Review Metabolic Characteristics of Hashimoto's Thyroiditis Patients and the Role of Microelements and Diet in the Disease Management-An Overview

Review

Metabolic Characteristics of Hashimoto's Thyroiditis Patients and the Role of Microelements and Diet in the Disease Management-An Overview

Abstract: Hashimoto's thyroiditis is the most common autoimmune disease and the leading cause of hypothyroidism, in which damage to the thyroid gland occurs due to the infiltration of lymphocytes. It is characterized by increased levels of antibodies against thyroid peroxidase and thyroglobulin. In this review, we present the metabolic profile, the effectiveness of micronutrient supplementation and the impact of dietary management in patients with Hashimoto's thyroiditis. For this current literature review, the databases PubMed, Cochrane, Medline and Embase were reviewed from the last ten years until March twenty twenty-two. This article provides a comprehensive overview of recent randomized controlled trials, meta-analyses, and clinical trials. Many patients with Hashimoto's thyroiditis, even in the euthyroid state, have excess body weight, metabolic disorders, and reduced quality of life. Due to frequent concomitant nutritional deficiencies, the role of vitamin D, iodine, selenium, magnesium, iron and vitamin B twelve is currently debated. Several studies have underlined the benefits of vitamin D and selenium supplementation. There is still no specific diet recommended for patients with Hashimoto's thyroiditis, but a protective effect of an anti-inflammatory diet rich in vitamins and minerals and low in animal foods has been suggested. There is insufficient evidence to support a gluten-free diet for all Hashimoto's thyroiditis patients. Pharmacotherapy, along with appropriate nutrition and supplementation, are important elements of medical care for patients with Hashimoto's thyroiditis. The abovementioned factors may decrease autoantibody levels, improve thyroid function, slow down the inflammatory process, maintain proper body weight, relieve symptoms, and prevent nutritional deficiencies and the development of metabolic disorders in patients with Hashimoto's thyroiditis.

One. Introduction

Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis or autoimmune thyroiditis, is a chronic inflammation of the thyroid gland with still incompletely defined etiopathogenesis. Hashimoto's thyroiditis is the most common autoimmune disease and endocrine disorder, as well as the leading cause of hypothyroidism in iodine-sufficient countries. The incidence of Hashimoto's thyroiditis is a growing trend. The diagnosis of Hashimoto's thyroiditis is determined by biochemical (positive circulating thyroid autoantibodies) and imaging tests (hypoechogenic inhomogeneous thyroid structure in ultrasonography) with characteristic clinical features. Hashimoto's thyroiditis is characterized by the production of anti-thyroid peroxidase antibodies and anti-thyroglobulin antibodies. Circulating anti-thyroid peroxidase antibodies are found in about ninety percent of Hashimoto's thyroiditis patients. Anti-thyroglobulin antibodies are less sensitive (positive in about sixty to eighty percent of patients) and less specific than anti-thyroid peroxidase antibodies. As a result of inflammation, thyroid follicles are destroyed and replaced by small lymphocytes, which significantly reduces the echogenicity of the thyroid parenchyma in the ultrasound image. Hashimoto's thyroiditis predominantly affects the female population of any age, with an increased incidence in the middle-aged. Women are about eight times more likely to develop Hashimoto's thyroiditis than men. In addition, it is also more common in Whites and Asians than in African-Americans.

The pathogenesis of Hashimoto's thyroiditis is related to lymphocytic intrathyroidal infiltration of T and B cells, especially of CD four positive Th one and the production of antithyroid antibodies. This leads to chronic inflammation and in consequence to fibrosis and gradual atrophy of the thyroid tissue. Hashimoto's thyroiditis is associated with various thyroid functional states ranging from euthyroid, subclinical to overt hypothyroidism. The overt hypothyroidism is expressed by an increase in thyrotropin and a decrease in free thyroid hormone levels.

Hashimoto's thyroiditis negatively affects wellbeing and quality of life, because thyroid hormones are responsible for the rate of basal metabolism, metabolism of carbohydrates, proteins, and fats, in addition to thermogenesis. Clinical symptoms usually occur as a result of hypothyroidism and are characterized by local and systemic manifestations. Hashimoto's thyroiditis affects various systems, including the cardiovascular, gastrointestinal, pulmonary, hematopoietic, reproductive, neuropsychiatric, as well as the skin. The symptoms of Hashimoto's thyroiditis are non-specific (concentration problems, chronic fatigue, weakness, dry skin, changes in body weight and constipation) and they depend on the severity of Hashimoto's thyroiditis. Mood and anxiety disorders are also common in patients with Hashimoto's thyroiditis. The cross-sectional study conducted by Yalcin et al. indicates that autoimmunity of the thyroid gland may have an impact on impaired health-related quality of life, depression and anxiety in euthyroid patients with Hashimoto's thyroiditis independent of levothyroxine substitution. Some studies reported that even euthyroid Hashimoto's thyroiditis patients have an increased predisposition to depression and anxiety disorders.

The exact mechanisms underlying autoimmune thyroiditis pathogenesis are not fully understood. Multiple factors from the external environment and the genetic background contribute to the pathogenesis of Hashimoto's thyroiditis. These genetic, environmental, and existential factors provoke the immune system to produce antibodies to thyroid antigens. The most important factors associated with this disease are summarized in Table one.

Several genes have been involved in Hashimoto's thyroiditis pathogenesis, including genes of the immune response (coded in the Human Leukocyte Antigen complex) and thyroid function. Other immunoregulatory genes are involved in the development of Hashimoto's thyroiditis, including the single nucleotide polymorphisms in cytotoxic T lymphocyte-associated antigen four, protein tyrosine phosphatase non-receptor type twenty-two, and CD forty.

Among the environmental factors are insufficient or excessive iodine intake, infections, or the intake of certain medications. Several of the currently used anticancer drugs, such as interferon alpha, may cause autoimmune thyroid dysfunction. The role of smoking and alcohol consumption in the etiopathogenesis of Hashimoto's thyroiditis is still not clear. The data suggest that moderate alcohol consumption may protect against Hashimoto's thyroiditis and the development of overt hypothyroidism. Furthermore, some studies indicate that smoking decreases the levels of thyroid autoantibodies and the risk of hypothyroidism. However, the mechanism for these protective effects of smoking and drinking remains unclear and must be elucidated. In recent years, the influence of stress on the development and course of Hashimoto's thyroiditis has also been investigated. Some studies suggest that stress is involved in the pathogenesis of Hashimoto's thyroiditis, while other evidence indicates that it has no effect. A randomized controlled trial by Markomanolaki et al. showed that managing stress is also important in treating Hashimoto's thyroiditis patients. After eight weeks of stress management intervention, patients demonstrated a reduction in anti-thyroglobulin antibody titers, decreased levels of stress, depression, anxiety and improved lifestyle. Additionally, the adequate levels of vitamin D and selenium may help prevent or delay the onset of Hashimoto's thyroiditis. Moreover, the risk of Hashimoto's thyroiditis is increased in other autoimmune diseases.

The therapy of hypothyroidism as a result of HT is a daily, oral administration of synthetic thyroid hormone-levothyroxine, at a dosage of one point six to one point eight micrograms per kilogram of body weight. The substitution therapy must be taken for life in order to maintain normal T S H levels. In addition to the use of L T four, an appropriate diet and supplementation may be an important aspect of the treatment process. Selenium supplementation is associated with a significant decrease in T P O Ab. On the other hand, inadequate dietary selenium intake may exacerbate HT. Moreover, recent data demonstrated that vitamin D supplementation may have a beneficial effect on the course of HT.

In this review, based on the current literature, the influence of micronutrients and the effectiveness of selected types of diets in the treatment of HT were assessed. We investigated the relationship between micronutrient supplementation, including vitamin D and selenium, and Hashimoto's thyroiditis. It has also not been established whether a gluten-free diet is necessary or whether any other diet may be of benefit in HT patients. Nutritional and supplementation guidelines for patients with Hashimoto's thyroiditis to improve health and quality of life and reduce the incidence of complications have still not been developed. Moreover, there was a need to summarize the current knowledge about the effect of overweight or obesity on the risk of metabolic disorders and the role of oxidative stress in HT patients. Their influence on the course of Hashimoto's thyroiditis has not been elucidated. We have tried to present a comprehensive view of these patients.