Hashimoto thyroiditis

Hashimoto thyroiditis 

Updated: 10/13/2022

© Jun Wang, MD, PhD

General features
  • Autoimmune disease
  • Predominantly women, more common in mid age
  • More common in white
  • Most common cause of sporadic goiter in children with sufficient iodine supply
  • Higher clustering of other autoimmunity diseases
  • Higher risk for thyroid carcinoma and lymphoma
Pathogenesis
  • Complex genetic background: HLA-DR5, HLA-DR3, CTLA4, protein tyrosine phosphatase-22 (PTPN22)
  • Autoantibody against multiple thyroid proteins, anti-thyroid peroxidase and anti-thyroglobulin antibodies
  • Autoimmune destruction of follicular cells by activated CD8+ T cells, cytokine-mediated process or autoantibodies
Clinical presentations
  • Adults
Painless, gradual thyroid failure due to autoimmune destruction
May initially have transient hyperthyroidism
  • Children
Variable hypothyroidism and reversion to euthyroidism
Must monitor thyroid function
Key laboratory findings
  • Levels of TSH, T3 and T4 associated with status of thyroid functional
  • Thyroid autoantibodies:  Anti-TPO (anti-thyroid peroxidase) and anti-Tg (anti-thyroglobulin) antibodies
Pathological features
  • Extensive lymphocytic infiltrate with germinal center formation
  • Destructed follicles
  • Follicular cells with granular eosinophilic cytoplasm
Treatment
  • Pharmacotherapy: Thyroid hormone replacement
  • Surgery: Large goiter, malignant tumor, cosmetic reasons
  • Excellent prognosis if treated early



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