Andrew Louis has asked a few questions about the disease which we'll go into one by one.
1. Why do we assess the success or failure of the treatment by measuring TSH levels? Why not T3 or T4?
With Hashimoto's thyroiditis, one has some residual thyroid function, just not enough to produce sufficient quantities of T4 and T3, which are therefore low. The level of TSH (which orders the thyroid to produce T4 and T3) will be higher than normal, which is fundamentally analogous to the body screaming at the thyroid to produce more hormones. This screaming does work a bit, as it forces what remains of the thyroid gland to work harder and make more of the thyroid hormones.
If you replace T4 a little, but not completely, you may end up with normal T4 levels - but only because the pituitary, via TSH, is still forcing the functional parts of the gland to work harder than normal. Only when T4 has been completely replaced will this screaming match stop, and the TSH will return to normal.
This is why TSH is a better measure of the success, or failure, of our treatment than T4.
2. Do patients benefit from T3 replacement?
In theory, giving T4 alone should be enough, since the body naturally converts some T4 to the more potent T3. However, some studies suggest that patients report feeling better, symptomatically, when given T3 together with their T4. More studies are needed on this at present, but it might be worth a try in some patients. However, taking T3 alone is not recommended, because T3 has a much shorter half-life than T4. This means that T3 would have to be taken 3-4 times per day and you would have to cope with levels of T3 that would fluctuate quite a lot (which can cause odd symptoms).
3. Can patients with Hashimoto's thyroiditis have normal TSHs and yet be symptomatic?
No, not for all intents and purposes. Autoimmune destruction of the gland will reduce its output of T4 and T3. This should stimulate the pituitary to produce more TSH than normal, as a way of signalling to the (remaining) thyroid to up its production levels.
However, it is possible to suffer from hypothyroidism despite normal TSH levels, although this is rare. It involves some sort of anterior pituitary pathology, whereby this gland is unable to produce enough TSH for that patient, even though the TSH is still within population norms. T4 will be low in this case, providing for an easy measurement. This is not, however, Hashimoto's thyroiditis.
4. Is there a benefit between the synthetic and the natural preparations of thyroid replacement hormones?
'Natural' preparations are made from the thyroid tissues of other animals. However, they are not recommended, as the quantity and potency of the thyroid hormones can vary greatly between batches. Anyway, 'synthetic' levothyroxine is identical to thyroxine, which is the natural version of this hormone made by your own thyroid gland.
5. Since Hashimoto's disease is chronic, why have a a lifetime of monitoring and dose changes? Why not simply remove the thyroid all together?
Alas, removing the gland wouldn't avoid a lifetime of monitoring and potential dose changes. In fact, a treatment for many cases of hyperthyroidism involves removing the gland (either surgically or with radioactive iodine), thus rendering these patients hypothyroid as a consequence. And as with Hashimoto's thyroiditis, such people also need lifelong monitoring to get their thyroid hormone levels right. However, once they are stable, levels only need checking annually, or even less frequently.
Removing the gland also has several disadvantages. For one, no surgical procedure is without risk, especially when operating in the dangerous neck area. Furthermore, since there is some functional thyroid tissue remaining, it is best to leave it in place. The reason that the average person doesn't need to measure their thyroid hormone levels annually is because the body will naturally adjust its levels to match the demands of the time. As much as possible, this function should be left intact, even if it needs a little artificial supplementation. Removing the thyroid in its entirety would make the levels even harder to control.
6. How do the adrenal glands (and cortisol) relate?
Usually they don't really. However, Hashimoto's thyroiditis is associated with other autoimmune diseases in a minority of cases. One of these is Addison's disease, which is chronic insufficiency of the adrenal cortex. (It has many causes; this is just one of them.) This would result in low cortisol levels (but there are many other causes of this biochemical phenomenon too!).
7. I hear there are advances on the way to cure auto-immune disease. Do you know anything about this?
Auto-immune diseases can be treated by:
- Ignoring their cause and simply treating the symptoms - this is done in auto-immune thyroiditis and diabetes mellitus type 1, for instance. If you can get away with it safely, this is actually the best option.
- Trying to suppress the immune system in general - this rather drastic approach is reserved as a last resort against debilitating illnesses, but its place is well-established if used judiciously.
- Trying to modulate the immune system subtly - this newer approach is more promising, but amazingly difficult to get right. It can be done pharmacologically, or, even more recently, via gene therapy.
However, I'm not aware of any established and proven treatment options apart from replacing the missing thyroid hormones pharmacologically. The rest is either nonsense (as in some 'alternative' naturopathic remedies) or still being studied. However, I'm not an endocrinologist, so if you've heard of anything new, let me know and I'll look into it. :)