Lifelong thyroid hormone replacement therapy is required to treat the common chronic endocrinopathy, hypothyroidism. Nearly 130 years ago, such treatment started with crude desiccated extracts of animal thyroid glands, and this continued until synthetic levothyroxine became available in the 1980s.
Receptors for the thyroid hormones T3 (3,5,3-triiodothyronine); and T4 (thyroxine) are widely expressed in tissues and organs throughout the body, and deficiency may result in a plethora of symptoms affecting cardiovascular, neurological, cognitive and metabolic functions. The severity of symptoms may vary over a wide spectrum, with possible severe impacts on health and quality of life.
While the goal of treatment is to resolve a client’s signs and symptoms by achieving biochemical euthyroidism and resultant normalisation of the biochemical abnormalities associated with a hypothyroid state, the aetiology and the treatment of hypothyroidism across a lifespan is more complex than often realised. Levothyroxine is a drug with a narrow therapeutic index, and its absorption, transport, actions and metabolism may be influenced by a number of physiological and medical conditions and comorbidities. Regular long-term follow-up is required to avoid the consequences of under- or overtreatment, and some clients may continue to feel unwell despite being biochemically euthyroid.