Atrophic Thyroiditis

Abstract

Atrophic thyroiditis is an organ-specific autoimmune disease characterized by thyroid autoantibodies, functional hypothyroidism, and absence of goiter. Atrophic thyroiditis is a rare entity, which occurs between the ages of 40–60 years especially in elderly women. Immunogenetical analysis suggests that atrophic thyroiditis may be a distinct entity from Hashimoto’s disease. Genetic and environmental factors appear to interact leading to appearance of autoantigens with autoantibody formation. The frequency of HLA-DR8 and HLA-DQB1∗0302 is significantly increased in AT patients positive for TSH-binding inhibitor immunoglobulin compare with controls and goitrous autoimmune thyroiditis. Atrophic thyroiditis is a Th2 disease with blocking anti-TSH receptor antibodies. It has been suggested that Hashimoto's thyroiditis, primary myxedema or AT, and Graves’ disease are different expressions of a basically similar autoimmune process, and that the clinical appearance reflects the spectrum of the immune response in the particular patient. This response may include cytotoxic antibodies, stimulatory antibodies, blocking antibodies, or cell-mediated immunity. The clinical presentation varies from asymptomatic AT, overt hypothyroidism, and myxedema. The pathological features are atrophic thyroid gland with lymphocytic infiltration and fibrous tissue replacing normal thyroid parenchyma. There are no current diagnostic criteria for AT. We propose the following bases for AT diagnosis: clinic or subclinic hypothyroidism, positive thyroid stimulation blocking antibodies and thyroid ultrasound with diffuse low thyroid echogenicity associated with a reduced thyroid volume.

In asymptomatic AT, preventive thyroid replacement therapy is indicated in patients with elevated basal TSH levels. Overt hypothyroidism always requires hormonal substitution.