Do you feel comfortable discussing euthyroid-sick syndrome?
How are thyroid function tests in euthyroid-sick syndrome?
Let's start!
Severely ill patients often have ⬇️ TSH and ⬇️ free T4.
It was believed that the thyroid was working normally, and this condition was described as "euthyroid-sick syndrome".
It is now believed that these pts may also have acquired central hypothyroidism.
Regardless of it being central hypothyroidism or not, this condition is considered protective as it prevents tissue catabolism.
The body "tries" to avoid further stress by reducing the thyroid hormone.
Let's use a parallel: it is like an induced state of "hibernation".
Euthyroid-sick syndrome presents not only with ⬇️ TSH and ⬇️ free T4, but also ⬆️ reverse T3 (rT3).
rT3 is a metabolically inactive byproduct of T4.
Again, regardless of central hypothyroidism, there are other mechanisms to avoid thyroid hormones burden in severely ill pts.
How to treat? Do not give LT4/T3. Treat the baseline condition.
Clinical meaning: do not assess thyroid function tests in severely ill pts unless there is ⬆️ suspicion for thyroid dysfunction. Be careful in interpreting it!
Do you now feel comfortable discussing euthyroid-sick syndrome?
That is all folks!
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In endocrinology, the concept of "inappropriately normal" is the basis for the interpretation of several labs results.
Do you understand this concept? It is definitely one of the most important for understanding endocrine diseases.
Follow the 🧵
📢 Clinically, it means the problem is not with the hormone itself. It means the problem is with the "hormone coordinator", which may sound normal when it is actually failing to respond as it should.
Let's clarify it!
With few exceptions, hormones control their own secretion by a mechanism called "negative feedback".
Let's use an example:
- Thyroid secretes T3/T4 controlled by TSH.
- T3/T4 act in the pituitary controlling TSH secretion.
--> T3/T4 negatively impact TSH secretion
Sodium-glucose transport proteins (SGLT) are found both in the small intestines (SGLT1) and in the kidneys (SGLT2).
In the nephron, SGLT2 is the main responsible for the reabsorption of the filtered glucose. For this reason, its inhibition⬆️ glucosuria, decreasing hyperglycemia.
Phlorizin, a non-selective SGLT inhibitor, was isolated in the 1800s.
Why don't we use it?
- Instability;
- ⬇️ bioavailability;
- Inhibition of SGLT1, leading to ⬇️ intestinal glucose absorption and diarrhea
Biotin supplements are commonly used and do not change thyroid function.
On the other hand, biotin often causes lab assay interference mimicking Graves' disease:
⬇️ TSH
⬆️ fT4 and T3
⬆️ TRAb
TRAb is a marker of Graves' disease, the most common cause of thyrotoxicosis/hyperthyroidism, and has a high accuracy :
- Sensitivity: ~ 97%
- Specificity: ~ 99%
📢Beware that despite high reliability, TRAb result can be falsely elevated in the setting of biotin use