1. Modern medicine is rarely at a loss with the thyroid gland, perhaps the most biddable organ in the human body. We can turn it up, turn it down, even pull it out and replace it with drugs. We also have excellent diagnostic tools. But thyroid treatment isn’t always simple. Overtreating is common. Subclinical hypothyroidism is an area of confusion. And some symptoms of hypothyroidism — fatigue and weight gain — are so ubiquitous it can be tough convincing patients that their thyroid is functioning correctly.
2. Subclinical hypothyroidism: TSH is elevated (usually mildly: 5-10 mIU/L), T4 (thyroxine) is normal range. So is T3 (triiodothyronine), if tested. There’s little evidence that treatment helps, but there’s an argument that progression to overt hypothyroidism can be prevented. Estimates of prevalence range from 1% to 10%, with women overrepresented, and of these 3-20% will progress untreated. Others are resolving cases of thyroiditis that will improve.
3. Wait 2-3 months then test again. If subclinical hypothyroidism persists, test for thyroid peroxidase antibodies. These demonstrate an autoimmune process and progression risk. These patients stand to benefit from treatment. So do those with goitre, and women who are pregnant or trying. In others, don’t treat unless TSH exceeds 10 mIU/L.
4. Stop a moment to consider the possibility of adrenal insufficiency (Addison’s disease). This can cause high TSH, and should be ruled out before treatment as levothyroxine is dangerous in Addison’s disease. Domperidone or metoclopramide treatment can also raise TSH.
5. The goal should be to restore serum TSH not to the middle of the normal range, but to a low-normal value (0.3-0.6 mIU/L). This will require from 25 to 100 µg levothyroxine daily. This should put T4 in the upper-normal range (12-22 pmol/L).
6. Some patients will need a slightly higher thyroxine dose to get TSH down to low-normal. This can put their T4 in the 24-28 pmol/L range. This is, of course, exogenous subclinical hyperthyroidism. But it shouldn’t cause any problems, so long as you monitor T3 to be sure it’s in the middle of its reference range (1.0-2.2 nmol/l, aim for 1.6 or 1.7).
7. Malabsorption syndromes can weaken levothyroxine’s effect, necessitating a higher dose. So can cholestyramine, ferrous sulphate, and antacids. Anticonvulsants, rifampicin and sertraline increase levothyroxine metabolism. Required dose may change with age and should be increased about 50% in pregnancy.
8. Monitor TSH and T4 every 4-8 weeks until it stabilizes in target ranges. That done, hypothyroidism is controlled. But patients won’t see immediate improvement. It can take 3-6 months or even longer. And some will still complain that their T4 is too low and is causing fatigue. In the U.S., there are even organized patient groups pushing for higher T4 targets for their members.
9. Don’t be pushed. Too much levothyroxine can actually trigger weight gain, leading patients to believe they’re not getting enough. And TSH falling below 0.2 mIU/L exposes the patient to osteoporosis, cardiovascular risk and possible atrial fibrillation.
10. One option with the patient who feels undertreated is to substitute some triiodothyronine (T3). Give 10 µg daily, while reducing levothyroxine by 50 µg. But don’t let TSH or T3 stray beyond reference ranges. If, after all that, the patient is still experiencing fatigue or weight gain, it’s not the thyroid that’s causing it, and they may benefit from considering lifestyle issues.