The thyroid is a hormone-producing gland located at the base of the neck. It releases hormones that play a significant role in the control of metabolism and regulating other body functions such as breathing and heart rate amongst others. The Hashimoto's Thyroiditis is a condition where the body's immune system launches an attack against the thyroid gland. Typically, the immune system should attack only foreign materials such as pathogens. One of the most significant implications of the disease is that it results in hypothyroidism, a condition where the thyroid is unable to produce enough hormones to serve the body needs. In the United States, research has indicated that the Hashimoto's disease is the primary cause of hypothyroidism (Majumder, & Sanyal, 2012). The Hashimoto Thyroiditis is, therefore, a member of a group of conditions known as the autoimmune thyroid diseases (AITSs) hallmarked by the destruction of thyroid glands by antibody and cell-mediated immune responses.
Why the Topic Is Interesting
Understanding the Hashimoto's Thyroiditis is critical in two significant ways. First, it is a rare class of diseases that come as a result of the disorders in the immune system. The immune system composed of cell-mediated and the antibodies have an essential role in protecting the body against pathogens including bacteria, viruses, and fungal infections. However, in this scenario, an autoimmune reaction occurs where the immune cells attacks its own tissues leading to damage. Many of the immune deficiency diseases jeopardize the body's ability to fight pathogens thus making it vulnerable to infections. The second reason why the condition is worth analyzing is that it is the primary cause of hypothyroidism among people aged 6 and above in the US. It is, therefore, an infection that should be adequately understood because due to the effects it has on metabolism and other essential body functions such as the heart rate.
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Background Information
Causes
Although scientists have not yet figured out the real cause of Hashimoto’s disease, several factors play a critical role in the development of the disease. Scientists have associated genes with the causation of the autoimmune infection. Brix, & Hegedüs, (2012) asserted that many people with Hashimoto mostly have family members with the thyroid gland disease or any other autoimmune infection. As such, genetic factors have input in determining infection with the disease. Hormones have also been implicated in the disease with women having a prevalence that is seven times that of the men. Therefore, it means that sex hormones have a role in the development of Hashimoto's Thyroiditis. Research has also shown that many women develop thyroid problems in the first year following birth. Studies have shown that 20% of these women go-ahead to develop Hashimoto's disease after some years (Brix, & Hegedüs, 2012). Other factors associated with the disease include excessive iodine and exposure to radiation. Many thyroid diseases have been reported in people exposed to radiation such the atomic bombs in Japan and the Chernobyl nuclear accident amongst others.
Anatomy
Before assessing how the disease affects its morphology, it is first important to analyze the anatomy of the thyroid gland. The gland is a butterfly in shape and is located inferior to Adam's apple in front of the windpipe. It has two lobes joined in the middle by a bridge called the isthmus. A normal thyroid cannot be felt from the outside. The thyroid gland is rich in blood vessels and nerves passing through it. Attack by the immune cells normally results in an inflammation of the cells of the thyroid gland (Pyzik et al. 2015). As such, several morphological changes occur on the tissue. The obvious change noticed is on the gross appearance of the thyroid gland. The gland enlarges due to the inflammation of the cells which can be observed with the eye as goiter on the neck. Further histological changes also occur which can be seen microscopically. Histological changes primarily occur due to inflammation caused by the plasma cells and lymphocytes, some of which organize into a germinal center. One of the significant causes of inflammation is the resultant destruction of the thyroid follicles. Progressive fibrosis is also noted in histological experiments. Koprowski et al. (2012) indicated another anatomical change that can likely develop in a person with Hashimoto’s Thyroiditis is the development of the Hurthle Cells. The cells are characterized by a juicy eosinophilic cytoplasm and are usually a sign of metaplasia of the epithelial cells present in the thyroid gland due to 9njury inflicted by the inflammation. Other anatomical changes witnessed secondary to the inflammation include atrophy of the thyroid and the development of dense fibrotic bands due to the deposition of collagen. The goiter that results from Hashimoto disease is primarily painless. The continued destruction of the thyroid gland results in hypothyroidism.
Physiology
Before delving into the physiological development of the disease, critical to understanding is how a healthy thyroid gland works. The thyroid forms part of the endocrine system made of glands that produce, store, and release hormones into the blood to the cells to facilitate proper body functioning. The thyroid gland utilizes iodine from food to create two hormones including the triiodothyronine (T3) and Thyroxine (T4) (Gaberšček et al. 2015). The balance between T3 and T4 is maintained by the pituitary and the hypothalamus found in the brain. The thyroid gland is a vital tissue in the human body. The two hormones, T3 and T4 travel in the bloodstream and influence almost all the cells in the body. One of the vital functions of the hormones is that they regulate the speed of metabolism. They also control the heart rate and determine how fast the intestines digest food. Therefore, low levels of T3 and T4 means that the heart rate will be lower than normal and a person might develop increased weight or constipation due to poor digestion. On the contrary, high levels of T3 and T4 can lead to increased heart rate and weight loss or diarrhea. Pyzik et al. (2015) intimated that Hashimoto's disease occurs primarily due to the inflammation caused by the autoimmune response of the body's immune system. The inflammation results from the stimulation of the T helper cells and CD4 explicit to the thyroid gland. The accumulation of the CD4 and T helper cells coupled with several autoantibodies produced by plasma cells destroy the thyroid gland. The CD8 cells are responsible for apoptosis, one of the processes that result in the injury to the thyroid gland (Antonelli et al. 2015). Therefore, the primary immune process implicated in the development of the Hashimoto's Thyroiditis is known as the antibody-dependent cell-mediated autoimmune response. The T lymphocytes have a cytotoxic effect on the cells of the thyroid gland. The T lymphocytes can also result in the recruitment of macrophages all which have a negative impact on the functioning of the thyroid gland. Antonelli et al. (2015) asserted that Cytokines have an inflammatory effect that causes the enlargement of the thyroid gland. Due to this pathophysiology emanating from a fault in the body’s immune system, primary hypothyroidism occurs. The destruction of the thyroid gland leads to low production of the T3 and T4 hormones. The decrease in these hormones increases the levels of the Thyroid Releasing Hormone (TRH) and Thyroid Stimulating Hormone (TSH) resulting in a chemical imbalance in the body (Majumder, & Sanyal, 2012). Some of the clinical presentation that set in include decreased metabolism, cold intolerance, lethargy, fatigue, depression, irritability, and goiter among many others. Research has shown that hypothyroidism that results from this disease can affect almost all the body systems proceeding for months and years.
Research
Relevant Research on Hashimoto Thyroiditis
One of the studies going on today is on the role of selenium in the treatment of Hashimoto's. The thyroid gland is the tissue in the body that has the highest concentration of selenium. The purpose of selenium includes acting as an anti-inflammatory and antioxidant agent (Drutel, Archambeaud, & Caron, 2013). It is also vital in the activation and production of the thyroid hormone. Therefore, research has been ongoing on whether selenium supplements could play a critical role in the treatment of thyroid diseases including the Hashimoto's syndrome. Another study that has continued to develop in the area of Hashimoto disease is whether the infection has a connection with polycystic ovary syndrome (PCOS). PCOS primarily occurs due to an imbalance in the hormone levels in the body. Common symptoms for the disease include acne, menstrual irregularity, and excessive hair growth amongst others. PCOS is also implicated in other symptoms that include problems in the metabolism and difficulty during pregnancy. Therefore, research has focused on analyzing the relationship between women with Hashimoto’s and the likelihood that they will develop PCOS (Gaberšček et al. 2015).
Findings of the Research
The research on selenium has focused on its likelihood to treat an autoimmune disorder such as the Hashimoto's disease. Drutel, Archambeaud, & Caron, (2013) noted that studies conducted have indicated that indeed selenium can be beneficial in the management of a wide range of autoimmune disorders. In what was termed as the "Serena Study," the study found out that taking selenium was vital especially during pregnancy. It lowers some types of antibodies including TG and TPO thus reducing the likelihood of autoantibody reactions that could affect the well-being of the thyroid glands. In a research conducted by the Experimental and Clinical Endocrinology and Diabetes, the researchers postulated that women with PCOS have problems with the thyroid glands which produce hormones responsible for maintaining the metabolic process in the body. The research specifically found out that the Hashimoto’s Thyroiditis is three times more likely to occur among women with PCOs than those without it. The reason given is that Hashimoto’s leads to hormonal changes in the body which further creates an imbalance in hormones in the body. Gaberšček et al. (2015) asserted that the resultant chemical imbalance in the body is implicated in the high levels of infertility among women with PCOS.
Research Directions and Advancements
The disease has many grey areas that researchers should answer in a bid to reduce the prevalence, especially in the American population. First, the etiology of Hashimoto's Thyroiditis remains an area where more research should emphasize. Many research directions have attempted to illuminate the real causes of the disease, but currently, no single reason has been provided. Another study that is currently underway is the relationship between Hashimoto's and the heart disease. More research direction should shift to the treatment mechanism such as the effectiveness of the prophylactic L-thyroxine treatment which has remained under studies for a long time (Stone, Zen, & Deshpande, 2012). Also, more focus should be put on alternative therapies and treatment mechanism that are less invasive. Critical to appreciate is that the Hashimoto’s disease is an autoimmune disorder that occurs due to a fault in the body’s immune system. Therefore, research should emphasize on how well the faulty immune system can be modulated to avoid incidences of reoccurrence in people who have already received treatment on the disease.
References
Antonelli, A., Ferrari, S. M., Corrado, A., Di Domenicantonio, A., & Fallahi, P. (2015). Autoimmune thyroid disorders. Autoimmunity reviews, 14(2), 174-180. Brix, T. H., & Hegedüs, L. (2012). Twin studies as a model for exploring the etiology of autoimmune thyroid disease. Clinical Endocrinology, 76(4), 457-464. Drutel, A., Archambeaud, F., & Caron, P. (2013). Selenium and the thyroid gland: more good news for clinicians. Clinical Endocrinology, 78(2), 155-164. Gaberšček, S., Zaletel, K., Schwetz, V., Pieber, T., Obermayer-Pietsch, B., & Lerchbaum, E. (2015). Mechanisms in endocrinology: thyroid and polycystic ovary syndrome. European journal of endocrinology, 172(1), R9-R21. Koprowski, R., Zieleźnik, W., Wróbel, Z., Małyszek, J., Stępień, B., & Wójcik, W. (2012). Assessment of significance of features acquired from thyroid ultrasonograms in Hashimoto's disease. Biomedical engineering online, 11(1), 48. Majumder, A., & Sanyal, D. (2012). A case of simultaneous occurrence of Graves’ disease and Hashimoto's thyroiditis. Indian journal of endocrinology and metabolism, 16(Suppl 2), S338. Pyzik, A., Grywalska, E., Matyjaszek-Matuszek, B., & Roliński, J. (2015). Immune disorders in Hashimoto’s thyroiditis: what do we know so far? Journal of immunology research, 2015. Stone, J. H., Zen, Y., & Deshpande, V. (2012). IgG4-related disease. New England Journal of Medicine, 366(6), 539-551.
