Hashimoto's disease

In Hashimoto's thyroiditis is an autoimmune disease characterized by inflammation and damage to the thyroid tissue. Damage occurs because the body's immune cells mistakenly attack the thyroid tissue. Thyroid tissue damaged by immunologic factors is replaced by lymphocytes, plasma cells and fibrosis.  These patients usually present with a firm, diffuse goitre; in some the gland is nodular and then can also present as a solitary thyroid nodule.  Unlike many thyroid disorders, Hashimot's often progresses quietly and might not be noticed until significant damage has occurred. Additionally, if not properly managed, it increases the risk of heart problems and can raise the overall risk of death.

Hashimoto's thyroidosis (HT) is one of two autoimmune thyroid disorders and is the more common of the two. Both conditions involve the immune system attacking the thyroid gland but affect thyroid hormone levels differently. In HT, the immune system creates autoantibodies known as thyroid peroxidase antibodies (TPOAb) and thyroglobulin antibodies (TgAb), destroying thyroid tissue and resulting in hypothyroidism.

The other autoimmune thyroid condition is Graves’ disease, which involves the formation of autoantibodies against the thyroid-stimulating hormone (TSH) receptor. Graves’ disease leads to hyperthyroidism, or overactive thyroid function.  Although it is not common, it is possible for an individual to progress from HT to Graves’ disease (or vice versa) or have symptoms of both.

There are several recognized variants or subtypes of HT:

• Painless thyroiditis: Also called silent or lymphocytic thyroiditis, this variant involves thyroid inflammation without pain or tenderness.
• Painful thyroiditis: In this variant, the thyroid gland becomes swollen and painful, often accompanied by fever. It is also called subacute thyroiditis or De Quervain thyroiditis.
• Postpartum thyroiditis: This temporary form of thyroiditis can occur in women within the first year after giving birth. It may cause fluctuating levels of thyroid hormones, leading to periods of both hyper- and hypothyroidism, but it usually resolves on its own. If it persists, it is classified as Hashimoto’s.
• IgG4-related thyroiditis: This is a recently identified variant that can mimic other thyroid disorders and is characterized by the presence of IgG4 antibodies. It is considered systemic.
• Fibrous variant: Occurring in about 10 percent of HT cases, this variant is marked by extensive fibrosis replacing normal, functional thyroid tissue.
• Fibrotic and atrophic variant: This variant is characterized by extensive fibrosis and atrophy of the thyroid gland.
• Riedel thyroiditis: This is a rare, chronic, and progressively worsening form of thyroiditis marked by significant fibrosis that may spread beyond the thyroid gland, potentially compressing nearby structures. While its link to HT isn’t well understood, some researchers view it as a variant.
• Hashitoxicosis: In this type, thyroid hormones are released from damaged thyroid follicles, causing temporary periods of thyrotoxicosis from too much thyroid hormone. Typically, this condition is managed with beta blockers instead of levothyroxine and usually progresses to permanent hypothyroidism within three to 24 months.

Hashimoto's disease is the most common cause of goitrous hypothyroidism in adults and sporadic goitre in children. HT can occur at any age, including childhood and adolescence. It affects at least 14 million people in the United States and up to 7.5 percent globally (2024). 

Typically HT affects women between the ages of 30 and 50. The risk of developing HT is at least four times greater for women than men. Additionally, thyroiditis can occur after giving birth. About 20 percent of women who develop postpartum thyroiditis eventually develop HT.