Krish’s research group is focused on genetic and molecular endocrinology, exploring disorders including resistance to thyroid hormone (RTH) and PPARgamma gene defects associated with lipodystrophic insulin resistance. They have also shown how deficiency of human selenocysteine-containing proteins leads to a multisystem disease, including disordered thyroid hormone metabolism, and works on translating his discoveries to improve diagnosis and treatment of thyroid conditions.
Dare we live in hope!
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DippyDame
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Not really! This is old hat. RTH (genetic mutations of the TRBeta gene) was discovered by Sam Refetoff in the USA. It presents with elevated thyroid hormones and a non-suppressed TSH. i.e. blood tests are abnormal.
Chatterjee leads the UK centre of excellence for RTH and his team discovered RTH due to TRAlpha mutations. This is mercifully rare as the children present with severe abnormalities and may only survive a few years.
These are forms of RTH caused by genetic mutations of thyroid hormone receptors. I believe there are non-genetic forms of RTH which I have called ‘Acquired RTH’ or ‘ARTH’. I think by giving it a name it might help raise awareness. My hypothyroidism was caused by PBDEs which are endocrine disrupting chemicals (EDCs). PBDEs disrupt T3 binding in peripheral tissues but not in the pituitary, this is because the pituitary has receptors (TRB2) which are different to peripheral receptors (TRA1, TRB2). Thus the patient has clinical hypothyroidism with normal blood tests. I describe it here ibshypo.com/index.php/acqui... (click on the blue links at the bottom of each webpage).
Chatterjee was President of the BTA and during his time was more supportive of liothyronine prescribing than those that came before and after him.
I simply describe my condition as "a form of RTH"...."acquired" makes better sense and I know you have adopted this.
I agree, to be recognised this condition needs a name, it's the best way to start!
i have no idea what caused my ARTH.... but I know it exists. It may be genetic; a geneticist did suggest it may be the result of an as yet unrevealed variant.
For me, ARTH is the only explanation/ diagnosis that currently makes sense....after decades of slowly declining health and unhelpful tests, treatments etc etc.
The low cellular T3 caused by this condition needs to be recognised/understood by medics....serum FT3 as we know is not a helpful marker in this case. It appears to be too much of leap into the dark right now for current medical thinking....remembering Gordon Skinner et al
Those of us who now depend on high dose T3 mono know they were correct, but the very mention of T3 is too much for some medics to even contemplate....and current teaching and guidelines are against them!
I don't have your depth of knowledge but I do know enough to convince me that this is a growing problem which is causing misery for so many people.
We seem to be dealing with cellular rather than glandular hypothyroidism!
To quote Sinatra, " I did it my way"....but many things prevent that from being an option for the majority. NHS thinking for a start!
I cannot see any change occurring any time soon....the barriers are too strong... but with very faint hope I wondered if Chatterjee's support of lio might be a crack where a slither of light gets through!
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