Endocrinology
Hashimoto Thyroiditis
하시모토갑상선염
Chronic lymphocytic thyroiditis from anti-TPO/anti-Tg autoantibodies
- How common
- 10% women, 1% men
- Typical age
- Peak 30–60 yrs
What is it?
CD4+ T cells and autoantibodies infiltrate thyroid follicles, progressively destroying them.
Commonly affected: Thyroid follicular cells
How it develops
- Genetic + environmentalHLA-DR3/DR5, iodine excess, pregnancy
- T-cell activationTh1-mediated follicle attack
- Autoantibody productionAnti-TPO and anti-Tg antibodies
- Progressive destructionFollicular atrophy, fibrosis → hypothyroidism
Symptoms
- Hypothyroid symptomsFatigue, weight gain, cold intolerance
- Diffuse goiterFirm, enlarged thyroid
- Hashitoxicosis (transient)Initial transient hyperthyroid phase
- Other autoimmuneVitiligo, T1DM, rheumatic
- Painless glandDiffers from subacute thyroiditis
How it is examined
- TSH + Free T4High TSH, low T4
- Anti-TPO + anti-Tg95% positive anti-TPO
- Thyroid USHypoechoic heterogeneous, atrophic
Imaging
Plain X-ray not needed.
- Clinical+lab
Thyroid US is standard imaging.
- Heterogeneous, hypoechoic
Non-surgical care
- Levothyroxine replacementReplace once hypothyroid
- Observation (subclinical)Watch if TSH normal
- Selenium (controversial)May reduce antibody titers
- Screen other autoimmuneT1DM, adrenal insufficiency
Conservative options are generally tried first. Medications listed here can have side effects — discuss them with your prescriber.
When surgery is considered
Large goiter, compression, suspicious nodule
Procedures that may be discussed
- Thyroidectomy
Outlook
Lifelong replacement = normal life; small increase in thyroid lymphoma risk.