Hashimoto’s Thyroiditis

Most common cause of hypothyroidism in the United States.

A cause of non-endemic goiter.

An average of 1 to 1.5 in a 1000 people have this disease.

Women to men between 10:1 and 20:1

Most prevalent between 45 and 65 years of age.

Prevalence has been increasing dramatically over the past 50 years.

Occurrence in children is also not uncommon, especially in populations where iodine deficient diet is present.

Caused by inflammation and is an autoimmune process.

Chronic lymphocytic thyroiditis is an autoimmune disease in which the thyroid gland is attacked by a variety of cell- and antibody-mediated immune processes.

Often results in hypothyroidism with bouts of hyperthyroidism.

Symptoms include: weight gain, depression, sensitivity to heat and cold, paresthesia, fatigue, bradycardia, tachycardia, hypoglycemia, constipation, hypercholesterolemia,, migraines, muscle weakness, cramps, memory loss, mania, infertility, hair loss, panic attacks psychosis.

The thyroid gland may be enlarged, lobulated in Hashimoto’s thyroiditis, or nonpalpable.

Changes of the thyroid is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy.

Antibodies against thyroid peroxidase (TPO) and/or thyroglobulin cause destruction of follicles in the thyroid gland.

Histologically, seen as diffuse parenchymal infiltration by lymphocytes, particularly plasma B-cells, which can often be seen as secondary lymphoid follicles, and by thyroid atrophy with dense fibrotic bands of collagen.

May be associated with non-Hodgkin lymphoma.

Diagnosis is made by detecting elevated levels of anti-thyroid peroxidase antibodies in the serum.

Given the relatively non-specific symptoms of initial hypothyroidism it is often misdiagnosed.

Lab evaluation includes:thyroid-stimulating hormone (TSH), Free T3, Free T4, and the anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO) and anti-microsomal antibodies.

Early presentation may be associated with elevated levels of thyroglobulin.

A family history of thyroid disorders is common.

The HLA-DR5 gene most strongly implicated.

May be associated with CTLA-4(Cytotoxic T-lymphocyte Associated-4) gene polymorphisms.

Increased incidence in patients with chromosomal disorders, including Turner, Down’s, and Klinefelter syndromes.

Small percentage of patients have no antibodies present, and a percentage of the population may also have antibodies without developing Hashimoto’s thyroiditis.

Antibody-dependent cell-mediated cytotoxicity damages thyroid cells by activation of cytotoxic T-lymphocytes.

Hypothyroidism is treated with lifelong thyroid hormone replacement.

If untreated may lead to muscle failure, including possible heart failure.

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