Thyroid gland
Anatomy & development
* blood supply: ext. carotid a. -> superior thyroid artery
subclavian a. -> inferior thyroid artery
12-20g, highly vascular
medullary C cell : calcitonin»ý»ê
* ¹ß»ý
pharyngeal epitheliumÀÇ evagination
parathyroid gland : 3rd & 4th pharyngeal pouch¿¡¼ migration
fetal thyroid´Â ÀӽŠ10ÁÖ¿¡ iodine concentration & organification´É·Â ȹµæ
* transcription factor : Tg, TPO, NIS, TSH-R¿Í °°Àº thyroid-specific gene induction
Thyroid axis regulation
ant. pituitary thyrotrope cell¿¡¼ TSHºÐºñ : ¥á, ¥â subunits
¥á subunit : ´Ù¸¥ glycoprotein hormone(LH, FSH, hCG)¿Í À¯»ç
¥â subunit : TSH¿¡¸¸ À¯ÀÏ
Hormone synthesis, metabolism, and action
1. ÇÕ¼º
I- ----> I- ----> I ----> coupling --> release
(trapping) (organification)
1) Iodine metabolism and transport
iodide uptake normal : 10-25%, Graves' ds: 70-90%
NIS(Na+/I- symporter)¿¡ ÀÇÇØ ¸Å°³µÊ
iodine deficiency area¿¡¼ goiter, ½ÉÇϸé hypothyroidism, cretinismÀÌ ¹ß»ýÇÒ °¡´É¼ºÀÌ
³ô´Ù.
cf. cretinism : ¾ÆÀÌ¿¡°Ô¼ thyroid hormone or iodineÀÌ °ø±ÞµÇÁö ¾Ê¾ÒÀ» ¶§ mental &
growth retardationÀÌ ¹ß»ý
* ÇÏ·ç Çʿ䷮: ¼ºÀÎ 150 ug/d, ¾ÆÀÌ 90-120 ug/d, ÀÓ»êºÎ 200 ug/d
2) organification, coupling, storage, release
organification: TPO¿¡ ÀÇÇØ I- ¡æ I·Î oxidation
Tg + iodine => MIT, DIT
coupling: T3, T4
cf. organification & couplingÀ» blockÇÏ´Â antithyroid drug
: PTU, methymazole, mercaptoimidazole
release blocking agent: lithium, dexamethasone
3) TSH action
TSH-R(seven-transmembrane GPCR)À» ÅëÇÏ¿© thyroid functionÀ» Á¶ÀýÇÑ´Ù.
TSH-R´Â stimulatory G proteinÀÇ ¥á subunit(Gs¥á)¿Í ¿¬°áµÇ¾î adenylate cyclase¸¦
Ȱ¼ºÈ½Ã۰í cAMP»ý»êÀ» Áõ°¡½ÃŲ´Ù.
TSH´Â ¶ÇÇÑ phospholipase C¸¦ activation½ÃÄÑ phosphatidylinositol turnover¸¦ ÀÚ±ØÇÑ´Ù.
4) È£¸£¸ó ÇÕ¼º°ú ºÐºñ¿¡ ¿µÇâÀ» ¹ÌÄ¡´Â ÀÎÀÚ
TSH°¡ dominant hormonal regulatorÁö¸¸ ±× ¿Ü¿¡ ´Ù¾çÇÑ growth factor°¡ thyroid hormone
ÇÕ¼º¿¡ ¿µÇâÀ» ¹ÌÄ£´Ù.
: IGF-I, EGF, TGF-¥â, endothelin, various cytokines
¿¹¸¦ µé¸é, acromegaly¿¡¼ growth hormone°ú IGF-IÀÇ Áõ°¡´Â goiter¸¦ µ¿¹ÝÇϱ⵵ Çϰí,
multinodular goiterÀÇ ¼±ÇàÀÎÀÚ°¡ µÇ±âµµ ÇÑ´Ù.
¾î¶² cytokineµéÀº autoimmune thyroid disease¿Í °ü·ÃÇÏ¿© thyroid growth¸¦ ÀÏÀ¸Å°±âµµ
ÇÏ°í ¶Ç´Ù¸¥ °ÍµéÀº apoptosis¸¦ ÀÏÀ¸Å²´Ù. iodineÀº thyroid functionÀÇ important
regulatorÀε¥ ¿¹¸¦ µé¾î iodine deficiency¶§ thyroid blood flow°¡ Áõ°¡Çϰí NIS¿¡ ÀÇÇØ
uptake¸¦ ÀÚ±ØÇÑ´Ù.
iodine°ú´Ù½Ã ÀϽÃÀûÀ¸·Î thyroid iodide organificationÀ» ¾ïÁ¦Çϴµ¥ ÀÌ Çö»óÀ»
"Wolff-Chaikoff effect"¶ó Çϸç thyrotoxic crisisÄ¡·á¿¡ À̿밡´ÉÇÏ´Ù.
2. Thyroid hormone transport and metabolism
1) serum binding proteins
T4´Â T3º¸´Ù 20¹è ´õ ¸¹ÀÌ ºÐºñµÈ´Ù. µÑ´Ù TBG, transthyretin(TTR=thyroxine-binding
prealbumin, TBPA)¿Í °°Àº plasma protein°ú °áÇÕÇÏ¿© ¼øÈ¯ÇÑ´Ù.
TBG³óµµ´Â ¸Å¿ì ³·Áö¸¸(1-2mg/dL) high affinity(T4>T3)°¡ ÀÖ¾î hormoneÀº ´ë·« 80%°¡
°áÇյǾî ÀÖ´Ù. AlbuminÀº thyroid hormone¿¡ ´ëÇÑ affinity°¡ ³·Áö¸¸ ³óµµ°¡ ³ô´Ù(¡3.5
g/dL).
albuminÀº T4ÀÇ 10%, T3¿Í´Â 30%Á¤µµ °áÇյǾî ÀÖ´Ù.
¿©·¯ °¡Áö binding proteinÀÇ È¿°ú°¡ º¹ÇÕÀûÀ¸·Î ÀÛ¿ëÇÒ ¶§ ´ë·« T4ÀÇ 99.98%, T3ÀÇ 99.7%
°¡ protein°ú °áÇÕµÈ ÇüÅ·ΠÀÖ´Ù. T3°¡ T4º¸´Ù ´Ù¼Ò ´À½¼ÇÏ°Ô °áÇÕÇϹǷΠfree T3°¡ free
T4º¸´Ù ¸¹´Ù.
2) dysalbuminemic hyperthyroxinemia
X-linked TBG deficiency¶§ total T4 & T3 levelÀº ¸Å¿ì ³·´Ù. ±×·¯³ª free hormoneÀº Á¤»ó
À̸ç ȯÀÚ´Â euthyroid & normal TSH levelÀ» °®´Â´Ù.
estrogen°ú °°ÀÌ TBG levelÀÌ Áõ°¡µÈ °æ¿ì¿¡µµ free T3, T4´Â Á¤»óÀÌ´Ù.
TBG, TTR, and albuminÀÇ T4 and/or T3 affinity°¡ Áõ°¡ÇÑ °æ¿ì¿¡ euthyroid
hyperthyroxinemia or familial dysalbuminemic hyperthyroixinemia(FDH)¸¦ ÀÏÀ¸Å²´Ù.
À̺´Àº total T4 and/or T3´Â
Áõ°¡µÇ¾î ÀÖÀ¸³ª free hormone levelÀº Á¤»óÀÌ´Ù.
3) deiodinases
¨ç T4 -> T3(30%), rT3(40%), liver¿¡¼ conjugationµÇ¾î bile·Î ¹è¼³(20%)
¨è T3: thyroid gland¿¡¼ ÇÕ¼º(20%)
T4·ÎºÎÅÍ Àüȯ(80%)
monodeiodinationµÇ¾î T4->T3·Î ÀüȯµÈ´Ù.
T3´Â rapid clearance(1ÀÏ), T4´Â slow clearance(7ÀÏ)
* T4 -> T3 ¾ïÁ¦
: fasting, systemic illness or acute trauma,
oral contrast agents,
drug(PTU, propranolol amiodarone, glucocorticoid)
3. Thyroid hormone action
1) nuclear thyroid hormone receptors
thyroid hormone receptor(TRs) ¥á,¥â
µÑ´Ù ¸ðµç Á¶Á÷¿¡ ÀÖÀ¸³ª ¾çÀº ´Ù¼Ò Â÷À̰¡ Àִµ¥
TR¥á´Â brain, kidney, gonads, muscle, and heart¿¡ ÁÖ·Î ÀÖ°í
TR¥â´Â pituitary, liver¿¡ ¸¹´Ù.
TRsÀº central DNA-binding domain & C-terminal ligand-binding domainÀ» °¡Áö°í ÀÖ´Ù.
ÀÌ´Â thyroid response elements(TREs)¶ó´Â ƯÁ¤ DNA sequences(target geneÀÇ
promotor regions)¿¡ °áÇÕÇÑ´Ù.
thyroid hormoneÀº TR¥á, TR¥â¿¡ ¸ðµÎ °°Àº Á¤µµÀÇ Ä£È·ÂÀ¸·Î °áÇÕÇÏÁö¸¸ T3°¡ T4º¸´Ù
10-15¹è ´õ Å« ģȷÂÀ¸·Î °áÇÕÇÏ¿© Áõ°¡µÈ hormonal potency¸¦ ³ªÅ¸³½´Ù.
2) thyroid hormone resistance
autosomal dominant disorder·Î TR¥â receptor gene mutationÀ¸·Î ¹ß»ýÇÑ´Ù.
free thyroid hormone & TSH°¡ ºñÁ¤»óÀûÀ¸·Î Áõ°¡µÇ¾î ÀÖ´Ù.
Ưº°ÇÑ Ä¡·á´Â ÇÊ¿ä¾ø´Ù.
Áø´ÜÀÇ ¸ñÀûÀº hyperthyroidismÀ¸·Î ¿ÀÀÎÇÏ¿© ºÎÀûÀýÇÑ Ä¡·á¸¦ ÇÏ´Â °ÍÀ» ¹æÁöÇϴµ¥
ÀÖ´Ù.
Physical examination
* Pemberton's sign : large retrosternal goiter°¡ ÀÖÀ» ¶§ ÆÈÀ» µé¸é ¸ñÀ§·Î venous
congestion°ú È£Èí°ï¶õÀÌ ÀϾ´Â Çö»ó
Laboratory evaluation
1. Thyroid hormone ÃøÁ¤
4¼¼´ë TSH IRMA(immunoradiometric assay)´Â TSH levelÀ» 0.004 mU/LÀÌÇϱîÁö ÃøÁ¤°¡´É
Çϳª ½ÇÁ¦ ÀÓ»ó¿¡¼´Â 0.1 mU/LÀÌÇϱîÁö ÃøÁ¤°¡´ÉÇÑ ¹Î°¨µµ¸é ÃæºÐÇÏ´Ù.
serum total T4 & total T3¿¡ ´ëÇØ radioimmunoassay°¡ ³Î¸® »ç¿ëµÇ´Âµ¥ total T3 & T4´Â
¸¹Àº ÀÎÀÚ(illness, medications, genetic factors)ÀÇ ¿µÇâÀ» ¹Þ´Â´Ù. ±×·¯¹Ç·Î
free(=unbound) hormone levelÀ» ÃøÁ¤ÇÏ´Â °ÍÀÌ ´õ À¯¿ëÇÏ´Ù. Free thyroid hormone level
À» °£Á¢ÀûÀ¸·Î ÃøÁ¤ÇÏ´Â ¹æ¹ýÀ¸·Î total T4 or T3 ³óµµ ¹× THBR(thyroid hormone binding
ratio)·Î free T3 or free T4 index¸¦ °è»êÇÏ´Â ¹æ¹ýÀÌ Àִµ¥ THBRÀº T3-resin uptake test¸¦
ÅëÇØ ±¸ÇÑ´Ù.
total thyroid hormone levelÀº TBG°¡ Áõ°¡ÇÒ¶§ Áõ°¡Çϰí, TBG°¡ °¨¼ÒÇÒ ¶§ °¨¼ÒÇÑ´Ù.
TBG¡è: pregnancy, oral contraceptives, hormone replacement, tamoxifen
TBG¡é: androgen, nephrotic syndrome
´ëºÎºÐ thyrotoxicosis¸¦ È®ÁøÇϴµ¥ free T4 levelÇϳª·Î ÃæºÐÇÏ´Ù. T3 levelÀÌ Áõ°¡µÈ °æ¿ì
´Â 2-5%¿¡ ºÒ°úÇÏ´Ù(T3 thyrotoxicosis). ±×·¯¹Ç·Î free T3 levelÀº TSH°¡ ¾ïÁ¦µÈ ȯÀÚ¿¡¼
ÃøÁ¤ÇØ¾ß ÇÏÁö¸¸ normal free T4 levelÀ» º¸À϶§´Â ÃøÁ¤ÇÒ Çʿ䰡 ¾ø´Ù. free T3 levelÀº
hypothyroidismȯÀÚÀÇ 25%¿¡¼ Á¤»óÀ̹ǷΠÀÌ·± °æ¿ì¿¡ À¯¿ëÇÑ Á¤º¸¸¦ Á¦°øÇÏÁö ¸øÇÑ´Ù.
hypothalamic-pituitary disease·Î ÀÎÇÑ secondary hypothyroidismÀº ´Ù¾çÇÑ TSH levelÀ»
º¸À̱⠶§¹®¿¡ pituitary disease°¡ Àְųª ÀǽɵǴ °æ¿ì¿¡ thyroid functionÀ» Æò°¡ÇÔ¿¡
ÀÖ¾î TSH¸¦ »ç¿ëÇØ¼´Â ¾ÈµÈ´Ù.
<Âü°í>
* total T3 : 70-190 ng/dL, total T4: 5-12 ug/dL, TSH 0.4-5 uU/ml
* T3 resin uptake(T3RU) Á¤»ó 25-30%
TBG°¡ ÀÏÁ¤ÇÏ´Ù°í °¡Á¤Çϸé hyperthyroidism½Ã thyroid homoneºÐºñ°¡ Áõ°¡ÇϹǷÎ
T3RU°¡ Áõ°¡ÇÏ°í ¹Ý´ë·Î hypothyroidism¶§´Â °¨¼ÒÇÏ°Ô µÈ´Ù.
ÃøÁ¤¹ýÀÌ °£´ÜÇÏ°í °©»ó¼± ±â´É»óŸ¦ ºñ±³Àû Àß ¹Ý¿µÇÑ´Ù´Â ÀåÁ¡ÀÌ ÀÖÀ¸³ª
TBGÀÇ ¾ç¿¡ µû¶ó Àý´ëÀû ¿µÇâÀ» ¹Þ°í, T3, T4ÀÇ Á÷Á¢ ÃøÁ¤ÀÌ ¾Æ´Ï¹Ç·Î °£Á¢ÀûÀÎ °©»ó¼±
±â´É»óÅ Æò°¡¹æ¹ýÀÌ´Ù. ±×·¡¼ º¸´Ù Á¤È®È÷ °©»ó¼± ±â´É»óŸ¦ Æò°¡ÇϰíÀÚ FT4I(free T4
index)¸¦ ±¸ÇÏ°Ô µÈ´Ù.
* FT4I(Free T4 index)
TBGÁõ°¡(ÀÓ½Å, extrogenÅõ¿© µî)½Ã total T4´Â Áõ°¡Çϰí, T3RU´Â °¨¼ÒÇÏ°Ô µÈ´Ù.
ÀÌ µÎ°¡Áö °á°ú·ÎºÎÅÍ °£Á¢ÀûÀ¸·Î free T4¾çÀ» ¾Ë°íÀÚ FT4I¸¦ ±¸ÇÑ´Ù.
* FT4I = total T4 ¡¿ T3RU Á¤»óÄ¡ 5¡12
2. Thyroid dysfunction ¿øÀÎÀ» ±Ô¸íÇϱâ À§ÇÑ °Ë»ç
euthyroid womenÀÇ 5-15%, euthyroid menÀÇ 2%°¡ thyroid antibody¸¦ °¡Áö°í ÀÖÀ¸¸ç
À̵éÀº thyroid dysfunctionÀÌ »ý±æ À§ÇèÀÌ ³ô´Ù.
1) TPO antibody
autoimmune hypothyroismÀÇ ´ëºÎºÐ, Graves' diseaseÀÇ 80%¿¡¼ high level·Î Á¸Àç
2) TSI
Graves' disease¿¡¼ TSH-R¸¦ ÀÚ±ØÇÏ´Â Ç×ü
ÀÓ½ÅÁß 1st trimester¶§ maternal TSI levelÀÌ ³ôÀ» ¶§ neonatal thyrotoxicosis¸¦ ¿¹ÃøÇÏ´Â
µ¥ ÁÖ·Î »ç¿ëµÈ´Ù.
3) serum Tg level
thyrotoxicosis factitia¸¦ Á¦¿ÜÇÑ ¸ðµç ÇüÅÂÀÇ thyrotoxicosis¶§ Áõ°¡ÇÑ´Ù.
TgÃøÁ¤ÀÇ ÁÖ ¿ªÇÒÀº thyroid cancer f/u¿¡ ÀÖ´Ù.
total thyroidectomyÈÄ¿¡´Â TgÀÌ °ËÃâµÇ¾î¼± ¾ÈµÇ´Âµ¥ 1-2 ng/mLÀÌ»ó °ËÃâÀº incomplete
ablation or recurrent cancer¸¦ ÀǹÌÇÑ´Ù.
4) Radioiodine uptake and thyroid scanning
(1) RAIU
131IÀ» ¸ÔÀ̰í 24½Ã°£ÈÄ uptakeÁ¤µµ¸¦ ÃøÁ¤ (Á¤»ó 5-30%)
* hyperthyroidismÀÌÁö¸¸ RAIU°¡ °¨¼ÒµÈ °æ¿ì
i) painless chronic or subacute thyroiditis
(=spontaneous resolving hyperthyroidism)
ii) iodine-induced hyperthyroidism
iii) thyrotoxicosis factitia
iv) struma ovarii
(2) perchlorate discharge test: perchlorate¸¦ ¸ÔÀ̰í uptakeÁ¤µµ¸¦ º»´Ù.
organification defect¸¦ ã¾Æ³»´Â °Í
15%ÀÌÇÏ·Î ¶³¾îÁú ¶§ positive
: pendred disease, Hashimoto's thyroiditis, hyperthyroidismȯÀÚ PTUÄ¡·áÁßÀ϶§
5) thyroid ultrasound
10 MHz¸¦ »ç¿ëÇϸé spatial resolution & image quality°¡ ¿ì¼öÇÏ¿© 3mmÀÌ»óÀÇ nodule°ú
cyst¸¦ ¹ß°ßÇÒ¼ö ÀÖ´Ù. noduleÀ» ¹ß°ßÇÏ´Â °Í¿Ü¿¡ nodule size¸¦ monitorÇÒ¼ö ÀÖ°í FNA
biopsy ¹× cystic lesion aspiration¶§ guidingÇÒ¼ö ÀÖ´Ù.
Autoimmune basis of thyroid disease
1. ºóµµ
thyroid autoimmunity : several forms of thyroiditis, hypothyroidism, Graves' diseaseÀ¯¹ß.
ºÎ°Ë½Ã 20-40%¿¡¼ focal thyroiditis°¡ °üÂûµÇ´Âµ¥ TPO antibodyÀÇ Á¸Àç¿Í °°Àº
autoimmunityÀÇ serologic marker°¡ µ¿¹ÝµÈ´Ù. ÀÌ·¯ÇÑ Ç×ü´Â ³²ÀÚº¸´Ù´Â ¿©ÀÚ¿¡¼ 4-10¹è
´õ ÈçÇÏ´Ù.
¿©¼ºÀÇ 5%°¡ ºÐ¸¸ÈÄ self-limited postpartum(silent) thyroiditis¸¦ °æÇèÇϴµ¥ À̶§
ante-partum TPO antibody°¡ Á¸ÀçÇϸç postpartum thyroiditis¸¦ °æÇèÇÑ ¿©¼ºÀÇ 20%°¡±îÀÌ
ºÐ¸¸ÈÄ 5-10³âÈÄ¿¡ permanent hypothyroidismÀ¸·Î ¹ßÀüÇÑ´Ù.
2. susceptibility factors
´ëºÎºÐÀÇ autoimmune disorderó·³ genetic & environmental factor¿¡ ÀÇÇØ °áÁ¤µÈ´Ù.
¨ç genetic factors
monozygotic twins¿¡¼ Graves' disease concordance´Â 20-30%ÀÌ´Ù.
autoimmune polyglandular syndrome 2 = autoimmune thyroid dysfunction + other
autoimmune diseases(type 1 DM, addison's ds, pernicious anemia, vitiligo)
ÀÌ·¯ÇÑ autoimmune disorder group¿¡¼´Â ¸î°¡Áö genetic factor¸¦ °øÀ¯ÇÑ´Ù.
Graves' disease & ¹éÀο¡¼ÀÇ autoimmune hypothyroidismÀÇ °¡Àå Àß ¹àÇôÁø genetic risk
factor´Â HLA DR3ÀÌ´Ù. T-cell regulatory gene TCLA-4ÀÇ polymorphismÀÌ ¸î¸î Á¾Á·¿¡¼
¹ß°ßµÇ¾úÀ¸³ª °ü·Ã¼ºÀº ¾àÇÏ´Ù.
¨è environmental factors
i) sex hormone
thyroid autoimmunity°¡ ¿©¼º¿¡¼ ¿ì¼¼ÇÑ °ÍÀº sex steroidsÀÇ ¿µÇâ ¶§¹®ÀÏ °ÍÀ¸·Î »ý°¢
µÈ´Ù.
ii) smoking
Èí¿¬Àº Graves' disease¹ß»ý¿¡ À־ minor riskÀÌÁö¸¸ ophthalmopathyÀÇ ¹ß»ý¿¡
À־ major risk factorÀÌ´Ù.
iii) infection
congenital rubella syndromeÀ» Á¦¿ÜÇϰí´Â °¨¿°ÀÇ ¿ªÇÒ¿¡ ´ëÇØ È®¸³µÈ Áõ°Å°¡ ¾ø´Ù.
congenital rubella infectionÀº autoimmune hypothyroidism¹ß»ýÀ§ÇèÀ» Áõ°¡½ÃŰÁö¸¸
viral thyroiditis°¡ autoimmune thyroiditisÀ» À¯¹ßÇÏÁö´Â ¾Ê´Â´Ù.
3. Humoral factors
Graves' disease´Â TSH-R stimulating immunoglobulin(TSI)¿¡ ÀÇÇØ ¹ß»ýÇÑ´Ù.
TSI´Â ŹÝÅë°ú°¡ °¡´ÉÇÏ¿© transient neonatal thyrotoxicosis¸¦ ÀÏÀ¸Å°¸ç Graves' disease
¿©¼ºÀÇ 1-2%¿¡¼ ÇÕº´µÈ´Ù.
TSH functionÀ» blockÇÏ´Â Ç×ü´Â hypothyroidismÀ» ÀÏÀ¸Å°´Âµ¥ TSH-R blocking antibody
´Â autoimmune hypothyroidismÀ» °¡Áø ¾Æ½Ã¾Æ ȯÀÚÀÇ 20%¿¡¼ ¹ß°ßµÈ´Ù.
* Antibody¸¦ ÃøÁ¤ÇÏ´Â ¹æ¹ý
i) TBII(TSH-binding inhibiting immunoglobulin)
functional effect¿¡ ´ëÇÑ Á¤º¸¸¦ Á¦°øÇÏÁö ¸øÇϸç, ºñÀüÇüÀûÀΠȯÀÚ¿¡¼ TSH-R AbÀÇ Á¸Àç
¸¦ Áõ¸íÇϱâ À§ÇØ ÀÏÂ÷ÀûÀ¸·Î »ç¿ëÇÑ´Ù.
ii) Ab to Tg & TPO
thyroid autoimmunity marker·Î ÀÓ»óÀûÀ¸·Î À¯¿ëÇÏ´Ù.
4. Cell-mediated factors
autoimmune thyroid disease¿¡¼ activated circulating T cellÀÌ Áõ°¡µÇ¾î ÀÖÀ¸¸ç thyroid
gland´Â CD4+ and CD8+ T cellsÀÌ infiltrationµÇ¾î ÀÖ´Ù.
¶Ç, thyroid gland´Â cytokine-mediated upregulation of Fas(and possibly Fas ligand)¸¦
ÅëÇÏ¿© apoptosisµÈ´Ù.
infiltrating immune cells¿¡ ÀÇÇØ »ý¼ºµÈ cytokineÀº thyroid cell-surface moleculesÀ» ¹ßÇö
ÇÏ¿© ´ÙÀ½°ú °°Àº °á°ú¸¦ ÃÊ·¡ÇÑ´Ù.
i) engagement by immune cells(¿¹, adhesion molecules, HLA class I & II molecules)
ii) thyroid cellÀÚü¿¡ ÀÇÇÑ cytokine secretionÀ¯µµ
iii) NO production
iv) TSH-R inhibition, TPO, and Tg synthesis¸¦ ÅëÇÏ¿© thyroid hormone»ý»ê °¨¼Ò
cytokineÀº ¶ÇÇÑ thyroid-associated ophthalmopathy¿¡ Áß¿äÇÑ ¿ªÇÒÀ» ÇÑ´Ù.
extraocular muscle¿¡ activated T cellÀÌ Ä§ÂøÇÏ¿© cytokineÀ» ºÐºñÇÏ¿© fibroblast¸¦
activation½Ã۰í glycosaminoglycanÇÕ¼ºÀ» Áõ°¡½ÃÄÑ °á±¹ muscle swellingÀ» ÃÊ·¡ÇÑ´Ù.
º´ÀÇ Èı⿡´Â fibrosisµÈ´Ù.
Hypothyroidism
1. ¿øÀÎ Tab 330-4
iodine deficiency : mc cause
iodine sufficiency area¿¡¼´Â autoimmune ds(Hashimoto's thyroiditis), iatrogenic
cause(hyperthyroidism tx)°¡ mc cause
2. Congenital hypothyroidism
1/3000-4000 newborns
¾ö¸¶°¡ TSH-R blocking ab°¡ Àְųª antithyroid drugÀ» º¹¿ëÁßÀÏ ¶§ ÀϽÃÀûÀ¸·Î ¹ß»ý
*neonatal hypothyroidism
thyroid gland dysfunction(85%)
inborn errors of thyroid hormone synthesis(10-15%)
TSH-R Ab-mediated
F>M
1) ÀÓ»ó¹ßÇö(Tab 330-5: adult hypothyroidismÀÇ ÀüÇüÀû Ư¡)
Ãâ»ý½Ã ´ëºÎºÐ Á¤»óÀ̸ç 10% ¹Ì¸¸¿¡¼ ÀÓ»óÀû Ư¡À» º¸ÀδÙ.
: prolonged jaundice, feeding problems, hypotonia, enlarged tongue,
delayed bone maturation, umbilical hernia
Ä¡·á°¡ Áö¿¬µÇ¸é permanent neurologic damage°¡ ÃÊ·¡µÈ´Ù.
2) Áø´Ü ¹× Ä¡·á
TSH or T4 screening
Áø´ÜµÇ¸é T4¸¦ Åõ¿©(10-15 ug/kg/d)Çϰí TSH¸¦ monitoringÇÏ¸é¼ ¿ë·®À» Á¶ÀýÇÑ´Ù.
T4·Î Á¶±âÄ¡·á½Ã normal IQ levelÀ» À¯ÁöÇÒ¼ö ÀÖÀ¸³ª ´ëºÎºÐÀÇ severe hypothyroidism
ȤÀº Ä¡·á°¡ ¹ÌÈíÇÒ ¶§ subtle neurodevelopmental abnormality°¡ ¹ß°ßµÈ´Ù.
3. Autoimmune hypothyroidism
1) ºÐ·ù
i) goiter(Hashimoto's or goitrous thyroiditis) or at the later stages of the disease
ii) minimal residual thyroid tissue(atrophic thyroiditis)
¼¼È÷ °©»ó¼± ±â´ÉÀÌ ÀúÇÏµÇ¸é¼ º¸»ó±âÀüÀ¸·Î TSH°¡ Áõ°¡ÇÏ°Ô µÈ´Ù.
ÀϺΠȯÀÚµéÀº minor symptomÀ» °¡Áö´Âµ¥ ÀÌ·± »óŸ¦ "subclinical hypothyroidism"À̶ó
ÇÑ´Ù.
Èı⿡ free T4 levelÀº °¨¼ÒÇϰí, TSH levelÀº Á¡Â÷ Áõ°¡ÇÏ¸é¼ Áõ»óÀº ´õ¿í ¶Ñ·ÇÇØÁø´Ù.
(º¸Åë TSH>10 mU/L)
À̶§¸¦ "clinical hypothyroidism(=overt hypothyroidism)"À̶ó ÇÑ´Ù.
2) À¯º´·ü
annual incidence: F= 4/1000, M= 1/1000
subclinical hypothyroidismÀÌ¸é¼ TPO antibody(+)ÀÏ ¶§ clinical hypothyroidism
À¸·Î ÁøÇàÇÒ À§ÇèÀº ¸Å³â 4%ÀÌ´Ù.
3) pathogenesis
Hashimoto : marked lymphocyte infiltration, thyroid follicle atrophy
Atrophic thyroiditis: fibrosis°¡ more extensive, lymphocyte infiltrationÀº ´úÇÏ´Ù.
µÑ´Ù TSH-R blocking Ab(+) -> T cell mediated thyroid follicular destructionÃÊ·¡
4) ÀÓ»ó¹ßÇö
Hashimoto's thyroiditisÀÇ °æ¿ì hypothyroidism sxº¸´Ù goiter°¡ ¸ÕÀú ³ªÅ¸³´Ù.
Å©Áø ¾ÊÁö¸¸ irrgular & firmÇÏ´Ù.
atrophic thyroiditis³ª Hashimoto's thyroiditisÀÇ late stage´Â hypothyroidismÀÇ sx & sign
À¸·Î ¹ßÇöµÈ´Ù.
ÀüÇüÀû Ư¡Àº puffy face with edematous eyelids & nonpitting pretibial edemaÀÌ´Ù.
myocardial contractility & PR°¨¼Ò·Î SVÀÌ °¨¼ÒÇϰí, bradycardia°¡ »ý±ä´Ù.
peripheral resistace°¡ Áõ°¡ÇÏ¿© hypertension(ƯÈ÷ diastolic)ÀÌ »ý±ä´Ù.
pericardial effusion(30%)ÀÌ »ý±æ¼ö ÀÖÀ¸³ª cardiac function¿¡´Â Àå¾Ö¸¦ ÁÖÁö ¾Ê´Â´Ù.
carpal tunnel syndrome & other entrapment syndrome, slow tendon reflex relaxation,
pseudomyotonia
´Ù¸¥ autoimmune disease°¡ µ¿¹ÝµÇ±âµµ ÇÑ´Ù.
: ƯÈ÷ vitiligo, pernicious anemia, Addison's disease, alopecia areata, type 1 DM
thyroid-associated ophthalmopathy´Â Graves' disease¿¡¼ ÈçÇϸç autoimmune
hypothyroidism¿¡¼± 5%Á¤µµ¿¡¼ º¼¼ö ÀÖ´Ù.
5) Lab
* Fig 330-5 Hypothyroidism evaluation
TSH°¡ Áõ°¡ÇØ ÀÖÀ¸¸é free T4¸¦ ÃøÁ¤ÇÑ´Ù.
(°¨¼Ò½Ã clinical hypothyroidism, Á¤»ó½Ã subclinical hypothyroidism)
ÀÏ´Ü clinical or subclinical hypothyroidismÀ¸·Î Áø´ÜÀÌ µÇ¸é TPO Ab¸¦ ÃøÁ¤ÇÑ´Ù.
autoimmune hypothyroidismÀÇ 90-95%¿¡¼ ¾ç¼º
TBII : 10-20%
goiterÀÇ ¿øÀÎÀÌ Àǽɽº·´´Ù¸é È®ÁøÀ» À§ÇØ FNA¸¦ ½ÃÇàÇÒ¼öµµ ÀÖ´Ù.
other abnormal lab: CPK, cholesterol, TG¡è, anemia
6) °¨º°Áø´Ü
asymmetric goiter in Hashimoto's thyroiditis
: multinodular goiter or thyroid carcinoma¿Í È¥µ¿
-> USG½ÃÇàÇϸé solitary lesionÀÎÁö multinodular goiterÀÎÁö¸¦ º¼¼ö ÀÖ´Ù.
focal noduleÀ» Á¶»çÇÒ ¶§ FNA biopsy¸¦ ½ÃÇàÇÒ¼ö ÀÖ´Ù.
7) hypothyroidismÀÇ ´Ù¸¥ ¿øÀÎ
¨ç iatrogenic hypothyroidism
radioiodine tx 3-4°³¿ùÈÄ¿¡ transient hypothyroidismÀÌ »ý±æ¼ö ÀÖÀ¸¸ç À̶§´Â
cellular destruction¿¡ ÀÇÇÑ °ÍÀÌ ¾Æ´Ï¶ó radiation damage¿¡ ÀÇÇÑ °ÍÀ̹ǷΠ°¡¿ªÀûÀÌ´Ù.
subtotal thyroidectomyÈÄ mild hypothyroidismÀÌ »ý±æ¼ö Àִµ¥ ÀÌ ¶ÇÇÑ ¼ö°³¿ùÈÄ
ȸº¹µÈ´Ù.
¨è iodine deficiency
endemic goiterÀ¯¹ß
¸ð¼øµÇ°Ôµµ iodine excessÀ϶§µµ goiter & hypothyroismÀ» ÀÏÀ¸Å³¼ö ÀÖ´Ù(±âÀüÀº
Àß ¸ð¸§).
¿¹> amiodarone Ä¡·áȯÀÚÀÇ 13%, lithium
¨é secondary hypothyroidism
ant. pituitary hormonal deficiency
8) Ä¡·á
¨ç clinical hypothyroidism
residual thyroid functionÀÌ ¾øÀ»¶§ levothyroxine 1.5 ug/kg(100-150ug)
residual thyroid functionÀÌ ÀÖÀ¸¸é lower dose
60¼¼ ¹Ì¸¸, heart disease°¡ ¾øÀ» ¶§ : 50-100 ug(TSH level¿¡ µû¶ó Á¶Àý)
normal TSH levelÀ» ȸº¹ÇÑÈÄ 3-6°³¿ùÀÌ Áö³ª¾ß ¿ÏÀüÇÑ Áõ»óÀÇ È¸º¹À» °æÇèÇÑ´Ù.
TSH°¡ ³ô´Ù¸é 12.5-25 ugÁõ·®ÇÏ°í ³·´Ù¸é ¹Ý´ë·Î °¨·®ÇÑ´Ù.
TSH levelÀÌ stableÇÏ´Ù¸é ¸Å 2-3³â¸¶´Ù ÃøÁ¤°£°ÝÀ» ´Ã¸°´Ù. À̶§ compliance¸¦ À¯ÁöÇÏ´Â
°ÍÀÌ Áß¿äÇÏ´Ù.
* ¿ë·®À» ¿Ã·Á¾ß ÇÏ´Â °æ¿ì
: malabsorption(celiac disease or small-bowel surgery)
T4 Èí¼ö¸¦ ¹æÇØÇÏ´Â ¾à or clearance¸¦ Áõ°¡½ÃŰ´Â ¾à
(cholestyramine, ferrous sulfate, calcium supplement, lovastatin, aluminum hydroxide,
rifampin, amiodarone, carbamazepine, phenytoin)
¨è subclinical hypothyroidism
TPO Ab°¡ ¾ç¼ºÀ̸é overt hypothyroidismÀ¸·Î ÁøÇàÇÒ À§ÇèÀÌ ÀÖ´Ù.
TSH¸¦ Á¤»óȽÃŰ´Â °ÍÀ» ¸ñÇ¥·Î levothyroxine low dose(25-50ug/d)·Î Ä¡·á¸¦
½ÃÀÛÇÑ´Ù.
¨é special considerations
i) pseudotumor cerebri in children : rare
Ä¡·á ¼ö°³¿ùÈÄ °©Àڱ⠹߻ý
ii) hypothyroidism history³ª °¡´É¼º ³ôÀº ¿©¼º
ÀÓ½ÅÃʱ⿡ hypothyroidismÀº fetal neuronal development¿¡ ¾Ç¿µÇâÀ» ³¢Ä¡¹Ç·Î ÀÓ½ÅÀü
euthyroid state¸¦ À¯ÁöÇØ¾ß ÇÑ´Ù. ¿ë·®Àº 50%ÀÌ»ó Áõ·®ÇÏ¿´´Ù°¡ ºÐ¸¸ÈÄ¿£ ÀÌÀü level·Î
ÇÑ´Ù.
iii) ³ëÀÎ, ƯÈ÷ coronary artery disease°¡ ÀÖÀ» ¶§
12.5-25 ug/d·Î ½ÃÀÛÇÏ¿© TSH°¡ Á¤»óȵɶ§±îÁö 2-3°³¿ù¸¶´Ù Áõ·®
iv) emergency surgery
untreated hypothyroidism¿¡¼ ÀϹÝÀûÀ¸·Î ¾ÈÀüÇÏ´Ù.
v) myxedema coma : high mortality rate
³ëÀο¡¼ ÈçÈ÷ »ý±â°í º¸ÅëÀº respiratory impairment¿¡ ÀÇÇØ Ã˹ߵȴÙ.
drug(sedatives, anesthetics, antidepressant), pneumonia, CHF, MI,
GI bleeding or CVA, sepsis, cold exposure
hypoventilation(-> hypoxia, hypercapnia)ÀÌ pathogenesis¿¡ Áß½ÉÀû ¿ªÇÒÀ» ÇÑ´Ù.
hypoglycemia, dilutional hyponatremia¶ÇÇÑ myxedema ¹ß»ý¿¡ ±â¿©ÇÑ´Ù.
*Ä¡·á
a. levothyroxine 500 ug IV(loading) or via NG tube -> 50-100 ug/d
alternative, T3 IV or via NG tube 10-25 ug q 8-12 hr(ºÎÁ¤¸Æ À¯¹ß°¡´É)
T4(200ug) + T3(25ug) -> T4(50-100ug) + T3(10ug q 8hr)
b. supportive tx : metabolic disturbance±³Á¤(external warmingµî)
c. hydrocortisone(50mg q 6hr) IV
d. precipitating factorÄ¡·á
broad-spectrum antibioticsÁ¶±â»ç¿ë
ventilatory support
hypertonic saline or IV glucose : hyponatremia or hypoglycemiaÀÖÀ» ¶§
hypotonic fluid´Â »ç¿ëÇÏÁö ¸» °Í: reduced renal perfusion & inappropriate
vasopressin secretionÀ¸·Î water retentionÀ» ¾ÇȽÃų¼ö ÀÖÀ¸¹Ç·Î
Thyrotoxicosis
thyrotoxicosis : the state of thyroid hormone excess
hyperthyroidism: excessive thyroid function
Tab 330-6 ¿øÀÎ
Graves' disease
1) ¿ªÇÐ thyrotoxicosisÀÇ 60-80%, ÁÖ·Î iodine intake¿Í °ü·ÃÀÖ´Ù.
(high iodine intake = increased prevalence of Graves' disease)
20-50¼¼¿¡ ÈçÇÏ´Ù. ¿©¼º>³²¼º(10¹è)
2) º´ÀÎ
TSI¿¡ ÀÇÇØ ¹ß»ýÇÑ´Ù.
extrathyroidal manifestation(ophthalmopathy & dermopathy)˼ extraocular muscle & skin
¿¡ immunologically mediated fibroblast activation, glycosaminoglycans accumulation->
water trapping & edema·Î ÀÎÇÏ¿© »ý±ä´Ù. ³ªÁß¿¡´Â fibrosis°¡ µÎµå·¯Áø´Ù.
locally infiltrating T cell & macrophage¿¡¼ ³ª¿À´Â cytokine(IFN-¥ã, TNF, IL-1)¿¡ fibroblast
activationµÈ´Ù.
3) ÀÓ»ó¹ßÇö Tab 330-7 Thyrotoxicosis sx & sign
³ëÀο¡¼ thyrotoxicosisƯ¡ÀÌ maskµÇ°í ÁÖ·Î fatigue & weight loss°¡ ÁÖ·Î ³ªÅ¸³¯ ¼ö
ÀÖ´Ù.(="apathetic hyperthyroidism")
mc cardiovascular manifestation: sinus tachycardia
ÀÚÁÖ palpitation, ¶§·Î SVT°¡ µ¿¹ÝµÈ´Ù.
high COÀ¸·Î ÀÎÇÏ¿© bounding pulse, widened pulse pressure, aortic systolic murmur¸¦
ÀÏÀ¸Å°°í preexisting heart disease, ³ëÀο¡¼ angina or heart failure¸¦ ¾ÇȽÃų¼ö ÀÖ´Ù.
50¼¼ À̻󿡼 AF°¡ ÈçÇÏ´Ù.
thyrotoxicosis¸¸ Ä¡·áÇÏ¿´À» ¶§ NSRÀ¸·Î ÀüȯµÇ´Â °ÍÀº ¹Ý¼ö ¹Ì¸¸Àε¥ ÀÌ´Â ³ª¸ÓÁö¿¡¼
underlying cardiac problemÀÌ ÀÖÀ½À» ÀǹÌÇÑ´Ù.
skin : warm & moist, sweating, heat intolerance
Graves' ophthalmopathy: 75%¿¡¼ Áø´ÜÀüÈÄ 1³â³»¿¡ ÁÖ·Î »ý±â±â¸¸ ¶§·Î´Â thyrotoxicosis
°¡ »ý±â±â Àü¿¡ »ý±â±âµµ Çϰí, ¼ö³âÈÄ¿¡ »ý±â±âµµ ÇÑ´Ù.
thyroid dermopathy(<5%) : pretibial myxedema
thyroid acropathy(<1%)
4) Lab Fig 330-7
2-5%´Â T3¸¸ Áõ°¡ÇÑ´Ù(T3 thyrotoxicosis)
5) °æ°ú
Ä¡·áÇÏÁö ¾ÊÀ¸¸é ¾ÇȵǸç 10-30% mortality¸¦ º¸ÀδÙ.
Ä¡·áÈÄ remissionµÈ ȯÀÚÀÇ 10-15³âÈÄ hypothyroidismÀ¸·Î µÈ´Ù.
ophthalmopathy´Â thyroid disease°æ°ú¸¦ µû¸£Áö ¾Ê´Â´Ù.
: ù 3-6°³¿ù°£ ¾ÇȵǴٰ¡ ±×ÈÄ 12-18°³¿ù°£ plateau phase, ±×ÈÄ spontaneous
improvement
5%¿¡¼´Â fulminant·Î ÁøÇàÇÏ¿© interventionÀÌ ÇÊ¿äÇÏ´Ù(optin n. compression or corneal
ulceration)
extraocular m. fibrosis·Î ÀÎÇØ Èı⿡ diplopia¹ß»ý
RI Ä¡·áÈÄ eye disease°¡ ¾ÇȵǾú´Ù´Â ¿¬±¸°¡ ÀÖ´Ù(ƯÈ÷ smoker¿¡¼).
antithyroid drug or surgery´Â ophthalmopathy°æ°ú¿¡ ¾Ç¿µÇâÀ» ³¢Ä¡Áö ¾Ê´Â´Ù.
6) Ä¡·á
¨ç antithyroid drug(PTU, carbimazole, methimazole)
TPO inhibition½ÃÄÑ oxidation, organificationÀ» ÀúÇØÇÔ
Àß ¸ð¸£´Â ¾î¶² ±âÀü¿¡ ÀÇÇØ thyroid Ab levelµµ °¨¼Ò½ÃÅ´
i) PTU(1T=50mg) T4->T3 deiodination inhibition(minor benefit)
¹Ý°¨±â(90ºÐ) cf. methimazole(6hr)
100-200 mg q 6-8hr(300-600mg)
ii) carbimazole or methimazole(1T=5mg) 10-20mg q 8-12hr(20-60mg)
euthyroidismµµ´ÞÈÄ¿£ ÇÏ·ç Çѹø °¡´É
"block-replace regimen"
drug-induced hypothyroidismÀ» ÇÇÇϱâ À§ÇØ high dose antithyroid drug°ú
levothyroxineÀ» ÇÔ²² Åõ¿©ÇÏ´Â °ÍÀ» ¸»Çϴµ¥ Ãʱ⿣ remission rate°¡ ³ô´Ù°í
ÇÏ¿´À¸³ª ´Ù¸¥ ¿¬±¸¿¡¼´Â ¾Æ´Ï¾ú´Ù.
´ëºÎºÐ Ä¡·á½ÃÀÛÈÄ 6-8ÁÖÈÄ¿¡³ª euthyroidism¿¡ µµ´ÞÇϸç TSH´Â ¼ö°³¿ùµ¿¾È ¾ïÁ¦µÈ
»óÅ·ΠÀÖ´Ù. ±×·¯¹Ç·Î TSH°¡ Ä¡·á¹ÝÀÀÀÇ ¹Î°¨ÇÑ ÁöÇ¥·Î »ç¿ëµÉ¼ø ¾ø´Ù.
* À¯Áö¿ë·®
carbimazole or methimazole: 2.5-10mg, PTU: 50-100mg
* maximum remission rate: 30-50%(18-24°³¿ùÈÄ)
* severe hyperthyroidism & large goiter
Ä¡·áÁß´ÜÈÄ Àç¹ßÇϱ⠽¬¿ì³ª °á°ú¸¦ ¿¹ÃøÇϱâ´Â ¾î·Æ´Ù.
* common S/E : rash, urticaria, fever, arthralgia(1-5%)
ÀúÀý·Î ¾ø¾îÁö°Å³ª ´Ù¸¥ ¾àÀ¸·Î ¹Ù²Ù¸é ¾ø¾îÁø´Ù.
rare but major S/E: hepatitis, SLE-like syndrome, agranulocytosis(most important,
<1%)
¾àÁ¦¸¦ Áï½Ã Áß´ÜÇØ¾ß ÇÏ¸ç ´Ù½Ã »ç¿ëÇØ¼´Â ¾ÈµÈ´Ù.
¨è propranolol(20-40mg q 6hr) or atenolol
adrenergic system control, ƯÈ÷ antithyroid drugÀÌ effect¸¦ ³ªÅ¸³»±âÀü Ãʱ⿡ »ç¿ë
¨é anticoagulation with warfarin
AF°¡ µ¿¹ÝµÈ ¸ðµç ȯÀÚ¿¡¼ »ç¿ë
¨ê radioiodine
thyroid crisis risk°¡ ´Ù¼Ò ÀÖ´Ù. µû¶ó¼ antithyroid drugÀ» ÃÖ¼Ò 1°³¿ùÀÌ»ó Ä¡·áÇÔÀ¸·Î½á
ÇÇÇÒ¼ö ÀÖ´Ù. ¸ðµç ³ëÀÎ & cardiac problemÀִ ȯÀÚ¿¡¼ antithyroid drugÀ» °í·ÁÇÏ¿©¾ß
ÇÑ´Ù.
RIÅõ¿©Àü 3-5Àϰ£ antithyroid drugÀ» Áß´ÜÇÏ¿©¾ß Çϴµ¥ optimum iodine intake¸¦ ¾ò±â
À§ÇؼÀÌ´Ù.
*¿ë·® : È®¸³µÈ °ÍÀº ¾øÀ¸³ª ´ë·« 5 mCi-15mCi
RI°¡ full effect¸¦ ³ªÅ¸³»±â±îÁö 2-3°³¿ù°£Àº hyperthyroidismÀÌ Áö¼ÓÇϹǷΠÀÌ ±â°£¿¡´Â
Áõ»óÀ» Á¶ÀýÇϱâ À§ÇØ ¥â-blocker or antithyroid drugÀ» »ç¿ëÇÒ¼ö ÀÖ´Ù.
persistent hyperthyroidism¶§´Â 2nd dose·Î Ä¡·áÇϴµ¥ À̶§´Â first doseÈÄ 6°³¿ùÈÄ¿¡
½ÃÇàÇÑ´Ù.
Ä¡·áÈÄ hypothyroidismÀÇ ¹ß»ýÀº ¿ë·®°ú »ó°üÀÌ ÀÖÀ¸³ª ´ë·« ù 1³â¿¡ 10-20%, ±×ÈÄ¿£
¸Å³â 5%Á¤µµ µÈ´Ù. µû¶ó¼ ù 1³â°£Àº close F/UÀÌ ÇÊ¿äÇÏ°í ±× ÈÄ¿£ ¸Å³â TFT¸¦ ½ÃÇà
ÇÑ´Ù.
* pregnancy & breast feeding
radioiodine txÀº Àý´ëÀû ±Ý±â
Ä¡·á 6-12°³¿ùÈÄ¿¡ ÀӽŠȤÀº ¼öÀ¯´Â ¾ÈÀü
* severe ophthalmopathyȯÀÚ´Â ÁÖÀÇÇØ¾ß Çϴµ¥ ÀϺΠÀúÀÚµéÀº RIÄ¡·á½Ã Pd 40mg/d»ç¿ë
ÇÒ °ÍÀ» ±ÇÇÑ´Ù. ±×ÈÄ 2-3°³¿ù°£ tapering
¨ë subtotal thyroidectomy
¼ö¼úÀü antithyroid drugÀ¸·Î thyrotoxicosisÀÇ careful controlÇÊ¿ä
±×ÈÄ potassium iodide(3 drops SSKI orally tid) ÇÊ¿ä(¡ñvascularity¸¦ °¨¼Ò½Ã۱â À§ÇØ)
*major cx : bleeding, laryngeal edema, hypoparathyroidism, recurrent layngeal n.
damage
Àç¹ßÀ² < 2%
¨ì Graves' disease in pregnancy
transplancental transfer°¡ ÀûÀº PTU¸¦ ÀϹÝÀûÀ¸·Î »ç¿ë
ÀӽŽà TSH-R Ab°¡ °¨¼ÒÇϹǷΠlowest effective dose¸¦ »ç¿ëÇØ¾ß Çϸç last trimester
¿£ Ä¡·á Áߴܵµ °¡´ÉÇÏ´Ù. ±×·³¿¡µµ ºÒ±¸Çϰí TSH-R AbÀÇ tranplacental transfer°¡
µå¹°°Ô fetal thyrotoxicosis or neonatal thyrotoxicosis¸¦ ÀÏÀ¸Å³¼öµµ ÀÖ´Ù.
poor intrauterine growth, fetal HR > 60bpm, high levels of maternal TSH-RÀÏ ¶§
fetal thyrotoxicosisÀǽÉ
postpartum period´Â Graves' ds relapseÀÇ major risk time
low doses of antithyroid drugÀº breast feeding½Ã ¾ÈÀüÇÏ´Ù.
¨í thyrotoxic crisis, or thyroid storm
rare, life-threatening exacerbation of hyperthyroidism
fever, delirium, seizure, coma, vomiting, diarrhea, jaundice
* mortality rate ¡30%
ÁÖ»ç¸Á¿øÀÎ: cardiac failure, arrhythmia, or hyperthermia
* À¯¹ßÀÎÀÚ
acute illness(stroke, infection, trauma, DKA), surgery(ƯÈ÷ thyroid), or
untreated hyperthyroidism¿¡¼ RI tx
* Ä¡·á : supportive care
large dose PTU(600mg loading -> 200-300 mg q 6hr)
PTUÅõ¿© Çѽð£ÈÄ stable iodideÅõ¿©(Wolff-Chaikoff effect)
saturated solution of potassium iodide(SSKI 5 drops q 6hr)
or ipodate or iopanoic acid(0.5mg q 12hr)
propranolol 40-60mg q 4hr PO or 2mg IV q 4hr
* ophthalmopathy: mild or moderate¶§´Â Àû±ØÀû Ä¡·á°¡ ÇÊ¿ä¾ø´Ù.(¡ñÈçÈ÷
spontaneous improveµÇ¹Ç·Î)
periorbital edema: more upright sleeping position
severe ophthalmopathy(optic n. involvement or chemosis·Î ÀÎÇÑ corneal damage)
¶§´Â ÀÀ±Þ»óȲÀ¸·Î ¾È°úÀÇ»ç¿Í ÇùÁø: high-dose glucocorticoid(Pd 40-80mg/d)·Î 2/3
¿¡¼ short-term benefit, ¶§·Ð cyclosporine°ú combine
¸Å 1-2ÁÖ¸¶´Ù 5mg¾¿ tapering
ext. beam radiotherapy°¡ »ç¿ëµÇ¾î ¿ÔÀ¸³ª equivocal
* thyroid dermopathy: Ä¡·á°¡ ÇÊ¿ä¾ø´Ù.
Other causes of thyrotoxicosis
¨ç subacute or silent thyroiditis: circulating Tg, IL-6¡è
¨è thyrotoxicosis factitia : Tg¡é
¨é ectopic thyroid tissue(ƯÈ÷ ovarian teratoma = struma ovarii)
¨ê functional metastatic follicular carcinoma
¨ë amiodarone treatment(10%) ƯÈ÷ low iodine intake area¿¡
¨ì TSH-secreting pituitary adenoma
: TSHÀÇ ¥á subunit¡è
¨í toxic multinodular goiter
¨î hyperfunctioning solitary nodules
Thyroiditis
1. Acute thyroiditis : rare, supprative infection¶§¹®
1) mc cause: children & young adults - pyriform sinus
elderly - long-standing goiter & thyroid malignancy degeneration
2) DDx(thyroid pain)
subacute thyroiditis, rarely, chronic thyroiditis, hemorrhage into a cyst, malignancy
including lymphoma, rarely, amiodarone-induced thyroiditis or amyloidosis
3) Lab ESR¡è, WBC¡è, normal thyroid function, FNA: PMNL¡è, culture: organism(+)
4) Áï°¢ antibiotic tx
2. Subacute thyroiditis
= de Quervain's thyroiditis, granulomatous thyroiditis, or viral thyroiditis
: mumps, coxsackievirus, influenza, adenovirus, echovirus
30-50¼¼, F>M(3¹è)
1) º´Å»ý¸®
pathy inflammatory infiltrate with disruption of thyroid follicles and multinucleated giant
cells within some follicles
granuloma + fibrosis, Á¤»óÀ¸·Î ȸº¹Çϴµ¥ ¼ö°³¿ù ¼Ò¿ä
¨ç initial phase(thyrotoxic phase) Tg & thyroid hormone release
-> circulating free T4 & T3¡è, TSH suppression, RAIU¡é
¨è ¼öÁÖÈÄ hypothyroid phase: hypothyroism¹ß»ý, free T4¡é, TSH¡è, RAIU : Á¤»ó ȤÀº ¾à°£ ¡è
¨é recovery phase: thyroid hormone, TSH Á¤»óÈ
2) ÀÓ»ó¹ßÇö painful & enlarged thyroid, ¶§·Ð fever
º´±â¿¡ µû¶ó thyrotoxicosis or hypothyroidism
´ëºÎºÐ ¿ÏÀüÈ÷ ȸº¹µÇ³ª ÀϺο¡¼´Â permanent hypothyroidismÀÌ ¹ß»ýÇÒ¼öµµ Àִµ¥
ÀÌ·± °æ¿ì´Â ƯÈ÷ thyroid autoimmunity°¡ µ¿¹ÝµÈ °æ¿ìÀÌ´Ù.
3) Lab *3 distinctive phases(6°³¿ù °£°Ý)
thyrotoxic phase --> hypothyroid phase -> recovery phase
(IL-6¡è)
4) Ä¡·á
¨ç large dose aspirin(600mg q 4-6hr) or NSAID
¨è glucocorticoid : aspirin or NSAID·Î ºÒÃæºÐÇϰųª Áõ»óÀÌ Áö¼ÓµÇ¸é Pd 40-60mg/d
-> 6-8ÁÖ¿¡ °ÉÃÄ tapering
RAIU°¡ Á¤»óȵǸé Ä¡·á¸¦ Áß´ÜÇÑ´Ù(Áõ»óÀ¸·Î Ä¡·áÁß´Ü¿©ºÎ °áÁ¤ÇÏ´Â °Í ¾Æ´Ô)
¨é ¥â-blocker: thyrotoxic sx control
thyrotoxic phase¶§ antithyroid drugÀº »ç¿ëÇÏÁö ¾ÊÀ¸¸ç
hypothyroid phase¶§ low dose(50-100ug/d) levothyroxineÀ» »ç¿ëÇÒ¼ö ÀÖ´Ù.
3. Silent thyroiditis(=painless thyroiditis)
ÀÓ½ÅÈÄ 3-6°³¿ùÈÄ¿¡ °¡Àå ÈçÈ÷ ¹ß»ýÇϹǷΠpostpartum thyroiditis¶ó ÇÑ´Ù.
thyrotoxocosis phase(2-4ÁÖ) -> hypothyroidism(4-12ÁÖ) -> resolution
* subacute thyroiditis¿ÍÀÇ °¨º°Á¡: painless goiter, normal ESR, TPO Ab(+)
glucocorticoid´Â not indicated
severe thyrotoxic sxÀÌ ÀÖÀ» ¶§ propranolol 20-40mg tid or qid
hypothyroid phase¶§ thyroxine replacement(6-9°³¿ùÈÄ Áß´Ü), ±×ÈÄ annual F/U
4. Drug-induced thyroiditis
: IFN-¥á, IL-2, or amiodarone => painless thyroiditisÀ¯¹ß
¨ç IFN-¥á : chronic hepatitis B, CÀÇ Ä¡·áÁ¦·Î »ç¿ëµÇ¸ç 5%¿¡¼ thyroid dysfunctionÀ»
ÀÏÀ¸Å²´Ù.
painless thyroiditis, hypothyroidism, Graves' disease
¨è IL-2 : malignancyÄ¡·á¿¡ ÀÌ¿ëµÇ¸ç, thyroiditis, hypothyroidismÀÏÀ¸Å´
¨é amiodarone : amiodaroneÆí ÂüÁ¶
5. chronic thyroiditis
mc = Hashimoto's thyroiditis
Riedel's thyroiditis : rare disorder, Á߳⿩¼º¿¡¼ ¼¼È÷ ¹ß»ýÇÏ´Â painless goiter with
local sx(compression sx)
open biopsy·Î Áø´Ü, ¼ö¼úÀû Ä¡·á
Sick euthyroid syndrome
1. Á¤ÀÇ
acute, severe illness°¡ ÀÖÀ» ¶§ underlying thyroid disease°¡ ¾ø´Â »óÅ¿¡¼ circulating
TSH or thyroid hormone level¿¡ ÀÌ»óÀ» ÃÊ·¡ÇÏ´Â °ÍÀ» ¸»ÇÑ´Ù.
ÀÌ·¯ÇÑ hormonal change¸¦ ÀÏÀ¸Å°´Â ´ëÇ¥Àû ¿øÀÎÀº "cytokine release"ÀÌ´Ù.
acutely ill patient¿¡¼ thyroid disorder°¡ °·ÂÈ÷ ÀǽɵÇÁö ¾Ê´Â´Ù¸é routine TFT´Â ÇÏÁö
¸»¾Æ¾ß ÇÑ´Ù.
2. ÇüÅÂ
1) low T3 syndrome(total & free T3 °¨¼Ò) with normal T4 & TSH level : most common
T3°¨¼ÒÁ¤µµ´Â illness severity¿Í ºñ·Ê
T4->T3·ÎÀÇ Àüȯ½ÇÆÐ·Î rT3Áõ°¡
TRH stimulation¿¡ ´ëÇÑ TSHÀÇ ¹ÝÀÀÀº Á¤»ó
2) low T4 syndrome
very sick patient¿¡¼ total T4 & T3 level¸ðµÎ °¨¼ÒµÇ¸ç poor prognosis
TBG°¡ °¨¼ÒÇϱ⠶§¹®À̸ç, free T4´Â Á¤»ó level
TSH levelÀº <0.1 ¡ >20 mU/L±îÁö ´Ù¾ç
TRH¿¡ ´ëÇÑ TSHÀÇ ¹ÝÀÀÀº blunting
3. ¿¹
1) acute liver disease: TBG releaseÁõ°¡·Î óÀ½¿¡´Â total T3, T4 levelÀÌ Áõ°¡µÇ´Ù°¡
liver failure°¡ ÁøÇàµÇ¸é¼ Á¡Â÷ subnormal
2) acutely ill psychiatric patientÀÇ 5-30%¿¡¼ ÀϽÃÀûÀ¸·Î total & free T4Áõ°¡, normal T3,
TSH °¨¼Ò, Á¤»ó, ȤÀº Áõ°¡
3) HIV infection
Ãʱ⿣ T3, T4Áõ°¡, ÁøÇàÇÏ¸é¼ T3°¨¼Ò, TSH´Â º¸Åë Á¤»ó
4) renal disease
T3¡é, rT3 normal ¡ñÀß ¸ð¸£´Â ¾î¶² ±âÀüÀ¸·Î liver·ÎÀÇ uptake°¡ Áõ°¡ÇϹǷÎ
4. Áø´Ü
thyroid diseaseÀÇ °ú°Å·ÂÀÌ ÀÖ´ÂÁö È®ÀÎ.
acutely illness severityÆò°¡
5. Ä¡·á
thyroid hormoneÄ¡·á¿¡ ´ëÇØ¼´Â controversial. ´ëºÎºÐÀÇ ÀúÀÚµéÀº È£¸£¸óÀ» Åõ¿©ÇÏÁö
¸»°í thyroid functionÀ» monitoringÇÒ °ÍÀ» ÃßõÇÑ´Ù.
Amiodarone effects on thyroid function
1) °³¿ä
amiodaroneÀº type III antiarrhythmic agent·Î ±¸Á¶ÀûÀ¸·Î thyroid hormone°ú °ü·ÃÀÖÀ¸¸ç,
iodineÀÌ 39%³ª ÇÔÀ¯µÇ¾î ÀÖ´Ù. µû¶ó¼ ÀϹÝÀûÀÎ amiodarone¿ë·® 200mg/d¿¡´Â »ó´ç·®ÀÇ
iodineÀÌ ÇÔÀ¯µÇ¾î plasma & urinary iodine levelÀÌ 40¹èÀÌ»ó Áõ°¡ÇÑ´Ù. adipose tissue¿¡
ÀúÀåµÇ¹Ç·Î ¾àÀ» Áß´ÜÈÄ¿¡µµ 6°³¿ù ÀÌ»ó high iodine levelÀÌ Áö¼ÓµÈ´Ù. amiodaroneÀº
deiodinase activity¸¦ ¾ïÁ¦Çϰí, thyroid hormone antagonist·Î¼ ÀÛ¿ëÀ» ÇÑ´Ù.
2) multiple effects
¨ç acute, transient changes in thyroid function
¨è hypothyroidism : °¨¼ö¼º Àִ ȯÀÚ¿¡¼
¨é thyrotoxicosis i) Jod-Basedow effect
ii) thyroiditis-like condition
iii) autoimmune Graves' disease induction
óÀ½¿£ ÀϽÃÀûÀ¸·Î T4°¡ °¨¼ÒÇÏ´Ù°¡ ±×ÈÄ iodine-dependent suppression of the
thyroid(Wolff-Chaikoff effect), deiodinase activity, thyroid hormone receptor actionÀÇ
inhibitory effects°¡ µÎµå·¯Áø´Ù. ±× °á°ú TFT¸¦ ½ÃÇàÇϸé T4¡è, T3¡é, rT3¡è, TSH ÀϽÃÀûÀ¸·Î
Áõ°¡(20mU/L±îÁö)
TSH´Â 1-3°³¿ùÈıîÁö Á¤»óÈ È¤Àº ¾à°£ °¨¼Ò
3) amiodarone-induced thyrotoxicosis(AIT)
low-iodine intake Áö¿ª¿¡¼± 10%, high-iodine intake Áö¿ª¿¡¼± 2%
°©»ó¼± È£¸£¸óÀÌ Áõ°¡ÇÔÀ¸·Î½á underlying arrhythmia & coronary a. disease¸¦ ¾ÇȽÃŲ´Ù.
¨ç type 1 AIT : underlying thyroid abnormality(+)(preclinical Graves' ds or nodular goiter)
Jod-Basedow phenomenon¿¡ ÀÇÇØ thyroid hormone synthesis¡è
¨è type 2 AIT : no intrinsic thyroid abnormality
drug-induced lysosomal activation -> destructive thyroiditisÀ¯¹ß
ÀúÀý·Î ȸº¹Çϰųª hypothyroidismÀ» À¯¹ßÇÒ¼ö ÀÖ´Ù.
IL-6 level¡è¡è(type 1 AIT¿¡¼´Â ¾à°£ Áõ°¡)
AIT¿¡¼± amiodaroneÀ» Áß´ÜÇØ¾ß ÇÑ´Ù. ±×·¸Áö¸¸ ¹Ý°¨±â°¡ ±æ±â ¶§¹®¿¡ Áï½Ã Áß´ÜÈ¿°ú°¡
³ªÅ¸³ªÁø ¾Ê´Â´Ù. type 1 AIT¿¡¼ high dose antithyroid drugÀ» »ç¿ëÇÒ¼ö ÀÖÁö¸¸ º¸Åë
È¿°ú´Â ¾ø´Ù.
* Ä¡·á
i) potassium perchlorate 200mg q 6hr : thyoid iodide content¸¦ °¨¼Ò½Ã۱â À§ÇØ
»ç¿ëµÇ³ª agranulocytosis¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Ù.
ii) glucocorticoid: subacute thyroiditis¿¡¼Ã³·³ Åõ¿©ÇÑ´Ù.
iii) lithium: thyroid hormone release block
iv) near-total thyroidectomy : thyoid hormone levelÀ» ±Þ°ÝÈ÷ °¨¼Ò½Ã۸ç most effective
long-term solution
Thyroid function in pregnancy
* factors
¨ç transient hCG increase(1st trimester)
TSH-RÀÚ±Ø -> TSH¡é(ÀÓ½ÅÁ߹ݱîÁö)
transient gestational hyperthyroidism and/or hperemesis gravidarumÀ» ÀÏÀ¸Å°±âµµ ÇÑ´Ù.
¨è estrogen¿µÇâÀ¸·Î TBGÁõ°¡
1st trimester¶§ Áõ°¡µÇ¾î Àӽų»³» Áö¼Ó
¨é urinary iodine excretionÁõ°¡
marginal iodine sufficiency area¿¡¼ thyroid hormone productionÀå¾ÖÃÊ·¡
ÀÓ½ÅÁß iodine intake(<50ug)°¡ ºÎÁ·ÇÑ ¿©¼ºÀº goiter¹ß»ýÀ§ÇèÀÌ ³ôÀ¸¸ç, maternal and fetal
hypothyroidism, neonatal goiter¸¦ ¿¹¹æÇϱâ À§ÇØ iodine º¸ÃæÀÌ ÇÊ¿äÇÏ´Ù.
Àӽſ©¼ºÀÇ 2-3%¿¡¼ maternal hypothyroidismÀÌ ¹ß»ýÇϸç ÀÚ³à ¹ß´Þ Áö¿¬À» ÃÊ·¡ÇÒ
À§ÇèÀÌ ³ô´Ù.
ÀÓ½ÅÁÖ thyroid hormone ¿ä±¸·®Àº 25-50 ug/d Áõ°¡ÇÑ´Ù.
cf. TSH, thyroid H: ŹÝÅë°ú¡¿
Goiter and nodular thyroid disease
goiter: thyroid gland enlargement
biosynthetic defect, iodine deficiency, autoimmune disease(Graves' disease,
Hashimoto's thyroiditis), nodular diseaseÀÏ ¶§ goiter¸¦ ÀÏÀ¸Å³¼ö ÀÖ´Ù.
nodular thyroid disease´Â ÈçÇÏ´Ù: ¼ºÀο¡¼ P/E·Î 3-7%, USG·Î´Â 25%¿¡¼ ¹ß°ß
1. Diffuse nontoxic(simple) goiter
1) ¿øÀÎ ¹× º´ÀÎ
iodine deficiency¿¡ ÀÇÇØ °¡Àå ÈçÈ÷ ¹ß»ýÇϸç Àα¸ÀÇ 5%ÀÌ»óÀÌ »ý±æ ¶§ endemic goiter¶ó
ÇÑ´Ù.
2) ÀÓ»ó Áõ»ó ¹× Áø´Ü
´ëºÎºÐ ¹«Áõ»óÀ̸ç Å©±â°¡ ³Ê¹« Å©¸é compression sxÀ» ÀÏÀ¸Å³¼ö ÀÖ´Ù.
substernal goiter´Â thoracic inlet obstructionÀ» ÀÏÀ¸Å³¼ö ÀÖ´Ù.
TFT : iodine deficiency¿¡¼ total T4¡é, normal T3
³ëÀο¡¼ low TSH levelÀÏ ¶§ undiagnosed Graves' disease or thyroid autonomy
°¡´É¼ºÀ» »ý°¢Çغ¸¾Æ¾ß ÇÑ´Ù(subclinical thyrotoxicosis)
low uninary iodine levels(<100 ug/L) : iodine deficiencyÁø´Ü
thyroid scan: ÀϹÝÀûÀ¸·Î ÇÊ¿äÄ¡ ¾ÊÀ¸¸ç uptake°¡ Áõ°¡µÈ´Ù.
USG: P/E¿¡¼ noduleÀÌ ¸¸Á®ÁöÁö ¾Ê´Â´Ù¸é diffuse goiter Áø´Ü¸ñÀûÀ¸·Î´Â ÇÊ¿äÄ¡ ¾Ê´Ù.
3) Ä¡·á
iodine deficiency: iodine or thyroid hormone replacement
other cause: levothyroxine young-100(ug/d), elderly(50ug/d)
3-6°³¿ù ³»¿¡ ÈçÈ÷ significant regressionµÇ¸ç ±×ÈÄ¿¡´Â Àß ÀϾÁö ¾Ê´Â´Ù.
2. Nontoxic multinodular goiter
1) ¿øÀÎ ¹× º´ÀÎ
Àα¸ÀÇ 1-12%, ¿©¼º¿¡¼ ´õ ÈçÇÏ°í ³ªÀ̰¡ µé¸é¼ Áõ°¡ÇÑ´Ù.
iodine-deficient region¿¡¼ ´õ ÈçÇÏÁö¸¸ iodine-sufficient region¿¡¼µµ ¹ß»ýÇÑ´Ù.
=> multiple genetic, autoimmune, environmental influence°¡ °ü¿©ÇÔÀ» ÀǹÌ
2) ÀÓ»ó¹ßÇö
´ëºÎºÐ ¹«Áõ»óÀ̸ç, ¼ö³âÀÌ»ó¿¡ °ÉÃÄ »ý±â°í ÁøÂûÀ̳ª, ¸ñÀÌ Ä¿Á® ¹ß°ßµÈ´Ù.
³Ê¹« Å©¸é compressive sxÀ» ÀÏÀ¸Å²´Ù.
sudden pain¹ß»ý½Ã nodule³»·ÎÀÇ hemorrhage °¡´É¼ºÀÌ ¸¹À¸³ª, ¹Ýµå½Ã invasive
malignancy°¡´É¼ºµµ »ý°¢ÇØ¾ß ÇÑ´Ù. hoarseness(=laryngeal nerve paralysis)¶§µµ
malignancy¸¦ ÀǽÉÄÉ ÇÑ´Ù.
3) Áø´Ü
MNG´Â thyroid cancer or more aggressive caÀÇ ¼±ÇàÀÎÀÚ°¡ ¾Æ´Ï´Ù.
nodular lesion¿¡ ´ëÇØ ¸ðµÎ biopsy¸¦ ÇÒ ¼ö´Â ¾øÀ¸¸ç dominant or enlarging noduleÀÌ
malignancy°¡ ÀÇ½ÉµÉ ¶§ biopsy¸¦ ½ÃÇàÇÑ´Ù.
4) Ä¡·á
¨ç ´ëºÎºÐ º¸Á¸Àû Ä¡·á¸¦ Çϸç T4 suppressionÀº goiter size¸¦ ÁÙÀ̴µ¥ °ÅÀÇ È¿°ú°¡ ¾ø´Ù.
¸¸¾à levothyroxineÀ» »ç¿ëÇÑ´Ù¸é low dose(50ug)À¸·Î ½ÃÀÛÇϰí excessive suppression
µÇÁö ¾Êµµ·Ï ÇÑ´Ù. contrast agent³ª ´Ù¸¥ iodine-containing substance´Â ÇÇÇϵµ·Ï ÇÑ´Ù.
(¡ñJod-Basedow effect¸¦ ÀÏÀ¸Å³ À§Ç輺ÀÌ Áõ°¡ÇϹǷÎ)
¨è RI
»ç¿ëºóµµ°¡ Áõ°¡µÇ°í Àִµ¥ goiter size¸¦ ÁÙ¿©ÁÖ°í autonomy regionÀ» ¼±ÅÃÀûÀ¸·Î
ablation½Ã۱⠶§¹®ÀÌ´Ù.
´ë·« 0.1 mCi/tissue 1g(10-29 mCi), ÇÊ¿ä½Ã repeat tx, ´ëºÎºÐÀÇ È¯ÀÚ¿¡¼ 40-50%
reduction
radiation-induced thyroid swelling & tracheal compressionÀº µå¹°Áö¸¸ »ý±æ¼ö Àִµ¥
ÀÌ·± acute compression¹ß»ý½Ã glucocorticoid or surgery°¡ ÇÊ¿äÇÒ¼öµµ ÀÖ´Ù.
radiation-induced hypothyroidismÀº µå¹°°í posttreatment autoimmune thyrotoxicosis
°¡ 5%¿¡¼ »ý±æ¼ö ÀÖ´Ù.
¨é ¼ö¼ú : highly effectiveÇÏÁö¸¸ ´Ù¼ÒÀÇ À§Ç輺ÀÌ ÀÖ´Ù.
3. Toxic multinodular goiter
pathogenesis´Â nontoxic MNG¿Í µ¿ÀÏÇϳª °¡Àå Å« Â÷ÀÌ´Â toxic MNG¿¡´Â functional
autonomy°¡ ÀÖ´Ù´Â °ÍÀÌ´Ù.
goiter¿ÜÀÇ ÀÓ»ó¹ßÇöÀº subclinical hyperthyroidism or mild thyrotoxicosis
³ëÀο¡¼ ÈçÇϰí, AF or palpitations, tachycardia, nervousness, tremor, or weight loss°¡
»ý±æ ¼ö ÀÖ´Ù.
iodine, contrast dye exposure°¡ thyrotoxicosis¸¦ ¾ÇȽÃų¼ö ÀÖ´Ù.
TSH¡é, T4 Á¤»ó ȤÀº ¾à°£ Áõ°¡, T3Áõ°¡Á¤µµ°¡ T4Áõ°¡Á¤µµº¸´Ù Å©´Ù.
thyroid scan: heterogenous uptake with multiple regions(increase or decrease)
24hr RI uptake : Áõ°¡¡¿
* Ä¡·á
i) antithyroid drug + ¥â-blocker
=> goiter¸¦ ´õ Å©°Ô ÇÒ¼ö ÀÖÀ¸¸ç spontaneous remissionÀº ÀϾÁö ¾Ê´Â´Ù.
ii) RI
iii) op : definite treatment, ¼ö¼úÀü antithyroid drugÀ¸·Î euthyroid state¸¦ ¸¸µé¾î¾ß ÇÑ´Ù.
4. Hyperfunctioning solitary nodule(=toxic adenoma)
pathogenesis : TSH-R signaling pathway¸¦ ÀÚ±ØÇÏ´Â mutation
ÀÏÂ÷ÀûÀ¸·Î receptor transmembrane domain¿¡¼ Gs¥á¿¡ constitutive receptor coupling
-> cAMP level¡è -> thyroid follicular cell proliferation & function¡è
90%À̻󿡼 TSH-R or Gs¥á subunit geneÀÇ activating mutation(+)
thyrotoxicosis : mild
thyroid scan: definitive diagnostic test
* Ä¡·á
i) RI ablationÀÌ treatment of choice
10-29 mCi, 75%¿¡¼ 3°³¿ù³» thyrotoxicosis±³Á¤
hypothyroidism <10%(5³â³»)
ii) surgical resection(enucleation or lobectomy) : effective
iii) medical tx: antithyroid drug +¥â-blocker
thyroid functionÀ» Á¤»óȽÃų¼ö ÀÖÀ¸³ª long-term tx·Î´Â ÀûÇÕÇÏÁö ¾Ê´Ù.
iv) ethanol injection : ÀϺμ¾ÅÍ¿¡¼ ¼º°øÀûÀ¸·Î ½ÃÇà
5ȸ ÀÌ»ó repeat injectionÀÌ ÇÊ¿äÇÏÁö¸¸ nodule size¸¦ °¨¼Ò½Ã۰í, normal thyroid
functionÀ» ȹµæÇÏ¿´´Ù.
Thyroid cancer
Tab 330-9 ºÐ·ù
Tab 330-10 thyroid noduleȯÀÚ¿¡¼ cancer risk factor
* ÀϹÝÀûÀÎ poor prognosis
<20¼¼ or >65¼¼, male
1. Pathogensis & genetic basis
¨ç radiation
¨è TSH & growth factor
¸¹Àº ȯÀÚ¿¡¼ thyroid cancer°¡ TSH receptor¸¦ ¹ßÇöÇϹǷΠTSH¿¡ ¹ÝÀÀÇÑ´Ù.
µû¶ó¼ thyroid cancer¿¡¼ T4 suppressionÇÏ´Â rationale°¡ ¿©±â¿¡ ÀÖ´Ù.
TSH receptorÀÇ residual expressionÀº 131I therapy½Ã¿¡ uptake¸¦ Áõ°¡½ÃŲ´Ù.
¨é oncogene & tumor suppressor genes
RET gene on chromosome 10
MEN type 2¿¡¼ÀÇ MTC : point mutation
papillary cancer: rearrangement
2. Well-differentiated thyroid cancer
1) papillary cancer(mc)
* Ư¡Á÷ÀÎ cytologic features: psammoma bodies, papillary structure formation
multifocal, local invasion, bone, lung metastasis, slow growth, ÈçÈ÷ early stage(I, II)¿¡
Áø´ÜµÇ°í excellent prognosis
2) follicular cancer
iodine-deficient regions¿¡¼ ´õ ÈçÇÏ´Ù.
vessel, nerve, adjacent structure¿¡ÀÇ invasionÀ¸·Î benign°ú malignancy°¡ °áÁ¤µÇ¹Ç·Î
FNA·Î Áø´ÜÇϱâ´Â ¾î·Æ´Ù.
hematogenous spreadÇϹǷΠ¸¹Àº ȯÀÚ¿¡¼ stage IV¿¡¼ Áø´ÜµÇ¹Ç·Î PTCº¸´Ù ¿¹Èİ¡
³ª»Ú´Ù.
* poor prognostic features
: distant metastasis, >50¼¼, >4cm, Hurthle cell histology, marked vascular invasion
3) Ä¡·á
¨ç surgery
stage IÀÏ ¶§ lobectomy ȤÀº near-total thyroidectomy»çÀÌ¿¡ »ýÁ¸·üÀº À¯»çÇÏ´Ù.
lobectomy´Â hypoparathyroidism, recurrent laryngeal nerve injuryÀÇ À§ÇèÀº ³·Áö¸¸,
residual lobe ¶§¹®¿¡ Tg levelÀ» monitorÇÒ¼ö ¾ø°í, 131I WBSÀ» ½ÃÇàÇÒ¼ö ¾ø´Ù.
±×¿Ü¿¡µµ RI scan or tx°¡ ÇÊ¿äÇÏ´Ù¸é ³²Àº thyroid tissueÁ¦°Å¸¦ À§ÇÑ Àç¼ö¼úÀÌ ÇÊ¿äÇÏ´Ù.
µû¶ó¼ ÀúÀÚµéÀº Àç¹ßÀ» Æò°¡Çϱâ À§ÇØ RI scan°ú TgÀ» ÃøÁ¤ÇÒ¼ö ÀÖ´Â near-total
thyroidectomy¸¦ ´õ ¼±È£ÇÑ´Ù.
¨è TSH suppressive tx
´ëºÎºÐÀÇ tumor°¡ TSH-responsvieÇϹǷΠTSH¿¡ ´ëÇÑ levothyroxine suppressionÀÌ
thyroid cancerÄ¡·áÀÇ ±âº»ÀÌ´Ù.
Ä¡·á¸ñÇ¥´Â excess thyoid hormoneÀ¸·Î ÀÎÇÑ ºÎÀÛ¿ë(AF, osteopenia, anxiety, other
thyrotoxicosis Áõ»ó)ÀÌ ¾ø´Â »óÅ¿¡¼ °¡´ÉÇÑ TSH¸¦ ¾ïÁ¦ÇÏ´Â °ÍÀÌ´Ù.
Àç¹ßÀ§ÇèÀÌ ³·À» ¶§, TSH 0.1-0.5 IU/L
Àç¹ßÀ§ÇèÀÌ ³ôÀ» ¶§, complete TSH suppresion
¨é radioiodine tx
RI uptake´Â ÀÏÂ÷ÀûÀ¸·Î sodium iodide symporter¿Í TSH stimulation¿¡ ÀÇÇØ °áÁ¤µÈ´Ù.
near-total thyroidectomyÈÄ thyroid tissue°¡ ³²¾ÆÀÖÀ»¼ö Àִµ¥, thyroid bed¿Í
parathyroid glandÁÖº¯ÀÌ Æ¯È÷ ±×·¸´Ù. °á°úÀûÀ¸·Î normal thyroid tissue¸¦ Á¦°ÅÇϰí,
residual tumor cellÀ» Ä¡·áÇϱâ À§ÇØ 131I ablationÀÌ ÇÊ¿äÇÏ´Ù.
* indications
i) larger papillary tumor¿¡¼ ÁÖÀ§ LN·ÎÀÇ spread
ii) follicular tumor
iii) metastasis evidence(+)¿¡¼ thyroid ablation & RI tx½ÃÇà
* 131I thyroid ablation & treatment
¼ö¼úÈÄ ¼öÁÖ°£ liothyronine(25ug bid or tid)·Î Ä¡·áÇÑ´Ù.
±×´ÙÀ½ thyroid hormoneÀ» ²÷´Â´Ù.
ÀÌ»óÀûÀ¸·Î´Â TSH>50 IU/L(3-4ÁÖÀÌ»ó)ÀÌ µÈ »óÅ¿¡¼ Ä¡·áÇÏ´Â °ÍÀÌ ÁÁ´Ù.
ÃÖ´ë outpatient dose: 29.9 mCi
known reisidual cancerȯÀÚ¿¡¼´Â ´õ ¸¹Àº ¾çµµ »ç¿ë
* 131I whole body scan(4-5 mCi)
residual tissue¸¦ È®ÀÎÇϰí ablationÀ» ÇÒ°ÍÀÎÁö guidance¸¦ Á¦°øÇÑ´Ù.
* F/U whole body scanning & Tg determination(Tab 330-12)
initial F/U: ¼ö¼ú ¹× thyroid ablationÈÄ 6°³¿ùÈÄ
initial scanÀÌ negative À̰í TgÀÌ ³·À¸¸é 1³âÈÄ¿¡ repeat
1³âÈÄ¿¡µµ ¿©ÀüÈ÷ negativeÀ̸é suppressive tx¸¦ ½ÃÇàÇϰí
¸Å 6-12°³¿ù¸¶´Ù Tg¸¦ checkÇÑ´Ù.
2nd F/U scanÀÌ negativeÀ̸é labÀÌ Á¤»óÀÎÇÑÀº further scanÀº ´õ ÇÊ¿äÄ¡ ¾Ê´Ù.
Tg >5-10 ng/mLÀ̰í scan negativeÀÏ ¶§ large dose 131I Ä¡·á¸¦ ÃßõÇÑ´Ù.
3. Anaplastic & other forms of thyroid cancer
1) anaplastic thyroid cancer
poorly differentiated & aggressive cancer, poor prognosis, 6°³¿ù³» »ç¸Á
RI uptake´Â ¹Ì¹ÌÇÏÁö¸¸ Ä¡·áÀûÀ¸·Î ÀÌ¿ëÇØº¼¼ö´Â ÀÖ´Ù.
CTx(antracycline & paclitaxel)¸¦ ½ÃÇàÇϱ⵵ ÇÏÁö¸¸ ÈçÈ÷ È¿°ú ¾ø´Ù.
external radiationÀ» ½ÃµµÇغ¼¼öµµ ÀÖ´Ù.
2) thyroid lymphoma
ÈçÈ÷ Hashimoto's thyroiditis¿¡¼ ¹ß»ýÇϰí rapid expanding thyroid massÀÏ ¶§ ÀǽÉÇÑ´Ù.
diffuse large cell lymphoma°¡ °¡Àå ÈçÇÑ typeÀ̰í
biopsy¸¦ Çϸé small cell lung cancer³ª ATC¿Í ±¸º°ÀÌ ¾î·Æ´Ù.
ext. radiation¿¡ highly sensitiveÇϰí spread dsÀ̹ǷΠinitial tx·Î surgical resectionÀ»
ÇÏ¿©¼´Â ¾ÈµÈ´Ù.
´Ù¸¥ ÇüÅÂÀÇ lymphoma Ä¡·á¿¡ µû¸¥´Ù.
3) medullary thyroid cancer(5-10%)
sporadic or familial
* familial: MEN-2A, 2B, MTC without MEN
* more aggressive
MEN-2B > 2A
familial > sporadic
* s-calcitonin¡è: residual or recurrent disease marker
* ¸ðµç ȯÀÚ¿¡¼ MET mutation testÇÏ´Â °ÍÀÌ ÁÁ°í, mutationÀ» °¡Áö´Â family member¿¡
´ëÇØ¼´Â genetic counselingÇÑ´Ù.
* Ä¡·á : surgical
RI uptake°¡ µÇÁö ¾ÊÀ¸¹Ç·Î RIÄ¡·á´Â ÇÏÁö ¾ÊÀ¸¸ç
ext. RT & CTx¸¦ palliation¸ñÀûÀ¸·Î ½ÃÇàÇÒ¼ö ÀÖ´Ù.