Epidemiology

• Hashimoto disease is the most common form of thyroiditis and the most frequent cause of hypothyroidism in the US.
• Iodine deficiency is the most common cause of hypothyroidism worldwide.
• Sex: ♀ > ♂ (7:1)
• Age of onset: occurs in all age groups; most prevalent in women aged 30–50 years

Etiology

Pathophysiology

• Associations with HLA-DR3, and DR5 have been proposed.
• Cellular (especially T cells) and humoral immune responses are activated → active B lymphocytes produce thyroid peroxidase antibodies (TPOAbs) and thyroglobulin antibodies (TgAbs) → destruction of thyroid tissue

Clinical features

• Early-stage
  • Primarily asymptomatic
  • Goiter: nontender or painless, rubbery thyroid with moderate and symmetrical enlargement
  • Hashitoxicosis may occur: transient thyrotoxicosis due to follicular rupture of hormone-containing thyroid tissue that manifests with signs of hyperthyroidism (e.g., irritability, heat intolerance, diarrhea)
• Late-stage
  • Thyroid may be normal-sized or small if extensive fibrosis has occurred.
  • Signs of hypothyroidism (e.g., cold intolerance, constipation, fatigue)

Diagnostics

• Thyroid function tests (TFTs)
  • Early-stage: Transient hashitoxicosis may appear (↓ TSH, ↑ FT3, and ↑ FT4).
  • Progression: subclinical hypothyroidism (mildly ↑ TSH; normal FT3 and FT4)
  • Late-stage: overt hypothyroidism (↑ TSH; ↓ FT4 and ↓ FT3)
• Thyroid antibodies
  • Anti-TPOAbs (formerly anti-microsomal antibodies): positive in up to 95% of patients
  • Anti-TgAbs: positive in 60–80% of patients
• Fine-needle aspiration
  • Indications: patients with focal nodules to exclude malignancy (see “Workup of thyroid nodules”)
  • Findings: diffuse lymphocytic infiltration (cytotoxic T lymphocytes) with germinal centers, oncocytic-metaplastic cells (Hurthle cells), and fibrotic tissue

Differential diagnostics

• Differential from Subacute thyroiditis

Treatment