Autoimmune thyroiditis (Hashimoto’s thyroiditis)

Thyroiditis, or inflammation of the thyroid gland, has many causes. The most common cause is autoimmune thyroiditis (Hashimoto’s thyroiditis). This chronic inflammatory thyroid disease is caused by the presence of an abnormal antibody in the blood, and white blood cells that attack and damage the thyroid cells. The end result of the so-called “autoimmune” destruction is hypothyroidism, due to the complete absence of thyroid cells. However, in many patients, the reserve of the thyroid gland is sufficient to prevent hypothyroidism.

Clinical features

Patients with autoimmune thyroiditis (AIT) are traditionally young or middle-aged women. They often have no symptoms other than mild thyroid pressure and fatigue. In the early stages there is a slightly patchy hard goiter, sometimes a little sensitive. Pain occurs in about 10% of cases.

Laboratory tests

The diagnosis of “autoimmune thyroiditis” is confirmed by a specific picture of the detection of high levels in the blood of antibodies that act against the patient’s own thyroid proteins. The diagnosis can be definitively established with a thyroid biopsy. The needle is inserted into the thyroid gland, some cells are selected and a smear is made on a glass object. The doctor will see a lot of blood lymphocytes in the smear, which indicates the inflammatory nature of the reaction in the thyroid gland.


If the diagnosis is already established, then for the treatment of AIT, thyroid hormone replacement therapy (L-Thyroxine) is performed, even if the thyroid function is normal at the moment. Thyroid hormone is prescribed for the following reasons:

1) it reduces the goiter by suppressing the production of thyroid-stimulating hormone (TSH) by the pituitary gland;

2) it prevents the development of thyroid insufficiency and the corresponding decrease in thyroid hormone levels, since this disease can progress over time;

3) it appears to have a neutralizing effect on blood lymphocytes that cause damage and destruction of the thyroid gland.

The dose of L-Thyroxine is the same as for hypothyroidism, although slightly higher doses may be needed to reduce the goiter. Many patients, especially young people, are concerned about the goiter itself, which can remain for several years before it disappears. In most patients, the goiter shrinks within 6 to 18 months. When the gland contracts, it does not function, and the patient may develop hypothyroidism if not treated. Therefore, treatment with L-Thyroxine for AIT should be continued throughout life. Patients with AIT should meet with an endocrinologist at least once a year to make sure that the dose of L-Thyroxine is correct and that the goiter is reduced.

Subacute thyroiditis

Subacute thyroiditis is about ten times less common than autoimmune thyroiditis. It is a transient form of thyroiditis that causes hyperthyroidism but does not require radioactive iodine treatment or removal of the thyroid gland.

There is evidence that subacute thyroiditis is caused by a viral infection, since most patients had an upper respiratory tract infection several weeks before the onset of thyroiditis. This disease occurs in the form of small epidemics, traditionally associated with known viral infections.

Clinical features

The main symptoms are painful swelling of the thyroid gland and symptoms of hyperthyroidism. These symptoms include heat intolerance, nervousness, palpitations, and weakness. Hyperthyroidism is caused by a leak of thyroid hormones from thyroid cells damaged by a viral infection. This is a temporary condition, because after the end of the viral infection, the thyroid cells return to normal. On examination, the patient has a very sensitive, swollen thyroid gland and mild signs of hyperthyroidism.

Laboratory tests

Hyperthyroidism develops in about half of patients with subacute thyroiditis. In such patients, the diagnosis can be confirmed by the establishment of high levels of thyroid hormones in the blood. The erythrocyte sedimentation rate (ESR), which is a very useful test in all this disease, is very high (over 80). Radioiodine uptake analysis gives very low results. Normal values ​​for this test are 15-20%. In subacute thyroiditis, absorption is traditionally less than 1%. This is due to the fact that the cells infected with the virus are “sick” and unable to absorb iodine.


Mild forms of the disease are treated with anti-inflammatory foods to relieve inflammation, swelling, and pain. Patients with severe symptoms may be given steroid hormones (cortisone). In most cases, the patient recovers within a few days. In some people, the disease lasts longer and sometimes recurs. In about a quarter of patients, due to significant damage to thyroid cells, a short-term stage of hypothyroidism occurs, which may require treatment with L-Thyroxin. Ultimately, the cells regenerate and L-Thyroxin treatment can be discontinued.

Asymptomatic thyroiditis

Another cause of hypothyroidism, which is almost as common as subacute thyroiditis, is “silent” thyroiditis. It is so named because there are no symptoms or signs of thyroid inflammation. The patient develops hyperthyroidism and may have the same symptoms as those with Graves-Basedow hyperthyroidism.

Postpartum thyroiditis

Postpartum thyroiditis is common in women who have recently had a baby and have a history of thyroid disease. In many ways, asymptomatic and postpartum thyroiditis are similar to autoimmune thyroiditis, except that the gland is traditionally regenerated and thyroid hormone treatment is required for only a few weeks. However, it differs from subacute thyroiditis in that it often recurs.

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