Grave's disease

• What is Grave’s Disease
• Statistics on Graves Disease
• Risk Factors for Graves Disease
• Progression of Graves Disease
• Symptoms of Graves Disease
• Clinical Examination of Graves Disease
• How is Graves Disease Diagnosed?
• Prognosis of Graves Disease
• How is Graves Disease Treated?
• Graves Disease References

What is Graves Disease

Graves’ Disease is the most common cause of hyperthyroidism or thyrotoxicosis (increased activity of the thyroid gland). The thyroid gland is a butterfly-shaped gland, located just inferior to the larynx, or voice box. It’s right and left lateral lobes lie on either side of the trachea, or windpipe. Connecting the lobes is a mass of tissue called the isthmus, that lies in front of the windpipe. Microscopic sacs called thyroid follicles comprise most of the thyroid gland. The walls of each of these thyroid follicles is made up by two types of cells, follicular cells and parafollicular (or C) cells. The follicular cells produce the thyroid hormones, called thyroxine, or T4, and T3. Thyroid hormones control body metabolism. Regulation of metabolism is critical in controlling mood, weight and mental and physical energy levels. Parafollicular cells produce the hormone calcitonin, which helps to regulate the levels of calcium in the body.

Statistics on Graves Disease

Graves’ Disease is the most common cause of hyperthyroidism, affecting 2-5% of females at some time, with a female:male ratio of 7:1. The disease has a peak incidence between the ages of 20 and 40 years of age.

Risk Factors for Graves Disease

Graves’ Disease is an autoimmune disease. Autoimmune diseases are where the immune system attacks certain tissues of the body, and in Graves Disease that causes overactivity of the thyroid gland. It is caused by the body’s production of antibodies against the thyroid TSH (thyroid stimulating hormone) receptor, which results in continuous stimulation of the thyroid gland to synthesize and secrete excess quantities of the thyroid hormones, T4 and T3. There is also a genetic component to the disease, with its development being linked to the presence of certain genes in individuals. Graves’ Disease (and Hashimoto’s thyroiditis) is sometimes associated with other autoimmune disorders, including insulin dependent diabetes mellitus, pernicious anemia, collagen diseases, and rheumatoid arthritis.

Progression of Graves Disease

Graves’ disease is characterized by hyperthyroidism and one or more of the following: goiter, exophthalmos (protrusion of the eyeballs), and pretibial myxoedema (swelling on the shin above the lateral bone of the ankle). The disease is chronic with a fluctuating course, many patients show a pattern of alternating relapse and remission; perhaps only 40% of patients have a single episode. Many patients eventually become hypothyroid. The disease may remit spontaneously.

How is Graves Disease Diagnosed?

Your doctor will need to perform the following investigations, most of which are possible from a simple blood test. Investigations include a full blood count, liver function tests, urea and electrolytes, and creatinine levels.

Prognosis of Graves Disease

Graves disease is a chronic illness without a true cure. None of the management options for this disorder actually remove the underlying immunologic disorder. Therefore, the prognosis of the disorder is very much dependent upon the form of therapy chosen.

How is Graves Disease Treated?

Treatment consists of three possibilities: radioiodine, antithyroid drugs and surgery. 1) Radioactive iodine. Iodine-131 in an empirical dose accumulates in the thyroid and destroys the gland by local radiation, taking several months to be fully effective. 2) Antithyroid drugs. These include carbimazole and propylthiouracil. These drugs inhibit the formation of thyroid hormones. 3) Subtotal thyroidectomy. Thyroidectomy can be performed only in patients who have previously been rendered euthyroid.

Graves Disease References

1. Kumar, P & Clark, M. 1999, Clinical Medicine, WB Saunders, London.
2. Oxford Handbook of Clinical Medicine.
3. Robbins, S. 2001, Pathologic Basis of Disease, WB Saunders, New York.
4. The Merck Manual www.merck.com