$Unique_ID{BRK03788} $Pretitle{} $Title{Graves' Disease} $Subject{Graves' Disease Basedow Disease Parry Disease Exophthalmic Goiter Hashimoto's Thyroiditis} $Volume{} $Log{} Copyright (C) 1988, 1989, 1991, 1992 National Organization for Rare Disorders, Inc. 560: Graves' Disease ** IMPORTANT ** It is possible that the main title of the article (Graves Disease) is not the name you expected. Please check the SYNONYM listing to find the alternate names and disorder subdivisions covered by this article. Synonyms Basedow Disease Parry Disease Exophthalmic Goiter Information on the following diseases can be found in the Related Disorders section of this report: Hashimoto's Thyroiditis General Discussion ** REMINDER ** The information contained in the Rare Disease Database is provided for educational purposes only. It should not be used for diagnostic or treatment purposes. If you wish to obtain more information about this disorder, please contact your personal physician and/or the agencies listed in the "Resources" section of this report. Graves' Disease is a disease affecting the thyroid gland. It is thought to occur as a result of an imbalance in the immune system. This disorder causes increased thyroid secretion (hyperthyroidism), enlargement of the thyroid gland (goiter) and protrusion of the eyeballs. Symptoms Symptoms of Graves' Disease include eyes that bulge from the head, producing a characteristic startled appearance. Development of an enlarged thyroid gland (goiter) and increased thyroid secretion (hyperthyroidism) also occurs. This in turn may result in swelling of the legs and eyes, extreme sensitivity to light, irregular heart beat, clubbing of the fingers, and the development of breasts in males (gynecomastia). It may also cause heat intolerance, emotional instability, weight loss or hyperactivity. Symptoms may occur as a single incident, and then go into remission, or recurrent attacks may occur. Causes The exact cause of Graves' Disease is not known. It is thought to be inherited as an autosomal recessive trait. (Human traits including the classic genetic diseases, are the product of the interaction of two genes for that condition, one received from the father and one from the mother. In recessive disorders, the condition does not appear unless a person inherits the same defective gene from each parent. If one receives one normal gene and one gene for the disease, the person will be a carrier for the disease, but usually will show no symptoms. The risk of transmitting the disease to the children of a couple, both of whom are carriers for a recessive disorder, is twenty-five percent. Fifty percent of their children will be carriers, but healthy as described above. Twenty-five percent of their children will receive both normal genes, one from each parent and will be genetically normal.) Graves' Disease may also be a disease of the autoimmune system. (Autoimmune disorders are caused when the body's natural defenses (antibodies) against invading organisms suddenly begin to attack perfectly healthy tissue). Excessive levels of thyroid hormone cause the symptoms of Graves' Disease. Affected Population Graves' Disease is a rare condition affecting females more often than males. It can occur at any age and in almost any part of the world. A 1987 survey of 924 hyperthyroid patients from 17 thyroid centers in six European countries indicated that sixty percent of hyperthyroid patients have Graves' Disease. Related Disorders Symptoms of the following disorders can be similar to those of Graves' Disease. Comparisons may be useful for a differential diagnosis: Hashimoto's Thyroiditis or Lymphoid Thyroiditis is believed to be an autoimmune disorder which can destroy the thyroid gland and produce below normal amounts of thyroid hormone secretion (hypothyroidism). Some individuals appear to have both Hashimoto's Disease and Graves' Disease at the same time. Hashimoto's Disease can occur at any age but is most common in the third to fifth decades of life, and is more common in women than men. It is characterized by an enlarged thyroid gland that is infiltrated with lymphocytes. Eventually, the thyroid may be completely destroyed. Treatment with drugs to reduce antithyroid antibody formation is the treatment of choice. Therapies: Standard Treatment of Graves' Disease in adults usually involves the use of radioactive iodine. However, in children and pregnant women, drugs that reduce release of thyroid hormone are preferred. Antithyroid drugs are usually either propylthiouracil or methimazole. In patients that need further drug treatment to control the release of thyroid hormone, scientists suggest the use of thyroxine alone or in conjunction with other drug therapy. Genetic counseling may be of benefit for patients and their families. Other treatment is symptomatic and supportive. Surgery as a method of treatment for Graves' Disease is usually reserved for patients in whom the other forms of treatment have not been successful. Lifelong follow-up is necessary if the thyroid is removed. Therapies: Investigational Clinical trials are underway to study the myocardial 31-phosphate imaging in hyperthroidism. Interested persons may wish to contact: Paul W. Ladenson, M.D. Division of Endocrinology and Metabolism, Blalock 904 600 N. Wolfe St. Baltimore, MD 21205 (301) 955-3663 to see if further patients are needed for this research. Clinical trials are underway to study the physiologic determinants of exercise capacity in hyperthyroidism. Interested persons may wish to contact: Wade Martin Washington University School of Medicine 4566 Scott Ave., Campus Box 8113 St. Louis, MO 63110 (314) 362-2392 to see if further patients are needed for this research. This disease entry is based upon medical information available through January 1992. Since NORD's resources are limited, it is not possible to keep every entry in the Rare Disease Database completely current and accurate. Please check with the agencies listed in the Resources section for the most current information about this disorder. Resources For more information on Graves' Disease, please contact: National Organization for Rare Disorders (NORD) P.O. Box 8923 New Fairfield, CT 06812-1783 (203) 746-6518 Graves Disease Foundation P.O. Box 130 Mentone, AL 35984 National Graves Disease Foundation 320 Arlington Rd. Jacksonville, FL 32211 (904) 724-6744 The Thyroid Foundation of America, Inc. Massachusetts General Hospital, ACC 630 Boston, MA 02114 American Thyroid Association Endocrine/Metabolic Service 7D Washington, DC 20307 800-542-20207 The Thyroid Foundation of Canada CD/Box 1597 Kingston, Ontario Canada K71 5C8 The Paget's Disease Foundation (and other diseases of bone resorption) 200 Varick St., Suite 1004 New York, NY 10014-4810 (212) 229-1582 (800) 23-PAGET National Digestive Diseases Information Clearinghouse Box NDDIC Bethesda, MD 20892 (301) 468-6344 For genetic information and genetic counseling referrals: March of Dimes Birth Defects Foundation 1275 Mamaroneck Avenue White Plains, NY 10605 (914) 428-7100 Alliance of Genetic Support Groups 35 Wisconsin Circle, Suite 440 Chevy Chase, MD 20815 (800) 336-GENE (301) 652-5553 References MENDELIAN INHERITANCE IN MAN, 7th ed.: Victor A. McKusick; Johns Hopkins University Press, 1986. Pp. 1280. INTERNAL MEDICINE, 2nd Ed.: Jay H. Stein, ed.-in-chief; Little, Brown and Co., 1987. Pp. 1927-1931, 2302. GRAVES' DISEASE. MANIFESTATIONS AND THERAPEUTIC OPTIONS. K. F. McFarland, et al.; Postgrad Med, (March, 1988, issue 83 (4)). Pp. 275-282. HIGH SERUM PROGESTERONE IN HYPERTHYROID MEN WITH GRAVES' DISEASE. K. Nomura, et al.; J Clin Endocrinol Metab (January, 1988, issue 66 (1)). Pp. 230-232. GRAVES' DISEASE ASSOCIATED WITH HISTOLOGIC HASHIMOTO'S THYROIDITIS. S.A. Falk, et al.; Otolaryngol Head Neck Surg (February, 1985, issue 93(1)). Pp. 86-91. ADMINISTRATION OF THYROXINE IN TREATED GRAVES' DISEASE: EFFECTS ON THE LEVEL OF ANTIBODIES TO THYROID-STIMULATION HORMONE RECEPTORS AND ON THE RISK OF REOCCURRENCE OF HYPERTHYROIDISM. K. Hashizume, et al., N Eng J Med, (April 4, 1991, issue 324). Pp. 947-953. TREATMENT FOR GRAVES' DISEASE; TELLING THE THYROID TO REST., P.W. Ladenson, N. Eng J Med, (April 4, 1991, issue 324). Pp. 989-900.