Graves’ disease is mainly resulted from hyperthyroidism. It is most prevalent in 3rd to 4th decade of life, and the incidence ratio of the Graves’ disease is much higher in females (Men: 2 out of every 1,000s vs. Women: 20 out of every 1,000s). Clinical manifestations of hyperthyroidism vary depend on patient’s age.
Thyroid gland secretes thyroid hormones, triiodothyronine (T3) and thyroxine (T4); these hormones regulate the body metabolism.
Autoimmune disease occurs when your immune system triggers an immune response against your own tissue. In Graves’ disease, its pathogenesis is played by the stimulation of immunoglobulin G antibody against the thyroid-stimulating hormone receptor. This eventually activates the thyroid gland. It is also possible to have mutations in the gene encoding the TSH receptor leading to hyperthyroidism. The activated thyroid gland secretes high level of thyroid hormones, triiodothyronine (T3) and thyroxine (T4), although the actual plasma level of TSH is decreased via the hypothalamus-pituitary gland-thyroid gland negative feedback loop.
Infection by Yersinia
enterocolitica: still elusive… but!! Shares a similarity in structure with
TSH-rc à may trigger ‘autoimmune response.’
The treatment is targeted at controlling the hyperactive thyroid gland, and the rapid preventive treatment is the most efficient method to treat the Graves’ disease.
The available reversible treatment options are; orbital radiation, surgical decompression, and intravenous or oral systemic glucocorticoids. But, relapses are common…. If mild symptom of the Graves’ disease: Selenium therapy or Rituximab (RTX) therapy
Beta-blocker is used to treat symptoms associated with the Graves’ disease, such as rapid heart rate, sweating, and anxiety. It blocks the beta-adrenergic receptors on cells of sympathetic nerve system, and it weakens the effect of stress hormones by inhibiting the release of epinephrine and other neurotransmitters.
Irreversible therapies:
Radiation therapy or surgery; if performed, it is required to take thyroid hormone replacement therapy for the rest of life.
Radioactive iodine treatment:
Performed by taking iodine pill (every 24 hours) to shrink the enlarged thyroid gland, and to decrease the plasma concentration of thyroid hormones (T3 and T4) and TSH. It can make eye problems associated with the Graves’ disease worse.
Surgical removal of thyroid gland:
Recommended
only if the disease process is severe or more conservative methods have failed.
References:
Abraham P, Avenell A, McGeoch SC, Clark LF, Bevan JS. Antithyroid drug regimen for treating Graves' hyperthyroidism. Cochrane Database of Systematic Reviews 2010, Issue 1.
Minakaran N, Ezra DG. Rituximab for thyroid‐associated ophthalmopathy. Cochrane Database of Systematic Reviews 2013, Issue 5. Art. No.: CD009226. DOI: 10.1002/14651858.CD009226.pub2.
Peixoto MB, Buescu A, Goncalves MRB, Albernaz MDS et al. Antithyroid drugs for the treatment of graves disease: A randomized clinical trial. Endocrinologist 2006; 16: 344-8.
Thanks so much for posting this! I know we got to discuss Grave's disease a bit in class, but this definitely clears up some of my questions about it! While reading your blog you mentioned that mutations in the gene encoding the TSH receptor could lead to hyperthyroidism. I was always under the impression that hyperthyroidism could lead to Grave's disease. I wondered if you found anything that specified that relationship? Does Grave's disease lead to hyperthyroidism or does hyperthyroidism lead to Grave's disease or does it not matter?
ReplyDeleteThank you for your comment, Sara! Graves' disease is a pathological condition of the hyperthyroidism. I am not 100% sure about the genetical etiology of the disease; however, when I took pathology last year, my professor told me about the genetic implications. He stated that it is still elusive, but the gene coding region of the HLA chromosome may get mutated, and it may lead into the hyperthyroidism due to the compromised TSH-receptors in the thyroid glad. You may think of it as diabetes mallatus type 2, which is another kind of the autoimmune disorder. Graves' disease is indeed resulted from the autoimmune system in our body by producing antibodies against the TSH receptors in the thyroid gland. Therefore, the sensitivity of the receptors to the hypophyseal TSH would be compromised, and it would eventually lead to an enlargement of the gland to compensate the compromise.
ReplyDeleteThank you again!
Best,
Minwoo