Hashimoto’s thyroiditis,

Thyroiditis refers to inflammation of the thyroid gland. Hashimoto’s thyroiditis, named after the Japanese physician Hakaru Hashimoto, is a common condition primarily affecting women. Also known as chronic lymphocytic thyroiditis, it is an autoimmune disease where the immune system attacks the thyroid gland. This leads to chronic inflammation and eventually causes hypothyroidism (underactive thyroid). While the exact causes are not fully understood, genetic, environmental, and immunological factors are believed to contribute. Below are the primary causes and contributing factors:

Genetic Factors

  1. Inherited Predisposition:
    • Hashimoto’s often runs in families. Having close relatives with Hashimoto’s or other autoimmune diseases increases the risk.
  2. Specific Genes:
    • Certain gene variants, often related to immune system regulation, can heighten susceptibility to autoimmune diseases, including Hashimoto’s.

Environmental Factors

  1. Iodine Intake:
    • Both iodine deficiency and excessive iodine intake can influence the development of Hashimoto’s. High iodine levels may trigger an autoimmune reaction in predisposed individuals.
  2. Infections:
    • Some viral or bacterial infections can activate the immune system, potentially triggering an autoimmune response against the thyroid.
  3. Stress:
    • Chronic stress is considered a potential trigger for autoimmune diseases, as it impacts immune system regulation.

Immunological Factors

  1. Misguided Immune Response:
    • In Hashimoto’s, the immune system produces antibodies against thyroid tissue, such as thyroid peroxidase antibodies (TPO antibodies). These antibodies attack the thyroid, causing inflammation and gradual tissue destruction.
  2. Dysfunction of Regulatory T-Cells:
    • Regulatory T-cells, which help maintain immune balance, may malfunction and contribute to autoimmune diseases like Hashimoto’s.

Hormonal Fluctuations

  1. Gender and Hormones:
    • Hashimoto’s is more common in women, particularly during hormonal changes such as puberty, pregnancy, and menopause. This suggests that female hormones may play a role in its development.

Other Contributing Factors

  1. Age:
    • While Hashimoto’s can occur at any age, it is most commonly diagnosed in middle-aged adults.
  2. Other Autoimmune Diseases:
    • Individuals with autoimmune conditions like Type 1 diabetes or rheumatoid arthritis are at increased risk of developing Hashimoto’s.

The development of Hashimoto’s thyroiditis is multifactorial, involving genetic predisposition, environmental triggers, and immune dysregulation. This complex interaction leads the immune system to attack the thyroid, ultimately causing hypothyroidism. Early diagnosis and treatment are essential for managing symptoms and preventing complications.

Symptoms and Progression

The disease typically begins slowly and without noticeable symptoms, as pain is not a characteristic feature. Some patients report a sense of tightness or a lump in the throat. Occasionally, during early stages, the inflammation can cause an excessive release of thyroid hormones into the bloodstream, resulting in transient hyperthyroidism. More commonly, however, the condition progresses to hypothyroidism over several years.

Laboratory Investigations

  • TSH (Thyroid-Stimulating Hormone):
    • Elevated TSH is a hallmark of hypothyroidism and the most sensitive early indicator of thyroid dysfunction.
  • Free T4 and Free T3:
    • These tests measure unbound thyroid hormones in the blood. In Hashimoto’s, free T4 and T3 are often low or normal, with an elevated TSH.
  • Thyroid Antibodies:
    • Anti-TPO Antibodies (Thyroid Peroxidase Antibodies): These are typically elevated in Hashimoto’s and support the diagnosis.
    • Anti-Tg Antibodies (Thyroglobulin Antibodies): These may also be elevated but are less specific than TPO antibodies.

Long-Term Effects and Treatment

In most patients, Hashimoto’s leads to a gradual reduction in thyroid size and function over the years. Eventually, the thyroid becomes incapable of producing sufficient hormones, necessitating hormone replacement therapy. Regular monitoring of laboratory values is recommended to detect when hormone supplementation is needed. Since there is no treatment targeting the immune cells attacking the thyroid, current therapy focuses on replacing lost thyroid function.

  • Lifelong Hormone Replacement:
    • Hormone replacement with levothyroxine (T4) is typically required for life. When appropriately dosed, this therapy restores physical and mental functionality, without causing weight gain or other complications.

Diagnosis

The diagnosis is based on:

  1. Laboratory tests (TSH, free T4/T3, thyroid antibodies).
  2. Typical ultrasound findings of the thyroid gland.
  3. A thyroid scan (scintigraphy) is unnecessary and only results in avoidable radioactive exposure.

Ultrasound Findings

Hashimoto’s thyroiditis presents characteristic patterns in thyroid ultrasound imaging, which, along with laboratory results, suffice for diagnosis.

Treatment

Treatment with thyroid hormones follows the same principles as for hypothyroidism:

  • Levothyroxine (T4) is administered, and dosage is adjusted to maintain optimal TSH levels.

Conclusion

Hashimoto’s thyroiditis is a chronic autoimmune disease that causes progressive damage to the thyroid gland, often leading to hypothyroidism. Although it cannot be cured, appropriate hormone replacement therapy ensures normal physical and mental performance. With proper management, patients can lead full, healthy lives without significant complications.

Ultrasound image of highly active Hashimoto’s thyroiditis.

Typical ultrasound image of highly active Hashimoto’s thyroiditis. On the left, a transverse section, and on the right, a longitudinal section of the thyroid gland, which appears much darker and more irregular than normal due to inflammation.

Selenium in Autoimmune Thyroiditis

Smaller studies have shown positive effects of supplementing with the trace element selenium on both well-being and antibody levels in autoimmune thyroiditis.

A 2001 study by a Munich research group demonstrated that daily intake of 200 µg selenium can reduce TPO antibodies by up to 36%. This suggests a potential immunomodulatory approach to treating this autoimmune condition. Previously, treatment was limited to hormone replacement therapy with thyroid hormone tablets.

Selenium Basics

  • Like iodine, selenium is a trace element essential for the body.
  • The human body cannot produce selenium; it must be obtained through diet. However, selenium content in soil varies greatly, leading to frequent deficiencies.
  • Soils in Central Europe generally have lower selenium concentrations, contributing to lower dietary selenium intake in these regions.

Selenium Deficiency

  • Blood selenium levels can be measured, but the test is costly and complex.
  • It is estimated that individuals living in urban environments with normal environmental exposures require 100–200 µg of selenium per day.
  • In Germany, the average selenium intake is currently around 40 µg per day, which is insufficient for optimal health.

Role in Autoimmune Thyroiditis

  • Selenium is a component of antioxidant enzymes that neutralize free oxygen radicals released during inflammatory processes.
  • These enzymes reduce oxidative damage and may help protect thyroid cells from destruction in thyroiditis.

Selenium Supplementation

  • Selenium is available as standalone preparations, including tablets or liquid forms.
  • Daily doses up to 2000 µg have shown no adverse effects with short-term use.
  • Symptoms such as hair loss, graying of hair, nail loss, headaches, liver damage, stomach issues, or garlic-like breath occur only with long-term use exceeding 500 µg/day. These symptoms typically resolve within 1–2 weeks after discontinuation.
  • Various selenium supplements are available over the counter. As dietary supplements, they are not covered by health insurance.
  • The Munich study used 200 µg sodium selenite per day, not selenium yeast.