Back داء غريفز Arabic Qreyv xəstəliyi AZ Базедова болест Bulgarian গ্রেভ রোগ Bengali/Bangla Malaltia de Graves-Basedow Catalan Gravesova–Basedowova nemoc Czech Basedows sygdom Danish Morbus Basedow German ގްރޭވްސް ބަލި DV Νόσος Γκρέιβς Greek
| Graves' disease | |
|---|---|
| Other names | Toxic diffuse goiter, Flajani–Basedow–Graves disease |
 | |
| The classic finding of exophthalmos and lid retraction in Graves' disease | |
| Specialty | Endocrinology |
| Symptoms | Enlarged thyroid, irritability, muscle weakness, sleeping problems, fast heartbeat, weight loss, poor tolerance of heat,[1] anxiety, tremor of hands or fingers, warm and moist skin, increased perspiration, goiter, changes in menstrual cycle, easy bruising, erectile dysfunction, reduced libido, frequent bowel movements, bulging eyes (Graves' ophthalmopathy), thick red skin on shins or the top of foot (pretibial myxedema)[2] |
| Complications | Graves' ophthalmopathy[1] |
| Causes | Unknown[3] |
| Risk factors | Family history, other autoimmune diseases[1] |
| Diagnostic method | Blood tests, radioiodine uptake[1][4] |
| Treatment | Radioiodine therapy, antithyroid and beta blocker medications, thyroid surgery[1] |
| Frequency | 0.5% (males), 3% (females)[5] |
Graves' disease, also known as toxic diffuse goiter or Basedow’s disease, is an autoimmune disease that affects the thyroid.[1] It frequently results in and is the most common cause of hyperthyroidism.[5] It also often results in an enlarged thyroid.[1] Signs and symptoms of hyperthyroidism may include irritability, muscle weakness, sleeping problems, a fast heartbeat, poor tolerance of heat, diarrhea and unintentional weight loss.[1] Other symptoms may include thickening of the skin on the shins, known as pretibial myxedema, and eye bulging, a condition caused by Graves' ophthalmopathy.[1] About 25 to 30% of people with the condition develop eye problems.[1][4]
The exact cause of the disease is unclear, but symptoms are a result of antibodies binding to receptors on the thyroid causing over-expression of thyroid hormone.[3] Persons are more likely to be affected if they have a family member with the disease.[1] If one monozygotic twin is affected, a 30% chance exists that the other twin will also have the disease.[6] The onset of disease may be triggered by physical or emotional stress, infection, or giving birth.[4] Those with other autoimmune diseases, such as type 1 diabetes and rheumatoid arthritis, are more likely to be affected.[1] Smoking increases the risk of disease and may worsen eye problems.[1] The disorder results from an antibody, called thyroid-stimulating immunoglobulin (TSI), that has a similar effect to thyroid stimulating hormone (TSH).[1] These TSI antibodies cause the thyroid gland to produce excess thyroid hormones.[1] The diagnosis may be suspected based on symptoms and confirmed with blood tests and radioiodine uptake.[1][4] Typically, blood tests show a raised T3 and T4, low TSH, increased radioiodine uptake in all areas of the thyroid, and TSI antibodies.[4]
The three treatment options are radioiodine therapy, medications, and thyroid surgery.[1] Radioiodine therapy involves taking iodine-131 by mouth, which is then concentrated in the thyroid and destroys it over weeks to months.[1] The resulting hypothyroidism is treated with synthetic thyroid hormones.[1] Medications such as beta blockers may control some of the symptoms, and antithyroid medications such as methimazole may temporarily help people, while other treatments are having effect.[1] Surgery to remove the thyroid is another option.[1] Eye problems may require additional treatments.[1]
Graves disease develops in about 0.5% of males and 3.0% of females.[5] It occurs about 7.5 times more often in women than in men.[1] Often, it starts between the ages of 40 and 60, but can begin at any age.[6] It is the most common cause of hyperthyroidism in the United States (about 50 to 80% of cases).[1][4] The condition is named after Irish surgeon Robert Graves, who described it in 1835.[6] A number of prior descriptions also exist.[6]
- ^ a b c d e f g h i j k l m n o p q r s t u v w x "Graves Disease". www.niddk.nih.gov. August 10, 2012. Archived from the original on April 2, 2015. Retrieved 2015-04-02.
- ^ "Graves' disease". Autoimmune Registry Inc. Archived from the original on 15 June 2022. Retrieved 15 June 2022.
- ^ a b Menconi F, Marcocci C, Marinò M (2014). "Diagnosis and classification of Graves disease". Autoimmunity Reviews. 13 (4–5): 398–402. doi:10.1016/j.autrev.2014.01.013. PMID 24424182.
- ^ a b c d e f Brent GA (June 2008). "Clinical practice. Grave disease". The New England Journal of Medicine. 358 (24): 2594–605. doi:10.1056/NEJMcp0801880. PMID 18550875.
- ^ a b c Burch HB, Cooper DS (December 2015). "Management of Graves Disease: A Review". JAMA. 314 (23): 2544–54. doi:10.1001/jama.2015.16535. PMID 26670972.
- ^ a b c d Nikiforov YE, Biddinger PW, Nikiforova LD, Biddinger PW (2012). Diagnostic pathology and molecular genetics of the thyroid (2nd ed.). Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins. p. 69. ISBN 9781451114553. Archived from the original on 2017-09-08.