Euthyroid Hyperthyroxinemia – Euthyroid Conditions

by Carlo Raj, MD

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    00:01 A topic that you want to be extremely comfortable with is called euthyroid conditions in laboratory investigation.

    00:09 As simple as this may seem, there are certain things that you want to take at a dissection that is going to help you differentiate one type of thyroid pathology from the another.

    00:18 Do not underestimate what I have to tell you now.

    00:23 This brings us to our first discussion of euthyroid.

    00:27 Break it up.

    00:28 Eu- prefix – normal.

    00:30 Thyroid.

    00:32 A pathology is going to lie within hyperthyroxinemia.

    00:38 Break this up.

    00:39 When you say thyroxinemia, referring to your T4 in your blood; in this case, we have hyper.

    00:46 So, how could you possibly have a normal thyroid state and be hyperthyroxinemic? The discussion now brings us back to our physiologic point of view of thyroid binding globulin.

    01:02 Remember the definition of total? Total is bound plus free.

    01:08 What is the component that makes up majority of your total? It is the bound.

    01:13 So, therefore, euthyroid hyperthyroxinemia, due to, in general, increased binding protein.

    01:23 What is this specifically for thyroid hormone? Thyroid binding globulin.

    01:27 Coming from where? The liver.

    01:29 Your emphasis and focus should be on, well, what is then causing liver to increase is thyroid binding globulin.

    01:39 Before we go at there, abnormalities.

    01:42 T4 - binding.

    01:45 Majority of your T4 is bound thyroid binding globulin.

    01:49 Transthyretin.

    01:51 Albumin.

    01:56 The most common cause - MCC of hyperthyroxinemia would be TBG excess.

    02:01 What is that going to do to your total? Total what? Total T4.

    02:08 Increases it.

    02:09 Why? What then binds to my TBG? T4 does.

    02:13 I’ll show you this.

    02:16 Remember, the majority of your thyroid hormone being released into circulation is T4.

    02:22 It has to be bound to TBG.

    02:25 Whenever TBG is found to be in excess, you would then expect there to be a total in T4.

    02:32 Hence, hyperthyroxinemia.

    02:35 What about that T3? Well, as far as the normal functioning, or the functioning of the body, it is within normal state.

    02:45 Euthyroid.

    02:47 It could be hereditary.

    02:50 Estrogen.

    02:53 Whenever you find a patient in a hyperestrogenic state, such as pregnancy or contraceptive pills that may contain estrogen… Estrogen works in liver to increase glycosylation of TBG.

    03:08 When you increase your TBG, you’re going to then decrease the clearance.

    03:13 So, therefore, with all this TBG that resides within your circulation, guess what it’s going to bind to.

    03:21 T4.

    03:22 So, you increase in the bound faction of your thyroid hormone, thus, what do you do to your total? You’re increasing it.

    03:33 Keep your bound and total separate.

    03:36 Resulting in hyperthyroxinemia.

    03:39 What other conditions might then result in increase or excess TBG? Hepatitis.

    03:46 Drugs such as Methadone, tamoxifen; a porphyria pathology, in biochemistry that you’ve heard it called acute intermittent porphyria - often times you’ll find euthyroid hyperthyroxinemia; reduced thyroxin deiodination, such as amiodarone or propranolol, could all result in euthyroid hyperthyroxinemia.

    04:11 What do you mean by deiodination? The conversion of T4 to T3.

    04:15 It’s not taking place effectively.

    04:21 I want to show you a picture here of what’s important to you clinically.

    04:27 You’re going to use this picture so that you can then first understand normal, then understand what’s happening in a state here of euthyroid hyperthyroxinemia and truly when you read a stem of a question or you’re dealing with the patient and you’re having discussion with your attending, you know what he or she is referring to.

    04:50 Let’s begin on the left here where it’s perfectly normal.

    04:54 The huge blocks that you’re seeing here, the blocks is your TBG – thyroid binding globulin.

    05:05 Coming from where? The liver.

    05:07 What is that TBG going to bind to? T4.

    05:12 Stop.

    05:14 Now, you’re left with T3.

    05:17 You’re going to be using clinically or interpreting what’s known as a thyroid hormone binding resin.

    05:26 You want to keep your resin, which is what you’re going to interpret clinically, separate from your TBG, which are these blocks that you’re seeing bound to T4.

    05:38 As long as you’re within normal state and you have adequate and normal amounts of TBG, then the resin is going to bind exactly as to what it needs to with T3.

    05:54 Let us now move on to the right side of this illustration.

    05:59 And the right half is then showing you euthyroid hyperthyroxinemia.

    06:03 What is the difference between the pathology on the right versus the physiology on the left? You’ll notice, please, that you have increased number of these blocks.

    06:15 How did this occur? Oh, maybe it was estrogen or a patient that was in a hyperestrogenism state.

    06:24 When you increase your TBG, you’re going to bind more T4.

    06:29 When you bind more T4, what faction of your total have you increased? The bound.

    06:36 What happens to total? It increases it.

    06:38 Therefore, what do you call this? Hyperthyroxinemia.

    06:42 But, why is it euthyroid? You’re still euthyroid because even though you’re robbing your T4 out of circulation, your thyroid gland and your anterior pituitary, the axis, is going to respond accordingly to start increasing thyroid hormone production to bring it back to normal.

    07:04 What do I mean by that? What is the active form of most hormones? Free.

    07:11 Free thyroid hormone.

    07:13 Free calcium.

    07:14 Free cortisol.

    07:17 So, when you rob your free faction, this is then interpreted as being hypo.

    07:24 Your feedback mechanism in your axis is immediately going to respond so that it can replenish the free.

    07:32 Your state of euthyroid.

    07:34 That picture on the right is probably one of the most important pictures that you want to be able to interpret.

    07:40 In pregnancy, in pregnancy, with the increased estrogen, you’re then going to increase your TBG.

    07:48 You’re going to then bind and remove the free faction of T4 out of circulation.

    07:53 Are you picturing that? Thus, immediately during pregnancy, the mother is then going to start increasing her production of her thyroid hormone so that you bring or she brings the thyroid hormone back, free faction back up to normal.

    08:09 And of course, that is absolutely critical to occur or otherwise the foetus is going to feel the effects of hypothyroidism and you cannot have that.

    08:20 Last little point that I’ll make here.

    08:23 I want you to focus upon the resin there.

    08:25 And at the end of this section, I’m going to walk you through a table where that resin, which is binding T3 will then tell you what’s actually happening in a patient that is differentials for euthyroid.

    08:40 Understand these two pictures for now.

    08:43 I’m going to build and build and build upon these until we finally come to a table where I’ll summarize everything for you clearly.

    About the Lecture

    The lecture Euthyroid Hyperthyroxinemia – Euthyroid Conditions by Carlo Raj, MD is from the course Thyroid Gland Disorders.

    Included Quiz Questions

    1. Increased binding proteins
    2. Increased T4
    3. Increased conversion of T3 to T4, leading to decreased T3
    4. Decreased estrogen leading to decreased binding proteins
    5. Decreased albumin leading to increased TBG binding to T4
    1. An increased concentration of estrogen
    2. Hepatitis
    3. Acute intermittent porphyria
    4. Amiodarone excess
    5. Methadone
    1. Progesterone-only contraceptives
    2. Methadone
    3. Amiodarone
    4. Propanolol
    5. Zanoxifen
    1. Increased estrogen increases the level of thyroid-binding globulin (TBG), decreases free T4, and leads to increased T4 production.
    2. Increased estrogen increases the level of TBG, decreasing bound T3.
    3. Delivery of the thyroid hormone to the fetus decreases the available thyroid hormone for the mother, leading to increased production.
    4. Increased TBG due to decreased bound T4 leads to a spike in estrogen until TBG levels even out.
    5. Decreased TBG due to increased delivery of T4 to the fetus leads to increased production of TBG.
    1. 99%
    2. 16%
    3. 75%
    4. 15%
    5. 80%

    Author of lecture Euthyroid Hyperthyroxinemia – Euthyroid Conditions

     Carlo Raj, MD

    Carlo Raj, MD

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