Thyroid Replacement Therapy
Hypothyroidism is a condition classified by an underactive thyroid gland — when the thyroid does not produce enough hormones. There are various treatments available depending on the cause of insufficient hormone production, but the standard of care is the same — initiating thyroid hormone replacement therapy.
To best understand the purpose of thyroid hormone replacement therapy, it helps to appreciate the role and interaction of T3 and T4 — the two primary thyroid hormones.
T3 and T4
The full name of T3 is triiodothyronine, and T4’s full name is tetraiodothyronine or thyroxine. T3 and T4 control your body’s metabolism. If you don’t have enough of these hormones, then your metabolism slows down. Your metabolic rate dictates how quickly you process food, how fast your heart beats, how much heat your body produces — and even how quickly you can think. In essence, T3 and T4 are in charge of how your body uses energy.
T3 and T4 are not equal in strength; T3 is the more active hormone of the two. While T3 is stronger, taking synthetic T4 hormone has been considered the standard treatment for hypothyroidism. The reason for this is that most of the T3 in our bodies actually used to be T4. When T4 hormones come into contact with other cells in the bloodstream, they give up an iodine atom to interact with those cells. When T4 loses an iodine atom, it becomes T3.
When this T4 to T3 conversion occurs, T3 then conveys the metabolic “message” to the other cells throughout the body. The benefit of taking only T4 therapy is that you’re allowing your body to perform some of the actions it is meant to do, which is taking T4 and changing it into T3. The half-life of T4 is also longer compared to T3 (7 days versus 24 hours), which means that it will stay for a longer time in your body after ingestion.
However, there is a growing consensus among experts that providing a supplement of both T3 and T4 is beneficial for many patients who have had a total thyroidectomy (removal of the entire thyroid gland).
The Purpose of Thyroid Hormone Replacement Therapy
If you are prescribed a form of thyroid hormone replacement therapy, the goal is to compensate for the lack of hormone secreted by your thyroid gland. In most cases, you will take a daily dose of T4 (or T3 and T4) in a pill taken orally.
But it’s important to understand that every patient’s therapy may be different. There is no cookie-cutter dosage or treatment plan when it comes to thyroid hormone replacement therapy. How the body absorbs the hormones, along with the amount of hormones needed to help the body function properly, is very varied. Your treatment plan will be individualistic. As such, you should expect some degree of adjustment when it comes to finding the dosage and form of therapy that works best for you.
Though synthetic T4 supplements have been the most prescribed form of thyroid hormone replacement therapy, there are a variety of forms, including animal thyroid supplements. Synthetic T3 is also occasionally given as part of treatment, most often after thyroid surgery, when waiting for radioiodine ablation in cases of cancer, or because the entire thyroid has been removed.
Thyroid hormone replacement therapy is a very individualized treatment process, and it is highly effective when prescribed properly. The goal of thyroid hormone replacement, in most cases, is to normalize your thyroid-stimulating hormone (TSH) levels. You and a doctor will discuss what treatment option will best alleviate your hypothyroid symptoms, allowing you to live a healthy, normal life.
Hypothyroidism is a common condition with an annual incidence of 3.5/1000 in women and 0.6/1000 in men. The prevalence increases with age. In areas, without iodine deficiency, the common causes of chronic hypothyroidism are autoimmune thyroid disease, thyroidectomy, radiotherapy (both radioiodine therapy and external beam radiotherapy), congenital disorders, and disorders of thyroid hormone metabolism. Secondary hypothyroidism occurs with some pituitary and hypothalamic diseases.
Diagnosis
Patients may not present with the typical clinical features of hypothyroidism. They may have vague symptoms such as tiredness. The diagnosis can be made by finding a persistently elevated serum concentration of thyroid-stimulating hormone (TSH). The serum-free thyroxine (fT4) concentration will below. Measuring tri-iodothyronine (fT3) adds little to the diagnosis or monitoring of hypothyroidism.
In secondary hypothyroidism, the pituitary fails to produce TSH appropriately so measurement of TSH is unhelpful. The diagnosis is suggested by a low fT4 and features of a pituitary disorder.
In subclinical hypothyroidism, the TSH is elevated (usually to 5-10 mIU/L) but the fT4 is normal. The typical symptoms of hypothyroidism are often absent.
The cause of primary hypothyroidism in an adult will usually be determined from a history of thyroidectomy or radiotherapy or finding high titers of antithyroid antibodies (thyroid peroxidase, anti-microsomal, or antithyroglobulin antibodies). The use of lithium and iodine-containing preparations (such as amiodarone) can cause drug-induced hypothyroidism.
Providing patients with a copy of the laboratory results which confirm their need for thyroxine often proves helpful for the patient and future treating doctors.
Treatment
Primary hypothyroidism is treated by giving the patient replacement thyroxine, usually for life. Liothyronine rarely needs to be used unless there is life-threatening hypothyroidism. Alternative sources of thyroid hormones such as thyroid extracts should be avoided.
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