The younger patients suffering from Graves’ disease usually present with the typical symptoms of thyrotoxicosis. Most of the symptoms are due to increased activation of the sympathetic system [5]. In the elderly age group, there may be no symptoms or only subtle ones.

Patients suffering from Graves' disease may have the following complaints on history:

• Weight loss
• Blurred vision, diplopia, photophobia
• Retro-orbital discomfort and painful eye movements
• Reduced visual acuity
• Amenorrhea in females; and erectile dysfunction and gynaecomastia in men
• Loose, frequent stools

• Pruritis and skin changes
• Pretibial myxedema

• Restlessness, anxiety and insomnia [6]
• Tremors
• Increased sweating
• Intolerance to heat

Physical exam may demonstrate the following findings:

• Thyroid gland: The thyroid gland is always diffusely enlarged and is non-tender. A bruit may be auscultated over it.
• Integumentary system: The hair become fine. The skin is warm. There may be areas of hyperpigmentation on it. Pretibial myxedema is often present [7].
• Opthalmologic findings: There may be lid retraction, lid lag, proptosis, ophthalmoplegia and loss of visual acuity and color vision. Eye findings are present in around 50% of the patients.
• Limbs: The limbs may show clubbing and fine tremors. Proximal myopathy can also be seen in some cases.

Graves’ disease, if left untreated, results in a state of life threatening thyrotoxicosis which is known as thyroid storm [8]. Even with early recognition and aggressive therapy, the mortality of this condition is 20% [9]. It results in various complications including weight loss with catabolism of bone and muscle, cardiac complications and psycho-cognitive complications. Graves’ disease is also associated with dermopathy, ophthalmopathy and acropathy.

Various tests are helpful in establishing any diagnosis related to the thyroid gland.

• In Graves’ disease, free T4 and T3 levels are usually elevated. There are certain conditions (such as toxic nodular goiter) in which only T3 levels are elevated. Such conditions are called T3 toxicosis.
• TSI (thyrotropin receptor anti-bodies) are mostly used as diagnostic test for Graves’ disease. Assays for TSI are mostly positive.
• Serum antibodies against collagen XIII are high in active Graves’ ophthalmopathy [11].
• Other markers include antithyroglobulin antibodies and antithyroidal peroxidase antibodies.

The treatment of Graves’ disease depends upon symptoms and thyrotoxic states. Treatment options include drugs, surgery and radiation.

Medication

• Anti-thyroid drugs such as carbimazole and propylthiouracil interfere with the normal functioning of the thyroid gland.
• beta-blockers are used to treat the symptoms caused by hyper-functioning of the sympathetic system.

Surgery

Either total or subtotal thyroidectomy is performed to reduce the mass of the active thyroid gland.

Radioactive Iodine

In the United States, radioactive iodine is given as first line therapy. Its dose usually ranges from 5-15 mCi. Thyroid function tests usually show improvement after 6 to 8 weeks of therapy. Radioactive iodine is absolutely contraindicated in pregnancy.

Many patients remain well after a single course of anti-thyroid drugs, but recurrence can happen at any time. Radioactive iodide is very effective, but often results in abnormally low levels of thyroid hormones (hypothyroidism). Surgery can also cause low levels of thyroid hormones.

The eye signs of Graves' disease tend to improve with anti-thyroid drug treatment. However, some element of the staring appearance often remains.

Normally thyroid gland releases its hormones (T3 and T4) under actions of thyroid stimulating hormone (TSH) that is produced by the pituitary gland in brain. In Graves' disease, abnormal antibodies are produced that are capable of mimicking the action of thyroid stimulating hormone. As a result, the levels of thyroid hormones T3 and T4 are increased. All these conditions collectively result into condition like Graves’ disease.

Moreover there are various other etiological factors that trigger increased thyroid hormone release such as thyroid surgery, trauma to thyroid gland, thyroid adenoma and thyroid carcinoma.

The prevalence of Graves’ disease varies in different areas around the world. Graves’ disease is most common cause of hyperthyroidism in the United States. These patients often have a family history of autoimmune diseases involving the thyroid gland which include Hashimoto thyroiditis, postpartum thyroiditis, Riedel thyroiditis and others [1]. Graves' disease is also commonly associated with non-thyroid conditions including diabetes mellitus type 1, myasthenia gravis, pernicious anemia, systemic lupus erythematosus, vitiligo and Sjogren syndrome [2].

The prevalence of maternal thyrotoxicosis is 1 case per 500 persons approximately in United States. In the United Kingdom, the incidence was reported to be 80 cases 100,000 per year in women [3].

Worldwide, Graves’ disease represents 60 to 90% of all causes of thyrotoxicosis. In one study, the incidence was reported to be around 100 to 200 cases per 100,000 population annually.

The hormones released by thyroid gland regulate the body metabolism and control the rate at which food is converted into energy form. The rate of metabolism is directly dependent on the amount of thyroid hormones released. If for some reason, there is an excessive production of hormones, the body metabolism is enhanced to very higher levels producing symptoms like sweating, trembling, weight loss in hyperthyroid individuals.

Graves’ disease is an autoimmune disorder mediated by autoantibodies that are capable of binding and stimulating the receptor for thyroid stimulating hormone on the thyroid gland [4]. Continued stimulation of the thyroid gland results in hypertrophy of the gland and overproduction of its hormones.

Binding of these antibodies to similar antigen retro-orbital connective tissue causes the ocular symptoms of Graves' disease.

There is no way to prevent Graves' disease as it is genetically mediated.

Graves’ disease is an autoimmune disorder characterized by hyperthyroidism due to circulating autoantibodies that are capable of stimulating the thyroid gland. It most commonly results in increased thyroid gland (twice or more of its size) due to increased synthesis of thyroid hormones by hyperfunctioning thyroid follicles.

Graves’ disease is a disorder in which the thyroid gland becomes overactive because bof stimulation by the body’s own antibodies. The symptoms seen in Graves’ disease include protuberance of eyes, heat intolerance, muscular weakness, increased sweating and anxiety.

It most commonly occurs in young individuals. There is no definitive prevention to this disease. Treatment can be done through drugs, surgery or radiation with favorable results.

1. Boelaert K, Newby PR, Simmonds MJ, et al. Prevalence and relative risk of other autoimmune diseases in subjects with autoimmune thyroid disease. The American journal of medicine. Feb 2010;123(2):183 e181-189.
2. Cruz AA, Akaishi PM, Vargas MA, de Paula SA. Association between thyroid autoimmune dysfunction and non-thyroid autoimmune diseases. Ophthalmic plastic and reconstructive surgery. Mar-Apr 2007;23(2):104-108.
3. Vanderpump MP, Tunbridge WM, French JM, et al. The incidence of thyroid disorders in the community: a twenty-year follow-up of the Whickham Survey. Clinical endocrinology. Jul 1995;43(1):55-68.
4. Jacobson EM, Tomer Y. The CD40, CTLA-4, thyroglobulin, TSH receptor, and PTPN22 gene quintet and its contribution to thyroid autoimmunity: back to the future. Journal of autoimmunity. Mar-May 2007;28(2-3):85-98.
5. Chen JL CH, Tseng YJ, Chu WC. Hyperthyroidism is characterized by both increased sympathetic and decreased vagal modulation of heart rate: evidence from spectral analysis of heart rate variability. Clinical endocrinology. 2006;64(6):611-616.
6. Bunevicius R, Prange AJ, Jr. Psychiatric manifestations of Graves' hyperthyroidism: pathophysiology and treatment options. CNS drugs. 2006;20(11):897-909.
7. Schwartz KM, Fatourechi V, Ahmed DD, Pond GR. Dermopathy of Graves' disease (pretibial myxedema): long-term outcome. The Journal of clinical endocrinology and metabolism. Feb 2002;87(2):438-446.
8. Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinology and metabolism clinics of North America. Dec 2006;35(4):663-686, vii.
9. Burch HB, Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinology and metabolism clinics of North America. Jun 1993;22(2):263-277.
10. Riis AL, Jorgensen JO, Gjedde S, et al. Whole body and forearm substrate metabolism in hyperthyroidism: evidence of increased basal muscle protein breakdown. American journal of physiology. Endocrinology and metabolism. Jun 2005;288(6):E1067-1073.
11. De Bellis A, Sansone D, Coronella C, et al. Serum antibodies to collagen XIII: a further good marker of active Graves' ophthalmopathy. Clinical endocrinology. Jan 2005;62(1):24-29.