Radioactive Iodine Uptake in Thyroid diseases - USMLE Forums
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  #1  
Old 12-04-2009
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Thyroid Radioactive Iodine Uptake in Thyroid diseases

It's wise to remember that not all cases of hypothyroidism are associated with decreased Iodine uptake and not all cases of hyperthyroidism are associated with increased Iodine uptake.

Examples of hyperthyroidism with increased uptake:
  • Typically Grave's disease as the autoantibodies stimulate TSH receptor sensitivity enhancing the uptake.
  • Secondary and tertiary hyperthyoroidism where the elevated TSH levels also stimulate the uptake.
  • Toxic adenoma in which the overactive adenoma need to take Iodine to support the production of T4.
Example of hyperthyroidism with decreased uptake:
  • Factitious hyperthyroidism in which the exogenous T4 causes feedback inhibition on the TSH secretion.
  • Any other exogenous thyroxine sources such as struma ovarii.
  • Iodine induced thyroid toxicosis.
  • Release of thyroid hormone by destructive process e.g. temporary hyperthyroidism seen in subacute thyroiditis.
  • Toxic Nodular Adenoma, the nodule is active (causing hyperthyroidism) but the rest of the gland is with decreased uptake due to suppressed TSH.
Example of hypothyroidism with increased uptake:
  • Thyroid hormone receptor insensitivity in which the T4 has no peripheral effects (hence the hypothyroidism) and no feedback effects (hence the elevated TSH and increased uptake).
Example of hypothyroidism with decreased uptake:
  • Hashimoto, De Quervain, and Reidle thyroditis are all associated with decreased Iodine uptake.

Thyroid carcinoma may variable be hyperthyroid/hypothyroid and Cold/Hot on radioactive Iodine uptake tests.

Last edited by rasheed; 02-07-2010 at 03:08 PM.
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Old 07-16-2010
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Thumbs Up Nice

That's wonderful.

Thank you very much
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Old 07-22-2010
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thnx a lot , really its a valuable info......
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Old 07-22-2010
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Smile thank you rasheed, for nice information.you such help increse our knowledge day by day.

Thank you rasheed for nice information.
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Old 11-15-2010
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Default great work

thnx a lot for these valuable information
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Old 01-20-2011
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any one can please explain how this is possible? "decreased RAIU in Iodine induced thyroid toxicosis "?
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Old 01-20-2011
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Dear Rasheed and my doctor friends, now that we have a list, let us discuss on each point. who wants to start first?
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Old 01-20-2011
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Quote:
Originally Posted by hana View Post
any one can please explain how this is possible? "decreased RAIU in Iodine induced thyroid toxicosis "?
Right? We would normally think of a thyrotoxicosis with decreased RAIU as resulting from some destructive process causing the gland to release thyroid hormone, and of iodine as suppressing t3 and t4 release, like when we use it for emergency treatment of thyroid storm. It is weird that RAIU is decreased in thyrotoxicosis from iodine excess. Merck Manual posits:
Quote:
Originally Posted by Merck Manual
Excess iodine ingestion causes hyperthyroidism with a low thyroid radioactive iodine uptake. It most often occurs in patients with underlying nontoxic nodular goiter (especially elderly patients) who are given drugs that contain iodine (eg, amiodarone, iodine-containing expectorants) or who undergo radiologic studies using iodine-rich contrast agents. The etiology may be that the excess iodine provides substrate for functionally autonomous (ie, not under TSH regulation) areas of the thyroid to produce hormone. Hyperthyroidism usually persists as long as excess iodine remains in the circulation.
But you'd still think that those areas would be taking up the I131... Maybe it's that the radioactive iodine is out-competed by the excess iodine that has already been taken up by the gland?
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Old 01-21-2011
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Default confusing IODIDE/IODINE

OK.
I share what is my understanding and I will be so happy if anyone can contribute to this discussion. I have seen so many confusions not only in this forum but others and no one since could get to an agreement. let's solve it here, hopefully

Well, whenever "THYROID FOLLICULAR CELLS IN THYROID GLAND" increase their activity to make more thyroid hormones we can expect to see increased RADIOACTIVE IODINE UPTAKE-RAIU-.

In case of exogenous thyroid hormones or stromal thyroid, since the thyroid gland cells are not the source of thyroid synthesis, so it is logical to expect not only normal RAIU but even decreased b/c TSH is suppressed and thyroid is totally relaxing there doing nothing!!

OK, so we can have hyperthyroidism W/O increased RAIU. granted.
but about this part of rasheed's not i am not sure "
Toxic Nodular Adenoma, the nodule is active (causing hyperthyroidism) but the rest of the gland is with decreased uptake due to suppressed TSH"

Those nodules that are active are using I, RIGHt? they are just independently do it so I would expect to see high RAIU at areas that those nodules are hyperactive, but at same time since TSH is low I expect low RAIU by normal parts of gland,,,so maybe a patchy RAIU pattern? not just totally decreased RAIU??? WHAT DO YOU THINK GUYS?

Other point as rasheed says "Release of thyroid hormone by destructive process e.g. temporary hyperthyroidism seen in subacute thyroiditis" here the PREFORMED STORED hormones are released, they have already used Iodine before so now they are just released and of course we can not expect increased RAIU, moreover, since TSH IS LOW so RAIU is even low!

My big confusion is about Iodine itself;
I do not understand why Iodine can work differently in different situations such as;

1- KI is one of treatments for thyrotoxiocsis,,,so Iodine here inhibits THYROID SYNTHESIS ?
how about I131? it inhibits thyroid function. Why? b/c of again excess Iodine in it same as KI or the radioactive part destroys thyroid gland?!
2- A person with endemic goiter is exposed to Iodine by any means; traveling to rich Iodine AREA, receiving medications containing Iodine, radiocontrast media,,,,,_now he develops TRANSITIONAL HYPERTHYROIDISM! HOW? MECHANISM?
is it the Iodine induced thyrotoxicosis they are talking about ? or is it Plummer diz? please explain in your own words, I have read so many articles yet confused.

Thanks again
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Old 01-21-2011
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Quote:
Originally Posted by hana View Post
Those nodules that are active are using I, RIGHt? they are just independently do it so I would expect to see high RAIU at areas that those nodules are hyperactive, but at same time since TSH is low I expect low RAIU by normal parts of gland,,,so maybe a patchy RAIU pattern? not just totally decreased RAIU??? WHAT DO YOU THINK GUYS?
I didn't say totally decreased uptake, I said increased in the nodule and decreased in the rest of the gland, so you are right about the patchy appearance.
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Old 01-21-2011
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Default wolf chaikoff vs jod basedow

first we need to understand the basis of wolf chaikoff effect.
due to increased exposure to iodine in a hyperthyroid state, the enzyme deiodinase or peroxidase are inhibited. but this effect is temporary as there is an escape phenomenon for this effect involving the inactivation of the sodium iodide symporter channel. the escape phenomenon takes about ten days to appear. wolf chaikoff effect (in the form of Lugol's iodine or KI)
has been utilised in case of hyperthyroid emergencies before the antithyroid drugs came into picture.
the hypothyroid effect of I131 should be due to its radioablative effect as we know that the conc. of KI required to produce hypothyroidism is very high (1.4 grams in 100 ml of water)

now jod basedow effect:
it is hyperthyroidism on exposure to iodine, in an abnormal thyroid tissue (preclinical Graves or nodular goitre). "thirsty thyroid drinks more and more iodine to produce more of thyroxine".
but there is an additional mechanism of drug induced hyperthyroidism. it is evident by the use of Amiodarone. the mechanism involves lysosomal activation resulting in release of stored thyroxine.
so the person in endemic areas will have predominant hyperthyroidism due to increased iodine uptake.
whereas the person on amiodarone will have hyperthyroidism due lysosomal activation as well.
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Old 01-21-2011
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Quote:
Originally Posted by rasheed View Post
I didn't say totally decreased uptake, I said increased in the nodule and decreased in the rest of the gland, so you are right about the patchy appearance.
you are right,my misunderstanding was b/c the explanation was under "Example of hyperthyroidism with decreased uptake;" section.
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Old 01-21-2011
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Quote:
Originally Posted by manphnx View Post
first we need to understand the basis of wolf chaikoff effect.
due to increased exposure to iodine in a hyperthyroid state, the enzyme deiodinase or peroxidase are inhibited. but this effect is temporary as there is an escape phenomenon for this effect involving the inactivation of the sodium iodide symporter channel. the escape phenomenon takes about ten days to appear. wolf chaikoff effect (in the form of Lugol's iodine or KI)
has been utilised in case of hyperthyroid emergencies before the antithyroid drugs came into picture.
the hypothyroid effect of I131 should be due to its radioablative effect as we know that the conc. of KI required to produce hypothyroidism is very high (1.4 grams in 100 ml of water)

now jod basedow effect:
it is hyperthyroidism on exposure to iodine, in an abnormal thyroid tissue (preclinical Graves or nodular goitre). "thirsty thyroid drinks more and more iodine to produce more of thyroxine".
but there is an additional mechanism of drug induced hyperthyroidism. it is evident by the use of Amiodarone. the mechanism involves lysosomal activation resulting in release of stored thyroxine.
so the person in endemic areas will have predominant hyperthyroidism due to increased iodine uptake.
whereas the person on amiodarone will have hyperthyroidism due lysosomal activation as well.
..."as we know that the conc. of KI required to produce hypothyroidism is very high (1.4 grams in 100 ml of water",,,well no i did not know that and that is why i had problem understanding this part.so iodid in "very high "doses is able to supress thoes enzymes and help reducing thyroid hormones synthesis. now i get why diet iodid do not cause hypO while KI does! is my undestanding right? i know i have OCD

ABOUT I 131,SO IT IS THE RADIAOACTIVE part that damages...then how we do thoes testes to check RAIU ? should not radioactive i damages thyroid here aswell?

jodbasedow; i like thirsty mechanism,clear

amiodarone,new concept for me!i thought its just b/c of idodine in it.

but how about plummer? FA says it happens inI deprivation situation followed by iodine restoration. my q; does it have to happen after I restoration? or if person lets say have endemic goiter for years and never leave that area,can he still develope TOXIC multinoduar goiter-plummer-?
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Old 01-22-2011
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yes u got that right hana. about the ocd part, every one has an OCD, ur lucky that urs is related to studies. jokes apart
now coming to ur question about RAIU. there is a big difference between therapeutic use and diagnostic use of Radioactive I131.
for diagnostic scans like RAIU the dose given is about 3-5 mCI.
but for full ablation the doses are between 50-100 mCi.
so u see, the low dose iodine 131 is just like normal iodine which acts as a tracer. thats it and the effects of radiations are minimal.

ur second question that the effect of amiodarone on thyroid is due to iodine itself. as this drug has high conc. of iodine its effects can be similar to high doses of iodine. but it itself causes two types of effects. amiodarone induced thyrotoxicosis type 1 (AIT I) which is nothing but Jod Basedow and Second AIT Type II which is due to lysosomal activation.

ur next question whether endemic goiter can turn into multinodular goiter:
endemic goiter is a diffuse type of goiter and mostly the patients present with just a big lump in neck region i.e. cosmetic reasons and not hypothyroid symptomatology. if u do the lab reports u will see either TSH is normal or TSH is slightly raised and not markedly raised (due to increased sensitivity of the TSH receptors on thyroid)
so if u give iodine the goiter will reduce depending on the duration of the disease (that is why iodine supplements are given along with thyroxine replacements in treatment of endemic goiter)
now if u find TSH to be low in a suspected case of endemic goiter, u should reconsider the diagnosis as it can be a case of subclinical graves or plummers or tertiary adenoma. and these are the cases that have a very thirsty thyroid.
so i wont consider whether it is endemic goiter or multinodular goiter, without the TSH levels as treatment protocol changes.
there is a possibility of transformation of an endemic goiter of long duration changing into toxic goiter only if thyroid has been stimulated by high TSH levels for a long duration of time. this is tertiary adenoma. but it will remain subclinical until it is exposed to iodine.
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Old 06-15-2011
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HEY GUYS...

Every time u put a text on this forums.. PLEASE. PLLLLEEEASE include the source ok?... seems like if u all guys were researchers and put your investigations to be read.
thanks
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