Hi all, I have been slowly adding tiromel t3 to my 175mcg levo dose to try and improve remaining symptoms, the worst being over-reaction to external temperature change (sweating) and bouts of heavy sweating for no reason at all. A few other milder symptoms remain. After reaching 25mcg I had a breakthrough with the random sweating, at rest, going away but not great improvement in other circumstances, mood also improved. I,ve been 'medichecks' testing at each stage. I am now taking 62.5mcg which having seen posts here seems a very high dosage. The tests show only a very minor improvement in ft3, which I don't understand (t3 now at 48% range. I will provide results from no t3 to now. I am male, 59yrs, 6.0ft and 105kg.
I notice the translated tiromel instructions state for mild hypothyroidism 1 to 3 tablets going by tests and symptoms. So I can increase to 75mcg ?. bit worried as I see people here feeling better on 12.5mcg but I am definitely improving. All tests were done to the guidance on here i.e 24hrs from t4, 9hrs after half t3 dose. Comments and advice would be much appreciated, thanks #itsaminefield
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ade1961
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25mcg of T3 is equal - in its effect - to 100mcg of levothyroxine. I think you may be on a larger total dose of thyroid hormones than you realise i.e. (25mcg of T3 = 100 + 175 levo is total 275 mcg of thyroid hormones.
Tiromel is T3 and 25mcg, as stated above, is approx 100mcg of T4 - in its effect.
I agree, it seems excessive. So why doesn't it reflect in the test and why do the tiromel manufacturers advise 1 to 3 tablets of 25mcg for hypothyroidism, any ideas please
I am not medically qualified so cannot prove what is stated but would assume that 3 x 25mcg T3 plus 100 levo (approx dose 75 mcg of T3 plus 100 levo would be for a person who had 'thyroid hormone resistance'. I must also state I am not medically qualified.
Thank you shaws, I also am a little confused and that's why I posted. The translated instructions for 'tiromel' are available here and I hope to get answers, they state, as above, 1 to 3 tablets as normal dose for mild hypothyroidism, tests and symptoms confirming. I have no symptoms of over-replacement, just an improvement of symptoms(getting expensive though)I hope perhaps the experts can comment.
Yes but the tiromel instructions are talking about just their T3 as a replacement dose (the 3 tablets.) but you are also taking quite a bit of T4. Normally getting overheated is associated with overactive thyroid. Sorry its such a minefield isn’t it. I take just t3 myself. Good luck 😎
But you cannot treat yourself as being hypothyroid when on 175mcg thyroxine? Hypo may be the underlying condition but replacement T4 takes you out of that bracket and gives a different base line to work with. Excess sweating is usually associated with being hyper.
Your TSH results are coming down which suggests overtreatment?
How are you feeling generally? If you stretch your hands out is there any tremor? Energy levels? Weight loss?
It’s important to note symptoms as well as test results. We’re all different!
Resistance to Thyroid Hormone (RTH) or Impaired Sensitivity to Thyroid Hormone.
For those who have certain unusual test results and effects from levothyroxine, this paper does consider causes.
Note that as they did not find DIO2 mutations, this is something which could be dismissed on those grounds. A doctor who has some idea of DIO2, sees a negative result, and assumes all is well. Clearly that would be wrong but it is a real problem with the interpretation and management of those who have had a DIO2 test. If it is positive, it just might unlock sensible treatment. If not, you might get dismissed even more forcefully.
Thyroid . 2020 Jun 5. doi: 10.1089/thy.2019.0825. Online ahead of print.
Identification of Resistance to Exogenous Thyroxine in Humans
Nerea Lacámara 1 , Beatriz Lecumberri 2 , Beatriz Barquiel 3 , Arancha Escribano Muñoz 4 , Isabel González-Casado 5 , Cristina Alvarez-Escolá 6 , Fernando Aleixandre 7 , Francisco Morales 8 , Rocío Alfayate 9 , MariaCarmen Bernal 10 , Raquel Miralles 11 , Ilgin Yildirim 12 , Ahmet Gökhan Özgen 13 , Juan Bernal 14 , Pere Berbel 15 , Jose Carlos Moreno 16
• PMID: 32498666
• DOI: 10.1089/thy.2019.0825
Abstract
Background:
Thyroxine (T4) to triiodothyronine (T3) deiodination in the hypothalamus/pituitary is mediated by deiodinase type-2 (D2) activity. Dio2(-/-) mice show central resistance to exogenous T4. Patients with Resistance to Exogenous Thyroxine (RETH) have not been described.
Aim:
To identify hypothyroid patients with TSH unresponsiveness to levothyroxine (L-T4) and to characterize the clinical, hormonal and genetic features of human RETH.
Methods:
We investigated hypothyroid patients with elevated TSH under L-T4 treatment at doses leading to clinical and/or biochemical hyperthyroidism. TSH and free T4 (fT4) were determined by chemiluminescence, and total T4, T3 and reverse T3 (rT3) by radioimmunoassay. TSH/fT4 ratio at inclusion and T3/T4, rT3/T4 and T3/rT3 ratios at follow-up were compared with those from patients with resistance to thyroid hormone (RTH) due to thyroid hormone receptor-β (THRB) mutations. DIO2, including the Ala92-D2 polymorphism, selenocysteine binding protein 2 (SECISBP2) and THRB were fully sequenced.
Results:
Eighteen hypothyroid patients (9 of each sex, 3-59 years) treated with L-T4 showed elevated TSH (15.5±4.7 mU/L; reference range [RR]: 0.4-4.5), fT4 (20.8±2.4 pmol/L; RR: 9-20.6) and TSH/fT4 ratio (0.74±0.25; RR: 0.03-0.13). Despite increasing L-T4 doses from 1.7±1.0 to 2.4±1.7 µg/kg/day, TSH remained elevated (6.9±2.7 mU/L). Due to hyperthyroid symptoms, L-T4 doses were reduced, and TSH increased again to 7.9±3.2 mU/L. In the euthyroid/hyperthyrotropinemic state, T3/T4 and T3/rT3 ratios were decreased (9.2±2.4 -RR: 11.3-15.3- and 2.5±1.4 -RR: 7.5-8.5-, respectively) whereas rT3/T4 was increased (0.6±0.2; RR: 0.43-0.49), suggesting reduced T4 to T3 and increased T4 to rT3 conversion. These ratios were serum T4-independent and were not observed in RTH patients. Genetic testing was normal. The Ala92-D2 polymorphism was present in 7 of 18 patients, but allele dose did not correlate with RETH.
Conclusions:
Human RETH is characterized by iatrogenic thyrotoxicosis and elevated TSH/fT4 ratio. In the euthyroid/hyperthyrotropinemic state, it is confirmed by decreased T3/T4 and T3/rT3 ratios, and elevated rT3/T4 ratio. This phenotype may guide clinicians to consider combined T4+T3 therapy in a targeted fashion. The absence of germline DIO2 mutations suggests that aberrant posttranslational D2 modifications in pituitary/hypothalamus or defects in other genes regulating the T4 to T3 conversion pathway could be involved in RETH.
1 Erasmus University Medical Center, Rotterdam, The Netherlands.
2 Wellcome-MRC Institute of Metabolic Science, University of Cambridge, Cambridge, United Kingdom.
3 Erasmus University Medical Center, Rotterdam, The Netherlands. Electronic address: t.j.visser@erasmusmc.nl.
Abstract
BACKGROUND:
Thyroid hormone (TH) acts via nuclear thyroid hormone receptors (TRs). TR isoforms (TRα1, TRα2, TRβ1, TRβ2) are encoded by distinct genes (THRA and THRB) and show differing tissue distributions. Patients with mutations in THRB, exhibiting resistance within the hypothalamic-pituitary-thyroid axis with elevated TH and nonsuppressed thyroid-stimulating hormone (TSH) levels, were first described decades ago. In 2012, the first patients with mutations in THRA were identified. Scope of this review: This review describes the clinical and biochemical characteristics of patients with resistance to thyroid hormone alpha (RTHα) due to heterozygous mutations in THRA. The genetic basis and molecular pathogenesis of the disorder together with effects of levothyroxine treatment are discussed.
CONCLUSIONS:
The severity of the clinical phenotype of RTHα patients seems to be associated with the location and type of mutation in THRA. The most frequent abnormalities observed include anemia, constipation, and growth and developmental delay. In addition, serum (F)T3 levels can be high-normal to high, (F)T4 and rT3 levels normal to low, while TSH is normal or mildly raised. Despite heterogeneous consequences of mutations in THRA, RTHα should be suspected in subjects with even mild clinical features of hypothyroidism together with high/high-normal (F)T3, low/low-normal (F)T4, and normal TSH.
From the extremely small changes to your blood test results, two things occur to me: either you're barely absorbing the Tiromel, or it's possible you've got a 'bad batch' - there have been a few reported cases of people buying certain batches of Tiromel that did not appear to contain the correct amount of active T3.... I think SeasideSusie knows more about this?
Thank you seasidesusie, the same thought had crossed my mind about the validity of the tiromel and supplier ! - blister pack expiry date 08 2023, 16V069, numbers on the cardboard pack - (01)08699514017004 and (21) 221612005109215 I'm afraid I have disposed of the previous packs
I haven't heard that there is a problem with that batch.
On the box, besides the long number you've given above, there should also be the lot number which should be the same as the number on the blister pack.
However, all those batches I have been notified of have lot numbers beginning with 20 and their expiry dates have been 2021 and 2022. From the lot numbers I have seen, the first two numbers go up rather than down, so I'm surprised you've got a batch beginning with 17 rather than 20, that would suggest possibly an older batch but I can't be 100% sure of that.
If you want to send me a private message giving me the name of your supplier, I will see if I have any feedback on them
Thanks seasidesusie, there is no lot number on the outside cardboard after the long number, the 'part numbers' on the cardboard and blister pack match, 16v069. It's late so i'll pm you tomorrow, as if it isn't hard enough eh !
Maybe there's another simpler reason... maybe your body needs more time to adjust on the changes. Not sure if this is correct, and on the timeframe you have increased the dose but I have noticed this on myself also: changing your dose will indeed affect your TSH within the 6-8 weeks period but the related ft3/ft4 change is followed long after that (around 16 weeks in myself). So maybe the gradual increase you did on your dose was too soon.
Thanks for your reply Jonathan1956, I follow the protocol of Paul Robinson's patient manual. I did split dose but found that taking all t3 in the morning with t4 more convenient with no noticeable difference. T4 only, did clear up the worst of my symptoms,(morning anxiety and low mood). Heat intolerance and sweating had been a symptom for me for many years and continued to get worse on t4 only. Adding t3 was a urica break through, I stopped sweating inappropriately but it does still happen on exercise and sudden external temperature change. This was why I continued to raise t3 which may be a mistake because after about 37.5mcg I haven't really noticed an improvement. So although blood tests show only a small increase in ft3, it doesn't seem to reflect the good result in symptoms. I suspect it may be impossible to totally relieve all the symptoms of Hypothyroidism as it is described as the thermostat of the body, so I just try to get as best as I can. I posted because I expected to see a large increase in ft3 but it hasn't moved up much. I,ve decided to reduce t3 to 37.5mcg and wait a longer period to blood test.
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