Thyroid diseases are common, and most can be safely and effectively managed in primary care. Two of the most common reasons for thyroid function testing are fatigue and obesity, but the vast majority of affected patients do not have hypothyroidism. There is no plausible basis for the assertion that hypothyroidism commonly occurs despite normal thyroid function tests. In primary hypothyroidism all patients, except the elderly and those with ischaemic heart disease, can safely be started on a full replacement dose of thyroxine; the aim is to restore thyroid stimulating hormone (TSH) to normal.
The profound benefit of achieving appropriate levels of thyroid hormone in patients with hypothyroid cannot be overstated: The aim of the present study was to evaluate the impact of hypothyroidism on the autonomic regulation of the cardiovascular system by analyzing sympathetic and parasympathetic influences on the heart and the effect of thyroxine replacement. Thirty newly diagnosed female hypothyroid patients with mean age 32.73 +/- 9.98 years were recruited from the Thyroid Clinic, GTB Hospital, Delhi. Various Autonomic function tests to assess Basal heart rate variability, parasympathetic activity (E:I Ratio, 30:15 Ratio, Valsalva Ratio) and sympathetic activity (Postural Challenge test, Sustained handgrip test) were done before and after attainment of euthyroidism. There was significant increase in parasympathetic activity on achieving euthyroid state. The sympathetic activity too significantly improved after L-thyroxine supplementation. Lipid profile parameters significantly decreased after achieving euthyroid state. Our findings are consistent with previous reports that thyroxine therapy appears to restore the efferent vagal activity and alters the relative contribution of systems that maintain resting blood pressure and heart rate.
T3 affects almost every physiological process in the body, including growth and development, metabolism, body temperature, and heart rate. Production of T3 and T4 (the prohormone to T3) is induced by thyroid-stimulating hormone (TSH), which originates in the pituitary gland. This process is regulated by closed-loop feedback process: high concentrations of T3 and/or T4 in blood plasma TSH production in the pituitary gland. As concentrations diminish, pituitary production of TSH increases; thus a feedback system is constantly in place which regulates the concentration of thyroid hormones circulating in the bloodstream.
Liothyronine is the most potent form of thyroid hormone. It is marketed as Cytomel and often referred to as T3. Cytomel and other commercial drugs are synthetic versions of the body's own natural T3 hormone. In the body it increases the basal metabolic rate (BMR), increases protein synthesis (except at extremely high doses where increased protein synthesis is exceeded by even more greatly increased protein degradation), and increases sensitivity to catecholamines. Thyroid hormones are essential to proper development and differentiation of all cells. They also directly regulate dietary protein, fat, and carbohydrate metabolism, which is the determining factor in how dietary intake affects cellular energy production. In comparison to levothyroxine (T4), T3 has a faster onset and shorter half-life, possibly due to less plasma protein binding to thyroxine-binding globulin and transthyretin.
T3 binds to thyroid receptors found on the nuclei of cells. The thyroid hormones, however, are not very lipophilic and typically are thus unable to pass through the cellular phospholipid bilayers. Specific transporter proteins on the cell membranes exist, allowing the T3 and T4 to pass into the cells. Thyroid receptor gene transcription is controlled by elements which respond to environment, making it a process governed by epigenetics. Also of note is that tissue sensitivity to thyroid hormone is modulated through the thyroid receptors themselves. T3 elevates BMR thereby increasing oxygen and energy consumption. T3 acts on most tissues excluding the spleen and testis.
Selenium deficiency may play a role in thyroid issues: Inadequate supply of the essential trace element selenium (Se) has been associated with predisposition for, or manifestation of, various human diseases such as Keshan and Kashin-Beck disease, cancer, impaired immune function, neurodegenerative and age-related disorders and disturbances of the thyroid hormone axis. Se deficiency in combination with inadequate iodine contributes to the pathogenesis of myxedematous cretinism. The recent identification of various distinct selenocysteine-containing proteins, encoded by 25 human genes, provides information on the molecular and biochemical basis of beneficial and possible adverse effects of this trace element. The thyroid gland is among the human tissues with the highest Se content per mass unit similar to other endocrine organs and the brain.