Recent Advances in Autoimmune Thyroid Diseases

Abstract

Autoimmune thyroid disease (AITD) includes hyperthyroid Graves disease, hypothyroid autoimmune thyroiditis, and subtle subclinical thyroid dysfunctions. AITD is caused by interactions between genetic and environmental predisposing factors and results in autoimmune deterioration. Data on polymorphisms in the AITD susceptibility genes, related environmental factors, and dysregulation of autoimmune processes have accumulated over time. Over the last decade, there has been progress in the clinical field of AITD with respect to the available diagnostic and therapeutic methods as well as clinical consensus. The updated clinical guidelines allow practitioners to identify the most reasonable and current approaches for proper management. In this review, we focus on recent advances in understanding the genetic and environmental pathogenic mechanisms underlying AITD and introduce the updated set of clinical guidelines for AITD management. We also discuss other aspects of the disease such as management of subclinical thyroid dysfunction, use of levothyroxine plus levotriiodothyronine in the treatment of autoimmune hypothyroidism, risk assessment of long-standing antithyroid drug therapy in recurrent Graves' hyperthyroidism, and future research needs.

The value of preoperative antithyroidperoxidase antibody as a novel predictor of recurrence in papillary thyroid carcinoma

“…As the main pathogenic pathway underlying CLT is the breakdown of immune tolerance toward the thyroid gland, with TPO and Tg being the main targets, the diffuse infiltration by lymphocytes of the thyroid gland occurs in the affected patients leading to a progressive destruction of the parenchyma . This immune reaction may promote a tumorigenic microenvironment by persistently releasing inflammatory molecules that can increase tumor cell proliferation, promote angiogenesis, and reduce apoptosis . However, a unique feature of CLT is that although it is a risk factor for PTC, it also has a protective effect against clinical stage and recurrence in PTC.…”

Current Concepts in Endocrinology for Clinicians and Medical Students. Hashimoto’s Thyroiditis: clinical and subclinical thyroid dysfunction

“…The hypothyroidism is traditionally defined as deficient thyroidal production of thyroid hormone by factors affecting the thyroid gland itself; the fall in serum concentrations of thyroid hormone causes an increased secretion of TSH resulting in elevated serum TSH concentrations and, can also be caused by insufficient stimulation of the thyroid gland by TSH, due to factors directly interfering with pituitary TSH release or indirectly by diminishing hypothalamic thyrotropin-releasing hormone (TRH) release (Lee HJ, 2015;Yoo WS, 2016;Mincer, DL, 2017).…”

“…The most common antibodies are anti-thyroid peroxidase (TPO) and anti-thyroglobulin (TG) and, in some cases it is possible to detect thyroid stimulating hormone (TSH) receptor blocking antibodies (anti-TSHR) (Pyzik A, 2015;Antonelli A, 2015;Chistiakov DA, 2005). The etiology of HT is still poorly understood, but the autoimmunity against thyroid antigens has been related to the genetic and environmental factors and the disorder is prevalent in individuals aged > 60 years, with a female/male ratio ranging from 5:1 to 10:1 (Yoo WS, 2016).…”

Articles inEndocrinology and Metabolismin 2016

“…In the September issue of Endocrinology and Metabolism , special reviews on thyroid diseases were published [10111213]. Of particular note, Yi [10] introduced the revised 2016 Korean Thyroid Association guidelines for thyroid nodules and cancers, focusing on the differences from the 2015 American Thyroid Association guidelines in her review.…”