THYROID DYSFUNCTIONS AND ITS MONITORING

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About Authors:
Pathak Namita*, Kothiyal Preeti, Dr. Prashant Mathur
Department of Clinical Pharmacy,
Shri Guru Ram Rai Institute of Technology and Sciences,
Dehradun, Uttarakhand, India, 248001
pathak_namita@ymail.com

Abstract
The prevalence of hypothyroidism is three times higher among women than men. The prevalence in an unselect­ed community population of young, middle aged and elderly individuals is about 1.4 percent and the estimated annual incidence rate is one to two per 1,000 women. Surveys of geriatric populations have yielded estimated prevalence rates for overt hypothyroidism of 0.2 percent to 3 percent. The presentation of symptoms in the elderly may be atypical or absent. The prevalence of subclinical hypothyroidism is estimated to be between 4.0–8.5% of the adult US population without known thyroid disease, and the prevalence increases with age. Up to 20% of women over the age of 60 are estimated to have subclinical hypothyroidism. Caucasians are more likely to have subclinical hypothyroidism than non-Caucasians. The risk is highest in those with type I diabetes mellitus, a family history of thyroid disease or head/neck cancers treated with external beam radiation. Other risk factors include previous radioactive iodine treatment or thyroid surgery. Interestingly, about 20% of patients on thyroid medications are both over re­placed and under replaced. Because of the high incidence of thyroid disease, The American Thyroid Association recommends measuring thyroid function on all adults beginning at age 35 years and every 5 years thereafter noting that more frequent screening may be appropriate in high risk groups. The treatment of subclinical hypothyroidism has been controversial but more recent data suggest there are increased risks of ischemic heart disease in untreated patients and that a more aggressive approach to treat­ ment would be appropriate.7 In contrast, subclinical hyperthyroidism has more well understood risks of atrial fibrillation and flutter and so should be more ag­gressively treated.

REFERENCE ID: PHARMATUTOR-ART-2049

PharmaTutor (ISSN: 2347 - 7881)

Volume 1, Issue 2

Received On: 31/10/2013; Accepted On: 08/11/2013; Published On: 20/12/2013

How to cite this article: Pathak N, Kothiyal P, Thyroid Dysfunctions and its Monitoring, PharmaTutor, 2013, 1(2), 23-38

Introduction
The thyroid gland, located below the larynx, is the largest endocrine organ, and is essential to mammalian life. The thyroid gland produces hormones, which help in the regulation of metabolism, growth and development, and even reproduction1. To maintain normal thyroid function, the hypothalamus and the pituitary gland both impact thyroid status. Known as the hypothalamic-pituitary-thyroid axis, this link between the three is what regulates proper thyroid hormone synthesis and release. The system is a negative-feed process in which the level of circulating thyroid hormone (both T4 and T3) signals the hypothalamus to synthesize and release thyroid-releasing hormone (TRH) or suppress it. The level of thyroid-releasing hormone in turn balances the release of TSH. When more TSH is needed, thyroid-releasing hormone binds to receptors in the pituitary gland that cause the release of TSH. The release of TSH causes the thyroid to stimulate the expression of the sodium/iodide symporter (NIS), which is responsible for iodide transport and therefore iodine uptake, the enzyme thyroid peroxidase, and thyroglobulin. In addition, TSH also helps in the generation of H2O2. All of these uses of TSH cause more thyroid hormones to be produced and released2. Less TSH causes less thyroid hormone to be produced and released from the thyroid gland, causing TRH suppression.


Figure 1. Hypothalamic-Pituitary-Thyroid axis.

Within the thyroid gland, thyroid hormone synthesis requires iodine and the enzyme thyroid peroxidase to turn thyroglobulin (Tg) into thyroxine and triiodothyronine, T4 and T3, respectively. Thyroxine and triiodothyronine are then released into the bloodstream, where they are part of protein synthesis and metabolic processes in a multitude of cells and tissues The regulation of thyroid hormones is a complex process. In a person with healthy thyroid function, the presence of excess or lack of iodine, for example, leads the thyroid gland to make and release more or less of its hormones. The level of hormone in circulation signals the suppression or the synthesis of other hormones like TRH and TSH that in turn help maintain thyroid hormone balance. Since thyroid hormones are not water-soluble they bind to proteins when they are released from the thyroid gland. The majority travels in the bloodstream bound to the proteins thyroxine-binding globulin (TBG), thyroxine-binding prealbumin (TBPA) and albumin. Free thyroxine, fT4, is the small amount (about 0.03%) of thyroid hormone that is not bound to a protein3. Similarly, fT3 is the triiodothyronine that is not bound to a protein. While there is more thyroxine in the thyroid gland and circulating in the body, triiodothyronine (T3) is the bioactive form of the two. In addition to being released from the thyroid gland, T3 and 3, 3’, 5’-triiodothyronine (rT3) are also formed from thyroxine locally in the cells by deiodination. Greer (1990)3 states that in individuals with healthy thyroid function 20% of T3 is produced in the thyroid gland, while 80% is formed from thyroxine peripherally (p. 236).

THYROID FUNCTION
The term euthyroid is used to refer to individuals with normal thyroid function. Different studies use some combination of the following criteria to decide who is considered euthyroid. Most studies will primarily check for thyroid autoantibodies, TSH levels, fT4 levels and previous thyroid disease as elements to determine thyroid status4-6. If all information is readily available to the investigators, a person can be determined euthyroid if:
(1) they do not have a previous or current diagnosis of thyroid disorders or dysfunction.
(2) are not taking thyroid hormone therapy or medications for thyroid diseases.
(3) Do not have positive thyroid autoantibodies (anti-Tg and TPOAb) in the Serum.
(4) Have TSH levels, fT4 levels and fT3 levels within the reference ranges.

Abnormal thyroid function, which leads to the body making too little or too much hormone, can be due to different issues. Autoimmune thyroid disorders (AITD) are largely attributed to genetics7, while other forms of hypothyroidism and hyperthyroidism can be iodine-induced8 or caused by medications that interfere with thyroid function. Hypothyroidism occurs when the thyroid gland does not make enough thyroid hormones. It can be detected through serum TSH tests that show levels of TSH above the reference range. The most severe form of hypothyroidism is myxedema, where the body starts to shut down. This form of hypothyroidism may occur after many years of a person suffering from the dysfunction9. On the other hand, hyperthyroidism occurs when the body makes too much thyroid hormone and the thyroid gland is said to be “overactive”. The dysfunction can be diagnosed through serum TSH, T4, and T3 tests, which reveal low levels of TSH and higher levels of T4 and T3 than the reference ranges. Besides autoimmune disease, hyperthyroidism can be caused, temporarily, by lower overall immune response (e.g. when a person is fighting a viral infection), the individual is suffering from thyroid inflammation (thyroiditis), or due to a thyroid nodule or goiter forming10. In addition to these diseases, an individual can develop thyroid cancer. Thyroid nodules can be either benign or cancerous. A thyroid ultrasound and biopsy is used to diagnose cancer, and a sensitive test is used to check for thyroid carcinoma re-occurrence, where serum thyroglobulin (Tg) levels are examined. While thyroid cancer is a common endocrine-related cancer, it is rare that a person is diagnosed as having this type of carcinoma. According to the American Thyroid Association (2008a)11, the incidence of thyroid cancer in the United States is 20,000 cases per year. Thyroid carcinoma can be managed through surgical removal of the thyroid and continued use of thyroid hormone therapy.

Factors That Affect Thyroid Function
Different factors affect thyroid function. The present study was able to include urinary iodine concentration, gender, age, smoking and race as variables in the analysis due to their known potential to be confounders when studying thyroid function. Additionally, education, physical activity level, daily caloric intake and poverty status were included because they are known risk factors for BMI. While other known risk factors of thyroid function are known, these are not included in the study due to the unavailability of data.

Iodine
Studies have shown that iodine is a vital component of thyroid hormone synthesis, and therefore is of critical importance in thyroid function12. Without the proper balance of iodine intake, thyroid function suffers greatly. Iodine is needed in thyroid hormone synthesis to turn thyroglobulin into thyroxine or triiodothyronine, T4 or T3, respectively. Too little iodine will cause the thyroid gland to produce less hormone, while too much will lead to an excess of hormone. Iodine deficiency is still a big problem across the world 13.The effects range from different size goiters to the very serious complication called cretinism. Since the 1990’s, the U.S. has been considered iodine sufficient. However, excess iodine intake is of concern because it may lead to thyroid dysfunction. The effects of excess iodine intake range from hyperthyroidism to hypothyroidism and chronic autoimmune thyroiditis (CAT)14. Research shows that in populations where there is iodine deficiency or excess, overt hyperthyroidism and hypothyroidism exist15. For example, in areas of iodine deficiency such as in Aalborg, Denmark where there is a moderate iodine deficiency, and in Copenhagen, Denmark where there is a mild iodine deficiency, 16Pedersen et al. (2002), found that incidence rates of overt hyperthyroidism were much higher in Aalborg than those in Copenhagen. The reverse was also true, where more cases of overt hypothyroidism existed in Copenhagen than in Aalborg16. Some studies have found iodine intake to be directly related to serum TSH levels17,14,18. Laurberg et al. (1998),19 found that serum TSH levels were low in Jutland, Denmark, an area known to have low iodine intake levels, whereas Iceland, an area known to have high iodine intake levels had high TSH values. Similarly, 20 Vejbjerg et al. (2009) also found higher median serum TSH levels after iodine intake increased in the population due to mandatory salt iodization.

While iodine deficiency causes more damage than iodine excess, both extremes are detrimental to a population’s health. In studies of thyroid hormones and obesity, iodine may be a key component in understanding this relationship.

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