Open access peer-reviewed chapter - ONLINE FIRST
Abstract
Hashimoto’s thyroiditis is the most common type of thyroiditis, an inflammatory disease of the thyroid gland. Antibodies that the body normally produces against substances foreign to the body, together with the immune system, attack the thyroid cells and cause inflammation and damage to the thyroid gland. Thus, the thyroid gland cannot fulfill its function, and the level of hormones it secretes decreases over time. It is familial and is mostly seen in women between the ages of 30–50. Hashimoto’s thyroid is one of the causes of “hypothyroidism”, a condition in which the thyroid gland is underactive. The thyroid hormone, which regulates the body’s metabolic rate and thus affects all tissues, decreases over time in these patients, and the risk of hypothyroidism increases with age. Another problem that Hashimoto’s thyroid can cause in the thyroid gland is nodule formation. In general, enlargement of the thyroid gland is common, especially in the beginning, and this may be accompanied by nodule formation in the process. Hashimoto’s thyroid should be detected early, and thyroid hormone levels should be monitored at regular intervals and replaced with medication if necessary. With close follow-up and treatment, patients do not experience adverse effects related to Hashimoto’s thyroid.
Keywords
- Hashimoto’s thyroiditis
- hypothyroidism
- thyroid antibodies
- thyroid peroxidase
- chronic autoimmune thyroiditis
1. Introduction
In areas with adequate iodine, Hashimoto’s thyroiditis is the primary reason for hypothyroidism. Hashimoto initially described this condition in 1912, and it primarily affects women, impacting approximately 10% of the population. As individuals age, the prevalence of this disease rises [1]. We now acknowledge Hashimoto’s thyroiditis as an autoimmune thyroid disorder with a rising incidence [2].
Presently, Hashimoto’s thyroiditis is the primary cause of hypothyroidism [3], and patients with this condition face an elevated risk of cardiovascular diseases and malignancies [4]. The disease’s progression involves lymphocytic infiltration and autoimmune damage to the thyroid gland. Nearly all patients with this disease exhibit elevated serum antibody levels against thyroid antigens, along with extensive lymphocytic infiltration primarily involving thyroid-specific B and T cells.
The disease typically involves follicular destruction, which results from a combination of genetic predisposition and environmental factors. Despite their distinct clinical presentations, the familial link between Graves’ disease and the occasional transition from Graves’ disease to Hashimoto’s thyroiditis suggests a related pathophysiological connection between these two disorders [5].
Here, we discuss the etiological factors and pathophysiological changes that contribute to the development of the disease. Diagnostic methods, various treatment strategies, and important considerations in patient management are also discussed.
2. Epidemiology
Over the last three decades, there has been a significant rise in the occurrence of Hashimoto’s thyroiditis [6]. Presently, Hashimoto’s thyroiditis ranks among the most prevalent thyroid disorders, affecting 0.3–1.5 cases per 1000 people [7]. Over 10% of women test positive for antibodies related to Hashimoto’s thyroiditis, and around 2% experience clinical symptoms.
Although Hashimoto’s thyroiditis is less common among Pacific Islanders, individuals of white ethnicity have a higher incidence compared to those of black ethnicity [8].
The prevalence of the disease increases with age. The exact reasons behind the elevated prevalence of Hashimoto’s thyroiditis in women remain unclear. However, potential factors include similarities to animal models of other autoimmune diseases and the influence of X chromosome inactivation and fetal microchimerism due to female sex hormone exposure [9].
Hashimoto’s thyroiditis can present itself in three ways: on its own, in conjunction with other autoimmune diseases like type 1 diabetes mellitus and Sjögren syndrome, or paired with other thyroid conditions. It is worth noting that within this last category, the incidence of papillary thyroid cancer can vary between 0.5% and 30%.
The development of Hashimoto’s thyroiditis has been linked to climatic factors. For instance, Siberian women exhibit a greater density of thyroid peroxidase (TPO) antibodies compared to the overall population [10]. Additionally, Hashimoto’s thyroiditis may be more prevalent in specific conditions, including myasthenia gravis (MG) and systemic sclerosis.
Hashimoto’s thyroiditis serves as a typical illustration of organ-specific autoimmune conditions and frequently coexists with other autoimmune diseases within the same patient or family, implying a shared genetic foundation [11]. Notably, Hashimoto’s thyroiditis and systemic lupus erythematosus were the initial diseases where a genetic underpinning for autoimmunity, specifically associated with MHC class II genes, was established during the early 1970s.
Despite extensive research spanning four decades, only a handful of susceptibility genes have been pinpointed for Hashimoto’s thyroiditis, each exerting a modest influence on the disease phenotype via mechanisms that remain unclear [12].
3. Etiology
There are primary and secondary causes.
3.1 Primary Hashimoto’s disease
The most prevalent type of Hashimoto’s thyroiditis is the primary form, which includes cases where no specific causes can be identified. This form encompasses a clinical and pathological spectrum comprising six main variants: the classical form, fibrous variant, IgG4-related variant, juvenile form, Hashitoxicosis, and painless (or silent) thyroiditis [13].
The latter variant may occur sporadically or postpartum. The typical clinical presentation involves enlargement of the thyroid gland (goiter), with or without hypothyroidism. Pathologically, all these variants share a common feature: pronounced lymphocytic infiltration within the thyroid gland.
3.2 Secondary Hashimoto’s disease
These forms involve identifiable etiological agents. More frequently, it results from medical intervention and the use of immunomodulatory medications. A case in point is interferon-alpha, which, when used to treat hepatitis C viral infection, can trigger or worsen thyroiditis [14].
Recent progress in cancer immunotherapy has revealed various immune-related adverse events, including thyroiditis, associated with the use of monoclonal antibodies that block CTLA-4 or cancer vaccines.
4. Pathogenesis
The development of Hashimoto’s thyroiditis involves a complex, multistep process influenced by genetic, environmental, and immunological factors. In essence, the breakdown of immune tolerance toward normal thyroid cells results in the production of antibodies targeting thyroid tissue, leading to thyroid gland destruction. The initial inflammatory changes occur when genetically susceptible individuals encounter the aforementioned environmental factors.
Following this, cells expressing major histocompatibility complex (MHC) class 2 antigens, including dendritic cells and macrophages, infiltrate the thyroid gland. These cells present the thyroid’s autoantigens to the immune system for recognition and processing. Among the various potential auto-antigens, thyroglobulin, the primary protein produced in thyroid tissue, plays a central role in the disease’s pathogenesis [15]. Notably, thyroglobulin protein encompasses approximately 40 distinct epitope types critical to the disease process [16].
In the disease’s pathogenesis, thyroid peroxidase an enzyme responsible for iodine oxidation serves as a crucial autoantigen. Moreover, 180 different types of thyroid peroxidase antibodies have been identified to date. Studies have confirmed that antibodies against the thyrotropin receptor and the sodium iodide symporter, which have been detected in patients with autoimmune thyroid disease, do not play a significant role in the pathogenesis of this condition.
Initially, a functional alteration occurs in B cells, leading to the production of autoantibodies in the disease process. Furthermore, T cell dysfunction contributes to the disturbance of immune balance targeting thyroid tissue [17]. Hence, we can infer that both cellular and humoral immunity play a role in the development of Hashimoto’s thyroiditis. Cellular immunity has been found in Hashimoto’s patients with CD8+ T cells against thyroglobulin and TPO [18].
Nevertheless, only a small proportion (approximately 2–3%) of CD8+ cells specifically target TG/TPO, indicating that the majority are not thyroid antigen-specific. Furthermore, recent studies have revealed that cell death in autoimmune thyroiditis is not only dependent on cytotoxicity but also on apoptotic processes. “Suppressor T cells”, a specialized population of CD8+ cells, are thought to be able to inhibit harmful immune responses. It is hypothesized that Hashimoto’s thyroiditis involves altered function of T cell suppressors targeting specific thyroid antigens. Certain functions attributed to T suppressor cells are also carried out by T regulatory cells [19].
A key hallmark of Hashimoto’s thyroiditis is the generation of specific antibodies targeting thyroid tissue [20]. In most cases, Hashimoto’s patients produce autoantibodies against thyroglobulin (TG) and thyroid peroxidase (TPO). Furthermore, analyzing anti-TPO antibodies proves valuable in predicting the development of hypothyroidism. A recent description of Hashimoto’s includes a variant known as IgG4 thyroiditis, characterized by the presence of IgG4-positive cells within the context of a systemic autoimmune disorder [21].
Several studies have reported elevated serum levels of Th1 cells, as well as IL-17 and IL-22 cytokines, in individuals with Hashimoto’s thyroiditis [22]. Evidence indicates that IL-12 cytokine levels are elevated in 56% of Hashimoto’s patients [23]. A recent study proposed that circulating exosomes actively contribute to the pathogenesis of Hashimoto’s thyroiditis (HT) [24]. Exosomes possess the ability to transport bioactive molecules to other cells, impacting biological processes. They participate in diverse cellular functions, including antigen presentation, inflammatory activation, autoimmune conditions, and tumor metastasis. Hashimoto-specific exosomes can present antigens to dendritic cells (DCs), triggering DC activation through the NFκB signaling pathway by binding to TLR2/3. This process may disrupt CD4+ T lymphocyte differentiation and potentially contribute to the development of Hashimoto’s thyroiditis.
A similar process has been observed in systemic lupus erythematosus; however, further studies are necessary to validate this hypothesis in Hashimoto’s patients. Hashimoto’s thyroiditis (HT) frequently coexists with other autoimmune disorders, suggesting a potential shared poly-autoimmune origin. In a large prospective study involving 3209 patients with Graves’ disease, Ferrari and colleagues investigated the association of this thyroid disorder with other autoimmune conditions.
A significant proportion of Graves’ patients (16.7%) presented with additional autoimmune diseases, including vitiligo, autoimmune gastritis, rheumatoid arthritis, polymyalgia rheumatica, multiple sclerosis, and celiac disease. Notably, some patients were diagnosed with three or more associated autoimmune disorders [25].
5. Symptoms and diagnosis
The current diagnostic criteria for Hashimoto’s thyroiditis involve evaluating clinical features, detecting serum antibodies against thyroid antigens (primarily thyroperoxidase and thyroglobulin), and assessing the thyroid sonogram. Radioactive iodine uptake and cytological examination of thyroid aspirate are infrequently employed in the diagnostic process.
5.1 Clinical features
Hashimoto’s thyroiditis (HT) manifests with both local and systemic symptoms, as well as features specific to different forms of the disease. Local symptoms arise due to pressure on cervical structures near the thyroid gland. These include dysphonia (caused by involvement of the recurrent laryngeal nerve), dyspnea (due to tracheal constriction), and dysphagia (resulting from pressure on the esophagus).
Systemic symptoms emerge from thyroid gland dysfunction, leading to primary hypothyroidism. Given the far-reaching impact of thyroid hormones on various organs and tissues, the signs and symptoms of hypothyroidism are diverse and variable.
5.1.1 Gastrointestinal system
Hypothyroid patients frequently report constipation as their primary complaint. Reduced peristalsis can occasionally result in pseudo-obstruction or ileus. Additionally, gallbladder hypotonia and alterations in bile composition may contribute to an increased risk of bile duct stone formation.
5.1.2 Skin involvement
Hypothyroid patients commonly exhibit skin alterations, including dryness, coldness, yellowness, and thickening. These changes arise from the accumulation of hydrophilic mucoproteins, such as hyaluronic acid, in the skin, leading to myxedema. Additionally, sweat gland atrophy contributes to these manifestations. Hair becomes coarse and prone to falling out, while nails become thin and brittle.
5.1.3 Cardiovascular system
Hypothyroidism is characterized by classic signs, including bradycardia and reduced amplitude of cardiac waves on electrocardiogram. These manifestations result from decreased ventricular contractility, increased peripheral resistance, and their combined impact on cardiac output. Cardiomegaly may be present, often accompanied by pericardial effusion. Additionally, hypothyroid patients frequently experience coronary artery disease, likely influenced by the effects of thyroid hormones on lipid metabolism. Notably, hypothyroidism leads to reduced levels of cholesterol and LDL cholesterol, both recognized as atherogenic factors.
5.1.4 Skeletal muscles
The muscles appear hypertrophic due to the myxedematous infiltration of the connective tissue. The contraction and relaxation times are delayed and may cause pain and cramps.
5.1.5 Pulmonary system
Common respiratory abnormalities are bradypnea and hypoxia. These are caused by obstruction of the upper airways by enlarged soft tissues, weakness of the respiratory muscles, decreased chest wall and lung compliance, increased capillary permeability, and pleural effusion. Respiratory failure may occur in patients with myxedematous coma.
5.1.6 Hematopoietic system
Anemia is common in hypothyroidism. It can be normocytic (due to decreased renal secretion of erythropoietin), hypochromic, and microcytic (due to impaired iron absorption) or megaloblastic (due to gastric atrophy with B12 vitamin malabsorption).
5.1.7 Reproductive system
Oligomenorrhea and/or menometrorrhagia are common. Menstrual cycles are often anovulatory due to impaired conversion of estrogen precursors. Hypothyroidism during pregnancy has been associated with an increased rate of miscarriage.
5.1.8 Urinary system
Fluid retention caused by decreased glomerular filtration has been described.
5.1.9 Neuro-psychiatric system
Patients with Hashimoto’s thyroiditis (HT) often experience difficulty concentrating, memory loss, and depression. A more contentious issue is Hashimoto’s encephalopathy, which was first reported in 1966 [26]. It manifests insidiously, resembling truncal ataxia associated with spino-cerebellar degeneration. Additionally, paroxysmal dyskinesia has been documented [27]. Over time, patients develop cognitive impairments affecting episodic memory, attention, executive function, and visual–spatial abilities, while retaining naming ability. Diagnostic criteria remain unclear, necessitating a diagnosis based on excluding other potential causes of encephalopathy in patients with HT.
5.2 Clinical variants
Hashimoto’s thyroiditis (HT) typically presents in the fifth decade of life and is more prevalent in women. The thyroid gland exhibits enlargement and firmness. Approximately 75% of patients are euthyroid at the time of diagnosis, while the remaining minority display a spectrum of dysfunction ranging from subclinical hypothyroidism (characterized by elevated TSH levels but thyroid hormones within the normal range) to overt hypothyroidism. The fibrous variant of HT, also more common in women but occurring at older ages, often presents with symptomatic goiter. The thyroid’s lobulated appearance can resemble benign nodules.
Most patients with HT experience hypothyroidism and require prompt thyroid hormone replacement. In advanced age, this fibrous variant progresses to a severe form of thyroid atrophy, clinically manifesting as idiopathic myxedema. Although the thyroid gland is non-palpable, patients exhibit hypothyroid symptoms that may be challenging to distinguish from age-related signs.
The IgG4-associated variant of HT, akin to the classic form, typically emerges in the fifth decade of life but at a younger age [28]. Unlike the disproportionately high female-to-male ratio of the classic form, this variant affects both sexes equally. Despite synthetic thyroid hormone administration, the IgG4-associated variant often follows a more aggressive course, leading to persistent subclinical hypothyroidism in many patients.
The juvenile form of Hashimoto’s thyroiditis (HT) typically appears before the age of 18, with the average age at referral being 11 [29]. While it is more prevalent in females, the ratio of females to males is lower. A majority of children show signs of goiter, but they usually do not exhibit any symptoms.
At the point of diagnosis, 43% of children have normal thyroid function (euthyroid), 24% have mild (subclinical) hypothyroidism, 21% have severe (overt) hypothyroidism, 9% have severe (overt) hyperthyroidism, and 3% have mild (subclinical) hyperthyroidism [30]. The disease progression can vary, including periods of remission, relapse, and eventual progression to permanent hypothyroidism.
The Hashitoxicosis variant, initially described by Fatourechi in 1971 [31], combines the clinical features of Graves’ hyperthyroidism with the pathological appearance of HT. The initial hyperthyroid phase closely resembles Graves’ disease, characterized by high thyroid uptake of radioactive iodine and the presence of thyroid-stimulating immunoglobulins. However, hyperthyroidism is transient, eventually transitioning to permanent hypothyroidism within a period of 3 to 24 months.
Silent thyroiditis, also known as painless thyroiditis, refers to a lymphocytic inflammation affecting the thyroid gland. It may manifest sporadically or more frequently within a year after childbirth. These two forms share indistinguishable characteristics, with the second form, associated with pregnancy, being termed postpartum thyroiditis. In regions with higher dietary iodine intake [32], painless thyroiditis tends to be more prevalent.
Scientifically, it is described as exhibiting a triphasic model, involving an initial phase of thyrotoxicosis, followed by hypothyroidism, and ultimately leading to recovery. Postpartum thyroiditis occurs in approximately 8% of all pregnancies [13], although estimates may vary based on the studied population and the frequency of follow-up.
Thyrotoxicosis, which typically occurs two to five months after delivery, has a duration of approximately one month. It is generally mild and seldom necessitates treatment, although beta-blockers can be employed. The underlying mechanism for the elevation in serum thyroid hormone levels is not excessive production by the thyroid gland (hyperthyroidism). Instead, it results from the release of previously synthesized hormones from thyroid follicles, triggered by destructive inflammation. Consequently, antithyroid drugs are not recommended during this phase.
Following thyrotoxicosis, a hypothyroid phase ensues, lasting approximately two to six months. During this period, symptoms are mild, and patients may be mistakenly attributed to postpartum depression. Fortunately, most women (80%) eventually recover normal thyroid function within a year after delivery. However, permanent hypothyroidism is more likely in women with multiple pregnancies and a history of postpartum thyroiditis.
5.3 Thyroperoxidase antibodies
Thyroid peroxidase antibodies serve as the optimal serological marker for diagnosing Hashimoto’s thyroiditis (HT). These antibodies are present in approximately 95% of HT patients, whereas they are rare in healthy individuals. In the context of postpartum thyroiditis, thyroid peroxidase antibodies also play a unique role by increasing the risk of hypothyroidism and long-term thyroid dysfunction in pregnant women who have them at the beginning of pregnancy.
The correlation between thyroid peroxidase antibody levels and the number of autoreactive lymphocytes infiltrating the thyroid is evident. Additionally, it relates to the degree of sonographic hypoechogenicity. On the other hand, thyroglobulin antibodies, which constitute the most abundant protein in the thyroid gland, are less sensitive than thyroid peroxidase antibodies (positive in only 60–80% of HT patients) and less specific (positive in a higher proportion of healthy controls).
Despite this, they serve their own purposes. In clinical practice, both antibodies are simultaneously assessed and fluctuate together following treatment interventions. Interestingly, thyroid antibodies exhibit poor correlation with each other. The interplay between thyroglobulin and thyroid peroxidase antibodies represents distinct facets of the autoimmune response against the thyroid gland.
Thyroglobulin antibodies might signify an initial, more innate immune response, whereas thyroid peroxidase antibodies could represent a subsequent adaptive immune response, a type of immune intensification. In line with this theory, thyroglobulin antibodies are anticipated to be present at the beginning of a disease that is inherently associated with thyroiditis.
Indeed, in mouse models of spontaneous autoimmune thyroiditis, thyroglobulin antibodies emerge before thyroid peroxidase antibodies. The commencement of disease is seldom seen in human autoimmune diseases. For instance, in the case of HT, the majority of patients have been living with the disease for a minimum of 7 years before they are clinically diagnosed. Hence, in humans, thyroid peroxidase antibodies are predicted to be more prevalent and elevated compared to thyroglobulin antibodies.
5.4 Ultrasonography
Among patients with thyroid conditions, neck ultrasound has become the most commonly employed imaging technique [33]. In Hashimoto’s thyroiditis (HT), there is a characteristic reduction in echogenicity, distinguishing it on ultrasound. The normal thyroid gland, composed of varying-sized thyroid follicles, scatters ultrasound, causing the lobes to appear bright.
Conversely, in HT, the destruction of thyroid follicles by small lymphocytes results in a significant decrease in echogenicity, making the thyroid parenchyma similar to the adjacent strap muscles.
Different forms of HT exhibit distinct characteristics; for example, the IgG4-associated variant [34] displays more pronounced hypoechogenicity, while the fibrous variant shows irregularity and nodularity due to collagen fiber accumulation. Thyroid ultrasound also allows for the measurement of the thyroid gland’s volume. The field of thyroid ultrasound is rapidly advancing, with ongoing efforts to improve visual impressions, facilitate point-of-use applications for endocrinologists and surgeons, and integrate with Doppler or elastography for additional information.
Lastly, ultrasound is commonly used in various centers to guide needle placement during fine needle aspiration, enhancing precision in targeting thyroid nodules.
5.5 Thyroid function tests, radioiodine uptake, and fine needle aspiration
The assessment of thyroid function in patients with HT is conducted by measuring the levels of serum thyrotropin (TSH) and free thyroxine (FT4). TSH serves as the most crucial indicator for monitoring thyroid function as its levels precisely adjust to the slightest changes in circulating thyroid hormones. Due to the variability in results, the 24-hour thyroid radioactive iodine uptake is seldom employed for diagnosing HT.
However, it proves beneficial in painless thyroiditis. During the hyperthyroid phase of this HT variant, contrary to what is expected in hyperthyroidism, the radioiodine uptake is reduced rather than increased. This is because the rise in circulating thyroid hormones is attributed to the destruction of thyroid follicles and the release of preformed thyroid hormones (thyrotoxicosis), not due to the enhanced function of the thyroid gland (hyperthyroidism).
Fine needle aspiration is commonly performed when a thyroid nodule is present in the patient. The majority of thyroid nodules are genuine neoplastic nodules, and most of them are benign tumors. However, in the fibrous variant of HT, considering that the dense keloid-like fibrosis disrupts the thyroid structure and gives the gland a lobular appearance, “pseudo-nodules” may be present. When thyroid antibodies and a nodule are present, it becomes challenging to determine whether the patient has two coexisting thyroid diseases or only the fibrous variant of HT.
Hence, fine needle aspiration is carried out, and the interpretation of the cytological results can be challenging. HT cytology typically presents a polymorphic lymphoid cell population (small mature lymphocytes, larger active lymphocytes, and occasionally plasma cells) along with Hurtle cells. Lymphocytes frequently interact with thyroid cell groups; this characteristic is believed to be beneficial in differentiating HT from thyroid neoplasms [35].
However, in some aspirates, there are no lymphoid cells, and they are composed almost entirely of Hurtle cells, which complicates the determination of whether these cells are Hurtle cells found in HT or those found in other oncocytic lesions of the thyroid, such as oncocytic adenomatoid nodule, Hurtle cell adenoma, or Hurtle cell carcinoma [36].
For these aspirates that are primarily composed of Hurtle cells, the cytopathologist employs the term “atypia of undetermined significance” [37] to denote the features that are neither benign nor malignant. Despite the Bethesda system’s recommendation for this category being conservative treatment and the fact that most of these Hurtle cell lesions are benign [38], numerous patients are referred to a surgeon, and thyroidectomy is frequently performed.
6. Treatment
The primary objective of HT treatment is to manage hypothyroidism, which involves the oral intake of a synthetic hormone, Levo-Thyroxine 4 (L-T4), at a dosage of 1.6–1.8 micrograms per kilogram of body weight. Lifelong substitution therapy is necessary to achieve normal levels of circulating thyrotropin (TSH).
In certain cases, L-T4 therapy might not be needed, and mere clinical observation could suffice. The use of glucocorticoids has been debated as they can control thyroiditis and rapidly enhance thyroid function, but the risks linked with high dosage and prolonged treatment are believed to surpass the benefit [39].
However, the short-term usage of prednisolone may offer a longer-term advantage in the IgG4 disease subgroup [40]. In recent times, the supplementary role of a specific diet in managing HT has been scrutinized. Overconsumption of iodine has been proposed to trigger thyroid autoimmunity in genetically susceptible individuals by amplifying the immunogenicity of thyroglobulin [41].
Therefore, even though a supplement suitable for a total intake of 250 g/day during pregnancy is advised, high iodine supplementation in HT should likely be avoided as it could pose a risk.
Selenium, which is involved in various selenoproteins, plays a crucial role in the homeostasis of human thyroid hormones, but the effectiveness of selenium supplementation in HT patients is a matter of debate [42].
The oral intake of selenium in the form of seleno-methionine could be advantageous for HT patients with a selenium deficiency and is expected to shield the thyroid gland from autoimmune damage. Numerous studies have demonstrated an association between Vitamin D deficiency and the pathogenesis and hypofunction of the thyroid in HT [43].
Given the affordability and minimal side effects of oral vitamin D supplementation, it may be advisable to screen and supplement HT patients for vitamin D deficiency, with clinical necessity dictating monthly monitoring of calcium and 25[OH]D levels [42].
The scope of HT surgery is restricted in the presence of a nodule with cervical anatomical structures or features of malignant transformation [44]. However, thyroidectomies performed on HT patients tend to have more complications than other thyroid disorders [45]. Looking ahead, the transplantation of the thyroid gland has been proposed as a solution to hypothyroidism, but further studies are required for confirmation [46].
7. Conclusions
In this section, we delved into the epidemiology, assumed pathogenesis, diagnosis, and treatment of Hashimoto’s thyroiditis. We also explored other autoimmune diseases and potential complications. Hashimoto’s thyroiditis often serves as a model for autoimmune disease in many respects. We also highlighted how environmental exposure can alter genetic susceptibility. As is the case with many subjects, increased knowledge often leads to more questions about what we understand. Consequently, HT remains a disease with an unknown pathogenesis, intricate and continually evolving, awaiting prevention strategies or novel treatment methods.
Financial support and sponsorship
The author reports no funding sources for this article.
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