Hormone replacement therapy often is focused on hormones such as estrogens, progesterone, DHEA and testosterone, but optimal hormone balance cannot be achieved without correcting thyroid hormone imbalances. The complexity of the relationships can be summarized as follows: menopause may modify the clinical expression of some thyroid diseases, particularly the autoimmune ones; and thyroid function is not directly involved in the pathogenesis of the complications of menopause. However, coronary atherosclerosis and osteoporosis may be aggravated in the presence of hyperthyroidism or hypothyroidism. Also, the effects of postmenopausal estrogen replacement on thyroxine requirements in women with hypothyroidism should be considered.
Thyroid hormone (T4, thyroxine) is produced by the thyroid gland in response to the release of thyroid stimulating hormone (TSH) from the pituitary gland. Triiodothyronine (T3), the active form of thyroid hormone is produced predominantly outside the thyroid parenchyma secondary to peripheral tissue deiodination of thyroxine (T4), with <20% being secreted directly from the thyroid. In hypothyroidism, either the thyroid’s ability to make and release T4, or the body’s ability to convert T4 to T3, becomes compromised often showing up in the form of elevated TSH.
With aging, the main changes regarding thyroid physiology and function are a reduction of thyroid iodine uptake, free thyroxine and free triiodothyronine synthesis, and catabolism of free thyroxine while reverse triiodothyronine (R-T3; a non-usable form of T3) increases. The level of thyroid stimulating hormone remains normal with sometimes a tendency to higher limits. These changes are present in both sexes without distinction.
The original form of thyroid hormone replacement was desiccated thyroid extract (Armour Thyroid®) which contained both T4 and T3 and was the only available treatment for hypothyroidism for almost 50 years. Levothyroxine sodium is synthetic form of T4 and has replaced desiccated thyroid for the treatment of primary hypothyroidism with the aim of relieving symptoms and normalizing serum TSH. Many physicians note that despite apparently adequate replacement therapy with levothyroxine, some hypothyroid patients remain symptomatic. Studies suggest that replacement therapy for hypothyroidism with levothyroxine alone does not ensure normal thyroid levels in all tissues, and that a combination of levothyroxine and T3 may be required for optimal thyroid replacement therapy. However, the only commercially available form of T3 for replacement
therapy is synthetic liothyronine sodium. This immediate release formulation is rapidly absorbed and may result in higher than normal T3 concentrations throughout the body, causing serious side effects including heart palpitations. Because immediate release T3 is quickly metabolized, replacement of T3 with synthetic liothyronine requires multiple daily doses. Due to dosing problems and the significant potential for side effects, typically liothyronine is prescribed only in exceptional circumstances. Research indicates there is a need for sustained-release T3 preparations in order to avoid adverse cardiac effects. A study published in the New England Journal of Medicine reported that treatment with T4 plus T3 improved the quality of life for most hypothyroid patients.
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