Autoimmune Hashimoto’s Thyroiditis and Hypothyroidism: Novel Aspects

Abstract

Autoimmune Hashimoto’s thyroiditis is an organ specific autoimmune disorder. It affects the thyroid gland and it is characterized by the presence of antibodies to thyroid proteins, namely, thyroid peroxidase, TPOab and thyroglobulin, Tgab and thyroid tissue invasion by lymphocytes. The presence of Hashimoto’s thyroiditis may be associated with normal thyroid function or hypothyroidism. In many cases of Hashimoto’s thyroiditis with normal thyroid function may progress to subclinical hypothyroidism or overt hypothyroidism. Risk factors for the development of Hashimoto’s thyroiditis are genetic and environmental. Genetic factors are HLA-DR4, CD40, CTLA-4 and PTP-N22 and genetic factors related to thyroglobulin gene and TSH receptor gene. Environmental factors include the presence of iodine excess in the environment, infectious agents such as hepatitis C virus and the SARS-CoV-2 virus, smoking, alcohol, selenium deficiency, drugs such as amiodarone, interferon-a, highly active antiretroviral therapy and immune checkpoint inhibitors. Female sex is also a risk factor for Hashimoto’s thyroiditis. The disease runs a variable course. Presently there are experimental efforts to pause or reverse the autoimmune process which leads to Hashimoto’s thyroiditis and may progress to the destruction of the thyroid gland. Hypothyroidism is treated by the administration of thyroxine usually for life.