A dive into the literature– the complexities of Hashimoto’s Thyroiditis

For my Capstone project, I am focusing on Hashimoto’s Thyroiditis, a type of hypothyroidism in the form of an autoimmune disease. The first category by which I organized my literature from my search included papers that gave information about the disease. Many of these papers were older as they were some of the first published that talked about the signs, symptoms, and clinical findings of the disease. Many of the signs and symptoms associated with the disease include those of any generic hypothyroidism: fatigue, weight gain, fluid retention in the face and neck, feeling cold, irregular heart rates, and heavy menstrual flow in women. Additionally, the thyroid gland can develop abnormal lobes. These papers were critical for many of the developments made in

The gene that is associated with Hashimoto’s is Cytotoxic T-lymphocyte Antigen-4 (CTLA-4) while the gene is found on chromosome 2 and not a sex chromosome, the majority of people who suffer from Hashimoto’s disease are women.  Those who have the disease have the gene downregulated— an inhibitory signal is sent to T cells reducing the function of T-lymphocytes. Another interesting finding from my literature search was that those who already suffer from other autoimmune diseases such as type 1 diabetes and celiac disease are more at risk for developing this form of hypothyroidism. Progressive downregulation of the gene can lead to low T3/T4 levels and compensatory low TSH levels.

While much of the known causes for Hashimoto’s disease are genetic, there are some preventable environmental factors that I have found throughout my search. High iodine intake as well as selenium deficiency can cause hypothyroidism—specifically Hashimoto’s Thyroiditis. It is for this reason that for my first section of literature searches, I chose to focus on the biochemical, cellular, and genetic causes of Hashimoto’s Thyroiditis

The next section that I categorized in my literature search included the papers discussing the protein abnormalities associated with the disease. To me, these papers were the most interesting as they related the most to biochemistry and contained the most recent research in the field of endocrinology. Part of what makes Hashimoto’s Thyroiditis an autoimmune disease is that antibodies that are produced attack the enzymes in the thyroid, the thyroid itself, and also work against some of the thyroid hormones. Autoantibodies can work against thyroid peroxidase, thyroglobulin as well as block the TSH receptors found in the thyroid. Additionally inflammatory cytokines can destroy thyroid tissue. These protein abnormalities are in fact what allows the disease to be diagnosed—high serum levels of anti-thyroid peroxidase are usually what seals in the diagnosis along with the symptoms of hypothyroidism. My literature search revealed other protein abnormalities such as vitamin D receptor polymorphisms, Fas and its ligand behaving abnormally, and abnormal fetal/maternal protein expression combinations.

While I think that my literature search is a good start, I would like to look more into different treatment options for the disease to learn how the drug molecules can interact with these abnormal antibodies. I am excited to see where the literature can take me now that I have a solid foundation built for this project!

 

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