As a primary care PA, I see patients with all sorts of endocrine disorders. While diabetes dominates, thyroid and parathyroid disorders, and hormonal issues are all typical fare. Of all the thyroid patients I see, those with low or hypothyroidism, make up the majority. Rarely do I refer to an endocrine specialist, and though I’m no specialist myself, I feel that there are a lot of misconceptions about managing hypothyroidism and I see some pretty weird stuff coming from other clinicians.
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The most common issue I see is the treatment of asymptomatic patients with a “less than ideal” TSH, which has been defined as around 2 mIU/L. These are patients with what would otherwise be called subclinical hypothyroidism. Many of these folks tell me that they’re not even sure why they take thyroid medication, they were only told they needed it. How does that happen? My guess is that routine blood tests showed a TSH between 5 and 10 mIU/L and without a second thought, levothyroxine was prescribed.
Besides the risks of treatment (and over-treatment), this decision now commits the patient to several lifelong consequences including regular blood tests, increased pill burden, and the costs associated with more frequent follow-up.
Who should be treated for hypothyroidism?
Patients with classic symptoms such as fatigue, constipation, and cold intolerance, however, should be treated even a less-than-impressive TSH. Patients with a TSH over 10 mIU/L should be treated as should those with the combination of an elevated TSH and suppressed free T4–this is classic primary hypothyroidism. I don’t manage thyroid disease in pregnant women, so I won’t comment on treating that population. I will also say that just because someone with asymptomatic subclinical hypothyroidism shouldn’t be reflexively treated with levothyroxine, this does not mean that they should not be monitored–such patients are at a higher risk of developing overt hypothyroidism later in life.
There are multiple reasons why an individual would suffer hypothyroidism, the most common, however, is chronic inflammation from the presence of antithyroid peroxidase antibodies (anti-TPO) otherwise known as Hashimoto’s thyroiditis. It is all too common to see patients placed on a thyroid supplement without measurement of anti-TPO antibodies. This helpful confirmation can also drive treatment decisions in those with subclinical hypothyroidism.
Not a Magic Bullet for Weight Loss
Another all-too-common slip I see is thyroid replacement medication being used as part of a weight-loss regimen, often combined with stimulants like phentermine. Besides being ineffective for weight loss, the concern for arrhythmia and coronary insufficiency is enough that levothyroxine carries a boxed warning, the FDA’s highest level of alert. The warning reads, “Thyroid hormones … either alone or with other therapeutic agents, should not be used for the treatment of obesity or for weight loss. In euthyroid patients, doses within the range of daily hormonal requirements are ineffective for weight reduction. Larger doses may produce serious or even life-threatening manifestations of toxicity, particularly when given in association with sympathomimetic amines such as those used for their anorectic effects”.
Forget the T3
The next unfounded practice I’ve repeatedly observed is using free T3 to diagnose and/or manage hypothyroidism. A diagnosis of hypothyroidism is confirmed with an elevated TSH and a depressed free T4. There’s no reason to order free T3 when assessing a patient with symptoms of hypothyroidism. It’s even less helpful when managing thyroid medication. Multiple organizations recommend treating to TSH alone yet patients and providers alike continue to insist on a “full thyroid panel” with TSH, free T3, and free T4. The American Association of Clinical Endocrinologists states: “Confirmatory total T4, free T4, and T3 levels do not have sufficient specificity to serve as therapeutic endpoints by themselves.” Free T3 assays are also highly variable as are T3 levels themselves. The American Thyroid Association states that “Measurement of free T3 is possible, but is often not reliable and therefore not typically helpful.” T3 levels can also be falsely elevated by birth control pills–and most of my hypothyroid patients are female, many of whom are on birth control pills!
The one test I’ll never order, however, is the reverse T3. Reverse T3 is an inactive metabolite of thyroxine and is helpful only in rare genetic thyroid conditions and the critically ill. Unfortunately, it’s becoming a favorite of “alternative” health practitioners to justify unregulated supplements.
So, sound off PAs: are you still routinely ordering free T3 to diagnose and manage hypothyroidism? Would you ever order reverse T3?
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