Graves Disease 

  • Author: Sai-Ching Jim Yeung, MD, PhD, FACP; Chief Editor: George T Griffing, MD   more...
 
Updated: Sep 30, 2011
 

Background

Graves disease, named after Robert J. Graves, MD,[1] circa 1830s, is an autoimmune disease characterized by hyperthyroidism due to circulating autoantibodies. Thyroid-stimulating immunoglobulins (TSIs) bind to and activate thyrotropin receptors, causing the thyroid gland to grow and the thyroid follicles to increase synthesis of thyroid hormone. Graves disease, along with Hashimoto thyroiditis, is classified as an autoimmune thyroid disorder.

In some patients, Graves disease represents a part of more extensive autoimmune processes leading to dysfunction of multiple organs (eg, polyglandular autoimmune syndromes). Graves disease is associated with pernicious anemia, vitiligo, diabetes mellitus type 1, autoimmune adrenal insufficiency, systemic sclerosis, myasthenia gravis, Sjögren syndrome, rheumatoid arthritis, and systemic lupus erythematosus.[2]

Graves ophthalmopathy is shown below.

Graves disease. Varying degrees of manifestations Graves disease. Varying degrees of manifestations of Graves ophthalmopathy.

Recent studies

Boelaert et al investigated the prevalences of and relative risks for coexisting autoimmune diseases in patients with Graves disease (2791 patients) or Hashimoto thyroiditis (495 patients). The authors found coexisting disorders in 9.7% of patients with Graves disease and in 14.3% of those with Hashimoto thyroiditis, with rheumatoid arthritis being the most common of these (prevalence = 3.15% and 4.24% in Graves disease and Hashimoto thyroiditis, respectively). Relative risks of greater than 10 were found for pernicious anemia, systemic lupus erythematosus, Addison disease, celiac disease, and vitiligo. The authors also reported a tendency for parents of patients with Graves disease or Hashimoto thyroiditis to have a history of hyperthyroidism or hypothyroidism, respectively.[3]

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Pathophysiology

In Graves disease, B and T lymphocyte-mediated autoimmunity are known to be directed at 4 well-known thyroid antigens: thyroglobulin, thyroid peroxidase, sodium-iodide symporter, and the thyrotropin receptor. However, the thyrotropin receptor itself is the primary autoantigen of Graves disease and is responsible for the manifestation of hyperthyroidism. In this disease, the antibody and cell-mediated thyroid antigen-specific immune responses are well defined. Direct proof of an autoimmune disorder that is mediated by autoantibodies is the development of hyperthyroidism in healthy subjects by transferring thyrotropin receptor antibodies in serum from patients with Graves disease and the passive transfer of thyrotropin receptor antibodies to the fetus in pregnant women.

The thyroid gland is under continuous stimulation by circulating autoantibodies against the thyrotropin receptor, and pituitary thyrotropin secretion is suppressed because of the increased production of thyroid hormones. The stimulating activity of thyrotropin receptor antibodies is found mostly in the immunoglobulin G1 subclass. These thyroid-stimulating antibodies cause release of thyroid hormone and thyroglobulin that is mediated by 3,'5'-cyclic adenosine monophosphate (cyclic AMP), and they also stimulate iodine uptake, protein synthesis, and thyroid gland growth.

The anti-sodium-iodide symporter, antithyroglobulin, and antithyroid peroxidase antibodies appear to have little role in the etiology of hyperthyroidism in Graves disease. However, they are markers of autoimmune disease against the thyroid. Intrathyroidal lymphocytic infiltration is the initial histologic abnormality in persons with autoimmune thyroid disease and can be correlated with the titer of thyroid antibodies. Besides being the source of autoantigens, the thyroid cells express molecules that mediate T cell adhesion and complement regulation (Fas and cytokines) that participate and interact with the immune system. In these patients, the proportion of CD4 lymphocytes is lower in the thyroid than in the peripheral blood. The increased Fas expression in intrathyroidal CD4 T lymphocytes may be the cause of CD4 lymphocyte reduction in these individuals.

Several autoimmune thyroid disease susceptibility genes have been identified: CD40, CTLA-4, thyroglobulin, TSH receptor, and PTPN22.[4, 5] Some of these susceptibility genes are specific to either Graves disease or Hashimoto thyroiditis, while others confer susceptibility to both conditions. The genetic predisposition to thyroid autoimmunity may interact with environmental factors or events to precipitate the onset of Graves disease.

Two new susceptibility loci were found: the RNASET2-FGFR1OP-CCR6 region at 6q27 and an intergenic region at 4p14.[6] Moreover, strong associations of thyroid-stimulating hormone receptor and major histocompatibility complex class II variants with persistently thyroid stimulating hormone receptor autoantibodies (TRAb)-positive Graves disease were found.

Graves disease patients a have higher rate of peripheral blood mononuclear cell conversion into CD34+ fibrocytes compared with healthy controls. These cells may contribute to the pathophysiology of ophthalmopathy by accumulating in orbital tissues and producing inflammatory cytokines, including TNF-alpha and IL-6.[7]

Pathophysiologic mechanisms are shown in the image below.

Pathophysiologic mechanisms of Graves disease relaPathophysiologic mechanisms of Graves disease relating thyroid-stimulating immunoglobulins to hyperthyroidism and ophthalmopathy. T4 is levothyroxine. T3 is triiodothyronine.
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Epidemiology

Frequency

United States

Graves disease is the most common cause of hyperthyroidism in the United States. A study conducted in Olmstead County, Minnesota estimated the incidence to be approximately 30 cases per 100,000 persons per year.[8] The prevalence of maternal thyrotoxicosis is approximately 1 case per 500 persons, with maternal Graves disease being the most common etiology. Commonly, patients have a family history involving a wide spectrum of autoimmune thyroid diseases, such as Graves disease, Hashimoto thyroiditis, or postpartum thyroiditis, among others.

International

Among the causes of spontaneous thyrotoxicosis, Graves disease is the most common. Graves disease represents 60-90% of all causes of thyrotoxicosis in different regions of the world. In the Wickham Study in the United Kingdom, the incidence was reported to be 100-200 cases per 100,000 population per year.[9] The incidence in women in the UK has been reported to be 80 cases 100,000 per year.[10]

Mortality/Morbidity

If left untreated, Graves disease can cause severe thyrotoxicosis. A life-threatening thyrotoxic crisis (ie, thyroid storm) can occur. Long-standing severe thyrotoxicosis leads to severe weight loss with catabolism of bone and muscle.[11] Cardiac complications and psychocognitive complications can cause significant morbidity. Graves disease is also associated with ophthalmopathy, dermopathy, and acropachy.

  • Thyroid storm is an exaggerated state of thyrotoxicosis.[12] It occurs in patients who have unrecognized or inadequately treated thyrotoxicosis and a superimposed precipitating event such as thyroid surgery, nonthyroidal surgery, infection, or trauma. When thyroid storm was first described, the acute mortality rate was nearly 100%. In current practice, with aggressive therapy and early recognition of the syndrome, the mortality rate is approximately 20%.[13]
  • Long-term excess of thyroid hormone can lead to osteoporosis in men and women. The effect can be particularly devastating in women, in whom the disease may compound the bone loss secondary to chronic anovulation or menopause. Bone loss is accelerated in patients with hyperthyroidism. The increase in bone loss can be demonstrated by increased urinary pyridinoline cross-link excretion. Serum calcium and phosphate, plasma FGF-23 were significantly higher in the patients with Graves disease than in healthy control subjects, suggesting that FGF-23 is physiologically related to serum phosphate homeostasis in untreated Graves disease.[14]
  • Hyperthyroidism increases muscular energy expenditure and muscle protein breakdown. These abnormalities may explain the sarcopenia and myopathy observed in patients with hyperthyroid Graves disease.
  • Cardiac hypertrophy has been reported in thyrotoxicosis of different etiologies. Rhythm disturbances such as extrasystolic arrhythmia, atrial fibrillation, and flutter are common. Cardiomyopathy and congestive heart failure can occur.[15]
  • Psychiatric manifestations such as mood and anxiety disorders are common.[16] Subjective cognitive dysfunction is often reported by Graves disease patients and may be due to affective and somatic manifestations of thyrotoxicosis, which remit after treatment of Graves thyrotoxicosis.[17]
  • Nonpitting edema is the most prevalent form of dermopathy (about 40%) and are primarily in the pretibial area. The nearly all (>95%) patients with dermopathy had ophthalmopathy.[18] Advanced forms of dermopathy are elephantiasis or thyroid acropachy. Severe acropachy can be disabling and can lead to total loss of hand function.
  • Progression of ophthalmopathy can lead to compromised vision and blindness. Visual loss due to corneal lesions or optic nerve compression can be seen in severe Graves ophthalmopathy.
  • Maternal Graves disease can lead to neonatal hyperthyroidism by transplacental transfer of thyroid-stimulating antibodies. Approximately 1-5% of children of mothers with Graves disease (usually with high TSI titer) are affected. Usually, the TSI titer falls during pregnancy.
  • Elderly individuals may develop apathetic hyperthyroidism, and the only presenting features may be unexplained weight loss or cardiac symptoms such as atrial fibrillation and congestive heart failure.

Race

  • In whites, autoimmune thyroid diseases are, based on linkage analysis, linked with the following loci: AITD1, CTLA4, GD1, GD2, GD3, HT1, and HT2. Different loci have been reported to be linked with autoimmune thyroid diseases in persons of other races.
  • Susceptibility is influenced by genes in the human leukocyte antigen (HLA) region on chromosome 6 and in CTLA4 on band 2q33. Association with specific HLA haplotypes has been observed and is found to vary with ethnicity.

Sex

  • As with most autoimmune diseases, susceptibility is increased in females. Hyperthyroidism due to Graves disease has a female-to-male ratio of 7-8:1.
  • The female-to-male ratio for pretibial myxedema is 3.5:1. Only 7% of patients with localized myxedema have thyroid acropachy.
  • Unlike the other manifestations of Graves disease, the female-to-male ratio for thyroid acropachy is 1:1.

Age

  • Typically, Graves disease is a disease of young women, but it may occur in persons of any age.
  • The typical age range is 20-40 years.
  • Most affected women are aged 30-60 years.
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Contributor Information and Disclosures
Author

Sai-Ching Jim Yeung, MD, PhD, FACP  Associate Professor, Department of Emergency Medicine, Department of Endocrine Neoplasia and Hormonal Disorders, MD Anderson Cancer Center, University of Texas Medical School at Houston

Sai-Ching Jim Yeung, MD, PhD, FACP is a member of the following medical societies: American Association for Cancer Research, American College of Physicians, American Medical Association, American Thyroid Association, and Endocrine Society

Disclosure: Nothing to disclose.

Coauthor(s)

Mouhammed Amir Habra, MD  Endocrine Fellow, Department of Endocrine Neoplasia and Hormonal Disorders, University of Texas MD Anderson Cancer Center

Mouhammed Amir Habra, MD is a member of the following medical societies: American College of Physicians, American Thyroid Association, and Endocrine Society

Disclosure: Nothing to disclose.

Alice Cua Chiu, MD  Associate Affiliate, Department of Internal Medicine, Division of Endocrinology, Bayshore Medical Center

Alice Cua Chiu, MD is a member of the following medical societies: American Medical Association and Endocrine Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Steven R Gambert, MD  Professor of Medicine, Johns Hopkins University School of Medicine; Director of Geriatric Medicine, University of Maryland Medical Center and R. Adams Cowley Shock Trauma Center

Steven R Gambert, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physician Executives, American College of Physicians, American Geriatrics Society, Association of Professors of Medicine, Endocrine Society, and Gerontological Society of America

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Kent Wehmeier, MD  Professor, Department of Internal Medicine, Division of Endocrinology, Diabetes, and Metabolism, St Louis University School of Medicine

Kent Wehmeier, MD is a member of the following medical societies: American Society of Hypertension, Endocrine Society, and International Society for Clinical Densitometry

Disclosure: Nothing to disclose.

Mark Cooper, MBBS, PhD, FRACP  Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University

Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD  Professor of Medicine, St Louis University School of Medicine

George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation

Disclosure: Nothing to disclose.

References

  1. Ellis H. Robert Graves: 1796-1852. Br J Hosp Med (Lond). Jun 2006;67(6):313. [Medline].

  2. Cruz AA, Akaishi PM, Vargas MA, de Paula SA. Association between thyroid autoimmune dysfunction and non-thyroid autoimmune diseases. Ophthal Plast Reconstr Surg. Mar-Apr 2007;23(2):104-8. [Medline].

  3. Boelaert K, Newby PR, Simmonds MJ, et al. Prevalence and relative risk of other autoimmune diseases in subjects with autoimmune thyroid disease. Am J Med. Feb 2010;123(2):183.e1-9. [Medline].

  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. J Autoimmun. Mar-May 2007;28(2-3):85-98. [Medline].

  5. Iwama S, Ikezaki A, Kikuoka N, et al. Association of HLA-DR, -DQ genotype and CTLA-4 gene polymorphism with Graves' disease in Japanese children. Horm Res. 2005;63(2):55-60. [Medline].

  6. Chu X, Pan CM, Zhao SX, et al. A genome-wide association study identifies two new risk loci for Graves' disease. Nat Genet. Aug 14 2011;43(9):897-901. [Medline].

  7. Douglas RS, Afifiyan NF, Hwang CJ, et al. Increased generation of fibrocytes in thyroid-associated ophthalmopathy. J Clin Endocrinol Metab. Jan 2010;95(1):430-8. [Medline]. [Full Text].

  8. Furszyfer J, Kurland LT, McConahey WM, Elveback LR. Graves' disease in Olmsted County, Minnesota, 1935 through 1967. Mayo Clin Proc. Sep 1970;45(9):636-44. [Medline].

  9. Tunbridge WM, Evered DC, Hall R, et al. The spectrum of thyroid disease in a community: the Whickham survey. Clin Endocrinol (Oxf). Dec 1977;7(6):481-93. [Medline].

  10. 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. Clin Endocrinol (Oxf). Jul 1995;43(1):55-68. [Medline].

  11. Riis AL, Jørgensen JO, Gjedde S, et al. Whole body and forearm substrate metabolism in hyperthyroidism: evidence of increased basal muscle protein breakdown. Am J Physiol Endocrinol Metab. Jun 2005;288(6):E1067-73. [Medline].

  12. Nayak B, Burman K. Thyrotoxicosis and thyroid storm. Endocrinol Metab Clin North Am. Dec 2006;35(4):663-86, vii. [Medline].

  13. Burch HB, Wartofsky L. Life-threatening thyrotoxicosis. Thyroid storm. Endocrinol Metab Clin North Am. Jun 1993;22(2):263-77. [Medline].

  14. Park SE, Cho MA, Kim SH, Rhee Y, Kang ES, Ahn CW. The adaptation and relationship of FGF-23 to changes in mineral metabolism in Graves' disease. Clin Endocrinol (Oxf). Jun 2007;66(6):854-8. [Medline].

  15. Uchida T, Takeno K, Goto M, et al. Superior thyroid artery mean peak systolic velocity for the diagnosis of thyrotoxicosis in Japanese patients. Endocr J. Mar 6 2010;[Medline]. [Full Text].

  16. Bunevicius R, Prange AJ Jr. Psychiatric manifestations of Graves' hyperthyroidism: pathophysiology and treatment options. CNS Drugs. 2006;20(11):897-909. [Medline].

  17. Vogel A, Elberling TV, Hørding M, Dock J, Rasmussen AK, Feldt-Rasmussen U. Affective symptoms and cognitive functions in the acute phase of Graves' thyrotoxicosis. Psychoneuroendocrinology. Jan 2007;32(1):36-43. [Medline].

  18. Schwartz KM, Fatourechi V, Ahmed DD, Pond GR. Dermopathy of Graves' disease (pretibial myxedema): long-term outcome. J Clin Endocrinol Metab. Feb 2002;87(2):438-46. [Medline].

  19. Chen JL, Chiu HW, 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. Clin Endocrinol (Oxf). Jun 2006;64(6):611-6. [Medline].

  20. Kung AW. Clinical review: Thyrotoxic periodic paralysis: a diagnostic challenge. J Clin Endocrinol Metab. Jul 2006;91(7):2490-5. [Medline].

  21. Ryan DP, da Silva MR, Soong TW, et al. Mutations in potassium channel Kir2.6 cause susceptibility to thyrotoxic hypokalemic periodic paralysis. Cell. Jan 8 2010;140(1):88-98. [Medline]. [Full Text].

  22. Chung JO, Cho DH, Chung DJ, et al. Ultrasonographic features of papillary thyroid carcinoma in patients with Graves' disease. Korean J Intern Med. Mar 2010;25(1):71-6. [Medline]. [Full Text].

  23. Zaletel K, Krhin B, Gaberscek S, Pirnat E, Hojker S. The influence of the exon 1 polymorphism of the cytotoxic T lymphocyte antigen 4 gene on thyroid antibody production in patients with newly diagnosed Graves' disease. Thyroid. May 2002;12(5):373-6. [Medline].

  24. Zaletel K, Krhin B, Gaberscek S, Hojker S. Thyroid autoantibody production is influenced by exon 1 and promoter CTLA-4 polymorphisms in patients with Hashimoto's thyroiditis. Int J Immunogenet. Apr 2006;33(2):87-91. [Medline].

  25. Wang PW, Chen IY, Liu RT, Hsieh CJ, Hsi E, Juo SH. Cytotoxic T lymphocyte-associated molecule-4 gene polymorphism and hyperthyroid Graves' disease relapse after antithyroid drug withdrawal: a follow-up study. J Clin Endocrinol Metab. Jul 2007;92(7):2513-8. [Medline].

  26. Ban Y, Tozaki T, Taniyama M, Tomita M, Ban Y. Association of a C/T single-nucleotide polymorphism in the 5' untranslated region of the CD40 gene with Graves' disease in Japanese. Thyroid. May 2006;16(5):443-6. [Medline].

  27. Heward JM, Brand OJ, Barrett JC, Carr-Smith JD, Franklyn JA, Gough SC. Association of PTPN22 haplotypes with Graves' disease. J Clin Endocrinol Metab. Feb 2007;92(2):685-90. [Medline].

  28. Benvenga S, Guarneri F, Vaccaro M, et al. Homologies between proteins of Borrelia burgdorferi and thyroid autoantigens. Thyroid. 2004;14:964-6. [Medline].

  29. Gangi E, Kapatral V, El-Azami El-Idrissi M, et al. Characterization of a recombinant Yersinia enterocolitica lipoprotein; implications for its role in autoimmune response against thyrotropin receptor. Autoimmunity. Sep-Nov 2004;37(6-7):515-20. [Medline].

  30. Al-Muqbel KM, Tashtoush RM. Patterns of thyroid radioiodine uptake: Jordanian experience. J Nucl Med Technol. Mar 2010;38(1):32-6. [Medline].

  31. De Bellis A, Sansone D, Coronella C, et al. Serum antibodies to collagen XIII: a further good marker of active Graves' ophthalmopathy. Clin Endocrinol (Oxf). Jan 2005;62(1):24-9. [Medline].

  32. Cappelli C, Pirola I, De Martino E, Agosti B, Delbarba A, Castellano M. The role of imaging in Graves' disease: A cost-effectiveness analysis. Eur J Radiol. Apr 23 2007;[Medline].

  33. Markovic V, Eterovic D. Thyroid echogenicity predicts outcome of radioiodine therapy in patients with graves' disease. J Clin Endocrinol Metab. Sep 2007;92(9):3547-52. [Medline].

  34. Kubota S, Ohye H, Yano G, Nishihara E, Kudo T, Ito M. Two-day thionamide withdrawal prior to radioiodine uptake sufficiently increases uptake and does not exacerbate hyperthyroidism compared to 7-day withdrawal in Graves' disease. Endocr J. Oct 2006;53(5):603-7. [Medline].

  35. Bonnema SJ, Bennedbaek FN, Veje A, et al. Propylthiouracil before 131I therapy of hyperthyroid diseases: effect on cure rate evaluated by a randomized clinical trial. J Clin Endocrinol Metab. 2004;89:4439-44. [Medline].

  36. Read CH Jr, Tansey MJ, Menda Y. A 36-year retrospective analysis of the efficacy and safety of radioactive iodine in treating young Graves' patients. J Clin Endocrinol Metab. Sep 2004;89(9):4229-33. [Medline].

  37. Ceccarelli C, Canale D, Battisti P, Caglieresi C, Moschini C, Fiore E. Testicular function after 131I therapy for hyperthyroidism. Clin Endocrinol (Oxf). Oct 2006;65(4):446-52. [Medline].

  38. Rivkees SA, Dinauer C. An optimal treatment for pediatric Graves' disease is radioiodine. J Clin Endocrinol Metab. Mar 2007;92(3):797-800. [Medline].

  39. Bartalena L, Marcocci C, Bogazzi F, et al. Relation between therapy for hyperthyroidism and the course of Graves' ophthalmopathy. N Engl J Med. Jan 8 1998;338(2):73-8. [Medline].

  40. Bartalena L, Marcocci C, Bogazzi F, Panicucci M, Lepri A, Pinchera A. Use of corticosteroids to prevent progression of Graves' ophthalmopathy after radioiodine therapy for hyperthyroidism. N Engl J Med. Nov 16 1989;321(20):1349-52. [Medline].

  41. Bartalena L, Tanda ML, Piantanida E, Lai A, Pinchera A. Relationship between management of hyperthyroidism and course of the ophthalmopathy. J Endocrinol Invest. Mar 2004;27(3):288-94. [Medline].

  42. Macchia PE, Bagattini M, Lupoli G, et al. High-dose intravenous corticosteroid therapy for Graves' ophthalmopathy. J Endocrinol Invest. 2001;24:152-8. [Medline].

  43. Liao SL, Huang SW. Correlation of retrobulbar volume change with resected orbital fat volume and proptosis reduction after fatty decompression for Graves ophthalmopathy. Am J Ophthalmol. Mar 2011;151(3):465-9.e1. [Medline].

  44. Wakelkamp IM, Tan H, Saeed P, et al. Orbital irradiation for Graves' ophthalmopathy: Is it safe? A long-term follow-up study. Ophthalmology. Aug 2004;111(8):1557-62. [Medline].

  45. Dickinson AJ, Vaidya B, Miller M, Coulthard A, Perros P, Baister E. Double-blind, placebo-controlled trial of octreotide long-acting repeatable (LAR) in thyroid-associated ophthalmopathy. J Clin Endocrinol Metab. Dec 2004;89(12):5910-5. [Medline].

  46. Wemeau JL, Caron P, Beckers A, et al. Octreotide (long-acting release formulation) treatment in patients with graves' orbitopathy: clinical results of a four-month, randomized, placebo-controlled, double-blind study. J Clin Endocrinol Metab. 2005;90:841-8. [Medline].

  47. Stan MN, Garrity JA, Bradley EA, Woog JJ, Bahn MM, Brennan MD. Randomized, double-blind, placebo-controlled trial of long-acting release octreotide for treatment of Graves' ophthalmopathy. J Clin Endocrinol Metab. Dec 2006;91(12):4817-24. [Medline].

  48. Durrani OM, Reuser TQ, Murray PI. Infliximab: a novel treatment for sight-threatening thyroid associated ophthalmopathy. Orbit. Jun 2005;24(2):117-9. [Medline].

  49. Salvi M, Vannucchi G, Campi I, Currò N, Dazzi D, Simonetta S. Treatment of Graves' disease and associated ophthalmopathy with the anti-CD20 monoclonal antibody rituximab: an open study. Eur J Endocrinol. Jan 2007;156(1):33-40. [Medline].

  50. Ebner R, Devoto MH, Weil D, et al. Treatment of thyroid associated ophthalmopathy with periocular injections of triamcinolone. Br J Ophthalmol. Nov 2004;88(11):1380-6. [Medline]. [Full Text].

  51. Finamor FE, Martins JR, Nakanami D, Paiva ER, Manso PG, Furlanetto RP. Pentoxifylline (PTX)--an alternative treatment in Graves' ophthalmopathy (inactive phase): assessment by a disease specific quality of life questionnaire and by exophthalmometry in a prospective randomized trial. Eur J Ophthalmol. Jul-Aug 2004;14(4):277-83. [Medline].

  52. Grodski S, Stalberg P, Robinson BG, Delbridge LW. Surgery versus Radioiodine Therapy as Definitive Management for Graves' Disease: The Role of Patient Preference. Thyroid. Feb 2007;17(2):157-60. [Medline].

  53. Pradeep PV, Agarwal A, Baxi M, Agarwal G, Gupta SK, Mishra SK. Safety and efficacy of surgical management of hyperthyroidism: 15-year experience from a tertiary care center in a developing country. World J Surg. Feb 2007;31(2):306-12; discussion 313. [Medline].

  54. Panzer C, Beazley R, Braverman L. Rapid preoperative preparation for severe hyperthyroid Graves' disease. J Clin Endocrinol Metab. May 2004;89(5):2142-4. [Medline].

  55. Erbil Y, Ozluk Y, Giris M, Salmaslioglu A, Issever H, Barbaros U. Effect of lugol solution on thyroid gland blood flow and microvessel density in the patients with Graves' disease. J Clin Endocrinol Metab. Jun 2007;92(6):2182-9. [Medline].

  56. Alsuhaibani AH, Carter KD, Policeni B, Nerad JA. Effect of orbital bony decompression for Graves' orbitopathy on the volume of extraocular muscles. Br J Ophthalmol. Sep 2011;95(9):1255-8. [Medline].

  57. Hiraiwa T, Ito M, Imagawa A, et al. High diagnostic value of a radioiodine uptake test with and without iodine restriction in Graves' disease and silent thyroiditis. Thyroid. Jul 2004;14(7):531-5. [Medline].

  58. Rivkees SA, Stephenson K, Dinauer C. Adverse events associated with methimazole therapy of Graves' disease in children. Int J Pediatr Endocrinol. 2010;2010:176970. [Medline]. [Full Text].

 
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Pathophysiologic mechanisms of Graves disease relating thyroid-stimulating immunoglobulins to hyperthyroidism and ophthalmopathy. T4 is levothyroxine. T3 is triiodothyronine.
Graves disease. Varying degrees of manifestations of Graves ophthalmopathy.
 
 
 
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