There are two primary dimensions in follow up treatment for thyroid cancer. The first is focused on preventing and identifying recurrence while the second, often overlooked in the quest to “beat cancer” is supporting your Quality of Life (QoL).
Some endocrinologists and other providers may not always be aware of the need to keep TSH low to reduce the risk of recurrence. At best, TSH needs to be maintained at the very low end of the range while high risk patients should have TSH suppressed to below 0.1 mU/L per American Thyroid Association (ATA) guidelines.
In order to achieve appropriate suppression, patients are often started on high levels of thyroxine (levothyroxine, T4) without regard for QoL. This may cause symptoms typical of overmedication (usually referred to as hyperthyroidism in the literature) while, at the same time, low levels of triiodothyronine (T3) may cause symptoms of low T3 syndrome, poor lipid and carbohydrate metabolism and affect cardiovascular, central nervous, and reproductive systems. And this may all occur while still not adequately suppressing TSH.
T3 can play an important part in long term treatment and support for thyroid cancer patients by both suppressing TSH and contributing to overall functioning and QoL. While thyroid hormone metabolism isn’t rocket science it is complex yet with the tools we have available it is a no brainer to evaluate both clinical and bio-chemical response to thyroid hormone replacement therapy. Failure to use all the options available, including testing for Free T3 levels and utilizing liothyronine (T3) to achieve suppression without the negative side effects of supraphysiological doses of T4 leaves many thyroid cancer patients with no resolution of symptoms and a greatly decreased QoL.
From 2015 American Thyroid Association Management Guidelines for Adult Patients with Thyroid Nodules and Differentiated Thyroid Cancer
[B44] What is the appropriate degree of initial TSH suppression?
(A) For high-risk thyroid cancer patients, initial TSH suppression to below 0.1 mU/L is recommended.
(Strong recommendation, Moderate-quality evidence)
(B) For intermediate-risk thyroid cancer patients, initial TSH suppression to 0.1– 0.5 mU/L is recommended.
(C) For low-risk patients who have undergone remnant ablation and have undetectable serum Tg levels, TSH may be maintained at the lower end of the reference range (0.5– 2mU/L) while continuing surveillance for recurrence. Similar recommendations hold for low-risk patients who have not undergone remnant ablation and have undetectable serum Tg levels.
(D) For low-risk patients who have undergone remnant ablation and have low-level serum Tg levels, TSH may be maintained at or slightly below the lower limit of normal (0.1–0.5 mU/L) while surveillance for recurrence is continued. Similar recommendations hold for low-risk patients who have not undergone remnant ablation, although serum Tg levels may be measurably higher and continued surveillance for recurrence applies.
(E) For low-risk patients who have undergone lobectomy, TSH may be maintained in the mid to lower reference range (0.5–2 mU/L) while surveillance for recurrence is continued. Thyroid hormone therapy may not be needed if patients can maintain their serum TSH in this target range.
(Weak recommendation, Low-quality evidence) applies to (B) through (E)
Many “Long Covid” symptoms are quite similar to those of hypothyroidism or, in the case of post-thyroidectomy patients, inappropriate thyroid hormone replacement. Researchers are aware that there is more to thyroid hormones than just T4.
From Physiological Role and Use of Thyroid Hormone Metabolites – Potential Utility in COVID-19 Patients
Thyroid hormones (TH) are endocrine hormones that influence nearly all cells of the human body. Deficiency and excess, hypothyroidism and hyperthyroidism, demonstrate the action of TH on fetal development, lipid and carbohydrate metabolism, growth, cardiovascular, central nervous, and reproductive systems. TH action is determined by the level of circulating hormones and their metabolites, serum binding (distribution) proteins, cellular transporters, type and amount of deiodinases (D), and expression of receptors.
From Circulation Low-T3 Syndrome – A Strong Prognostic Predictor of Death in Patients With Heart Disease
Metabolism of Thyroid Hormone
Thyroid hormone is indispensable for normal development and metabolism of most cells and tissues. Thyroid hormones are metabolized by different pathways: glucuronidation, sulfation, and deiodination, the latter being the most important.