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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