Blog # 4- Autoimmune Thyroid Diseases: Graves’ vs. Hashimoto’s- Why It is Important to Understand And What I Learned from Personal Experience

Comparing and contrasting Graves’ Disease and Hashimoto’s thyroiditis

(Featured Video Clip Credit Goes to, “Graves’ Disease and Hashimoto’s Thyroiditis”- YouTube. Published on Jul. 19, 2014. )

Website Links:

“Graves’ Disease”- American Thyroid Association Published 2019.

“Hashimoto’s Thyroiditis”- American Thyroid Association Published 2019.

I am going to use my own analogy to describe autoimmune disease in the context of the thyroid. Autoimmune disease is like the wall coming down that promotes the downfall of the structure because of invasions and trespassers outside the structure and inside the structure which results in a collapse. Within the structure you have people that you think you can trust, but in reality, either they are ready to fight against the structure, or, they are ready to flee away from the structure. In other words, the wall in this analogy symbolize the immune system. The invasions and trespassers symbolize the bacteria and viruses that try to attack the immune system. The structure symbolize the thyroid gland and the pituitary gland trying to operate its functions like it is supposed to. Unfortunately, the people which in this case symbolize the thyroid tissue, are either going to get overwhelmed because they are fighting, which hyperthyroidism produces too much thyroid hormone, or, they are going to get exhausted because they are trying to flee from the structure but it is trying to take control of operations again, which this is the concept of too little thyroid hormone, or hypothyroidism. The thyroid gland and the pituitary gland are not working properly which results in a struggle for the person medically regardless they have either hyperthyroidism or hypothyroidism, but then when you have antibodies attacking the immune system which impairs the thyroid gland, which can either result in Graves’ disease or Hashimoto’s thyroiditis.

Graves’ disease is an autoimmune condition in which because antibodies attack the immune system to impair the functioning thyroid gland, it results in the pituitary gland to send a false message to the thyroid gland that more thyroid hormone is needed. The condition was named after, “Robert Graves, an Irish physician, who described this form of hyperthyroidism about 150 years ago” (American Thyroid Association). The antibodies are responsible for linking to the thyroid cells which regulate the overproduction of thyroid hormone. Individuals diagnosed with Graves’ disease usually experience the following symptoms (note, they may not experience all the symptoms): Tachycardia; Palpitations; Fine Tremor (usually in hands); Insomnia; Weight Loss; Weak Muscle Tone; Rapid changes in mood (can experience anxiety and depression); and heat intolerance. Ophthalmology associated with Graves’, in which, “only 5% have moderate to severe inflammation of the eyes to cause temporary to permanent vision trouble” (American Thyroid Association). People with Graves’ ophthalmology may experience eye conditions such as diplopia (double vision) and blindness, especially if severe. Thickening of the skin is another problem that individuals with Graves’ disease may experience as well. Goiter, or a moderately to severely enlarged thyroid gland, is also indicative of this disease as well. Usually, Graves’ disease is confirmed when the following happens: 1.) Lab results show that the TSH (thyroid stimulating hormone) level is abnormally low and the levels of T4 (Triiodothyronine) and T3 (Thyroxine) are abnormally high; 2.) TSI (Thyroid Stimulating Immunoglobulin) is confirmed to be positive; and 3.) Radioactive Iodine Uptake and Scan confirms an elevated percentage in uptake in comparison to the normal functioning thyroid gland. I remember back in June 2015 when I was first diagnosed with Graves’ disease, I did experience tachycardia; hypertension; palpitations; hypertension; fine tremor (of hands); weight loss; tiredness; changes in mood like anxiety and depression; and intolerance to the heat. One treatment option for Graves’ disease is antithyroid medication. I was on Methimazole, which was meant to help bring thyroid levels back to normal. I was also on Atenolol, a beta blocker that was used to help with the tachycardia and palpitations. The endocrinologist stated to me there was the possibility for remission after two years, however, the chances of remission were small. While my thyroid levels were stable for a couple years, unfortunately the disease returned in September of 2017 in which the disease progressed, so another treatment option, which is something an individual may try, is radioactive iodine therapy. It is basically a pill you are given at the hospital or clinic to take, and it is designed to shrink and destroy the thyroid gland from producing more antibodies and more thyroid hormone. Generally, when people receive this treatment, it usually results in the treatment not being successful which causes the Graves’ disease to progress, or, the treatment results in the person eventually developing hypothyroidism, which would then require lifelong thyroid hormone replacement medication. Eventually, on April of 2018, after unsuccessful attempts of treating the disease with antithyroid medication and radioactive iodine therapy, I had my whole thyroid surgically removed (which is called a total thyroidectomy) to cure the Graves’ disease. Although the surgery was successful, I did experience temporary hypocalcemia (too little calcium) which required me to take temporary calcium supplements to get calcium levels back within the normal range. The surgeon stated that consequently, because I no longer have a thyroid gland, I was required to take thyroid hormone replacement medication for the rest of my life, but I was willing to accept this rather than letting the Graves’ disease progress to a point where it became debilitating, and, in rare cases, but possible, to the point the condition is fatal and death was a possibility. I was truly thankful to still be alive despite the reality that I would have hypothyroidism permanently, a condition in which cannot be cured, but, with proper management and treatment, one can still enjoy life, but even this is challenging for those, especially individuals with hypothyroidism and needing to take thyroid hormone replacement medication for the rest of their lives, including myself. In fact, since my surgery, it has been difficult for my doctor and my endocrinologist to find the right dosage for my thyroid hormone replacement medication (which the majority of people with hypothyroidism are on Levothyroxine, which is what I am on), so either I would experience symptoms of hyperthyroidism, or, symptoms of hypothyroidism as my body has been struggling to find the proper dose given my body is still adjusting to no thyroid gland.

Hashimoto’s Thyroiditis, another autoimmune condition of the thyroid gland, which, “is the most common cause of hypothyroidism in the United States” (American Thyroid Association). In the case of Hashimoto’s, the antibodies that link to the thyroid cells deregulate the production of thyroid hormone, resulting in too little thyroid hormone. Common symptomatology associated with Hashimoto’s thyroiditis, which is related to the symptoms of hypothyroidism, are, but not limited to the following: fatigue; weight gain; hypotension; bradycardia; constipation; cold intolerance; dry skin; anxiety and depression. Some people with this condition may also experience goiter as well (that is, if they have a thyroid gland). A diagnosis of Hashimoto’s thyroiditis is usually confirmed by the following: 1.) 1.) Lab results show that the TSH (thyroid stimulating hormone) level is abnormally high and the levels of T4 (Triiodothyronine) and T3 (Thyroxine) are abnormally low; 2.) TPO (Thyroid peroxidase antibodies) levels are confirmed to be positive. Generally, in terms of treatment, Levothyroxine is the recommended treatment by endocrinologists and physicians. Levothyroxine is a T4 (Triiodothyronine) medication that is designed to be converted into T3 (Thyroxine), which this conversion is essential in order to promote regulation of thyroid hormone to help treat the symptoms associated with the condition. Unfortunately, “when an insufficient dose is taken, serum TSH levels remain elevated” (American Thyroid Association), and this means there is the progression of hypothyroid symptoms. On the contrary, “If the dose is excessive, serum TSH will become suppressed and patients may develop symptoms of hyperthyroidism” (American Thyroid Association).

Some people have stated, “A thyroid is just a thyroid” Well, the reality is that, a thyroid is a major organ in your body that is essential for your body to function and to survive. The next time you do to the doctor’s and you get your metabolic panel done during routine labs, if your TSH levels and T4 and T3 levels are off, and you are symptomatic, your body is trying to tell you something, and most likely is that there is a thyroid problem and that you likely need follow up medical tests; and, if necessary based on a physical exam and re-evaluating metabolic panel, then treatment to address the hyperthyroidism or the hypothyroidism, or even, the Graves’ disease or the Hashimoto’s thyroiditis. Whatever you do, if you have a thyroid problem, do not leave it untreated, because it could be the difference between remaining alive, and not being alive. Hope you found this information insightful. Thought I would give a more deeper emphasis behind thyroid diseases, and the implications of these diseases. What thoughts do you have?

2 Replies to “Blog # 4- Autoimmune Thyroid Diseases: Graves’ vs. Hashimoto’s- Why It is Important to Understand And What I Learned from Personal Experience”

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