We've just had a letter published in the European Journal of Endocrinology in which we discuss what exactly does a diagnosis of SCH mean and is TSH a useful indicator in all cases. Our belief is that the term SCH covers a multitude of possibilities and more individual attention to the patient is more important, rather than just TSH.
Response: Subclinical hypothyroidism: To treat or not to treat. Eur J Endocrinol. 2020;183:D15-D24.
doi:10.1530/EJE-20-062tJuly 2021
European Journal of Endocrinology
Rudolf Hoermann, John Edward M Midgley, Rolf Larisch, Johannes W. Dietrich
Written by
diogenes
Remembering
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Congratulations to all the effort you and the scientists do to try to change the attitudes of many professionals who cannot figure out why patients' still complain when the reliance is upon TSH alone.
I think I can get away with printing the text here as it's only a letter:
We read with great interest the current debate on the controversial issues that have long surrounded the treatment of subclinical hypothyroidism (1). The fact that the two discussants disagreed so strongly in their approach to a prevalent problem, routinely faced by clinicians around the globe, may indicate severe shortcomings in the current approach. Although this controversy has started many year ago, it remains unresolved. Unlike in many other diseases, thyroid diagnosis has evolved through definition by exclusive reliance on a single biochemical measure, as opposed to symptomatic presentation of the disease.
In our opinion, the problem begins with the term and very definition of “subclinical hypothyroidism”. What is subclinical hypothyroidism? Is it a true disease or a mere laboratory constellation? According to current guidelines, the diagnosis of subclinical hypothyroidism is made when a confirmed TSH measurement has been obtained that exceeds the upper reference range of the pituitary hormone while the concentrations of thyroid hormones still remain within their reference range (2). Adding to the confusion, therapeutic targets have been separated from diagnostic criteria of the disease by recent guidelines (2). LT4 substitution has been recommended to be withheld in patients with diagnosed subclinical hypothyroidism unless their TSH concentration exceeds a much higher threshold (of 10 mIU/L or even up to 20 mIU/L) than he diagnostic threshold (of approx. 4 mIU/L) (2,3). This disease understanding has left clinicians with a conundrum to explain to many patients why they suffer from a disease, yet would not require any therapeutic intervention. This may be particularly difficult to accept for patients presenting with symptoms which are in their opinion suggestive of a thyroid condition.
Perhaps, it is time to consider a different approach, potentially more satisfying to clinicians. As implied in the original term “subclinical” the new strategy should re-focus on the clinical manifestation rather than the biochemistry. In recent year, the over-reliance on a TSHcentred diagnostic strategy has been strongly challenged (4,5). The apparent deficiencies of this approach and its lack of diagnostic specificity and reliability have been reviewed elsewhere (6). The problem is deeply rooted in the guiding principles of HPT regulation (7).
In patients with subclinical hypothyroidism due to autoimmune thyroiditis and sufficient intact thyroid tissue, thyroid regulation importantly includes, in addition to the classical feedback of circulating thyroid hormones onto pituitary TSH secretion, the feedforward control of TSH over preferential thyroidal triiodothyronine (T3) secretion (8). The system is designed to take pro-active action in anticipation rather than reactive to the event of a shortage of thyroid hormone supply to the body. The manifestation of a clinical disease is determined either by the success or failure of the central attempt at compensation. Measurement of a slightly elevated TSH in subclinical hypothyroidism, cannot reliably discriminate between the two outcomes. It must therefore be regarded as an ambiguous signal, unless all thyroid hormones and clinical endpoints are taken into account.
Subclinical hypothyroidism, as a laboratory constellation, has been implicated to increase the risk of cardiovascular mortality (9). This conclusion may also be premature, because slightly elevated TSH levels together with "normal" thyroid hormone concentrations may not necessarily indicate early thyroid failure (10). Alternatively, this may reflect an increase in the homeostatic set point of the hypothalamus-pituitary-thyroid axis (10). Set point adjustments frequently occur in association with chronic psychosocial stress or allostatic load.
Many Thank Yous Diogenes for all your time and Amazing Hard work to get thyroid patients *Optimally* dosed and not by TSH sole. Rather FT4 and FT3 are the telling and most useful markers that are very useful for us.
What does the last sentence mean? ie set point adjustments.. psychosocial stress etc. Does it relate to permanent downregulation of TSH( feedback htp etc) folowing very stressful life events. This is something I am very very intetrsted in.
Ongoing stress by whatever cause can affect the thyroid/pituitary parameters. The whole mechanism is thrown when this occurs. It's a type 2 load where the problem is pernicious and long-lasting, cementing the responses into a area it's difficult to get out of.
Thank you so much fit taking the trouble to reply, this is a subject thst interests me and many others, thinking that this might lead to Hypothyroidism which makrs us more stressed and so it goes on in downward spiral.
Thank you diogenes . This is another excellent argument and will hopefully lead to change. I was 'luckier' than some, that I only spent a year without treatment for subclinical hypothyroidism. I very much appreciate your and your colleagues work on our behalf.
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