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Hashimoto's thyroiditis, also known as chronic lymphocytic thyroiditis, Hashimoto's disease, and autoimmune thyroiditis is an autoimmune disease in which the thyroid gland is gradually destroyed. [7] [1] Early on, symptoms may not be noticed. [3] Over time, the thyroid may enlarge, forming a painless goiter. [3]
Hakaru Hashimoto (橋本 策, Hashimoto Hakaru, May 5, 1881 – January 9, 1934) [1] [2] was a Japanese doctor and medical scientist of the Meiji and Taishō periods. He is best known for publishing the first description of the disease that was later named Hashimoto's thyroiditis .
In areas where iodine-deficiency is not found, the most common type of hypothyroidism is an autoimmune subtype called Hashimoto's thyroiditis, with a prevalence of 1-2%. [40] As for hyperthyroidism, Graves' disease, another autoimmune condition, is the most common type with a prevalence of 0.5% in males and 3% in females. [41]
Hashimoto's thyroiditis is also known as chronic lymphocytic thyroiditis, and patients with this disease often complain about difficulty swallowing. This condition may be so mild at first that the disease goes unnoticed for years. The first symptom that shows signs of Hashimoto's thyroiditis is a goiter on the front of the neck.
It is associated with Hashimoto's thyroiditis, and was first described in 1966. It is sometimes referred to as a neuroendocrine disorder, although the condition's relationship to the endocrine system is widely disputed. It is recognized as a rare disease by the NIH Genetic and Rare Diseases Information Center. [1]
Hashitoxicosis, which can be abbreviated "Htx", [1] is a transient hyperthyroidism caused by inflammation associated with Hashimoto's thyroiditis disturbing the thyroid follicles, resulting in excess release of thyroid hormone. [2
The first sign of Ord's thyroiditis is the atrophy of the thyroid gland from the start this can be identified by ultrasound. [2] Another sign to help identify this disease is the presence of blocking anti-TSH receptors. Ord's thyroiditis can share symptoms with functional hypothyroidism. [3]
Hashimoto's thyroiditis [2] Thyroglobulin antigen Hypothyroidism, hard goiter, follicular thymitis Inflammatory bowel disease [2] Enteric microbiota and/or self antigens Hyperactivation of T-cells, cytokine release, recruitment of macrophages and other immune cells, inflammation Multiple sclerosis [2] Myelin antigens (e.g., myelin basic protein)