Editing Hypothyroidism (section)

==Causes==
Hypothyroidism is caused by inadequate function of the gland itself (primary hypothyroidism), inadequate stimulation by [[thyroid-stimulating hormone]] from the [[pituitary gland]] (secondary hypothyroidism), or inadequate release of [[thyrotropin-releasing hormone]] from the brain's [[hypothalamus]] (tertiary hypothyroidism).<ref name="Garber" /><ref name="Gaitonde2012">{{cite journal | vauthors = Gaitonde DY, Rowley KD, Sweeney LB | title = Hypothyroidism: an update | journal = American Family Physician | volume = 86 | issue = 3 | pages = 244–51 | date = August 2012 | pmid = 22962987 | url = https://www.aafp.org/linked_out?pmid=22962987 }}{{Dead link|date=August 2024 |bot=InternetArchiveBot |fix-attempted=yes }}</ref> Primary hypothyroidism is about a thousandfold more common than central hypothyroidism.<ref name="Persani2012" /> Central hypothyroidism is the name used for secondary and tertiary hypothyroidism since the hypothalamus and pituitary gland are at the center of thyroid hormone control.

[[Iodine deficiency]] is the most common cause of primary hypothyroidism and [[endemic goiter]] worldwide.<ref name=Garber/><ref name=Chakera/> In areas of the world with sufficient dietary iodine, hypothyroidism is most commonly caused by the autoimmune disease [[Hashimoto's thyroiditis]] (chronic autoimmune thyroiditis).<ref name=Garber/><ref name=Chakera/> Hashimoto's may be associated with a goiter. It is characterized by infiltration of the thyroid gland with [[T cell|T lymphocytes]] and [[autoantibody|autoantibodies]] [[Anti-thyroid autoantibodies|against specific thyroid antigens]] such as [[thyroid peroxidase]], [[thyroglobulin]] and the [[thyrotropin receptor|TSH receptor]].<ref name=Garber/>

After women give birth, about 5% develop [[postpartum thyroiditis]] which can occur up to nine months afterwards.<ref name="Stagnaro2012"/> This is characterized by a short period of [[hyperthyroidism]] followed by a period of hypothyroidism; 20–40% remain permanently hypothyroid.<ref name="Stagnaro2012">{{cite journal | vauthors = Stagnaro-Green A | title = Approach to the patient with postpartum thyroiditis | journal = The Journal of Clinical Endocrinology and Metabolism | volume = 97 | issue = 2 | pages = 334–42 | date = February 2012 | pmid = 22312089 | doi = 10.1210/jc.2011-2576 | type = Review | doi-access = free }}</ref>

[[Hashimoto's thyroiditis|Autoimmune thyroiditis (Hashimoto's)]] is associated with other [[autoimmune disease|immune-mediated diseases]] such as [[diabetes mellitus type 1]], [[pernicious anemia]], [[myasthenia gravis]], [[celiac disease]], [[rheumatoid arthritis]] and [[systemic lupus erythematosus]].<ref name=Garber/> It may occur as part of [[autoimmune polyendocrine syndrome]] ([[Autoimmune polyendocrine syndrome type 1|type 1]] and [[Autoimmune polyendocrine syndrome type 2|type 2]]).<ref name=Garber/>

[[Iatrogenesis|Iatrogenic]] hypothyroidism can be surgical (a result of [[thyroidectomy]], usually for [[thyroid nodule]]s or [[Thyroid cancer|cancer]]) or following [[radioiodine]] ablation (usually for [[Graves' disease]]).

{|class="wikitable" style = "margin-left:15px; text-align:center"
! Type of hypothyroidism
! Causes
|-
| Primary hypothyroidism<ref name=Garber/>
| Iodine deficiency (developing countries), autoimmune thyroiditis, [[subacute granulomatous thyroiditis]], [[subacute lymphocytic thyroiditis]], [[postpartum thyroiditis]], previous [[thyroidectomy]], [[acute infectious thyroiditis]],<ref name="Shrestha2015">{{cite book |last1=Shrestha |first1=ST |last2=Hennessey |first2=J |title=Acute and Subacute, and Riedel's Thyroiditis |date=December 2015 |publisher=MDText.com, Inc |pmid=25905408 |url=https://www.ncbi.nlm.nih.gov/books/NBK285553/}}</ref> previous [[Iodine-131|radioiodine]] treatment, previous [[external beam radiotherapy]] to the neck<br />Medication: [[Lithium pharmacology|lithium]]-based [[mood stabilizer]]s, [[amiodarone]], [[interferon alpha]], [[Tyrosine-kinase inhibitor|tyrosine kinase inhibitors]] such as [[sunitinib]]
|-
| Central hypothyroidism<ref name=Persani2012/>
| Lesions compressing the pituitary ([[pituitary adenoma]], [[craniopharyngioma]], [[meningioma]], [[glioma]], [[Rathke's cleft cyst]], [[metastasis]], [[empty sella syndrome|empty sella]], [[intracranial aneurysm|aneurysm]] of the [[internal carotid artery]]), surgery or radiation to the pituitary, drugs, injury, vascular disorders ([[pituitary apoplexy]], [[Sheehan syndrome]], [[subarachnoid hemorrhage]]), autoimmune diseases ([[lymphocytic hypophysitis]], polyglandular disorders), infiltrative diseases (iron overload due to [[hemochromatosis]] or [[Beta-thalassemia|thalassemia]], [[neurosarcoidosis]], [[Langerhans cell histiocytosis]]), particular inherited congenital disorders, and infections ([[tuberculosis]], [[mycosis|mycoses]], [[syphilis]])
|-
| [[Congenital hypothyroidism]]<ref name="Donaldson2013">{{cite journal | vauthors = Donaldson M, Jones J | title = Optimising outcome in congenital hypothyroidism; current opinions on best practice in initial assessment and subsequent management | journal = Journal of Clinical Research in Pediatric Endocrinology | volume = 5 Suppl 1 | issue = 4 | pages = 13–22 | year = 2013 | pmid = 23154163 | pmc = 3608009 | doi = 10.4274/jcrpe.849 | type = Review }}</ref>
| [[Thyroid dysgenesis]] (75%), [[thyroid dyshormonogenesis]] (20%), maternal antibody or radioiodine transfer<br />Syndromes: mutations (in ''[[GNAS complex locus]]'', ''[[PAX8]]'', ''[[NK2 homeobox 1|TTF-1/NKX2-1]]'', ''[[FOXE1|TTF-2/FOXE1]]''), [[Pendred's syndrome]] (associated with [[sensorineural hearing loss]])<br />Transiently: due to maternal iodine deficiency or excess, anti-TSH receptor antibodies, certain congenital disorders, neonatal illness<br />Central: pituitary dysfunction (idiopathic, [[septo-optic dysplasia]], deficiency of ''[[Pituitary-specific positive transcription factor 1|PIT1]]'', isolated TSH deficiency)
|}