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.
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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