The thyroid gland is a small, butterfly-shaped gland located in the base of the neck just below the Adam’s apple. While small in size, the thyroid gland has a crucial role as it controls the functioning of various vital body organs including the heart, brain, liver, kidneys and skin. Ensuring that the thyroid gland is healthy and functioning properly is critically important to the body’s overall well-being.
Here’s a quick review about hypothyroidism and hyperthyroidism, two conditions related to the thyroid gland, their diagnosis and treatment.
Hyperthyroidism and hypothyroidism refer to overactive thyroid and underactive thyroid, respectively. In the United States, about 1.2 percent of people suffer from hyperthyroidism while about 4.6 percent of the population aged 12 and older have hypothyroidism (1). Treatment depends on the cause and severity of the condition, but in many cases it requires lifelong treatment.
IMPORTANT ACTORS IN THE ENDOCRINE SYSTEM
Thyroid hormones, produced by the follicular cells of the thyroid gland, are part of the endocrine system. They are essential for the regulation of metabolism and play a crucial role in growth and neuronal development. There are two types of thyroid hormones: triiodothyronine (T3) and thyroxine (T4). Their synthesis is regulated by the thyroid-stimulating hormone (TSH) (2).
The function of the thyroid gland is to take iodine, which is found in many foods, and convert it into thyroid hormones. Every cell in the body relies on thyroid hormones for regulation of their metabolism. T4 and T3 bind to thyroid receptor proteins in the cell nucleus. This dynamic interaction causes metabolic effects through the modulation of DNA transcription and protein synthesis (2).
WHAT ARE THE RISK FACTORS FOR THYROID HORMONE IMBALANCE?
Hypothyroidism and hyperthyroidism are common conditions that affect people worldwide. Iodine nutrition is the main actor responsible when it comes to the risk for developing these diseases. However, there are many other factors – such as genetic susceptibility, age, and ethnicity, among others – that influence the development of these conditions (3).
The most common cause of hypothyroidism is an autoimmune disorder known as Hashimoto’s thyroiditis. This is a condition where thyroid cells are destroyed, leading to a slowing down of the metabolism. People with Hashimoto’s thyroiditis experience fatigue, depression, weight gain and dry skin, among other symptoms (4).
Graves’ disease is the most common form of hyperthyroidism. It is characterized by the production of antibodies that affect the TSH receptor. These antibodies bind to the TSH receptor and chronically stimulate its activity, triggering the secretion of T3 and T4. Rapid heartbeat, fatigue, weight loss and palpable goiter are some of the main symptoms. (5).
HOW ARE THYROID CONDITIONS DIAGNOSED AND TREATED?
Thyroid conditions are diagnosed by measuring the levels of TSH, T3, and T4 in the blood. TSH is synthesized by the pituitary gland, and a high concentration of this hormone is associated with low production of T4 and T3 – an underactive thyroid, or hypothyroidism (6). In contrast, high levels of T3 and T4 keep the levels of TSH low, a disorder that is frequently related to the development of hyperthyroidism (6).
The development of successful drugs for the treatment of hypothyroidism and hyperthyroidism is possible thanks to our understanding of binding interactions. The main goal of therapies for these conditions is to restore the euthyroid state.
In hypothyroidism, the oral synthetic thyroxine has contributed to the reversal of most of the clinical manifestations of the condition (7). Levothyroxine, a synthetic form of T4 is another treatment option. It is possibly the most renowned drug employed to treat hypothyroidism and different types of thyroid cancer (8).
In patients with hyperthyroidism, beta blockers, also called beta-adrenergic blocking agents, are medications used to improve the symptoms (like palpitations, anxiety and tachycardia) by blocking the action of some hormones such as adrenaline (9). For example, propranolol is a beta blocker that, in high doses, gradually reduces T3 concentrations (9). Methimazole, another treatment option, is an antithyroid drug that is used to treat Graves’ disease (10).
Fortunately, medication can help balance the lack of or the overproduction of T3 and T4 in almost all cases. This capability has improved the life of many patients. Today, research is being conducted to find a safe and definitive cure for these thyroid disorders.
Sources:
1. https://www.niddk.nih.gov/health-information/endocrine-diseases/
2. Rohit Sinha, MD, Paul M Yen, MD. Cellular action of thyroid hormones. De Groot LJ, Chrousos G, Dungan K, et al., editors. South Dartmouth (MA): MDText.com, Inc.; 2000-.
3. Taylor PN, et al. Global epidemiology of hyperthyroidism and hypothyroidism. Nat Rev Endocrinol. 2018 May;14(5):301-316. doi: 10.1038/nrendo.2018.18. Epub 2018 Mar 23.
4. Zeng R. Relationship between Hashimoto’s thyroiditis and papillary thyroid carcinoma in children and adolescents. Eur Rev Med Pharmacol Sci. 2018 Nov;22(22): 7778-7787. doi: 10.26355 / eurrev_201811_16401.
5. Fanning E, et al. Radioiodine treatment for graves’ disease: a 10-year Australian cohort study. BMC Endocr Disord. 2018 Dec 12;18(1):94. doi: 10.1186/s 12902-018-0322-7.
6. Ehlers M. Graves’ disease in clinical perspective. Front Biosci (Landmark Ed). 2019 Jan 1;24:35-47.
7. Mc Aninch E, Bianco A, The History and Future of Treatment of Hypothyroidism. Ann Intern Med. Author manuscript; available in PMC 2016 Aug 11. Published in final edited form as: Ann Intern Med. 2016 Jan 5; 164(1): 50–56. doi: [10.7326/M15-1799]
8. Wartofsky L. Levothyroxine: therapeutic use and regulatory issues related to bioequivalence. Expert Opin Pharmacother. 2002 Jun;3(6):727-32.
9. Wiysonge C, et al. Beta-blockers for hypertension. Cochrane Database Syst Rev. 2017 Jan 20; (1): CD002003. Published online 2017 Jan 20. doi: [10.1002/14651858.CD002003.pub5]
10. Rivkees S, et al. Adverse Events Associated with Methimazole Therapy of Graves’ Disease in Children. Int J Pediatr Endocrinol. 2010; 2010: 176970. Published online 2010 Mar 7. doi: [10.1155/2010/176970]
