50-year-old female experienced a slowly progressive painless symmetrical enlargement of the thyroid gland. In addition, she started to develop hypothyroidism. Presence of a stridor required thyroidectomy.
- Parenchyma diffusely infiltrated by a mononuclear inflammatory infiltrate containing small lymphocytes and plasma cells. Secondary lymph follicles with well-developed germinal centres are present throughout the gland.
- Many atrophic thyroid follicles exhibit epithelial cells with abundant eosinophilic granules (Hürthle or oxyphil cells). Follicles are partly destroyed, epithelial strands are formed.
- Immune histochemistry staining for IgM reveals the abundance of plasma cells.
Pathogenesis: cellular and humoral immune mechanisms contribute to this autoimmune disease that ultimately destroys the follicular epithelium. A well-known mechanism is the production of auto-antibodies against thyroglobulin and other follicular cell antigens. Presentation of auto-antibodies by follicle cells is followed by antibody-dependent cell-mediated cytotoxicity (ADCC) involving NK-cells (antibody-mediated (Type II) hypersensitivity). Hypothyroidism usually ensues, because the whole gland is uniformly affected.