Amiodarone.....again! Sorry....

[waveylines]

Hi Everyone,Appreciate your thoughts suggestion on this as am stuck....thank you.

I was put on Amiodarone for 4 weeks post surgery last September. So Amiodarone was stopped 7 months ago. I was on 3 3/4 grains of Armour Thyroid for Hypothyroidism before surgery. Been stable for years on this dose. 16yrs on NDT. Amiodarone completely messed up my thyroid hormones and I had to drop to one grain which was scary as my thyroid hormones shot way over range. Amiodsrines secondary effect is that it inhibits up take of thyroid hormones and conversion at cellular level. Effectively it creates a sort of blockade. Amiodarones half life is 150days approx. Its not really know when it leaves the body finally. Some report 8-12months. Many say it stays in the body for years! My endo (whose poorly now) told me its an unknown.

Nice says its contrary indicated for people with existing hypothyroidism but it was still prescribed for me....lol.

I'm stuck on 2 1/2 grains, been like it for about 3 months. I feel terrible keep crashing with typical hypo symptoms.

I've tried splitting the dose into two in the hope that more would get into cellular level. Helped with night time palpitations.

My blood test results just done are;

TSH: 0.005 supressed as usual.

Ft 4 19.6 (upper range limit 21.6)

Ft 3 5.4 (upper range limit 6.8)

6 weeks ago:

TSH 0.002

Ft4 20.4

Ft3 5.8

Same range

Not really a lot of room to move unless I try adding a bit of T3 in. Thoughts? But if it's a blockade would that make a difference?

I'm trialling changing split dose to 2 1/4 grain, plus 1/4grain at night. Still 2 1/2 grains per day.

Pulling my hair out with sheer frustration!

Any thought suggestions welcome.

Ps: B12, vit D etc all optimal. Take vit D with k2, b12 injection, b complex with folate. Vit C. I'm gluten free.

[greygoose]

I've tried splitting the dose into two in the hope that more would get into cellular level.

That's the wrong way round. Splitting the dose means there's less chance of getting some into the cells. You need to flood the receptors by taking it all in one go, to force some into the cells.

A blood test only tells you what's in the blood, not what's getting into the cells. So, reducing the dose on the basis of what's in the blood - where it doesn't do anything - when you know it's not getting into the cells, is illogical because it reduces the chance of any getting into the cells and actually doing something. Personally, I would not have reduced if I felt well on that dose. So, now that you've reduced and are not feeling well, maybe it's time to put the dose up again. Blood tests can be false friends at times like this, and should not rule over common sense.

[waveylines in reply to greygoose]

Thanks. I didn't feel wellGreygoose. My heart was racing, I was shakey on my usual dose. I could only tolerate 1 grain. Everytime I increase I get side effects which is why I'm stuck. I was post heart surgery so had to be careful. All good on the heart front. So I've tried three times to go to 2 3/4 but each time my heart races etc... its taken me ages to get this far. That's why I'm wondering about Liothyronine on top of my current ndt dose.....

I don't know anything about how to get past Amiodarone. Is it the same as cellular resistance? What I read was that amiodarone reduces conversion of T4 to T3 with in the cell as well as uptake. Nothing about how you manage it!!

[greygoose in reply to waveylines]

I don't know anything about Amioderone, either. I was just going by what you said. But, yes, if it affects conversion adding T3 might do the trick.

[waveylines in reply to greygoose]

Thanks Greygoose. I'll give T3 a go. I've found this situation very confounding!! Lol....

[waveylines in reply to greygoose]

I tweaked the same daily dose and reduced night time and increased morning......feel a bit better. Though now getting palpitations early morning again. All a balance. I think ure right a little bit of T3 in the morning could help.

[arTistapple]

I was wondering why we had not heard from you recently. Sounds like you have been working away at the problem in the background.

What GG says makes sense but the proof will be in the pudding. Get back to us ASAP and update us on your experiment. I am dealing with cardio now too. It’s a nightmare no-one seeming (especially NHS trained medics) to have a handle on thyroid issues underpinning (or not) our health.

I see the glee with which GP surgeries are being congratulated for cutting down on T3 prescriptions and instructions on NDT falling into the same category. It’s a bloody nightmare.

Really their drug bill (excluding off course all the other drugs they then need to prescribe due to lousy treatment of thyroid) is reduced by very little it seems to me.

Good Luck to both of us.

[waveylines in reply to arTistapple]

Sorry to hear you're having to deal with cardio now. I found my EP very good but the cardiologist was just hell bent on beta blockers!!

Yes am fighting on. Tedious and long winded......... still no thyroid meds!!! But been sent off to Wales by local nhs endo to see another Endo....Turns out you start the wait all over again if your nhs endo sends you elsewhere..... so am told it will be 2025 before I'll get seen!

[DizzyD]

Just read your post and comments of others which you posted over three months ago. As you know, re amiodarone I am in the same situation as yourself. Recently, I reintroduced small dose of NDT (half grain) alongside 75 levo which I was already on.

Having just read above research paper I suspect the addition of NDT is doing nothing....ie its being blocked.

Question is going by all comments i have read how can synthetic T3 get into cells when ohter hormones derived from NDT cannot?

Since sending last private msg to you I have been in constant afib and suspect t3 from NDT in my blood is not getting into cells and triggered the afib

WILL synthetic T3 actually get into my cells?

if it can I will dose small amount of t3 instead of the NDT.

thanks lovely

[waveylines in reply to DizzyD]

Hi Jean,T3 can get into your cells or you would die. Can't live without it. Has the Amiodarone damaged the receptors....well I believe it has. Endos I've seen believe Amiodarone has largely left my system so wont be affecfing me now.....10months since it was dropped. If that's the case why can Amiodarone cause harm years later????? What a nonsense they all spout.

I've put my ndt up by a quarter 2 3/4 grains. This because I had palpitations at night, hr 150 woke me. Scary. That has stopped with the increase. I weed for England too. However HR still tipping over 100 in the evening.

Am not convinced the blood tests help. Doesn't tell me what's happening at cellular level. I think I'm still under medicated as remain a whole grain lower than before.

I will need a further increase. My last blood tests showed low fT3.

I will increase agsin when I feel I can. I doubt I will get back to my original dose but if I could get to 3 1/4 grains I will be happy

I'm also looking at adding a tadge bit of lio on top of ndt .... But I'll do a blood trst to cross check whether ft3 remains low with the quarter increase. Hopefully it will rise.

None of the medical profession recognises this problem as a much longer issue. I've come to the conclusion even the good endos are blind.

Excuse my bluntness.

Ange

Xx

[waveylines in reply to waveylines]

I should add last blood test showed Ft4 20.7 (upper range 22.3) Ft 3 4.1 (upper range 6 8) Hence me increase of a quarter. Gives me a further T3 increase of 2.3 mcg approx and T4 increase of 17mcg. Little steps.

NEVER will I take it again even if thrusted on me in ICU post surgery. I will have it put on my notes. Intolerant of Amiodarone do not give.

It says do not prescribe for patients with Hypothyroidism on NICE guidelines.

Though NICE has also said the same for NDT! 🤣😂

[pennyannie in reply to waveylines]

Your blood tests now look similar to mine when on T4 monotherapy :

Maybe T3 is going to be a better way forward - though not sure if one can unblock that blocked by another drug :

Since the guidelines state ' not recommended for those who are hypothyroid ' maybe you can use this as a lever to get optimally medicated on T3 if, push comes to shove.

[waveylines in reply to pennyannie]

Had thought of this but in my ICB both Liothyronine and ndt are blacklighted. Levothyroxine IS the only treatment they offer, according to the Endo I saw.

[pennyannie in reply to waveylines]

So is there a case of medical negligence - as it's not recommended - but has been used - and you, the patient are just left to get on with the consequences.

It's just dreadful - for the sake of a guideline that is arbitrary and imposed haphazardly throughout the country - dependent on where you live -

where has common sense gone ?

[waveylines in reply to pennyannie]

Think that's a tricky area. Yes NICE say dont prescribe it to patients eith hypothyroidism but then say in certain situations it may be necessary. Medical negligence is big area.....and any legal firm will want to know the long term harm. As settlements are based on this. I doubt there's much money in it for them. They're not interested otherwise.

[pennyannie in reply to waveylines]

Well yes - of course, I understand,

it's made so difficult to prove anything and takes years - it's just a job for those in the business of representing you -

but it is a life sentence for the patient - who seems to get lost and just a name on the paperwork -

there appears no recourse - and where you live within the UK should not be the deciding factor and actually makes a mockery out of the whole issue of ' health care ' !

[helvella]

For interest:

Life-threatening amiodarone-induced thyrotoxicosis - Personalized approach to radical treatment

Abstract

Objective: Amiodarone is an iodine-rich molecule and an effective antiarrhythmic drug. It is a first-line treatment for patients with life-threatening ventricular arrhythmias and for prevention in patients at high risk. The use of amiodarone may cause serious adverse effects such as pharmacotherapy-resistant, life-threatening amiodarone-induced thyrotoxicosis (AIT)leading to rapid deterioration of the patient's condition.According to the European Thyroid Association (ETA) guidelines, emergency thyroidectomy is the first-line treatment option in these cases. ; however, is not always feasible in the clinical setting due to the high anesthetic risk.We aimed to assess the clinical course and results of urgent thyroidectomy and 131-I therapy in patients with severe AIT with worsening of cardiac status.

Methods: Retrospective analysis of the clinical course and outcomes of life-threatening AIT refractory to pharmacotherapy in patients hospitalized at a tertiary endocrinology center between 2014 and 2022.

Results: An electronic database search identified 75 patients hospitalized for severe AIT. At the time of AIT diagnosis, median Thyroid-stimulating hormone (TSH) concentration was 0.001 mIU/L (range 0.001-0.35), fT4 63.2 pmol/L (range 9.0 - >100), and fT3 10.2 pmol/L (range 3.8-49.3). All patients received optimal conservative treatment. Among them, 20 required urgent radical therapy due to worsening arrhythmias and/or AIT-related heart failure. In this group, 6 patients died before any radical treatment was applied, 6 underwent total thyroidectomy, while 8 patients were successfully treated with 131-I (in 6 cases after rhTSH stimulation). The median dose of 131-I used for the therapy was 784MBq (range 627-860). The decision to treat with 131-I despite low but detectable 131-I uptake (median value 6 %) was made in cases of significant contraindications to anesthesia due to refractory ventricular arrhythmias, exacerbation of severe heart failure unresponsive to cardiac treatment, myocardial infarction during AIT course, massive pulmonary embolism.

Conclusion: The decision regarding the optimal time and type of radical treatment of AIT refractory to pharmacotherapy is critical for patients management and should not be delayed. Urgent therapy with 131-I may be an effective therapeutic option in patients who are unsuitable for thyroidectomy due to the high risk of anesthesia.

Keywords: 131-I; AIT; Amiodarone; Salvage therapy; Thyrotoxicosis.

© 2024 Jagiellonian Univerity Medical College.

pubmed.ncbi.nlm.nih.gov/391...

[waveylines in reply to helvella]

Thanks yes seen this. This is for people who have a normal functioning thyroid to which Amiodarone induced over active thyroid. Partly induced by the thyroid producing more thyroid hormones as a result of the Amiodarine and exacerbated by the blockade that Amiodarone causes for up take and conversion as cellular level. It's a shocking drug!! Other patients normal thyroid functioning gland get round this by naturally adjusting their out put. From what I can gather and I'm mo medic/scientist it does so by lowering ft4 and increasing ft3. This is why I'm hindering if liothyronibe added in would help. The medical profession go on about how ndt has to high a ratio of T4 to T3 but it may actually gave helped a bit. However its fixed ratio so maybe more T3 would help counterbalance why Amiodarone does?

Am back up to 2 3/4s. Last time I tried this dose I had to lower at 5 weeks....due to symptoms of over treatment which resolved when lowered.

Blood tests just tells me what's in the blood not a great help as my problem is at cellular level. Though I will do a blood test before lowering if the same thing happens again and plan to do one at 6 weeks.

Fed up!!