Transcript of Q&A session

At our ‘Meet the  Experts’ joint BTA/BTF webinar held on 20 September 2023, our speakers Prof Simon Pearce and Dr Nicola Zammitt discussed different the management of hypothyroidism.

This is a transcript of the patient questions answered live by our experts and chaired by Dr Sam Finnikin and Prof Bijay Vaidya.


SP = Prof Simon Pearce, consultant endocrinologist, speaker

NZ = Dr Nicola Zammitt, consultant endocrinologist, speaker

SF = Dr Sam Finnikin, GP, co-chair

BV = Prof Bijay Vaidya, consultant endocrinologist, co-chair

During tonight’s presentation, you have shown why T3/T4 combination is not beneficial compared with T4 monotherapy. Despite that, why does the BTA/SfE’s consensus statement on the ‘Use of liothyronine (T3) in hypothyroidism’ recommend T3/T4 treatment for some people? (BV)

This is a really good question and an important one. I think the bottom line is, any doctor who decides they are going to stop treatment on a patient who is feeling well on a treatment is a bit stupid. So that is why the consensus statement says if you have a patient who is feeling well on combination therapy, and there is no obvious harm from that i.e. they do not have any of the things we are concerned about such as atrial fibrillation or osteoporosis, you should just carry it on. So that is why the statement is permissive. I see we got some flak recently in ‘Pulse’ magazine from a doctor about this apparent paradox but I think the bottom line is why would you change treatment for someone who is feeling well? (SP)

We have a question asking whether the aim of the consensus statement was to reduce the number of T3 prescriptions.  Could you explain what the BTA/SfE’s aims were for developing this statement, please? (BV)

The first thing to say is that a consensus guideline is exactly that. I suppose it is a kind of compromise view between a group of people. I think it is fair to say the people involved in writing the statement have a spectrum of views. Likewise, there may be a spectrum of opinion about why we wrote it.

I think there are a number of reasons. One is that it has been an issue for patients who wanted to know why we are not prescribing this. We felt there had been some additional studies since the last guideline; not necessarily that any of them were lending a huge amount of weight to changing what we were doing in terms of prescribing T3 much more widely but we thought that it would be sensible to update the guidance.

From my point of view, I also saw it as an opportunity to think more holistically about the person in front of us. The aim is not to remove prescriptions or to reduce choice for people.  I think the aim is to give clinicians the tools with which to navigate the conversations with these people a little bit better. For me, when I am meeting a person in clinic who is feeling unwell on levothyroxine I start off with a few ground rules. The first thing I say is that I am not as good as a normally functioning thyroid gland but I will listen and do my best and here is the process. Let’s start with ‘was the diagnosis right? Is there anything else? What are the symptoms you are getting?’ I think the consensus statement gives a framework for that. I think it is a much more positive document and is not suggesting we should  just pull the drug out of peoples’ hands. It is really saying how can we can look holistically at the problem to try and achieve patient wellbeing? That is my view but Simon might have a slightly different view on why we wrote it.(NZ)

I think that is exactly right. We were still seeing a lot of discontent amongst colleagues as well. I think primary care has been in a difficult position, and secondary care has been in a difficult position too. I do not think private practice is behaving very well in this regard. Certainly in our local area, a private practitioner will see a patient once, prescribe them T3 and tell the patient they are discharged and their GP can deal with it. That is not good practice. I felt it was important to update and also share some of the evidence that we have talked about today about why it is not a panacea to be started on T3 because reading some websites you would have thought that were true. (SP)

I have a question on that exact point. What should GPs do if patients come to them with a private practice prescription of T3 and wanting that to be prescribed on the NHS? (BV)

Well, I think if the GP thinks it is reasonable to continue and that there is a proven diagnosis of primary hypothyroidism i.e. the patient has got a couple of TSH readings over 10 and they feel good on the treatment, then that is fine. However, if the patient is 80 and feeling tired then it might not be very appropriate for that person to be on T3 because the hazards start to become much more. So, I think your choices are: refer the patient back to private care, get secondary NHS care involved or, if you think it is a reasonable thing on the basis of what you have seen and the patient clearly has a good response to T3, then it may be reasonable to continue. (SP)

I would agree with what Simon says and would also like to add that principle of doctors to ‘first do no harm.’ I think if we look at the TSH and it is within normal limits, I am much more comfortable. If we see we are suppressing the TSH, which might suggest we are overtreating someone, then there is evidence of potential harm and we would worry about atrial fibrillation and osteoporosis in the long run. How well has the patient responded? How robust was the original diagnosis? Is there any suggestion that we are doing the patient harm? If we are not doing harm, the patient is well and there is a robust diagnosis there, then keep going. (NZ)

I suppose the difficulty there is that we are caught between a rock and a hard place here in that the patient may be asking for T3, our prescribing guidelines say do not prescribe it, your consensus statement quite clearly says the patient must be seen by an NHS endocrinologist and the protocol that you showed Nicola has a very clear testing and trial of treatment and follow-up protocol but that may not have been followed by the private endocrinologist. So, in a situation where this lovely guidance has been written and not followed, and then we in NHS primary care are left to deal with it, we have two options. One is to say  ‘No, there is a well-written protocol here and you need to see an NHS endocrinologist’ which has been pointed out in the chat and we are all well aware that this can take a long time. Or, we can prescribe outside of our professional expertise in this contentious, and slightly tricky, area.  (SF)

The guidance clearly states that you should not do anything that you are uncomfortable with either in secondary or primary care. If you do not think it is warranted you are absolutely within your rights to say: ‘This is at my discretion.’ The General Medical Council (GMC) clearly says if you do not think this the right thing to do, you should not prescribe anything; whoever started it. So once you continue that prescription, you are effectively taking responsibility for it and you should not take responsibility for anything that you do not feel is right. (SP)

Local pathways are going to vary slightly depending on where you are. In Edinburgh,, where I work, there are a couple of endocrinologists who do private practice but also work in the NHS. We have agreed with our GP colleagues that if someone prescribes it in their private clinic but it is the same person who might see them in an NHS clinic then we would not draw a distinction. But if it is a private practitioner somewhere else and we do not have access to the original tests, and we are not sure whether the diagnosis was robust, then we would want to look at that. In terms of dealing with the volume of work, I think a lot of clinics across the country have moved towards giving virtual advice. So, quite often if GP colleagues contact me and say ‘This patient has moved over from America. She was diagnosed, her Thyroid Peroxidase (TPO) antibodies were positive. She is on T3, these were her original thyroid function tests. Are you happy for me to keep prescribing?’ I would think ‘Yes, you have told me the patient is well, you have given me evidence the diagnosis was robust. The TSH is not suppressed at the moment. Keep going.’ Sometimes we can do this virtually to try and reduce waiting times. (NZ)

Thanks for that. I think a lot of places are using that ‘Advice and Guidance’ protocol which is probably already a useful protocol for a way of doing it although it does often end up with Primary Care taking on more responsibility than our professional expertise would feel comfortable with. We are doing that because the NHS is stretched and to help our patients but it is difficult.

On a slightly more practical note; oestrogen - a lot of people will be taking thyroxine when it comes to menopause and starting on HRT. We have a couple of questions whether we should proactively titrate their thyroxine dose or whether we should measure it at a certain interval after starting HRT. Do you have any practical advice about managing thyroid conditions after starting HRT in people stable of thyroxine? (SF)

I do not proactively increase it. I think Simon’s idea of an information prescription that tells people these are stages in life when doses may need to be adjusted is a really good one. I know that patients often worry that clinicians are slaves to the blood results. What I try to explain to patients is that the blood tests and the normal values are really outer safety brackets. Regardless of whether they have gone on to HRT or not, if someone does not feel great on thyroxine and their TSH is towards the upper end of normal, and their T4 is towards the lower end of normal, actually it is perfectly reasonable to try increasing the dose. If they have just gone onto a medication that is oestrogen-containing that suggests there might be an underlying mechanism for that, then that seems sensible. I like Simon’s idea of an information prescription. I must admit I have not done that formally in the past but I will be giving consideration to doing that in the future. (NZ)

I think as well it is a bit unpredictable because, of course, the amount of increase in the thyroxine-binding globulin depends on the hepatic exposure to HRT to the oestrogens and that will be quite different for someone on a patch or transdermal prep compared with someone on an oral prep. You would expect a much bigger change for someone on an oral prep. (SP)

Thank you for that. (SF)

Just on the practical management: We have a couple of questions about TPO antibodies. What is the value of having TPO antibodies checked in a person with overt hypothyroidism? How would this change the management of the patients’ hypothyroidism? (BV)

It may not change the management in someone with ‘barn door’ overt hypothyroidism but it might inform some aspects of what we do. For example, someone might have ‘barn door’ overt hypothyroidism with a history that is suggestive of thyroiditis or postpartum thyroiditis. Knowing that the TPOs are positive means there is a slightly higher risk that the hypothyroidism is going to be permanent. To be honest, I would still give the patient the option of a trial off treatment after we have had them on levothyroxine for a year. So, it is not that it is necessarily going to wed me to a path but I think it informs that discussion with the patient. I think where you have got a fairly borderline set of thyroid function tests that might perhaps be subclinical hypothyroidism that will revert to normal, or a non-thyroidal illness that will go away, having negative TPOs would make me think ‘Perhaps this is not really genuine card-carrying hypothyroidism and let’s keep an open mind her.’ I have had at least two patients over the years who have felt unwell on levothyroxine and have always had negative TPOs. That enabled me to open the discussion by saying ‘Let’s be open-minded here. Your thyroid function tests are normal. Let’s take you off levothyroxine. Your thyroid function tests are still normal and you do not feel any worse. I am sorry that you do not feel any better but at least now we have ruled out the thyroid as the cause of your symptoms. Let’s now move on to thinking about what they are.’ I guess that is how I use TPOs. (NZ)

I do exactly as you do, Nicola. I do not have anything to add to that answer. (SP)

Just on the TPOs and the monitoring of subclinical hypothyroidism: It often seems to be quite young patients who have a diagnosis of subclinical hypothyroidism with positive or negative TPOs. If the TPOs are positive then this is more likely to become overt hypothyroidism as you say. The current advice is to monitor them annually and ask them to look out for any symptoms. If we have several years of normal thyroid function tests then surely we can stop monitoring them and just ask them to watch out for symptoms rather than proactively burdening them with an annual blood test? (SF)

I would say that might be ok but for a woman, if they are going to get pregnant, you need to be quite alert because you do not want them going into pregnancy with a raised TSH because that has definite adverse obstetric outcomes. I would still be thinking about occasional monitoring maybe not every year, but every three years or something. (SP)

I think maybe we have time for a short question. There was one about what is the role of vitamins or mineral supplements in the management of hypothyroidism. I suppose they are probably asking about vitamin D replacement, selenium or iodine. Nicola, do you recommend these? (BV)

People often ask me that and I do not. Selenium clearly has a role in thyroid eye disease and there is a study to back that up. If your thyroid does not work properly because it has been damaged by antibodies, then no amount of iodine is going to make that work better. Taking too much iodine, even with a normal thyroid, can cause abnormalities in thyroid function. So, I suppose I would caution against over-supplementation. If someone has vitamin D deficiency, they have vitamin D deficiency. If you live in Scotland, you probably should be on vitamin D replacement all the time anyway because there is so little sun that we do not make any and that is really government guidance as well. (NZ)

Well, Newcastle is not much better than Scotland for that! As part of my routine screening for people who are feeling tired on levothyroxine, I will measure vitamin D, ferritin and probably measure vitamin B12 as well just to make sure. I think there is a trial just about to be published, and I think it was actually released at the recent European Thyroid Association (ETA) meeting in Milan, showing that selenium does not actually make much difference to patients with Hashimoto’s thyroiditis in a large randomised study because there are a few small studies suggesting some positive benefits. (SP)

I think we can probably talk for a long time about vitamin D and the lack of evidence that it is associated with anything particularly. The fact is, much like the massive 5% -19% of people who have subclinical hypothyroidism on testing, if you go around testing people for vitamin D, you will find a massive number of people with low vitamin D quite frankly because there is not enough sunshine. I think before we go down a vitamin D rabbit hole we should probably wrap up.

I think that has been fascinating and thank you very much and thank you to all the people who have asked questions. Sorry that we have not got around to everything. I will hand back to Julia to close the session. Thank you. (SF)

MIMs learning 1 hour CPD module for healthcare professionals