Graves' disease differential diagnosis: Difference between revisions

Jump to navigation Jump to search
No edit summary
 
(17 intermediate revisions by 3 users not shown)
Line 1: Line 1:
__NOTOC__
__NOTOC__
{{Graves' disease}}
[[Image:Home_logo1.png|right|250px|link=https://www.wikidoc.org/index.php/Graves%27_disease]]
{{CMG}};{{AE}}{{MehdiP}}
{{CMG}};{{AE}}{{MehdiP}}
==Overview==
==Overview==
Graves' disease must be differentiated from other causes of hyperthyroidism. They include Thyroiditis, exogenous and ectopic hyperthyroidism, hashitoxicosis, toxic adenoma and toxic multi nodular goiter.


==Differentiating Graves' disease from other Diseases==
==Differentiating Graves' disease from other Diseases==


 
This table describes differential diagnosis for Graves' disease and the next table shows the the distinguishing features of diseases that may mimic Graves' diseases.
 
 


{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
{| style="border: 0px; font-size: 90%; margin: 3px;" align=center
Line 16: Line 15:
| style="background: #4479BA; padding: 5px 5px;" rowspan=5 colspan=1 |{{fontcolor|#FFFFFF|Thyroiditis}}
| style="background: #4479BA; padding: 5px 5px;" rowspan=5 colspan=1 |{{fontcolor|#FFFFFF|Thyroiditis}}
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Direct chemical toxicity with inflammation}}
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Direct chemical toxicity with inflammation}}
| style="padding: 5px 5px; background: #F5F5F5;" | Amiodarone, sunitinib, pazopanib, axitinib, and other tyrosine kinase inhibitors may also be associated with a destructive thyroiditis.
| style="padding: 5px 5px; background: #F5F5F5;" | [[Amiodarone]], [[sunitinib]], [[pazopanib]], [[axitinib]], and other [[tyrosine kinase inhibitors]] may also be associated with a destructive [[thyroiditis]].<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>
|-
|-
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Radiation thyroiditis}}
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Radiation thyroiditis}}
| style="padding: 5px 5px; background: #F5F5F5;" | Patients who treated with radioiodine, may develops thyroid pain and tenderness 5 to 10 days later, due to radiation-induced injury and necrosis of thyroid follicular cells and associated inflammation.
| style="padding: 5px 5px; background: #F5F5F5;" | Patients treated with [[radioiodine]] may develop thyroid pain and tenderness 5 to 10 days later, due to radiation-induced injury and necrosis of thyroid follicular cells and associated [[inflammation]].
|-
|-
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Drugs that interfere with the immune system}}
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Drugs that interfere with the immune system}}
| style="padding: 5px 5px; background: #F5F5F5;" | Interferon-alfa is well known for associated thyroid abnormality. It mostly lead to development of de novo antithyroid antibodies.
| style="padding: 5px 5px; background: #F5F5F5;" | [[Interferon alfa-2a clinical pharmacology|Interferon-alfa]] is a well known cause of thyroid abnormality. It mostly leads to the development of de novo antithyroid [[antibodies]].<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>
|-
|-
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Lithium}}
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Lithium}}
| style="padding: 5px 5px; background: #F5F5F5;" | Patients treated with lithium are at high risk to develop painless thyroiditis and Graves' disease.
| style="padding: 5px 5px; background: #F5F5F5;" | Patients treated with [[lithium]] are at a high risk of developing painless thyroiditis and Graves' disease.
|-
|-
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Palpation thyroiditis}}
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Palpation thyroiditis}}
| style="padding: 5px 5px; background: #F5F5F5;" | Manipulation of thyroid gland during thyroid biopsy or neck surgery and vigorous palpation during physical examination may cause transient hyperthyroidism.
| style="padding: 5px 5px; background: #F5F5F5;" | Manipulation of the thyroid gland during thyroid [[biopsy]] or neck surgery and vigorous palpation during physical examination may cause transient [[hyperthyroidism]].
|-
|-
| style="background: #4479BA; padding: 5px 5px;" rowspan=4 colspan=1 |{{fontcolor|#FFFFFF|Exogenous and ectopic hyperthyroidism }}
| style="background: #4479BA; padding: 5px 5px;" rowspan=4 colspan=1 |{{fontcolor|#FFFFFF|Exogenous and ectopic hyperthyroidism }}
Line 38: Line 37:
|-
|-
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Struma ovarii}}
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Struma ovarii}}
| style="padding: 5px 5px; background: #F5F5F5;" |Functioning thyroid tissue is present in an ovarian neoplasm.
| style="padding: 5px 5px; background: #F5F5F5;" |Functioning thyroid tissue is present in an [[ovarian neoplasm]].
|-
|-
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Functional thyroid cancer metastases}}
| style="padding: 5px 5px; background: #4479BA;" | {{fontcolor|#FFFFFF|Functional thyroid cancer metastases}}
| style="padding: 5px 5px; background: #F5F5F5;" |Large bony metastases from widely metastatic follicular thyroid cancer cause symptomatic hyperthyroidism.
| style="padding: 5px 5px; background: #F5F5F5;" |Large bony [[metastases]] from widely metastatic [[follicular thyroid cancer]] cause symptomatic hyperthyroidism.
|-
|-
| colspan="2" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Hashitoxicosis }}
| colspan="2" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Hashitoxicosis }}
|It is autoimmune thyroid disease who initially present with hyperthyroidism and a high radioiodine uptake caused by TSH-receptor antibodies similar to Graves' disease followed by the development of hypothyroidism due to infiltration of thyroid gland with lymphocytes and resultant autoimmune-mediated destruction of thyroid tissue similar to chronic lymphocytic thyroiditis.<ref name="pmid5171000">{{cite journal |vauthors=Fatourechi V, McConahey WM, Woolner LB |title=Hyperthyroidism associated with histologic Hashimoto's thyroiditis |journal=Mayo Clin. Proc. |volume=46 |issue=10 |pages=682–9 |year=1971 |pmid=5171000 |doi= |url=}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" |It is an autoimmune thyroid disease that initially presents with hyperthyroidism and a high radioiodine uptake caused by TSH-receptor antibodies similar to Graves' disease. It is then followed by the development of hypothyroidism due to the infiltration of thyroid gland with [[Lymphocyte|lymphocytes]] and the resultant autoimmune-mediated destruction of thyroid tissue, similar to chronic lymphocytic thyroiditis.<ref name="pmid5171000">{{cite journal |vauthors=Fatourechi V, McConahey WM, Woolner LB |title=Hyperthyroidism associated with histologic Hashimoto's thyroiditis |journal=Mayo Clin. Proc. |volume=46 |issue=10 |pages=682–9 |year=1971 |pmid=5171000 |doi= |url=}}</ref>
|-  
|-  
| colspan="2" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Toxic adenoma and toxic multinodular goiter}}
| colspan="2" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Toxic adenoma and toxic multinodular goiter}}
|Toxic adenoma and toxic multinodular goiter are result of focal/diffuse hyperplasia of thyroid follicular cells independent to TSH regulation. Finding single or multiple nodules in physical examination or thyroid scan.<ref name="pmid2040867">{{cite journal |vauthors=Laurberg P, Pedersen KM, Vestergaard H, Sigurdsson G |title=High incidence of multinodular toxic goitre in the elderly population in a low iodine intake area vs. high incidence of Graves' disease in the young in a high iodine intake area: comparative surveys of thyrotoxicosis epidemiology in East-Jutland Denmark and Iceland |journal=J. Intern. Med. |volume=229 |issue=5 |pages=415–20 |year=1991 |pmid=2040867 |doi= |url=}}</ref>
| style="padding: 5px 5px; background: #F5F5F5;" |Toxic adenoma and [[toxic multinodular goiter]] are results of focal/diffuse [[hyperplasia]] of thyroid follicular cells independent of TSH regulation. Findings of single or multiple [[nodules]] are seen on physical examination or thyroid scan.<ref name="pmid2040867">{{cite journal |vauthors=Laurberg P, Pedersen KM, Vestergaard H, Sigurdsson G |title=High incidence of multinodular toxic goitre in the elderly population in a low iodine intake area vs. high incidence of Graves' disease in the young in a high iodine intake area: comparative surveys of thyrotoxicosis epidemiology in East-Jutland Denmark and Iceland |journal=J. Intern. Med. |volume=229 |issue=5 |pages=415–20 |year=1991 |pmid=2040867 |doi= |url=}}</ref>
|-
|-
| colspan="2" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Iodine-induced hyperthyroidism  }}
| colspan="2" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Iodine-induced hyperthyroidism  }}
|It is uncommon but, can develop after an iodine load, such as administration of contrast agents used for angiography or computed tomography (CT) or iodine-rich drugs such as amiodarone.
| style="padding: 5px 5px; background: #F5F5F5;" |It is uncommon but can develop after an iodine load, such as administration of contrast agents used for angiography or computed tomography (CT), or iodine-rich drugs such as [[amiodarone]].
|-
|-
| colspan="2" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Trophoblastic disease and germ cell tumors }}
| colspan="2" rowspan="1" style="background: #4479BA; padding: 5px 5px;" |{{fontcolor|#FFFFFF|Trophoblastic disease and germ cell tumors }}
|
| style="padding: 5px 5px; background: #F5F5F5;" |[[Thyroid-stimulating hormone]] and [[HCG]] have a common alpha-subunit and a beta-subunit with considerable homology. As a result, [[HCG]] has weak thyroid-stimulating activity and high titer HCG may mimic hyperthyroidism.<ref name="pmid19605510">{{cite journal |vauthors=Oosting SF, de Haas EC, Links TP, de Bruin D, Sluiter WJ, de Jong IJ, Hoekstra HJ, Sleijfer DT, Gietema JA |title=Prevalence of paraneoplastic hyperthyroidism in patients with metastatic non-seminomatous germ-cell tumors |journal=Ann. Oncol. |volume=21 |issue=1 |pages=104–8 |year=2010 |pmid=19605510 |doi=10.1093/annonc/mdp265 |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;" | +
| 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;" | -
| 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;" | -
| 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;" | -
| 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;" | -
| 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;" | -
| 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;" | -
| 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;" | -
| 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;" | -
| 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;" | -
| 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;" | -
| 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
|}
|}



Latest revision as of 18:25, 25 February 2019

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

Overview

Graves' disease must be differentiated from other causes of hyperthyroidism. They include Thyroiditis, exogenous and ectopic hyperthyroidism, hashitoxicosis, toxic adenoma and toxic multi nodular goiter.

Differentiating Graves' disease from other Diseases

This table describes differential diagnosis for Graves' disease and the next table shows the the distinguishing features of diseases that may mimic Graves' diseases.

Disease Findings
Thyroiditis Direct chemical toxicity with inflammation Amiodarone, sunitinib, pazopanib, axitinib, and other tyrosine kinase inhibitors may also be associated with a destructive thyroiditis.[1][2]
Radiation thyroiditis Patients treated with radioiodine may develop thyroid pain and tenderness 5 to 10 days later, due to radiation-induced injury and necrosis of thyroid follicular cells and associated inflammation.
Drugs that interfere with the immune system Interferon-alfa is a well known cause of thyroid abnormality. It mostly leads to the development of de novo antithyroid antibodies.[3]
Lithium Patients treated with lithium are at a high risk of developing painless thyroiditis and Graves' disease.
Palpation thyroiditis Manipulation of the thyroid gland during thyroid biopsy or neck surgery and vigorous palpation during physical examination may cause transient hyperthyroidism.
Exogenous and ectopic hyperthyroidism Factitious ingestion of thyroid hormone The diagnosis is based upon the clinical features, laboratory findings, and 24-hour radioiodine uptake.[4]
Acute hyperthyroidism from a levothyroxine overdose The diagnosis is based upon the clinical features, laboratory findings, and 24-hour radioiodine uptake.[5]
Struma ovarii Functioning thyroid tissue is present in an ovarian neoplasm.
Functional thyroid cancer metastases Large bony metastases from widely metastatic follicular thyroid cancer cause symptomatic hyperthyroidism.
Hashitoxicosis It is an autoimmune thyroid disease that initially presents with hyperthyroidism and a high radioiodine uptake caused by TSH-receptor antibodies similar to Graves' disease. It is then followed by the development of hypothyroidism due to the infiltration of thyroid gland with lymphocytes and the resultant autoimmune-mediated destruction of thyroid tissue, similar to chronic lymphocytic thyroiditis.[6]
Toxic adenoma and toxic multinodular goiter Toxic adenoma and toxic multinodular goiter are results of focal/diffuse hyperplasia of thyroid follicular cells independent of TSH regulation. Findings of single or multiple nodules are seen on physical examination or thyroid scan.[7]
Iodine-induced hyperthyroidism It is uncommon but can develop after an iodine load, such as administration of contrast agents used for angiography or computed tomography (CT), or iodine-rich drugs such as amiodarone.
Trophoblastic disease and germ cell tumors Thyroid-stimulating hormone and HCG have a common alpha-subunit and a beta-subunit with considerable homology. As a result, HCG has weak thyroid-stimulating activity and high titer HCG may mimic hyperthyroidism.[8]


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

References

  1. 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.
  2. 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.
  3. 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.
  4. 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.
  5. 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.
  6. Fatourechi V, McConahey WM, Woolner LB (1971). "Hyperthyroidism associated with histologic Hashimoto's thyroiditis". Mayo Clin. Proc. 46 (10): 682–9. PMID 5171000.
  7. Laurberg P, Pedersen KM, Vestergaard H, Sigurdsson G (1991). "High incidence of multinodular toxic goitre in the elderly population in a low iodine intake area vs. high incidence of Graves' disease in the young in a high iodine intake area: comparative surveys of thyrotoxicosis epidemiology in East-Jutland Denmark and Iceland". J. Intern. Med. 229 (5): 415–20. PMID 2040867.
  8. Oosting SF, de Haas EC, Links TP, de Bruin D, Sluiter WJ, de Jong IJ, Hoekstra HJ, Sleijfer DT, Gietema JA (2010). "Prevalence of paraneoplastic hyperthyroidism in patients with metastatic non-seminomatous germ-cell tumors". Ann. Oncol. 21 (1): 104–8. doi:10.1093/annonc/mdp265. PMID 19605510.

Template:WH Template:WS