FAQ: Thyroiditis

By June 6, 2012 Thyroiditis No Comments


ATAWhat is the thyroid gland?

The thyroid gland located in the neck produces thyroid hormones which help the body use energy, stay warm and keep the brain, heart, muscles, and other organs working normally.



What is thyroiditis?
Thyroiditis includes a group of individual disorders that all cause thyroidal inflammation. As a result, there may be many different clinical presentations, from hypothyroidism to an enlarged thyroid (Goiter) to symptoms similar to hyperthyroidism.



What causes thyroiditis?
Thyroiditis results from an attack on the thyroid, causing inflammation and damage to the thyroid cells. Antibodies that attack the thyroid cause most types of thyroiditis. Certain drugs or an infection by a virus or bacteria may also cause Thyroiditis.



What are the clinical symptoms of thyroiditis?
There are no symptoms unique to thyroiditis. If the thyroiditis causes slow and chronic thyroid cell damage and destruction, leading to a fall in thyroid hormone levels in the blood, patients experience the symptoms of hypothyroidism (see Hypothyroidism brochure). If the thyroiditis causes rapid thyroid cell damage and destruction, the thyroid hormone that is stored in the gland leaks out, increasing thyroid hormone levels in the blood. These patients experience the symptoms of thyrotoxicosis, which are similar to hyperthyroidism (see Hyperthyroidism brochure). Pain in the thyroid can be seen in patients with subacute thyroiditis.

What are the types and clinical course of thyroiditis?

Hashimoto’s thyroiditis – Patients usually present with hypothyroidism, which is usually permanent.

Subacute, painless and post-partum thyroiditis – These disorders follow the same general clinical course of thyrotoxicosis followed by hypothyroidism. The thyrotoxic phase usually lasts for 1-3 months and is associated with symptoms including anxiety, insomnia, palpitations (fast heart rate), fatigue, weight loss, and irritability. Thyroidal pain in subacute thyroiditis follows the thyrotoxic phase. The hypothyroid phase typically occurs 1-3 months after the thyrotoxic phase and may last up to 9 –12 months. Typical symptoms include fatigue, weight gain, constipation, dry skin, depression and poor exercise tolerance. Most patients (80-95%) will have return of their thyroid function to normal within 12-18 months of the onset of symptoms.

Drug-induced and radiation thyroiditis – Both thyrotoxicosis and hypothyroidism may be seen. The thyrotoxicosis is usually shortlived. Drug-induced hypothyroidism often resolves with the cessation of the drug, while the hypothyroidism related to radiation thyroiditis is usually permanent.

Acute/Infectious thyroiditis – Symptoms may include thyroidal pain, systemic illness, painless enlargement of the thyroid and hypothyroidism. The symptoms usually resolve once the infection resolves.



How is thyroiditis treated?
Treatment depends on the type of thyroiditis and the clinical presentation.

Thyrotoxicosis – Beta blockers to decrease palpitations and reduce shakes and tremors may be helpful. Antithyroid medications (see Hyperthyroid brochure) are not used for the thyrotoxic phase of thyroiditis of any kind since the thyroid is not truly overactive.

Hypothyroidism – Treatment is initiated with thyroid hormone replacement for hypothyroidism due to Hashimoto’s thyroiditis (see Thyroid Hormone Therapy brochure). If thyroid hormone therapy is begun in patients with subacute, painless and post-partum thyroiditis, treatment should be continued for approximately 6-12 months and then tapered to see if thyroid hormone is required permanently.

Thyroidal pain – The pain associated with subacute thyroiditis usually can be managed with mild anti-inflammatory medications such as aspirin or ibuprofen. Occasionally, the pain can be severe and require steroid therapy with prednisone.

Further Reading

Further details on this and other thyroid-related topics are available in the patient information section on the American Thyroid Association® website at www.thyroid.org.


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