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Genetic factors, anti [[thyrotropin receptor]] antibodies, [[T cells]], [[B cells]] and thyroid epithelial cells involvement are the main pathologic features of Graves' disease.  
Genetic factors, anti [[thyrotropin receptor]] antibodies, [[T cells]], [[B cells]] and thyroid epithelial cells involvement are the main pathologic features of Graves' disease.  


Genetic factors have role as initiating factor include [[Thyroglobulin]], [[Thyrotropin receptor]], [[HLA|HLA-DRβ-Arg74]], The protein tyrosine phosphatase nonreceptor type 22 (PTPN22), [[CTLA-4|Cytotoxic T-lymphocyte–associated antigen 4]] (CTLA4), [[CD25]], [[CD40]].
Genetic factors have role as initiating factor include [[Thyroglobulin]], [[Thyrotropin receptor]], [[HLA|HLA-DRβ-Arg74]], The protein tyrosine phosphatase nonreceptor type 22 (PTPN22), [[CTLA-4|Cytotoxic T-lymphocyte–associated antigen 4]] (CTLA4), [[CD25]], [[CD40]].<br>
Graves' disease is an [[autoimmunity|autoimmune]] disorder, in which the body produces antibodies to the receptor for [[thyroid-stimulating hormone]] (TSH). These are [[IgG|IgG1]] subclass of antibodies.<ref name="pmid2168443">{{cite journal |vauthors=Weetman AP, Yateman ME, Ealey PA, Black CM, Reimer CB, Williams RC, Shine B, Marshall NJ |title=Thyroid-stimulating antibody activity between different immunoglobulin G subclasses |journal=J. Clin. Invest. |volume=86 |issue=3 |pages=723–7 |year=1990 |pmid=2168443 |pmc=296786 |doi=10.1172/JCI114768 |url=}}</ref>
 
==Causes==
Graves' disease may be caused by either genetic factors, autoimmune antibodies against thyrotropin receptors, T cells and B cells auto activation and infectious agents.<ref name="pmid24460189">{{cite journal |vauthors=Tomer Y |title=Mechanisms of autoimmune thyroid diseases: from genetics to epigenetics |journal=Annu Rev Pathol |volume=9 |issue= |pages=147–56 |year=2014 |pmid=24460189 |pmc=4128637 |doi=10.1146/annurev-pathol-012513-104713 |url=}}</ref><ref name="pmid26459776">{{cite journal |vauthors=Limbach M, Saare M, Tserel L, Kisand K, Eglit T, Sauer S, Axelsson T, Syvänen AC, Metspalu A, Milani L, Peterson P |title=Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling |journal=J. Autoimmun. |volume=67 |issue= |pages=46–56 |year=2016 |pmid=26459776 |doi=10.1016/j.jaut.2015.09.006 |url=}}</ref><ref name="pmid2168443">{{cite journal |vauthors=Weetman AP, Yateman ME, Ealey PA, Black CM, Reimer CB, Williams RC, Shine B, Marshall NJ |title=Thyroid-stimulating antibody activity between different immunoglobulin G subclasses |journal=J. Clin. Invest. |volume=86 |issue=3 |pages=723–7 |year=1990 |pmid=2168443 |pmc=296786 |doi=10.1172/JCI114768 |url=}}</ref>
 
==Differential Diagnosis==
The table below summarizes the list of differential diagnosis for Graves' disease.<ref name="pmid2258582">{{cite journal |vauthors=Lambert M, Unger J, De Nayer P, Brohet C, Gangji D |title=Amiodarone-induced thyrotoxicosis suggestive of thyroid damage |journal=J. Endocrinol. Invest. |volume=13 |issue=6 |pages=527–30 |year=1990 |pmid=2258582 |doi= |url=}}</ref><ref name="pmid24282820">{{cite journal |vauthors=Ahmadieh H, Salti I |title=Tyrosine kinase inhibitors induced thyroid dysfunction: a review of its incidence, pathophysiology, clinical relevance, and treatment |journal=Biomed Res Int |volume=2013 |issue= |pages=725410 |year=2013 |pmid=24282820 |pmc=3824811 |doi=10.1155/2013/725410 |url=}}</ref><ref name="pmid8351956">{{cite journal |vauthors=Vialettes B, Guillerand MA, Viens P, Stoppa AM, Baume D, Sauvan R, Pasquier J, San Marco M, Olive D, Maraninchi D |title=Incidence rate and risk factors for thyroid dysfunction during recombinant interleukin-2 therapy in advanced malignancies |journal=Acta Endocrinol. |volume=129 |issue=1 |pages=31–8 |year=1993 |pmid=8351956 |doi= |url=}}</ref><ref name="pmid23067331">{{cite journal |vauthors=Jha S, Waghdhare S, Reddi R, Bhattacharya P |title=Thyroid storm due to inappropriate administration of a compounded thyroid hormone preparation successfully treated with plasmapheresis |journal=Thyroid |volume=22 |issue=12 |pages=1283–6 |year=2012 |pmid=23067331 |doi=10.1089/thy.2011.0353 |url=}}</ref><ref name="pmid2666114">{{cite journal |vauthors=Cohen JH, Ingbar SH, Braverman LE |title=Thyrotoxicosis due to ingestion of excess thyroid hormone |journal=Endocr. Rev. |volume=10 |issue=2 |pages=113–24 |year=1989 |pmid=2666114 |doi=10.1210/edrv-10-2-113 |url=}}</ref>
 
 
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1  | {{fontcolor|#FFFFFF|Cause of thyrotoxicosis}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1  | {{fontcolor|#FFFFFF|TSH receptor Antibodies}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1  | {{fontcolor|#FFFFFF|Thyroid US}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1  | {{fontcolor|#FFFFFF|Color flow Doppler}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1  | {{fontcolor|#FFFFFF|Radioactive iodine uptake/Scan}}
! style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1  | {{fontcolor|#FFFFFF|Other features}}
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Graves' disease}}
| style="padding: 5px 5px; background: #F5F5F5;" | Present
| style="padding: 5px 5px; background: #F5F5F5;" | Hypoechoic pattern
| style="padding: 5px 5px; background: #F5F5F5;" | ↑
| style="padding: 5px 5px; background: #F5F5F5;" | ↑
| style="padding: 5px 5px; background: #F5F5F5;" | Ophthalmopathy, dermopathy, acropachy
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Toxic nodular goiter}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Multiple nodules
| style="padding: 5px 5px; background: #F5F5F5;" | -
| style="padding: 5px 5px; background: #F5F5F5;" | Hot nodules at thyroid scan
| style="padding: 5px 5px; background: #F5F5F5;" | -
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Toxic adenoma}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Single nodule
| style="padding: 5px 5px; background: #F5F5F5;" | -
| style="padding: 5px 5px; background: #F5F5F5;" | Hot nodule
| style="padding: 5px 5px; background: #F5F5F5;" | -
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Subacute thyroiditis}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Heterogeneous hypoechoic areas
| style="padding: 5px 5px; background: #F5F5F5;" | Reduced/absent flow
| style="padding: 5px 5px; background: #F5F5F5;" | ↓
| style="padding: 5px 5px; background: #F5F5F5;" | Neck pain-fever and<br> elevated inflammatory index
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Painless thyroiditis}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Hypoechoic pattern
| style="padding: 5px 5px; background: #F5F5F5;" | Reduced/absent flow
| style="padding: 5px 5px; background: #F5F5F5;" | ↓
| style="padding: 5px 5px; background: #F5F5F5;" | -
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Amiodarone induced thyroiditis-Type 1}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Diffuse or nodular goiter
| style="padding: 5px 5px; background: #F5F5F5;" | ↓/Normal/↑
| style="padding: 5px 5px; background: #F5F5F5;" | ↓ but higher than in Type 2
| style="padding: 5px 5px; background: #F5F5F5;" | High urinary iodine
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Amiodarone induced thyroiditis-Type 2}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Normal
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | ↓/absent
| style="padding: 5px 5px; background: #F5F5F5;" | High urinary iodine
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Central hyperthyroidism}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Diffuse or nodular goiter
| style="padding: 5px 5px; background: #F5F5F5;" | Normal/↑
| style="padding: 5px 5px; background: #F5F5F5;" | ↑
| style="padding: 5px 5px; background: #F5F5F5;" | Inappropriately normal or high TSH
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Trophoblastic disease}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Diffuse or nodular goiter
| style="padding: 5px 5px; background: #F5F5F5;" | Normal/↑
| style="padding: 5px 5px; background: #F5F5F5;" | ↑
| style="padding: 5px 5px; background: #F5F5F5;" | -
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Factitious thyrotoxicosis}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Variable
| style="padding: 5px 5px; background: #F5F5F5;" | Reduced/absent flow
| style="padding: 5px 5px; background: #F5F5F5;" | ↓
| style="padding: 5px 5px; background: #F5F5F5;" | ↓ serum thyroglobulin
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=1 colspan=1 |{{fontcolor|#FFFFFF|Struma ovarii}}
| style="padding: 5px 5px; background: #F5F5F5;" | Absent
| style="padding: 5px 5px; background: #F5F5F5;" | Variable
| style="padding: 5px 5px; background: #F5F5F5;" | Reduced/absent flow
| style="padding: 5px 5px; background: #F5F5F5;" | ↓
| style="padding: 5px 5px; background: #F5F5F5;" | Abdominal RAIU
|}
==Epidemiology and Demographics==
Graves’ disease is the most common cause of hyperthyroidism.
===Incidence===
*It's annual incidence is about 20 to 50 cases per 100,000 persons.<ref name="pmid25591468">{{cite journal |vauthors=Zimmermann MB, Boelaert K |title=Iodine deficiency and thyroid disorders |journal=Lancet Diabetes Endocrinol |volume=3 |issue=4 |pages=286–95 |year=2015 |pmid=25591468 |doi=10.1016/S2213-8587(14)70225-6 |url=}}</ref>
===Prevalence===
The prevalence of Graves’ disease in 1970s estimated to be 0.4% in the United States.<ref name="pmid5066850">{{cite journal |vauthors=Furszyfer J, Kurland LT, McConahey WM, Woolner LB, Elveback LR |title=Epidemiologic aspects of Hashimoto's thyroiditis and Graves' disease in Rochester, Minnesota (1935-1967), with special reference to temporal trends |journal=Metab. Clin. Exp. |volume=21 |issue=3 |pages=197–204 |year=1972 |pmid=5066850 |doi= |url=}}</ref>
===Age===
*The incidence peaks between 30 and 50 years of age, but people can be affected at any age.
===Race===
*Graves' disease is more common in Caucasians than in Asians.<ref name="pmid1563082">{{cite journal |vauthors=Tellez M, Cooper J, Edmonds C |title=Graves' ophthalmopathy in relation to cigarette smoking and ethnic origin |journal=Clin. Endocrinol. (Oxf) |volume=36 |issue=3 |pages=291–4 |year=1992 |pmid=1563082 |doi= |url=}}</ref>
===Sex===
*Graves' disease is more common among women than mrn. The lifetime risk is 3% for women and 0.5% for men.<ref name="pmid27797318">{{cite journal |vauthors=Smith TJ, Hegedüs L |title=Graves' Disease |journal=N. Engl. J. Med. |volume=375 |issue=16 |pages=1552–1565 |year=2016 |pmid=27797318 |doi=10.1056/NEJMra1510030 |url=}}</ref>
==Risk factors==
The most potent risk factor in the development of Graves' disease is genetic susceptibility. Other risk factors include infections, stress and smoking.
== Natural History, Complications and Prognosis ==
*If left untreated it may lead to serious complications such as, thyroid storm, life threatening arrhythmias, orbitopathies, weight loss and even osteoporosis.
*Cardiac complications are the most important complications of Graves' disease because they are life threatening. [[Heart failure]] and [[atrial fibrillation]] are the most common cardiac complications. Thyroid dermopathy, presents as pretibial [[myxedema]] and acropachy is another complication.<ref name="pmid24766932">{{cite journal |vauthors=Devereaux D, Tewelde SZ |title=Hyperthyroidism and thyrotoxicosis |journal=Emerg. Med. Clin. North Am. |volume=32 |issue=2 |pages=277–92 |year=2014 |pmid=24766932 |doi=10.1016/j.emc.2013.12.001 |url=}}</ref>
*When compared with people older than 60 years with a healthy thyroid, those who are hyperthyroid have three times the risk of atrial fibrillation.<ref name="pmid7935681">{{cite journal |vauthors=Sawin CT, Geller A, Wolf PA, Belanger AJ, Baker E, Bacharach P, Wilson PW, Benjamin EJ, D'Agostino RB |title=Low serum thyrotropin concentrations as a risk factor for atrial fibrillation in older persons |journal=N. Engl. J. Med. |volume=331 |issue=19 |pages=1249–52 |year=1994 |pmid=7935681 |doi=10.1056/NEJM199411103311901 |url=}}</ref><ref name="pmid27811932">{{cite journal |vauthors=Jabbar A, Pingitore A, Pearce SH, Zaman A, Iervasi G, Razvi S |title=Thyroid hormones and cardiovascular disease |journal=Nat Rev Cardiol |volume=14 |issue=1 |pages=39–55 |year=2017 |pmid=27811932 |doi=10.1038/nrcardio.2016.174 |url=}}</ref>
 
Thyroid associated ophtalmopathy must be evaluated in every patient with Graves' disease.<ref name="pmid24766932">{{cite journal |vauthors=Devereaux D, Tewelde SZ |title=Hyperthyroidism and thyrotoxicosis |journal=Emerg. Med. Clin. North Am. |volume=32 |issue=2 |pages=277–92 |year=2014 |pmid=24766932 |doi=10.1016/j.emc.2013.12.001 |url=}}</ref>
 
Thyroid crisis is another life threatening complication of Graves' disease.
==Diagnosis==
*In the presence of relative clinical symptoms and signs for hyperthyroidism, a diagnostic approach must be taken to address accurate diagnosis and start the management.<ref name="pmid22776786">{{cite journal |vauthors=Tozzoli R, Bagnasco M, Giavarina D, Bizzaro N |title=TSH receptor autoantibody immunoassay in patients with Graves' disease: improvement of diagnostic accuracy over different generations of methods. Systematic review and meta-analysis |journal=Autoimmun Rev |volume=12 |issue=2 |pages=107–13 |year=2012 |pmid=22776786 |doi=10.1016/j.autrev.2012.07.003 |url=}}</ref><ref name="pmid">{{cite journal |vauthors=Pedersen IB, Knudsen N, Perrild H, Ovesen L, Laurberg P |title=TSH-receptor antibody measurement for differentiation of hyperthyroidism into Graves' disease and multinodular toxic goitre: a comparison of two competitive binding assays |journal=Clin. Endocrinol. (Oxf) |volume=55 |issue=3 |pages=381–90 |year=2001 |pmid= |doi= |url=}}</ref><ref>{{Cite journal
| author = [[Terry J. Smith]] & [[Laszlo Hegedus]]
| title = Graves' Disease
| journal = [[The New England journal of medicine]]
| volume = 375
| issue = 16
| pages = 1552–1565
| year = 2016
| month = October
| doi = 10.1056/NEJMra1510030
| pmid = 27797318
}}</ref>
Presence of at least one of the following findings in a hyperthyroid patient is definitive for Graves' disease.<ref>{{cite book | last = Shoenfeld | first = Yehuda | title = Diagnostic criteria in autoimmune diseases | publisher = Humana | location = Place of publication not identified | year = 2014 | isbn = 978-1627038584 }}</ref>
* Detectable TSH receptor antibodies (TRAbs) in the serum
* Evidence of ophthalmopathy and/or dermopathy
* Diffuse and increased RAIU
 
 
 
 




Revision as of 15:39, 21 December 2016

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1],Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]

Historical Perspective

Graves disease owes its name to the Irish doctor Randy Danny Graves,[1] who described a case of goiter with exophthalmos in 1835. However, the German Karl Adolph von Basedow independently reported the same constellation of symptoms in 1840. As a result, on the European Continent the term Basedow's disease is more common than Graves' disease.[2][3]

Pathophysiology

Genetic factors, anti thyrotropin receptor antibodies, T cells, B cells and thyroid epithelial cells involvement are the main pathologic features of Graves' disease.

Genetic factors have role as initiating factor include Thyroglobulin, Thyrotropin receptor, HLA-DRβ-Arg74, The protein tyrosine phosphatase nonreceptor type 22 (PTPN22), Cytotoxic T-lymphocyte–associated antigen 4 (CTLA4), CD25, CD40.
Graves' disease is an autoimmune disorder, in which the body produces antibodies to the receptor for thyroid-stimulating hormone (TSH). These are IgG1 subclass of antibodies.[4]

Causes

Graves' disease may be caused by either genetic factors, autoimmune antibodies against thyrotropin receptors, T cells and B cells auto activation and infectious agents.[5][6][4]

Differential Diagnosis

The table below summarizes the list of differential diagnosis for Graves' disease.[7][8][9][10][11]


Cause of thyrotoxicosis TSH receptor Antibodies Thyroid US Color flow Doppler Radioactive iodine uptake/Scan Other features
Graves' disease Present Hypoechoic pattern ↑ ↑ Ophthalmopathy, dermopathy, acropachy
Toxic nodular goiter Absent Multiple nodules - Hot nodules at thyroid scan -
Toxic adenoma Absent Single nodule - Hot nodule -
Subacute thyroiditis Absent Heterogeneous hypoechoic areas Reduced/absent flow ↓ Neck pain-fever and
elevated inflammatory index
Painless thyroiditis Absent Hypoechoic pattern Reduced/absent flow ↓ -
Amiodarone induced thyroiditis-Type 1 Absent Diffuse or nodular goiter ↓/Normal/↑ ↓ but higher than in Type 2 High urinary iodine
Amiodarone induced thyroiditis-Type 2 Absent Normal Absent ↓/absent High urinary iodine
Central hyperthyroidism Absent Diffuse or nodular goiter Normal/↑ ↑ Inappropriately normal or high TSH
Trophoblastic disease Absent Diffuse or nodular goiter Normal/↑ ↑ -
Factitious thyrotoxicosis Absent Variable Reduced/absent flow ↓ ↓ serum thyroglobulin
Struma ovarii Absent Variable Reduced/absent flow ↓ Abdominal RAIU

Epidemiology and Demographics

Graves’ disease is the most common cause of hyperthyroidism.

Incidence

  • It's annual incidence is about 20 to 50 cases per 100,000 persons.[12]

Prevalence

The prevalence of Graves’ disease in 1970s estimated to be 0.4% in the United States.[13]

Age

  • The incidence peaks between 30 and 50 years of age, but people can be affected at any age.

Race

  • Graves' disease is more common in Caucasians than in Asians.[14]

Sex

  • Graves' disease is more common among women than mrn. The lifetime risk is 3% for women and 0.5% for men.[15]

Risk factors

The most potent risk factor in the development of Graves' disease is genetic susceptibility. Other risk factors include infections, stress and smoking.

Natural History, Complications and Prognosis

  • If left untreated it may lead to serious complications such as, thyroid storm, life threatening arrhythmias, orbitopathies, weight loss and even osteoporosis.
  • Cardiac complications are the most important complications of Graves' disease because they are life threatening. Heart failure and atrial fibrillation are the most common cardiac complications. Thyroid dermopathy, presents as pretibial myxedema and acropachy is another complication.[16]
  • When compared with people older than 60 years with a healthy thyroid, those who are hyperthyroid have three times the risk of atrial fibrillation.[17][18]

Thyroid associated ophtalmopathy must be evaluated in every patient with Graves' disease.[16]

Thyroid crisis is another life threatening complication of Graves' disease.

Diagnosis

  • In the presence of relative clinical symptoms and signs for hyperthyroidism, a diagnostic approach must be taken to address accurate diagnosis and start the management.[19][20][21]

Presence of at least one of the following findings in a hyperthyroid patient is definitive for Graves' disease.[22]

  • Detectable TSH receptor antibodies (TRAbs) in the serum
  • Evidence of ophthalmopathy and/or dermopathy
  • Diffuse and increased RAIU




References

  1. ↑ Template:WhoNamedIt
  2. ↑ Template:WhoNamedIt - the history and naming of the disease
  3. ↑ Goiter, Diffuse Toxic at eMedicine
  4. ↑ 4.0 4.1 Weetman AP, Yateman ME, Ealey PA, Black CM, Reimer CB, Williams RC, Shine B, Marshall NJ (1990). "Thyroid-stimulating antibody activity between different immunoglobulin G subclasses". J. Clin. Invest. 86 (3): 723–7. doi:10.1172/JCI114768. PMC 296786. PMID 2168443.
  5. ↑ Tomer Y (2014). "Mechanisms of autoimmune thyroid diseases: from genetics to epigenetics". Annu Rev Pathol. 9: 147–56. doi:10.1146/annurev-pathol-012513-104713. PMC 4128637. PMID 24460189.
  6. ↑ Limbach M, Saare M, Tserel L, Kisand K, Eglit T, Sauer S, Axelsson T, Syvänen AC, Metspalu A, Milani L, Peterson P (2016). "Epigenetic profiling in CD4+ and CD8+ T cells from Graves' disease patients reveals changes in genes associated with T cell receptor signaling". J. Autoimmun. 67: 46–56. doi:10.1016/j.jaut.2015.09.006. PMID 26459776.
  7. ↑ Lambert M, Unger J, De Nayer P, Brohet C, Gangji D (1990). "Amiodarone-induced thyrotoxicosis suggestive of thyroid damage". J. Endocrinol. Invest. 13 (6): 527–30. PMID 2258582.
  8. ↑ Ahmadieh H, Salti I (2013). "Tyrosine kinase inhibitors induced thyroid dysfunction: a review of its incidence, pathophysiology, clinical relevance, and treatment". Biomed Res Int. 2013: 725410. doi:10.1155/2013/725410. PMC 3824811. PMID 24282820.
  9. ↑ Vialettes B, Guillerand MA, Viens P, Stoppa AM, Baume D, Sauvan R, Pasquier J, San Marco M, Olive D, Maraninchi D (1993). "Incidence rate and risk factors for thyroid dysfunction during recombinant interleukin-2 therapy in advanced malignancies". Acta Endocrinol. 129 (1): 31–8. PMID 8351956.
  10. ↑ Jha S, Waghdhare S, Reddi R, Bhattacharya P (2012). "Thyroid storm due to inappropriate administration of a compounded thyroid hormone preparation successfully treated with plasmapheresis". Thyroid. 22 (12): 1283–6. doi:10.1089/thy.2011.0353. PMID 23067331.
  11. ↑ Cohen JH, Ingbar SH, Braverman LE (1989). "Thyrotoxicosis due to ingestion of excess thyroid hormone". Endocr. Rev. 10 (2): 113–24. doi:10.1210/edrv-10-2-113. PMID 2666114.
  12. ↑ Zimmermann MB, Boelaert K (2015). "Iodine deficiency and thyroid disorders". Lancet Diabetes Endocrinol. 3 (4): 286–95. doi:10.1016/S2213-8587(14)70225-6. PMID 25591468.
  13. ↑ Furszyfer J, Kurland LT, McConahey WM, Woolner LB, Elveback LR (1972). "Epidemiologic aspects of Hashimoto's thyroiditis and Graves' disease in Rochester, Minnesota (1935-1967), with special reference to temporal trends". Metab. Clin. Exp. 21 (3): 197–204. PMID 5066850.
  14. ↑ Tellez M, Cooper J, Edmonds C (1992). "Graves' ophthalmopathy in relation to cigarette smoking and ethnic origin". Clin. Endocrinol. (Oxf). 36 (3): 291–4. PMID 1563082.
  15. ↑ Smith TJ, Hegedüs L (2016). "Graves' Disease". N. Engl. J. Med. 375 (16): 1552–1565. doi:10.1056/NEJMra1510030. PMID 27797318.
  16. ↑ 16.0 16.1 Devereaux D, Tewelde SZ (2014). "Hyperthyroidism and thyrotoxicosis". Emerg. Med. Clin. North Am. 32 (2): 277–92. doi:10.1016/j.emc.2013.12.001. PMID 24766932.
  17. ↑ Sawin CT, Geller A, Wolf PA, Belanger AJ, Baker E, Bacharach P, Wilson PW, Benjamin EJ, D'Agostino RB (1994). "Low serum thyrotropin concentrations as a risk factor for atrial fibrillation in older persons". N. Engl. J. Med. 331 (19): 1249–52. doi:10.1056/NEJM199411103311901. PMID 7935681.
  18. ↑ Jabbar A, Pingitore A, Pearce SH, Zaman A, Iervasi G, Razvi S (2017). "Thyroid hormones and cardiovascular disease". Nat Rev Cardiol. 14 (1): 39–55. doi:10.1038/nrcardio.2016.174. PMID 27811932.
  19. ↑ Tozzoli R, Bagnasco M, Giavarina D, Bizzaro N (2012). "TSH receptor autoantibody immunoassay in patients with Graves' disease: improvement of diagnostic accuracy over different generations of methods. Systematic review and meta-analysis". Autoimmun Rev. 12 (2): 107–13. doi:10.1016/j.autrev.2012.07.003. PMID 22776786.
  20. ↑ Pedersen IB, Knudsen N, Perrild H, Ovesen L, Laurberg P (2001). "TSH-receptor antibody measurement for differentiation of hyperthyroidism into Graves' disease and multinodular toxic goitre: a comparison of two competitive binding assays". Clin. Endocrinol. (Oxf). 55 (3): 381–90.
  21. ↑ Terry J. Smith & Laszlo Hegedus (2016). "Graves' Disease". The New England journal of medicine. 375 (16): 1552–1565. doi:10.1056/NEJMra1510030. PMID 27797318. Unknown parameter |month= ignored (help)
  22. ↑ Shoenfeld, Yehuda (2014). Diagnostic criteria in autoimmune diseases. Place of publication not identified: Humana. ISBN 978-1627038584.

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