What is the cause of Hashimoto's thyroiditis?

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Last updated: September 11, 2025View editorial policy

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Causes of Hashimoto's Thyroiditis

Hashimoto's thyroiditis is caused by a complex interplay of genetic susceptibility, environmental triggers, and immune dysregulation that leads to autoimmune destruction of the thyroid gland.

Genetic Factors

  • HLA associations: Strong genetic predisposition linked to specific HLA-DR/DQ genes that can be either predisposing or protective 1
  • Sex-related factors: Women are affected 7-10 times more frequently than men, with X-chromosome inactivation patterns playing a significant role 2
  • Family history: Increased risk in individuals with family members who have autoimmune thyroid disorders

Environmental Triggers

  • Iodine exposure: Excessive iodine intake can trigger autoimmune thyroiditis in genetically susceptible individuals 1, 3

    • Highly iodinated thyroglobulin becomes more immunogenic
    • Universal salt iodization programs can have a transient effect on increasing incidence
  • Micronutrient deficiencies:

    • Selenium deficiency: Selenoproteins are essential for thyroid function and protection against oxidative stress 3
    • Iron deficiency: Impairs thyroid metabolism as thyroid peroxidase (TPO) is a heme-containing enzyme 3
    • Vitamin D status: Lower vitamin D levels are observed in Hashimoto's patients, though this may be a consequence rather than a cause 3
  • Infections: Viral or bacterial infections may trigger autoimmunity through molecular mimicry 4

  • Stress: Can act as an immune modulator that contributes to disease development 4

Immunological Mechanisms

  • Loss of self-tolerance: Breakdown of immune tolerance mechanisms leads to autoimmune attack on thyroid tissue 2

  • Lymphocytic infiltration: T-cell infiltration of the thyroid gland is the histological hallmark 5

  • Autoantibody production:

    • Thyroid peroxidase antibodies (TPO-Ab)
    • Thyroglobulin antibodies (TG-Ab)
  • Thyrocyte destruction: Progressive destruction of thyroid follicles leads to gradual atrophy and fibrosis of the gland 5

Associated Autoimmune Conditions

Hashimoto's thyroiditis frequently coexists with other autoimmune disorders 1:

  • Addison's disease
  • Vitiligo
  • Celiac disease
  • Autoimmune hepatitis
  • Myasthenia gravis
  • Pernicious anemia
  • Systemic lupus erythematosus (2.8-3% of HT patients)
  • Sjögren syndrome (2.8-7% of HT patients)
  • Rheumatoid arthritis (2-4% of HT patients)
  • Inflammatory bowel disease (2-11.4% of HT patients)

Clinical Implications

  • The multifactorial etiology explains why Hashimoto's thyroiditis presents with variable clinical courses:

    • Initial thyrotoxicosis (Hashitoxicosis) when stored hormones are released from destroyed follicles
    • Euthyroid phase when preserved thyroid tissue compensates
    • Progressive hypothyroidism as destruction advances
  • Understanding the causes helps guide monitoring and treatment:

    • Assessing iodine, selenium, iron, and vitamin D status
    • Screening for other autoimmune conditions
    • Monitoring thyroid function regularly
  • Patients with Hashimoto's thyroiditis have:

    • 1.6 times higher risk of papillary thyroid cancer
    • 60 times higher risk of thyroid lymphoma compared to the general population 2

The interplay between genetic susceptibility and environmental triggers in Hashimoto's thyroiditis underscores the importance of comprehensive evaluation and management of both thyroid function and associated autoimmune conditions.

References

Guideline

Thyroid Dysfunction Diagnosis and Treatment

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Research

Multiple Nutritional Factors and the Risk of Hashimoto's Thyroiditis.

Thyroid : official journal of the American Thyroid Association, 2017

Research

Hashimotos' thyroiditis: Epidemiology, pathogenesis, clinic and therapy.

Best practice & research. Clinical endocrinology & metabolism, 2019

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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