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US Endocrinology Highlights Hashimoto’s Thyroiditis in Adolescents Liliana R Santos, BSc, MD, 1,2,3 Paulo Fonseca, MD, 4,5 Rita Cardoso, MD 5 and Paula Soares,PhD 1,2,3,6 1. Instituto de Investigação e Inovação em Saúde, I3S, Universidade do Porto, Portugal; 2. Instituto de Patologia e Imunologia Molecular da Universidade do Porto (IPATIMUP), Porto, Portugal; 3. Faculdade de Medicina da Universidade de Porto, Porto, Portugal; 4. Hospital Pediátrico de Coimbra – Centro Hospitalar de Coimbra, EPE, Coimbra, Portugal; 5. Faculdade de Medicina da Universidade de Coimbra, Coimbra, Portugal; 6. Departamento de Patologia e Oncologia, Faculdade de Medicina da Universidade do Porto, Portugal Abstract Hashimoto’s thyroiditis (HT) is the most common cause of hypothyroidism in adolescence and mainly affects females. Being the archetype of an organ-specific T-cell-mediated disease, it is characterized by lymphocytic infiltration of the thyroid gland, damage to the thyroid follicular cells, and impaired ability to produce thyroid hormones. It may be associated with other autoimmune diseases and may arise in the context of congenital chromosomal aberrations. Symptoms of hypothyroidism develop insidiously. In adolescents the most common manifestation is the increase of the glandular volume. Hypothyroidism manifestations (asthenia, intolerance to cold, constipation, and/or skin and dry hair) are less common. The diagnosis is based on the presence of thyroid antibodies and characteristic imaging abnormalities on thyroid ultrasound. The treatment relies on the administration of synthetic thyroid hormones for patients with overt hypothyroidism or subclinical hypothyroidism and significant goiter. Keywords Hashimoto’s thyroiditis, adolescents, antibodies, hypothyroidism Disclosure: Liliana R Santos, BSc, MD, Paulo Fonseca, MD, Rita Cardoso, MD, and Paula Soares, PhD, have no conflicts of interest to declare. No funding was received for the publication of this article. Open Access: This article is published under the Creative Commons Attribution Noncommercial License, which permits any noncommercial use, distribution, adaptation, and reproduction provided the original author(s) and source are given appropriate credit. Received: August 11, 2015 Accepted: October 7, 2015 Citation: US Endocrinology 2015;11(2):85–8 Correspondence: Paula Soares, PhD, Institute of Molecular Pathology and Immunology of the University of Porto, Rua Dr Roberto Frias s/n, 4200-465 Porto, Portugal. E: Support: This research was supported by the Portuguese Foundation for Science and Technology. Further funding was obtained from the project “Microenvironment, metabolism and cancer” that was partially supported by Programa Operacional Regional do Norte (ON.2 – O Novo Norte) under the Quadro de Referência Estratégico Nacional (QREN) and the Fundo Europeu de Desenvolvimento Regional (FEDER IPATIMUP integrates the i3S Research Unit, which is partially supported by FCT, the Portuguese Foundation for Science and Technology. This work is funded by FEDER funds through the Operational Programme for Competitiveness Factors – COMPETE and National Funds through the FCT, under the projects “PEst-C/SAU/LA0003/2013.” The autoimmune thyroid diseases (AITD) comprise a series of interrelated conditions including Graves’ disease (GD) and Hashimoto’s thyroiditis (HT). AITD are the most prevalent diseases of the thyroid gland in the pediatric population, particularly in adolescence. 1 HT is the leading cause of goiter and hypothyroidism in children and adolescents in countries with adequate iodine supplementation. 2–3 In an American population aged between 11 and 18 years, five new cases were detected out of 1,000 adolescents screened every year. 4 It is a much more common condition in females than in males: 4:1 to 8:1 depending on the geographic region. 4–6 In the last decade, discoveries in molecular biology field have allowed new insight into the genes involved in the development of AITD. At least six susceptibility genes whose variants have been associated with AITD were identified: HLA-DR, CD40, CTLA-4, PTPN22, thyroglobulin (Tg), and thyroid stimulating hormone (TSH) receptor. 7 Genetic susceptibility accounts for 70% risk for disease that, once combined with environmental factors, play a crucial role in the initiation and progression of the disease. 8 Studies with immunoglobulin (Ig)-G4 autoantibody levels in juvenile thyroid disease patients showed evidence of heritability. 9 TOU CH MED ICA L MEDIA Etiology HT etiology is multifactorial. The susceptibility to the disease is determined by an interaction between genetic, environmental, and endogenous factors. 10,11 Genetic susceptibility is well evidenced by studies of monozygotic and dizygotic twins where the concordance rate for HT is around 38% for monozygotic and 0% for dizygotic twins. 12 Although genetic factors play a crucial role in the development of HT, nongenetic factors (environmental) are also involved. In immigrant populations from countries with a low incidence of diseases, this population adopts the new country’s incidence rate. 13 Strong evidence suggests iodine as the most significant environmental factor in the generation of thyroiditis. In fact, the prevalence of AITD increase in certain geographical regions, such as Japan and the US, and correlates with iodine intake. 14 The concentration of iodine in the thyroid is about 20 to 40 times higher than in the blood, since this element is essential to the synthesis of thyroid hormones. The process consists of the incorporation of iodine into tyrosine residues of Tg, leading to formation of derivatives of mono- and di-iodotyrosine, which subsequently undergo oxidation resulting in the production of the hormones T3 and T4. 15 Several studies suggest that the Tg iodization is crucial for recognition by the 57