Hashimoto’s Thyroiditis

Hashimoto’s Thyroiditis (HT) is a chronic inflammatory condition of the thyroid gland. It is a common cause of goiter and probably the most common cause of hypothyroidism in the United States.

We will discuss it on our Website because of its relative common occurrence and because on occasion it may be a surgically important disease. We don’t know the cause. It is much more common in women than men. Pregnancy may play a role in its development. It may be associated with other chronic inflammatory conditions such as lupus.

HT is an autoimmune disease. A useful way to think about it is that it’s like being allergic to your own thyroid gland. White blood cells (lymphocytes) invade the thyroid gland. The inflammation usually leads to enlargement of the gland. Irregularities and lobulations (pseudo-nodules) may occur.  Ultrasound of the thyroid may show hypo-dense areas ( a characteristic “moth-eaten appearance”). FNAmay reveal inflammatory cells but this is an inconsistent finding.

From a functional standpoint, most patients show normal thyroid function test (TFT) at the time of diagnosis. However, about 25% of patients will be hypothyroid at diagnosis. Over time most patients will develop hypothyroidism, either subclinical (elevated TSH only) or overt hypothyroidism (elevated TSH and decreased T-4). This may take years to develop. Uncommonly, some patients may develophyperthyroidism. This is rarely severe and usually transient. This variable function may be problematic for the patient and treating physician.


The diagnosis of HT is made by a combination of clinical findings. It may be suspected in a woman with a newly identified goiter. The TSH level may be slightly elevated and the gland may have a “moth-eaten” appearance on ultrasound. Antibody levels in the blood are checked. Most patients will have elevated anti-thyroid peroxidase levels. Many patients will also have elevated anti- thyroglobulin levels. A needle biopsy may reveal inflammatory cells. Sometimes the diagnosis isn’t made until the thyroid gland is removed and examined by a pathologist.


Generally, HT requires no specific treatment. Thyroid replacement therapy may be recommended as most patients progress to overt hypothyroidism. There is no consensus about this. If the patient has hypothyroidism, thyroid hormone replacement therapy is indicated. Immunosuppressive therapy, commonly given in some auto-immune disorders, is not indicated. Goiter, due to HT, is one of the few indications for a trial of suppressive thyroid hormone therapy. In this clinical situation, suppressive therapy with thyroid hormone may reduce the size of the goiter and help with local symptoms associated with the goiter. Unfortunately, suppressive therapy may have a variety of side effects including heart arrhythmia’s, sleep disturbance, and osteoporosis. For these reasons long term suppressive therapy may not be practical.

As in other patients with goiter, HT becomes a surgical issue if cancer is suspected or if local symptoms are a problem. FNA, is used to evaluate worrisome nodules. Unfortunately, FNA in HT may be problematic to interpret. The risk of false positives with FNA is higher in HT than in other clinical situation. Therefore, careful judgment is required in evaluating nodules in HT. This issue is further complicated by the fact that HT is associated with a higher risk of well-differentiated thyroid cancer and lymphoma of the thyroid gland. For this reason, life-long follow-up is required.

Generally, we try to avoid surgery in HT. The inflammatory response of the disease may lead to slightly increased risk of recurrent nerve injury and post-op hypoparathyroidism when surgery is required.  When surgery is needed, total thyroidectomy is appropriate. Leaving, thyroid tissue behind does not preserve function and the risk of complications goes up significantly if re-operation is required.

Surgery is indicated if there is a concern about cancer or for local symptoms. With the increased risk of cancer in HT, I tend to favor surgery if there is significant enlargement of the gland during follow-up. This is especially true if the TSH level has been adequately suppressed.