Background

• Hashimoto’s thyroiditis, which is also known as the chronic lymphocytic thyroiditis, is an autoimmune disorder that affects the thyroid gland. It is the most common cause of hypothyroidism in developed countries, particularly in women. 
• In Hashimoto’s thyroiditis condition, the immune system attacks the thyroid gland, leading to inflammation and damage. Over time, this can cause the thyroid gland to become enlarged and form a goiter, and it can also result in decreased thyroid hormone production, leading to hypothyroidism. 
• Symptoms of Hashimoto’s thyroiditis can include fatigue, weight gain, cold intolerance, dry skin, hair loss, and depression. Diagnosis is typically made through blood tests to measure thyroid hormone levels and thyroid antibodies, as well as a physical examination of the thyroid gland. 

Epidemiology

• Hashimoto’s thyroiditis is common cause of hypothyroidism in developed countries, with an estimated 1-2% prevalence in the general population. It is more common in women than men, with a female-to-male ratio of approximately 10:1. 
• The condition can occur at any age but is most commonly diagnosed in middle-aged women. It is also more common in individuals with a family history of autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, and lupus. 
• The incidence of Hashimoto’s thyroiditis varies by region and ethnicity, with higher rates reported in areas with higher iodine intake, such as Japan. In addition, certain genetic factors have been associated with an increased risk of developing the condition. 
• Overall, Hashimoto’s thyroiditis is a relatively common autoimmune disorder that affects a significant proportion of the population, mainly middle-aged women, and close monitoring and appropriate treatment are essential for optimal management of the condition. 

Anatomy

Pathophysiology

• Hashimoto’s disease is an autoimmune disorder characterized by lymphocyte infiltration, fibrosis. The current method of diagnosis involves a correlation of clinical symptoms with laboratory findings that show elevated TSH levels and normal-low thyroxine levels.  
• Interestingly, there is limited evidence to support the role of anti-TPO (antithyroid peroxidase) antibodies in pathogenesis of AITD (autoimmune thyroid disease). While anti-TPO antibodies could activate complement and invitro studies have shown that they can bind and destroy thyrocytes, there is no known correlation in human research studies between severity of the disease and levels of anti-TPO antibodies concentration in the serum. However, we know that a positive serum levels of anti-TPO antibody concentration is linked to the active phase of disease. Other theories propose that immune complexes containing the thyroid-directed antibodies may be responsible for thyroid destruction. 

Etiology

• The exact cause of Hashimoto’s thyroiditis is not fully understood, but it is believed to be a combination of genetic and environmental factors. 
• In individuals with a genetic predisposition to autoimmune disorders, exposure to specific environmental triggers may mistakenly cause the immune system to attack the thyroid gland. These triggers may include viral infections, radiation exposure, and certain medications. 
• In Hashimoto’s thyroiditis condition, the immune system produces antibodies that attack the thyroid gland, leading to inflammation and damage to the thyroid tissue. Over time, this can cause the thyroid gland to become enlarged and form a goiter, and it can also result in decreased thyroid hormone production, leading to hypothyroidism. 
• There may also be a link between Hashimoto’s thyroiditis and iodine intake. While iodine is necessary for producing thyroid hormone, excessive iodine intake can trigger or worsen autoimmune thyroiditis in susceptible individuals. In areas with low iodine intake, the condition is less common. 
• Overall, the etiology of Hashimoto’s thyroiditis is complex and multifactorial, and further research is needed to fully understand the underlying mechanisms and potential triggers of the condition. 

Genetics

Prognostic Factors

The prognosis for Hashimoto’s thyroiditis is generally good, particularly with appropriate treatment to replace thyroid hormone and manage related symptoms. However, certain factors may influence the prognosis for individuals with the condition. 

• Age at diagnosis: The younger the age at diagnosis, the higher the risk of developing complications such as nodules or thyroid cancer. 
• Severity of thyroid gland damage: Individuals with more severe thyroid gland damage, as indicated by higher thyroid peroxidase (TPO) antibodies and ultrasound evidence of thyroid gland fibrosis, may have a worse prognosis and require more aggressive treatment. 
• Presence of related autoimmune diseases: Individuals with other autoimmune diseases, such as type 1 diabetes, may have a higher risk of developing complications and require more frequent monitoring. 
• Compliance with treatment: Appropriate management of Hashimoto’s thyroiditis requires regular monitoring and adherence to thyroid hormone replacement therapy. Noncompliance with treatment can lead to worsening of symptoms and complications. 
• Family history of thyroid cancer: Individuals with a family history of thyroid cancer may have a higher risk of developing thyroid cancer, particularly if they have nodules or other suspicious findings on imaging studies. 

With appropriate treatment and regular monitoring, the prognosis for individuals with Hashimoto’s thyroiditis is generally reasonable. However, certain factors may increase the risk of complications and require more aggressive management. 

Clinical History

Hashimoto’s thyroiditis can present with many symptoms and clinical features. The age of onset, associated comorbidities or activity, and acuity of the presentation can vary depending on the individual. 

• Age group: Hashimoto’s thyroiditis can occur at any age, but it is most commonly diagnosed in middle-aged women.Although, it can also be seen in children and adolescents. 

Physical Examination

Physical examination is an essential component of diagnosing Hashimoto’s thyroiditis. The following are key findings that may be observed during a physical exam: 

• Goiter: Hashimoto’s thyroiditis can cause enlargement of the thyroid gland, leading to the formation of a goiter. A goiter may be visible or palpable in the neck and may be smooth or nodular in appearance. 
• Texture: The texture of the thyroid gland may be firm, rubbery, or even complex in cases of advanced fibrosis. 
• Tenderness: The thyroid gland may be tender to touch in cases of acute inflammation. 
• Lymphadenopathy: Enlarged lymph nodes in the neck may be palpable, particularly in cases of more severe inflammation or lymphocytic infiltration. 
• Other signs: Other signs of hypothyroidism, such as dry skin, brittle nails, and hair loss, may also be present. 

It is important to note that physical examination findings alone are insufficient for diagnosing Hashimoto’s thyroiditis, and further diagnostic testing, such as blood tests and imaging studies, is usually required for confirmation. 

Age group

Associated comorbidity

• Hashimoto’s thyroiditis is an autoimmune disorder often associated with other autoimmune diseases, such as type 1 diabetes, rheumatoid arthritis, and lupus. Additionally, certain activities, such as pregnancy and stress, may exacerbate symptoms in individuals with Hashimoto’s thyroiditis. 

Associated activity

Acuity of presentation

• The presentation of Hashimoto’s thyroiditis can range from asymptomatic to severe hypothyroidism. Some individuals may have no symptoms, while others may present with various symptoms, such as fatigue, weight gain, cold intolerance, constipation, dry skin, hair loss, and menstrual irregularities. In some cases, symptoms may be gradual, while in others, they may be more acute. 

Differential Diagnoses

The differential diagnosis of Hashimoto’s thyroiditis includes a variety of other thyroid disorders, as well as other conditions that can cause similar symptoms or laboratory abnormalities. These include: 

• Euthyroid sick syndrome: This condition in which thyroid function tests may be abnormal due to a non-thyroidal illness, but the patient is euthyroid and does not require thyroid hormone replacement therapy. 
• Goiter: Enlargement of the thyroid gland can be due to various causes, including iodine deficiency, nodular goiter, or thyroid cancer. 
• Graves disease (diffuse toxic goiter): This autoimmune disorder causes hyperthyroidism and is characterized by thyroid-stimulating immunoglobulins. 
• Hypopituitarism (panhypopituitarism): This is a condition in which the pituitary gland fails to produce sufficient hormones, which can lead to secondary hypothyroidism. 
• Lithium-induced goiter: Chronic lithium use can cause goiter and hypothyroidism. 
• Nontoxic goiter: Enlargement of the thyroid gland without associated hyper- or hypothyroidism can be due to various causes, including iodine deficiency or nodular goiter. 
• Polyglandular autoimmune syndrome type 1 and type 2: These are rare autoimmune disorders that can involve multiple endocrine glands, including the thyroid gland. 
• Thyroid cancer (lymphoma): Thyroid cancer can present with a thyroid nodule or with signs and symptoms of hyper- or hypothyroidism. 
• Toxic nodular goiter: This condition in which one or more nodules in the thyroid gland produce excess thyroid hormone, leading to hyperthyroidism. 

Laboratory Studies

Imaging Studies

Procedures

Histologic Findings

Staging

Treatment Paradigm

• The treatment of Hashimoto’s thyroiditis typically involves hormone replacement therapy to address the hypothyroidism resulting from the autoimmune thyroid gland attack.
• The goal of treatment is to normalize thyroid hormone levels, relieve symptoms, and prevent further thyroid gland damage. 

by Stage

by Modality

Chemotherapy

Radiation Therapy

Surgical Interventions

Hormone Therapy

Immunotherapy

Hyperthermia

Photodynamic Therapy

Stem Cell Transplant

Targeted Therapy

Palliative Care

• Some environmental factors can exacerbate or trigger Hashimoto’s thyroiditis, such as iodine deficiency or excess, exposure to radiation, and smoking. Avoiding these triggers or addressing underlying nutritional deficiencies can help improve the management of Hashimoto’s thyroiditis. 

• Hormone replacement therapy with levothyroxine (synthetic thyroid hormone) is the primary treatment for Hashimoto’s thyroiditis. The dose usually starts low and gradually increases until the desired thyroid hormone levels are achieved. Regular blood tests are advised to monitor thyroid hormone levels are necessary to adjust the medication dose as needed. 

• In some cases, nodules or goiters associated with Hashimoto’s thyroiditis may require intervention with a procedure such as fine-needle aspiration biopsy or surgery, particularly if they are causing symptoms or there is a concern for malignancy. 

• The management of Hashimoto’s thyroiditis typically involves two phases: the acute phase, which involves the initiation of hormone replacement therapy and monitoring for response and any potential side effects, and the maintenance phase, which involves ongoing monitoring of thyroid hormone levels, adjusting the medication dose as needed, and regular follow-up with a healthcare provider. 

Medication

Future Trends

Media Gallary

References

• https://www.ncbi.nlm.nih.gov/books/NBK459262/#article-22579.s3