Hashimoto’s thyroiditis

Overview

Hashimoto's thyroiditis, also known as Hashimoto’s syndrome, or chronic lymphocytic thyroiditis, is an autoimmune disease in which the thyroid gland is attacked by a variety of cell- and antibody-mediated immune processes. It was the first disease to be recognized as an autoimmune disease. It was first described by the Japanese specialist Hakaru Hashimoto in Germany in 1912.

Symptoms

Hashimoto's thyroiditis very often results in hypothyroidism with bouts of hyperthyroidism. Symptoms of Hashimoto's thyroiditis include Myxedematous psychosis, weight gain, depression, mania, sensitivity to heat and cold, paresthesia, fatigue, panic attacks, bradycardia, tachycardia, high cholesterol, reactive hypoglycemia, constipation, migraines, muscle weakness, cramps, memory loss, vision problems, infertility and hair loss.

The thyroid gland may become firm, large, and lobulated in Hashimoto's thyroiditis, but changes in the thyroid can also be nonpalpable. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy. Physiologically, antibodies against thyroid peroxidase (TPO) and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. Accordingly, the disease can be detected clinically by looking for these antibodies in the blood. It is also characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. It is associated with non-Hodgkin lymphoma.

Source:

Staecker, Hinrich; Thomas R. Van De Water; Van de Water, Thomas R. (2006). Otolaryngology: basic science and clinical review. Stuttgart: Thieme. p56

Causes

Chronic thyroiditis or Hashimoto's disease is a common thyroid gland disorder. It can occur at any age, but is most often seen in middle-aged women. It is caused by a reaction of the immune system against the thyroid gland.

The disease begins slowly. It may take months or even years for the condition to be detected. Chronic thyroiditis is most common in women and in people with a family history of thyroid disease. It affects between 0.1% and 5% of all adults in Western countries.

Hashimoto's disease may, in rare cases, be related to other endocrine (hormonal) disorders caused by the immune system. Hashimoto's disease can occur with adrenal insufficiency and type 1 diabetes. In these cases, the condition is called type 2 polyglandular autoimmune syndrome (PGA II).

Less commonly, Hashimoto's disease occurs as part of a condition called type 1 polyglandular autoimmune syndrome (PGA I), along with:

• Adrenal insufficiency (poor function of the adrenal glands)
• Fungal infections of the mouth and nails
• Hypoparathyroidism (underactive parathyroid gland)

 

Diagnosis

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

Given the relatively non-specific symptoms of initial hypothyroidism, Hashimoto's thyroiditis is often misdiagnosed as depression, cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, less frequently, as ED or an anxiety disorder. On gross examination, there is often presentation of a hard goitre that is not painful to the touch; other symptoms seen with hypothyroidism, such as periorbital myxedema, depends on the current state of progression of the response, especially given the usually gradual development of clinically relevant hypothyroidism. Testing for 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 can help obtain an accurate diagnosis. Earlier assessment of the patient may present with elevated levels of thyroglobulin owing to the transient thyrotoxicosis as inflammation within the thyroid causes damage to the integrity of thyroid follicle storage of thyroglobulin; TSH is concomitantly decreased.

Ultrasound imaging of the thyroid gland (right lobe longitudinal) in patient with Hashimoto Thyroiditis.

This exposure of the body to substantial amounts of previously isolated thyroid enzymes is thought to contribute to the exacerbation of tolerance breakdown, giving rise to the more pronounced symptoms seen later in the disease. Lymphocytic infiltration of the thyrocyte-associated tissues often leads to the histologically significant finding of germinal center development within the thyroid gland.

Hashimoto's when presenting as mania is known as Prasad's syndrome after Ashok Prasad, the psychiatrist who first described it.

Source:

Kumar, Vinay (2010). "24: The Endocrine System". Robbins and Cotran Pathologic Mechanisms of Disease (8th ed.). Philidelphia, PA: Elsevier. p. 1113.

Giannini, AJ (1986). The Biological Foundations of Clinical Psychiatry. New Hyde Park, NY: Medical Examination Publishing Company. p. 193–198. 

Simmons, PJ; Dellemarre, FG., Drexhage, HA. (July 1998). "Antigen-presenting dendritic cells as regulators of the growth of thyrocytes: a role of interleukin-1beta and interleukin-6". Endocrinology 139 (7): 3158–3186.

Prognosis

Prognosis of Hashimoto's Thyroiditis is good - most patients recover with treatment. 

Treatment

Hypothyroidism caused by Hashimoto's Thyroiditis is treated with thyroid hormone replacement agents such as levothyroxine or desiccated thyroid extract. A tablet taken once a day generally keeps the thyroid hormone levels normal. In most cases, the treatment needs to be taken for the rest of the patient's life. In the event that hypothyroidism is caused by Hashimoto's Thyroiditis, it is recommended that the TSH levels be kept under 3.0. As long as the patient's thyroid is active, the body will continue to attack it, and this can wreak havoc on the patient's TSH levels and symptoms.

Preliminary studies have suggested a correlation between Hashimoto's Thyroiditis and Celiac sprue. While it has not been rigorously explored, there is anecdotal evidence that a gluten-free diet may reduce the autoimmune response responsible for thyroid degeneration. A study published in January 2012 compared a group of confirmed celiac patients to a control group of healthy individuals, starting a gluten-free diet and continuing for one year. While there was a higher occurrence of thyroiditis found amongst the Celiac group, there was no reduction in their level of anti-TPO antibody, improvement in thyroid function, or change in thyroid volume reduction after one year without gluten. The study mentions that its results disagree with other studies.