Autoimmune thyroid disease

Abstract

Autoimmune thyroiditis (AIT) is not only one of the most prevalent human autoimmune diseases, but also the most frequent cause of primary hypothyroidism. It is characterized by lymphocytic infiltration of the thyroid gland with subsequent gradual destruction and fibrous replacement of thyroid tissue. Genetic predisposition, epigenetic modifications and environmental factors are suspected as disease triggers. Signs and symptoms of hypothyroidism include fatigue, bradycardia, constipation and cold intolerance. In subclinical hypothyroidism, symptoms may be absent. The diagnosis of AIT is based on the presence of antibodies against thyroid specific antigens, primarily anti-thyroid peroxidase antibodies and on a sonographically proven reduced echogenicity of the thyroid parenchyma. The diagnosis of concomitant hypothyroidism is primarily based on clinical signs and symptoms as well as measurement of thyroid-stimulating hormone (TSH)-concentration. Subclinical hypothyroidism is characterized by elevated TSH with normal serum free thyroxine (fT4) and triiodothyronine (fT3) levels, while in manifest hypothyroidism serum fT4 and fT3 levels are reduced. Levothyroxine (LT4) treatment in subclinical hypothyroidism is a controversy in the scientific literature and should be discussed individually. It not only depends on the level of TSH-elevation, but also on other factors, such as patient age, presence of comorbidities and clinical symptoms of hypothyroidism. In contrast, overt hypothyroidism and subclinical hypothyroidism with a TSH-level > 10 mIU/L is a strong indication for LT4 administration, aiming at rapid achievement of euthyroidism. In patients with dissatisfaction due to persistence of symptoms despite optimal LT4-treatment LT4/T3-combination therapy should be considered, based on expert opinion.