Anti-rheumatic drugs could prevent thyroid disease
Anti-rheumatic drugs used for rheumatoid arthritis might prevent the development of autoimmune thyroid disease, according to a new observational study by researchers from Karolinska Institutet published in the Journal of Internal Medicine.
It is well known that patients with rheumatoid arthritis (RA) are at increased risk of autoimmune thyroid diseases such as Hashimoto's disease and Graves' disease. While patients with RA are usually treated with immunomodulatory drugs that affect the immune system, such drugs are rarely used in autoimmune thyroid diseases.
Instead, such patients are treated with thyroid hormone to compensate for the changes in normal thyroid function that accompany autoimmune thyroid disease.
The researchers in the current study wanted to investigate whether immunomodulatory drugs that reduce inflammation in the joints of patients with RA might also reduce the risk of these patients developing autoimmune thyroid disease.
Previous studies in mice suggest that so-called DMARDs, a type of immune-modulatory drugs used to treat rheumatoid arthritis, can reduce inflammation in the thyroid gland. Still, knowledge of whether this effect also applies to humans is limited, according to the research team.
The researchers used data between 2006 and 2018 on over 13,000 patients with rheumatoid arthritis and their treatment, as well as data from over 63,000 individuals in a matched control group without rheumatoid arthritis.
The researchers found that the risk of developing an autoimmune thyroid disease among RA patients was lower after their onset of the rheumatic disease than before diagnosis.
The most pronounced reduction in the risk of autoimmune thyroid disease was seen in patients with rheumatoid arthritis treated with immunomodulatory drugs or "biological DMARDs". In these patients, the risk of autoimmune thyroid disease was 46 per cent lower than in the control group without rheumatoid arthritis.
"These results support the hypothesis that certain types of immunomodulatory drugs could have a preventive effect on autoimmune thyroid disease," says Kristin Waldenlind, researcher at the Department of Medicine, Solna, Division of Clinical Epidemiology, Karolinska Institutet, specialist in rheumatology at Karolinska University Hospital and first author of the study. She continues:
"Our results do not prove that it is the treatment with immunomodulatory drugs that led to the reduced risk of autoimmune thyroid disease, but provide support for this hypothesis. The results, if they can be replicated in further studies, open up the possibility of studying more directly in clinical trials whether the immunomodulatory drugs currently used for rheumatoid arthritis could also be used for the early treatment of autoimmune thyroid disease, i.e. for new areas of use of these drugs, known as drug repurposing."
The Swedish Research Council, the Swedish Heart-Lung Foundation and Vinnova mainly financed the study.
Publication
"Disease-modifying antirheumatic drugs and risk of thyroxine-treated autoimmune thyroid disease in patients with rheumatoid arthritis", Kristin Waldenlind, Bénédicte Delcoigne, Saedis Saevarsdottir, Johan Askling, Journal of Internal Medicine, online November 27, 2023, doi: 10.1111/joim.13743.
My late mother had both Hashi's and RA. They were both diagnosed in her 50s, but I can't remember which one was diagnosed first and how long the gap was between being diagnosed with each one.
It would be interesting to know if people who develop Hashi's first are at greater risk of getting RA than someone without Hashi's.
That’s v interesting! I was diagnosed with under active thyroid about 13 years ago and have taken Levothyroxine ever since.
Two years ago I had sudden pain in Achilles’ tendon followed a few weeks later by pain in opposite foot the swollen left hand and wrist which has spread to other wrist. I’ve been diagnosed with atypical inflammatory arthritis for which I take Sulfasalazine. It would be interesting to see how many others have a similar diagnosis. I’m now 61.
Very interesting article helvella thank you. I developed Graves’ disease in 2012 - 2013 was treated with block and replace for exactly a year that was followed by developing inflammatory arthritis in 2014 for which I was prescribed hydroxychloroquine (which is on your list) which I have been taking ever since.
The downside of treating Hashi with immunomodulatory drugs are the unwanted side effects, and if the triggers of Hashi are not removed, then as soon as meds such as DMARDs are reduced/stopped, Hashi inflammation/destruction risks returning.
We see many forum members managing their inflammatory conditions by removing gluten/dairy/etc from their diet and optimising natural anti-inflammories (such as Vit D). A good goal is to reduce elevated thyroid antibodies levels (a response to Hashi destruction) as these are not only indicative of the skewed immune response but risk contributing to further chronic inflammation making us more susceptible to other inflammatory conditions such as RA.
My sister has Hashi that was left to obliterate her thyroid gland. She later developed RA and was treated for five years with methotrexate which made her feel very nauseous ( a common side effect). Her choice was being crippled with swollen painful joints or feeling sick. However, after removing gluten and supplementing curcumin (and other natural anti-inflammatories) known to modulate those same inflammatory cytokines that drive both Hashi and RA, she has been off methotrexate meds for about a year, is very active and feels well.
I suspect I too have the beginnings of RA as get very achy if I don’t take my natural anti-inflammatories. I also suffered trigger finger after my TIA but that has completely gone now, except when I eat gluten!.
My biggest game changer was Kapparest by Biotics Research. It contains plant extracts shown to specifically target NF-kB inflammation which is the common denominator in Hashi & RA.
I initially took the the recommended six tablets a day under the care of a practitioner but can now maintain good inflammation levels with just two, and I use it cyclically. A few weeks on and few weeks off, and much less in summer as I find the sun very healing.
Funnily enough I've had a fair bit of genetic testing to evaluate how my body works best and much of Kapparest's ingredients are those same as recommended to best enhance my genetic disposition. Interesting isn't it.
Vit D is ultra important in the inflammatory stakes and also a serious immune modulator. Other naturals would be Vit D, Vit C, fish oils, garlic, and anything found in an antiflammatory diet really. I simply love berries and eat far too many nuts/seeds.
Also adequate T3 levels that act as a modulator of inflammation through their nuclear receptors.
A potential downside of your approach is the use of, as yet, unregulated and not fully tested supplements, which may cause liver damage, for example. A family member having rituximab infusions may be expected to have a further decade of life. Dietary approaches would not have been feasible (nor, I would hazard to guess, successful) when critically ill. The treatment appears to have reduced their preexisting autoimmune oral bullous pemphigoid to a non-issue which beforehand had led to dietary restriction (citrus fruit, for example) to avoid pain. With best wishes to you for safe and effective treatment.
'A potential downside of your approach is the use of, as yet, unregulated and not fully tested supplements, which may cause liver damage, for example'
Absolutely and why I use a practitioners knowledge regarding the more unknown supplements.And of course pharmaceutical drugs could also cause liver damage, etc in those susceptible or when prescribing care isn't properly monitored.
There is no one treatment to fit all and prescription immunomodulatory drugs certainly have their place but I do wonder how many others would benefit from supplementing plants before being prescribed these meds. Curcumin has received quite a lot of scientific research with very positive results.
well maybe true but regulated drugs can have horrendous effects.Methotrexate for example : The most frequently reported adverse reactions include ulcerative stomatitis, leukopenia, nausea, abdominal distress, malaise, undue fatigue, chills and fever, dizziness, and decreased resistance to infection. Drugs are not always fully tested either
Yes, indeed, and the aim is to have a system of controls to minimise the possibility of adverse events. Sadly, this is under high pressure. On a personal note, I had a TSH of 4.3 for my last test with no GP appointment available for over two months. With symptoms that I regard as myxoedema coma I decided to increase my dose. When I started treatment, nearly a decade ago, I was similarly left to fester, and I hope it's not a feature of thyroid treatment for the practice I attend.
Morning, a quick question, does removing gluten/dairy etc from your diet and optimising vit D etc help with reducing Graves antibodies? My TPOab have dropped considerably since removing gluten and supplementing Bs and D, my friend’s Graves antibodies are sky high and they were wondering if it would help them.
When I developed inflammatory arthritis in 2014 or 15 i decided enough was enough - that and having my photograph taken after we had driven from U.K. to the south of France with me eating baguettes, pains au raisins and croissants non stop all the way from Calais to the Mediterranean. My face looked like a massive puffy balloon, I was almost unrecognisable. At that point I sadly gave up the delicious French bread then when I got home I decided to go completely GF - I haven’t knowingly eaten gluten since then.
I was in the habit of doing home thyroid tests and first time I did it I noticed my antibody levels had gone down. Same with the next time I tested so I carried on and the levels kept dropping. Could have been the time for them ti drop but nothing on earth would make me go back to eating gluten again. If your friend is interested I would suggest she gets tested first - I didn’t! because once her antibodies start to fall she won’t want to eat gluten ever again.
I would also suggest she joins coeliac.org.uk/home/ they have a wonderful handbook of all gluten containing foods, ingredients and restaurants that are GF plus their website is really good. So for what it’s worth I’d tell her to try it.
Removing gluten (& possibly dairy) has helped many members with any form of AITD (autoimmune thyroid disease). Remember there has been found much cross over between Hashi and Graves disease. It's just we get tested for only one type and that becomes our label unless another type dictates a new diagnosis.
A competent immune system is about balance of killer T cells & the antibodies producing B cells, and the T helpers & T regulators that switch the immune system on and off, and are influenced by stress, poor gut health and poor liver function. Gluten is a well known trigger for autoimmunity where misdirected antibodies attack and damage own tissue whether its stimulating, blocking or causing fibrosis of the thyroid gland.
Apart from the actual gluten intolerance that causes unwanted inflammatory immune responses, once the gut is unwell the GALT fails to work correctly. GALT stands for 'gut associated lymphoid tissue' that houses part of the immune system just under the intestinal lining surface and helps immune cells mature. When a healthy functioning gut is absent, this part of the immune system becomes dysfunctional and effects other parts.
Although Isabella Wentz has Hashi, she clearly explains the effects of AITD and gluten. Maybe get your friend to read her book 'The Root Cause'.
there is also the alternative view that is is the faulty gut lining and poor microbiome that allows gluten into the blood stream which then does the damage to the thyroid not gluten per se
I was diagnosed with Rheumatoid arthritis and Hashimoto's 26 years ago at the same time. I have been on metherexate a DMARD for 26 years and Cimzia an anti tnf biological drug for 9 years. Also been taking thyroxine for 26 years . I have found when I have had to come off my rheumatoid medication when I have an infection my Hashimoto's symptoms seem to get worse and takes time to get back on track
Thank you! You have just answered a burning question for me (I think!) I've been quite ill and had to go off Cimzia some 2 months ago (flu for 4 weeks followed immediately by a UTI) and hadn't thought that the swallowing issue I am having might be due to a Hashi flare! I hope it subsides when I will finally be able to take my injections.
Yes I dont think gps and sometimes rheumatologist make the connection or believe it. However you know your own body and are fine tuned to changes Having more than one autoimmune condition which is often the case can be challenging to manage especially as they are treated in isolation.
I have first hand experience with Injectable Arthritis drugs …. 8 years ago I started one of those injectables and noticed about a month after starting that every time I had the shot I could taste it (had known thyroid nodules) my doctor never believed I could taste this injectable and after using this drug for 1 year I developed eye popping and horrendous swallowing issues eventually was diagnosed with thyroid cancer…. I always blamed this drug on my thyroid cancer but maybe what it was doing was trying to fix what was wrong … interesting and debatable.
I was diagnosed with RA 24 years ago and treated with Enbrel and then Cimzia... 9 years before being diagnosed with hypo and Hashis and put on Levo. Only wish I was one of those that the biologics worked to keep thyroid issues at bay...
My mother had symptoms of hypothyroidism in all the time I knew her (and maybe all her life previously) and she went onto developing RA after she'd gone through menopause.
She could never tolerate any of the RA drug treatments.
So, in her case: she had hypothyroidism decades (if not all her life) before she developed RA, and then was unable to tolerate any RA medication.
I wonder now, that if she'd been treated for hypothyroidism, she would then never have developed RA.
Hello, I think I must be missing something because I have a question relating to the two paragraphs quoted below - how do you determine a risk of developing something??? I can see how you might assess a likelihood of developing eg thyroid disease and I can see how you could determine the number of people/mice who did/didn't develop thyroid disease, but not how you know the risk of something developing in the future. Surely that would have to be retrospective and then a lot of other factors ruled out. Perhaps it was a retrospective study, a clinical audit perhaps?
"The researchers found that the risk of developing an autoimmune thyroid disease among RA patients was lower after their onset of the rheumatic disease than before diagnosis.
The most pronounced reduction in the risk of autoimmune thyroid disease was seen in patients with rheumatoid arthritis treated with immunomodulatory drugs or "biological DMARDs". In these patients, the risk of autoimmune thyroid disease was 46 per cent lower than in the control group without rheumatoid arthritis."
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