The Pathogenesis of Hashimoto's Thyroiditis: Further Developments in our Understanding

Some of you will recognise the second co-author of this paper - and not necessarily fondly.

Points that arise as I read it:

Apparently confortable with the term Hashimoto's thyroiditis (unlike much of the UK medicial profession)

Acceptance of significant genetic components.

Agreeing that there has actually been an increase in Hashimoto's.

Accepting that stress is a factor.

Accepting that both Thyroid peroxidase antibodies (TPOab) and Thyroglobulin antibodies (TGab) are found in the majority of sufferers and knowing this helps with management decisions.

Therapeutic clinical targets are still not known. Which rather takes the wind out of the sails of those who suggest that TSH is actually the only clinical target of relevance.

Above all - this damned Hashimoto's is complicated and much is still unknown.

Horm Metab Res. 2015 Sep;47(10):702-10. doi: 10.1055/s-0035-1548832. Epub 2015 Apr 16.

The Pathogenesis of Hashimoto's Thyroiditis: Further Developments in our Understanding.

Ajjan RA1, Weetman AP2.

Author information


Hashimoto's thyroiditis (HT) is part of a spectrum of thyroid autoimmune conditions and this review provides an update on the latest developments in the field. HT has a genetic predisposition with a number of immune-related and thyroid-specific genes conferring disease susceptibility. However, disentangling genes with protective and predisposing effect is a complex process that requires further work. The recent increase in the incidence of HT implicates environmental factors in disease pathogenesis including improved hygiene, increased dietary iodine intake, new treatment modalities and chemical agents. Additional unmodifiable predisposing factors include stress, climate, age and gender. Both cellular and humoral immunity play a role in HT pathogenesis. Defects in T regulatory cells and increased activation of follicular helper T cells may have a role in disease initiation/perpetuation. Infiltrating lymphocytes can be directly cytotoxic to thyroid follicular cells (TFC) or may affect cell viability/function indirectly through cytokine production, which alters TFC integrity and modulates their metabolic and immune function. Thyroid peroxidase and thyroglobulin antibodies are present in the majority of HT patients and help with management decisions. Antibodies against the sodium iodide symporter and pendrin are present in a minority with little known about their clinical relevance. In addition to immune cells, recent work has identified DNA fragments, generated following cell death, and micro RNA as potential factors in HT pathogenesis. Despite the large number of studies, the mechanistic pathways in HT are still not fully understood and further work is required to enhance our knowledge and identify novel preventative and therapeutic clinical targets.

© Georg Thieme Verlag KG Stuttgart · New York.



[PubMed - in process]

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15 Replies

  • Would love to read the full article

    Abstracys are always a pain

  • How did you find this Jazzw?


  • Follow "my" link to the PubMed listing. Then look towards the top right - there is a blue-coloured icon Thieme Connect under Full text links. Click on that and you end up on the Thieme Connect site, on the abstract. Look for a Full Text tab.

    Or use the link that I have sneakily edited into my original post. :-)

  • Sneaky link worked fine.Will read in full later after Tai Chi .

    Just keep remembering the first endo I saw " thyroid is simple" !

    Looks very interesting.

  • It would be good to see routine testing for HT in the presence of sore throats, swollen lymph nodes, exhaustion, strange general unwell-being, instead of being fobbed off with the "a virus and take some Floradix" diagnosis.

    I'm sure this pattern of ill health that many of us have PREVIOUSLY suffered is the prelude to what happens later.

    Until the ravaging effects of autoimmunity is recognised....when the drug companies finally target autoimmune conditions. ..(I'm sure it will be done..)..I don't suppose much will happen.

    I guess it is kinda encouraging...thank you for posting Rod,


  • It has ruined my life.

  • Its ruined the life of my husband ,our daughter and all 4 of her kids that's for sure and not done me much good coping with all of them

    Its a nonsense to say its maneagable or does not cause symptoms and a severe loss of quality of life even if you are on NDT

  • That's just terrible. I would be devastated if my kids got it. Thyroid meds don't help my symptoms..period. I have been homebound since 2008.

  • does NDT not help ????????

  • ndt makes me worse.

  • Maybe because you cant convert the t4 in it ?

    have you tried T3?

  • I don't convert well, but it made me hot , sweaty, shaky, heart racing, high blood pressure, rashes, swollen..on a small dose, i couldn't even raise. It flared up my immune system to produce more inflammation/cytokines. I am on t3 only now, feel like crap but not like that.

  • Amazing that they should still be researching a disease, which, according to my doctor is very simple and clear cut. If the tsh is below 1 the patient is overmedicated and the meds should be lowered. If tsh is over 30 the patient might feel a bit unwell according to my mums doc, but no cause for concern.

    I bet my mums doc and mine think all this new fangled research is a waste of time. :-)

    Thanks for posting Rod, i would show it to my doc but i dont think he would understand .

    G xx

  • "if TSH is over 30 the patient may feel a little unwell " !!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!!

    Should have seen my husband and daughter and granddaughters with a TSH of 2.9

    My husband was a wreck and very nearly lost his job he would fly off the handle or be curled up in a corner frozen cold wrapped in blankets barely able to walk let alone climb a flight of stairs

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