Autoimmune thyroiditis (Hashimoto’s thyroiditis) is the most common autoimmune disease. It most often manifests itself as hypothyroidism but may also present with euthyroidism or even hyperthyroidism. The etiopathogenesis of autoimmune thyroiditis is still unclear. However, in addition to genetic and epigenetic factors, many environmental factors are known to increase the risk of developing AIT. In this review, we aimed to collect and analyze data connected with environmental factors and autoimmune thyroiditis development. Our review indicates iodine intake, vitamin D deficiency, selenium deficiency, viral infections caused by Epstein–Barr Virus (EBV), Human parvovirus B19 (PVB19), Human herpesvirus 6A (HHV-6A) and Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), bacterial infection caused by Helicobacter pylori, microbiome disruption, medications such as interferon-alpha and tyrosine kinase inhibitors, as well as stress, climate, and smoking can influence the risk of the occurrence of autoimmune thyroiditis. Having knowledge of risk factors allows for making changes to one’s diet and lifestyle that will reduce the risk of developing the disease and alleviate the course of autoimmune thyroiditis.

SHBG is a glycoprotein that not only controls serum sex hormone levels but is also strongly correlated with metabolic syndrome, cardiovascular risk, thyroid function, gynecological conditions, and even the process of carcinogenesis. Synthesis of SHBG is controlled by many factors related to obesity, lipogenesis, inflammatory status, and genetic predisposition. By influencing the bioavailability of sex hormones, SHBG regulates their effects not only on the reproductive system, but also cardiomyocytes, vascular epithelium, and more. In this review, we aim to gather and summarize current knowledge on the physiology of SHBG and its association with cardiovascular disease, metabolic syndrome, DM 2, thyroid function, PCOS, hypogonadism, infertility, and its correlations with oral contraception. What is more, genetic alterations are mentioned to highlight SHBG as a potential new diagnostic marker. Furthermore, we assess the clinical usefulness of this parameter in the diagnosis and treatment of patients suffering from the above-specified conditions.

Down syndrome develops due to the presence of supernumerary chromosome 21. This diagnosis is made in approximately 1:800 live births. The tendency to develop autoimmune disorders like idiopathic arthritis, celiac disease, diabetes mellitus type 1, vitiligo and autoimmune thyroid disease is strongly expressed in patients with Down syndrome. Autoimmune thyroid diseases consisting of Hashimoto’s thyroiditis and Graves’ disease are specifically prevalent in patients with Down syndrome. The aim of our study is to collect available data connecting the pathogenesis and clinical course of autoimmune thyroid diseases in patients with Down syndrome of different ages and compare them to control groups. According to published data, the incidence ratio of Hashimoto’s thyroiditis diagnosis in patients with Down syndrome is elevated compared to in age-matched controls without this chromosomal aberration, similarly to Graves’ disease risk, which is also increased in a group of patients with Down syndrome. What is more, both Hashimoto’s thyroiditis and Graves’ disease are diagnosed at an earlier age than in the healthy population and are not correlated with gender or a family history of autoimmune diseases.