Columnist Dr Copperfield responds to NHS England’s updated guidance on treating hypothyroidism, which warns that liothyronine should only be prescribed by a specialist in a small number of patients
Now, I’ve got to be very careful here. For one thing, I’m aware that the very active thyroid lobby is probably poised with myxoedematous-fingers-on-mouse ready to direct venom my way if I mis-step. So just to clarify, anything that you might take exception to is a mistake, typo or misinterpretation of whatever I actually meant, which was something nice.
And second, last time I was in this situation, having what the pro-B12 lobby felt was a pop at them and what I thought was a balanced view on why the world has gone B12 bonkers, the forums wished severe B12 deficiency on me. So powerful was that hex that I actually ended up hospitalised with a B12 of 62 and a resolution never to be so sneery again.
Then again, I feel better now.
So it was with interest that I read the joint statement from the British Thyroid Association and Society for Endocrinology on the controversial subject of liothyronine (T3) in hypothyroidism. You know, that stuff that’s really expensive that unhappy hypothyroid patients treated with thyroxine and having completely normal TSH levels chew your ear off to get prescribed, while prescribing advisers chew the other one off to get you not to.
And there’s some good stuff in this guidance around what is a really tricky area. It points out, for example, that all hypothyroid treatments have a significant placebo effect. And that dissatisfaction with treatment might be because it wasn’t needed in the first place. And that the symptoms might be caused by other factors, which rings true given that we’re dealing here with fatigue, weight gain, brain fog et al, which have a billion and one aetiologies.
So far so pragmatic. But then something really weird happens. On the one hand, the guidance points out that ‘numerous randomised trials have failed to show a benefit of treatment regimes that combine liothyronine with levothyroxine over levothyroxine monotherapy’. And on the other, it says that ‘some hypothyroid patients do experience benefit during a trial with liothyronine’ – so, basically, it’s reasonable for a specialist to give it a try.
Hang on. Run that by me again. Thyroid treatments have a huge placebo response for symptoms that often have some other cause anyway, the evidence says liothyronine doesn’t work but you can give them a go if the patient wants? What just happened to science there????
Look, I’m sure that if I gave it a try, I’d have patients who insist that interferon alpha helps their URTI, but I’m not going to prescribe it because that would be insane. So what’s going on with liothyronine? Has the ‘E’ in ‘EBM’ suddenly become, ‘Errrr, OK, if you shout loud enough’? It’s just complete and utter non-science.
How very disappointing. Almost as disappointing as the fact that 1/3 of my eyebrows have just fallen out.
Dr Copperfield is a GP in Essex. Read more of his blogs here
Any idea why the treatment recommendations for treated T4 and TSH levels have changed significantly since 1990?
And, given that TSH is so frequently raised by other conditions, like acute infections, why can we not get T4 levels off the lab when we suspect that patient is hyperthyroid but TSH is raised by something else (like, er, liothyronine?)
I find this an interesting issue where non specific malaise leaves patient open to the walletectomy by snake oil salesman some of whom still have medical degrees. My cognitive dissonance is that some awkward challenging medical colleagues are responsible for moving things forward by challenging the accepted dogma. However I suspect many more of the awkward lot just cause problems and undermine good medical practice as there is money to be made in doubt and uncertainty. Deciding which side the awkward group lie on is a tricky determination. But we all know of clinics who’s prescribing recommendations we would decline to follow.
Evidence based medicine is dead, we live in the politics based medicine era where anything will be approved if there’s enough pressure from twitter or the politicians feel it will win votes…
As I understand it, when your sole source of Thyroxine is exogenous, then your level of T3 depends on your deiodinase activity on the T4 intake. It is thought that some patients lack the ability to effectively deiodinase their T4 to T3 and some of them feel the associated brain fog… in which case they may feel a benefit from T3 (or, I suppose, that benefit may be a placebo benefit…)
So I have a very few patients who, on the advice of an endocrinologist, have been allowed a trial of T3 and apparently benefited.
Interestingly there are trials afoot on the role of T3 in remyelination of demyelinated plaques in MS, which makes me wonder what on earth T3 does anyway. They don’t really teach us this stuff at medical school do they…..
Use the science Dylan
So if they lack such an enzyme why are they not Cretins from birth?
Evidence Schmevidence, whatever the science, and I totally agree that it’s mired in uncertainty, the good news is that you can write a letter authorising those who are completely fixed on T3 to buy it online from Europe for a fraction of what the contrived NHS cost is.