Hashimoto's thyroiditis overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Furqan M M. M.B.B.S[2]

Hashimoto’s thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease where the body’s own antibodies attack the cells of the thyroid. Hashimoto’s thyroiditis was first described by Hashimoto Hakaru in 1912. He named it struma lymphomatosa which was renamed as Hashimoto’s thyroiditis in 1931. Hashimoto’s thyroiditis can be classified as primary or secondary types. Rarely, Hashimoto’s thyroiditis can be categorized under the polyglandular syndromes. Hashimoto’s thyroiditis (HT) is characterized by lymphocytic infiltration of the thyroid gland and production of antibodies that recognize thyroid-specific antigens. The pathogenesis is not yet completely understood. Thyroid cells undergo atrophy or transform into a type of follicular cell rich in mitochondria called Hurthle cell. It is currently thought that the disease is caused by abnormalities in cellular and humoral immunity which results in a localized cell-mediated immune response directed toward the thyroid parenchymal cells. This results in the decreased production of thyroid hormones. Hashimoto’s thyroiditis is particularly common in middle aged women, Asians, and Whites. Hashimoto’s thyroiditis usually begins slowly and may progress to hypothyroidism. Complications include heart failure, lymphoma, myxedema, and cervical compression. A positive history of autoimmune diseases and certain drug use are suggestive of Hashimoto’s thyroiditis. The most common symptoms of Hashimoto’s thyroiditis include fatigue, constipation, and cold intolerance. Laboratory findings consistent with the diagnosis of Hashimoto’s thyroiditis usually include increased thyroid stimulating hormone, decreased free T3 and free T4, and anti-thyroid peroxidase antibodies. Ultrasound findings associated with Hashimoto’s thyroiditis are reduced echogenicity, glandular irregularities, and nodules. 24-hour iodine-123 uptake is decreased in Hashimoto’s thyroiditis. The mainstay of therapy for Hashimoto’s thyroiditis is synthetic levothyroxine. Corticosteroids and selenium can also be used in certain cases. Thyroidectomy is usually performed when the enlarged thyroid produces cervical compression symptoms and there is a high suspicion for malignancy.

Hashimoto’s thyroiditis was first described by Hashimoto Hakaru in 1912. He named it struma lymphomatosa which was renamed as Hashimoto’s thyroiditis in 1931.

On the basis of the etiology, Hashimoto’s thyroiditis can be classified as primary or secondary types. Rarely, Hashimoto’s thyroiditis can be categorized under the polyglandular syndromes.

Hashimoto’s thyroiditis (HT) is characterized by lymphocytic infiltration of the thyroid gland and production of antibodies that recognize thyroid-specific antigens.The pathogenesis is not yet completely understood. Thyroid cells undergo atrophy or transform into a type of follicular cell rich in mitochondria called Hurthle cell. It is currently thought that the disease is caused by abnormalities in cellular and humoral immunity which results in a localized cell-mediated immune response directed toward the thyroid parenchymal cells. This results in the decreased production of thyroid hormones.

Hashimoto’s thyroiditis may be caused by T cells and B cells auto activation, genetic factors, and autoimmune antibodies against thyrotropin receptors.

Hashimoto’s thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. Hashimoto’s thyroiditis must be differentiated from other causes of thyroiditis, such as De Quervain’s thyroiditis, Riedel’s thyroiditis, and suppurative thyroiditis. Hashimoto’s thyroiditis must also be differentiated from other diseases which cause hypothyroidism. As Hashimoto’s thyroiditis may cause transient thyrotoxic symptoms, the diseases causing thyrotoxicosis must also be considered in the differential diagnosis.

Hashimoto’s thyroiditis is particularly common in middle aged women, Asians, and Whites. Annually, there are around 22 per 100,000 individuals worldwide.

Common risk factors in the development of Hashimoto’s thyroiditis are family history, female gender, and other autoimmune diseases.

There is insufficient evidence to recommend routine screening for Hashimoto’s thyroiditis.

Hashimoto’s thyroiditis usually begins slowly and may progress to hypothyroidism. Complications include heart failure, lymphoma, myxedema, and cervical compression.

There are no established criteria for the diagnosis of Hashimoto’s thyroiditis. The diagnosis of Hashimoto’s thyroiditis is made on laboratory and pathological findings after the clinical suspicion. It includes the TPO antibodies, hypothyroidism, reduced echogenicity on the ultrasound, the presence of germinal centers and lymphocytic infiltration of the thyroid gland.

The hallmark of Hashimoto’s thyroiditis is hypothyroidism. A positive history of autoimmune diseases and certain drug use are suggestive of Hashimoto’s thyroiditis. The most common symptoms of Hashimoto’s thyroiditis include fatigue, constipation, and cold intolerance.

Patients with Hashimoto’s thyroiditis usually appear fatigued and have myxedema. Physical examination of patients with Hashimoto’s thyroiditis is usually remarkable for bradycardia, bradypnea and delayed reflexes.

Laboratory findings consistent with the diagnosis of Hashimoto’s thyroiditis usually include increased thyroid stimulating hormone, decreased free T3 and free T4, and anti-thyroid peroxidase antibodies.

The findings associated with ECG in Hashimoto’s thyroiditis are bradycardia and low voltage QRS complex.

The findings associated with Chest X ray in Hashimoto’s thyroiditis are pleural effusion and cardiomegaly.

Non-contrast CT may be used in Hashimoto’s thyroiditis to assess the tracheal or esophageal compression.

There are no MRI findings associated with Hashimoto’s thyroiditis.

Ultrasound findings associated with Hashimoto’s thyroiditis are reduced echogenicity, glandular irregularities, and nodules.

24-hour iodine-123 uptake is decreased in Hashimoto’s thyroiditis.

The histological analysis in Hashimoto’s thyroiditis may show inflammatory cell infiltration and hurthle cells. Fine needle aspiration cytology helps to differentiate between the benign and malignant nodules. ^[1][2]

The mainstay of therapy for Hashimoto’s thyroiditis is synthetic levothyroxine. Corticosteroids and selenium can also be used in certain cases.

Thyroidectomy is usually performed when the enlarged thyroid produces cervical compression symptoms and there is a high suspicion for malignancy.

There are no primary preventive measures available for Hashimoto’s thyroiditis.

There are no secondary preventive measures available for Hashimoto’s thyroiditis.

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