosis)
Late-stage
Thyroid may be normal-sized or small if extensive fibrosis has occurred.
Early-stage: transient hyperthyroidism possible (↓ thyroid stimulating hormone (TSH), ↑ free triiodothyronine (fT3), and ↑ free thyroxine (fT4))
Progression: subclinical hypothyroidism (↑ TSH; fT3 and fT4 normal)
Late-stage: overt hypothyroidism (↑ TSH; ↓ fT4 and ↓ fT3)[7]
Antibody detection
Anti-TPO antibody positive
Anti-Tg antibody positive
↑ Anti-microsomal antibodies
See thyroid antibodies.
Other laboratory tests
Lipid profile: ↑ LDL and ↓ HDL
CBC: ↓ Hb
Anti-TPO antibodies are also elevated in 70% of patients with Graves disease!
Ultrasound
Indications: to assess thyroid size, echotexture, and to exclude thyroid nodules
Results depend on the form of Hashimoto's thyroiditis.
Atrophic phenotype: reduction in thyroid size (mainly observed)
Goitrous phenotype: heterogeneous enlargement
Fine-needle aspiration
Radioactive iodine uptake test (RIUT): Radioactive iodine uptake is variable, often patchy and irregular with either an increase or decrease in 99mTc uptake. There is ↓ absorption of radioactive technetium (↓ 99mTc uptake) in the thyroid during transient hyperthyroidism
References:[1][3][7][6][8]
Pathology
Diffuse lymphocytic infiltration (cytotoxic T lymphocytes) with germinal center, oncocytic-metaplastic cells (Hurthle cells) and fibrotic tissue
References:[9][1]
Differential diagnoses
Subacute thyroiditis (de Quervain's thyroiditis)
Diffuse toxic goiter/ Grave's disease
Nontoxic/multinodular goiter
Maternal hypothyroidism (cretinism)
Riedel's thyroiditis ("Riedel's struma")
Rare, special form of autoimmune thyroiditis
Invasive fibrous growth beyond the thyroid tissue into surrounding tissue with destruction of thyroid tissue
Goiter; symptoms of compression
Surgery may be necessary because of compression.
References:[2][3][10][6]
The differential diagnoses listed here are not exhaustive.
Treatment
Levothyroxine (T4) replacement therapy
Life-long oral administration of L-thyroxine (T4)
Commence at a lower and more slow-acting dose with increasing severity of hypothyroidism because of the risk of cardiac side effects.
Life-long monitoring
Due to decline in T4 production with increasing age
Life-long monitoring of thyroid parameters (primarily TSH) is necessary to adjust treatment accordingly and avoid hyperthyroidism
References:[3]
Complications
Permanent hypothyroidism
Myxedema coma
Thyroid lymphoma (the risk is 60 times higher in patients with Hashimoto's thyroiditis)
References:[2][3][11]
We list the most important complications. The selection is not exhaustive.
Sources
last updated 12/05/2018
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