This paper on how to diagnose and treat central (pituitary-based) hypothyroidism is a useful discussion about the problem and the factors causing it. The paper is free to access
The diagnosis and management of central hypothyroidism in 2018
February 2019 Endocrine Connections 8(2)
DOI: 10.1530/EC-18-0515
Luca PersaniLuca PersaniBiagio CangianoBiagio CangianoMarco BonomiMarco Bonomi
Thank you diogenes Keep them coming. Merry Christmas to you and all and Best wishes for 2020.
That is very interesting to me. Despite the doubts of my Endo, I believe I have Central Hypothyroidism as my TSH was 2.9 with a T4 of 10 (12-22) on diagnosis. I also have the DIO2 ThAla gene as mentioned at the end of the article.
Many thanks for posting this diogenes . As my son has Pan-Hypopituitarism with Septo-Optic Dysplasia, this will be most useful to show his Endocrinologist at his next appointment, as just lately they have not been taking his FT3, which, of course, is the test to go by. I am most grateful for all the information you and your colleagues post for this group.
An interesting review which sadly emphasizes blood tests over signs and symptoms, particularly for therapy. It's encouraging to see the statement that central hypothyroidism should be considered in every subject with low fT4 and low or normal TSH.
They consider fT3 of little use but I believe fT3 is important. Rightly or wrongly central hypothyroidism is a term restricted to the more severe forms arising from genetic origin or physical damage. Milder forms may be proposed but are not investigated.
Therapy of central hypothyroidism is targeted at ‘restoring’ serum thyroid hormone levels – fT4 and perhaps fT3. Unfortunately, this does not restore TSH. TSH has two major roles: stimulating thyroidal secretion and stimulating deiodinase, especially type-2 deiodinase (D2) which regulates local T3 levels. Simply bringing serum fT4 and fT3 back to normal is not good enough, T3 in organs such as the brain and skeletal muscles (that depend on D2 generated T3) will remain low.
Central hypothyroidism is quite rare. Subnormal TSH secretion - fT3 and fT4 low normal with a non-elevated TSH is common. All three parameters can be within their reference intervals and the patient told their results are ‘normal’. Subnormal TSH secretion can occur after a period of hyperthyroidism if TSH is suppressed for some time. As a result, fT3 and fT4 are lower than they should be and crucially there is hypothyroidism in tissues reliant on D2 activity. T3 originating from D2 activity stays around the cell nucleus for several hours facilitating thyroid hormone action. T3 from the thyroid or tablets is the same molecule as T3 from D2 but it has come from a different place. Where the T3 comes from matters.
Thank you for this diogenes it's very interesting and will be useful to share with endocrinologist and GP!
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