We see lots of people who have their diagnoses flipped between hypothyroid and hyperthyroid. Sometimes it looks like a mistake. Other times the changes seem to be dismissed or disbelieved.
At least this is reported as real.
Case report peer-reviewed
Fluctuating Hyperthyroidism and Hypothyroidism in Graves’ Disease: The Swinging Between Two Clinical Entities
Cite this article as: Shrestha A, Adhikari N, Devkota S, et al. (August 05, 2022) Fluctuating Hyperthyroidism and Hypothyroidism in Graves’ Disease: The Swinging Between Two Clinical Entities. Cureus 14(8): e27715. doi:10.7759/cureus.27715
Abstract
Autoimmune thyroid disorders are frequently encountered in clinical practice and consist of a spectrum ranging from Graves’ hyperthyroidism to Hashimoto's hypothyroidism. Generally, patients with autoimmune thyroid disorders will lean towards one end of the spectrum or the other, with fluctuations between hyper- and hypothyroidism rarely seen. This is especially the case when persistent hyperthyroidism occurs after a prolonged period of hypothyroidism. Here, we present a case of a young female patient initially presenting with Graves’ disease with a previous history of hypothyroidism.
I suspect swinging between hypo and hyper happens more frequently than this paper suggests. In the UK we are lucky if we have TRAb measured. Testing separately for stimulating and blocking antibodies isn't done so we have no reference.I had hypo symptoms years before Graves diagnosis. As is common these symptoms were brushed aside, only TSH was measured and when top of range, I was told I did not have a thyroid problem.
After 6 years on B&R for Graves I now suspect I have Blocking TRAb dominating. I have no TPO or TG. I therefore assume the fluctuations are due to the balance of Stimulating and blocking TRAb.
I quite agree I was like a yo-yo - atropic autoimmune thyroiditis is one hell of a roller coaster ride. I suspect I have TRAB too as I look like I have TED years after my diagnosis with AAT. Why do they ignore antibodies when they are so important as to which darn disorder you have and what treatment is appropriate. It’s like they think playing pin the tail on the donkey with our health is acceptable practice.
Thanks for posting. 'Belief' really ought not to come into this! Science, as such, is not fixed, there is no 'All' of anything. It astounds me that they've such narrow, fixed views. Tragic!
Nice to see it in print . My suspicion is that if they routinely tested all hypothyroid patients for both stimulating and blocking forms of TRab, they would find it's not so rare to have some TRab involvement . Granted it is rare to find a hypo patient who gets such high levels of stimulating TRab that they then go full blown hyper and need no levo at all .... but what about the destabilising effects of somewhat milder levels of blocking or stimulating Trab ?
it is often said on here that hashi's hyper swing's are the cause of such fluctuations, but personally i don't believe hashi's destruction (dumping T4/T3 from follicles that are being damaged) is responsible for all of the weird fluctuations we see on the forum .. i think some of it is likely to be people who have milder levels of blocking or stimulating TRab fluctuating and confusing their picture.
I've never seen any detailed research showing actual T4/T3 results from what we would call a 'hashimoto's hyper swing' .. so how do we really know how long this dumping process might realistically last for? .. are we just guessing ?
I had my fT4 going way over range for at least a year, possible a lot longer, and it kept going up despite a reduced Levo dose ... then eventually coming down again. it wasn't high enough to make me feel hyper at al, but it messed with my bloods (and my GP's head, who clearly didn't believe i took the doses he prescribed).
Having TRab testing during this period might have proved very enlightening as somehow i just wouldn't expect a hashi's attack to last that long, but i could be wrong.
I got the impression from Tania that testing for the blocking sort is not readily available anymore , but the case study presented here seems to have managed to do it somehow with what looks to be TBII testing :
"TSH receptor binding inhibitory immunoglobulin (TSB Ab)" .... i'm assuming that's another way of writing TBII Thyrotropin binding inhibiting immunoglobulin ?
yes that one would tell you for sure about the stimulating antibodies but could not give any information about whether there were also blocking antibodies present.
Stimulating ones are definitely involved with TED ... i'm not sure if blocking ones are implicated in TED or not.
Yes I thought that might be the case. I suppose the blocking ones are why it fluctuates or could be one reason why it can fluctuate and go remission? Shame you can’t easily find out blocking ones
you probably know this already , just adding it here incase it's useful for other readers:
Stimulating ones fit into the TSH receptors and stimulate them just like TSH does , (including those TSH receptors in the eyes.. hence TED)
Blocking ones sit on top of the TSH receptors, stopping 'real' TSH from having any effect there , (hence no stimulation of thyroid, hence hypothyroidism ensues)
, but unlike hashi's damage , this sort of hypothyroidism is reversible ~ as soon as the blocking antibodies bugger off ,TSH can stimulate thyroid again as normal ~ hence apparent 'remission'
if you get more blocking ones than stimulating , you'll go hypo ..
if you get more stimulating than blocking , you'll go hyper..
if they all go away , or if they balance each other out , you'll appear to be in remission.
When blocking ones are causing hypothyroidism you would expect to see very high TSH levels .. because pituitary keeps pumping out TSH in response to low T4/T3 levels , but it's blocked from acting, so T4/T3 stay low , and so pituitary pumps more TSH out etc etc.
I've been blocked forever - and realised reading around these past few years that my Dad was medically discharged just before the end of WW 2 and I was born in 1947 and believe I inherited my Graves from him.
I remember my Mum saying - your Dad went into the Army a kind placid man- though a big heavyweight boxer who never was any good at it though pushed into it by his father - and came out a skinny rake with a filthy temper :
Growing up I thought it was all about not having enough money etc etc but it's evident to me now he had Graves and it did burn itself out as my sister 13 years my junior saw a kind placid man, heavyweight again, but no boxer, just a big soft Teddy bear whom I came to understand much better and loved dearly.
indeed .... army service +WW2 sounds like a very likely trigger for Graves.
my kids were only 8yrs apart , but i had to remind them the other day that even though i'm their mum.. they both experienced a very different person as mum.
Just for completeness, the old name of “long-acting thyroid stimulator” (LATS) hints at something, That is, the antibodies seem to get stuck and continue stimulating longer than does TSH.
The first example of such a disease was Graves’ disease, in which a “long-acting thyroid stimulator” was found to be an autoantibody reactive with the thyrotropin receptor on the surface of the thyroid epithelial cell. Some of these antireceptor antibodies cause uncontrolled stimulation of the thyroid cell with continued overproduction of the thyroid hormone. Other antibodies can bind the receptor and inhibit its action.
it's probably unethical to give people autoantibodies on purpose , but i'd like to see what happens if you give hypo patients blood transfusions with some stimulating TRab in .
and hyper patients transfusions with blocking ones.
I now know I was undiagnosed hypothyroid for as long as I can remember and my Graves was triggered 3 months after being attacked by a man I employed as my assistant manager.
My sister, 13 years my junior was diagnosed hypothyroid after the birth of her fourth child and I went again to be tested considering the genetic predisposition thinking - at last, but no, I wasn't hypothyroid when age 53.
It was insomnia and dry gritty eyes that sent me to the doctors when 56 as I had come to accept the total exhaustion build up over very many years and just saw that as part of ' me ' .
The Carbimazole eased my symptoms, I was well, and I continued to work.
I never thought of myself as hyper, my heart rate was stable and I didn't experience anything like I read on here and other forums - though whilst on the AT drug I did experience a brief period of weight loss whilst eating for England - felt marvellous and quite novel as I'd spent most of my life not eating in order to drop those same few pounds I'd put on a month earlier.
After the RAI thyroid ablation the weight piled on again and I have only lost weight since switching to self medicating with NDT.
Whilst we do not get the full blood antibody analysis at diagnosis and routinely no follow up of antibodies it's anyone's guess what is actually going on and I don't think anyone cares as there is currently no cure for this auto immune disease.
Mainstream medical have no answers and all the AT drug does is buy the patient time, in the hope that the immune system response calms down by itself, and as we now know the longer one stays on the AT medication the better the outcome for the patient though this new research tends to fly in face of current NHS and hospital guidelines.
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