Thyroiditis, or inflammation of the thyroid gland, has many causes. The most common cause is Hashimoto’s thyroiditis, first described by Dr Hashimoto in Japan. This is a chronic inflammatory disorder of the thyroid gland caused by abnormal blood antibodies and white blood cells attacking and damaging thyroid cells. The end result of this so-called “autoimmune” destruction is hypothyroidism or underactive thyroid functioning. Some patients are able to retain sufficient thyroid reserve to prevent hypothyroidism.
Patients with Hashimoto’s thyroiditis are usually, young, middle-aged or older women. They often have no symptoms apart from mild pressure in the thyroid gland and tiredness. In the early stages there is a goitre which is firm, slightly irregular, and sometimes slightly tender. Pain occurs in about 10% of cases. In the later stages the thyroid can become small and non palpable.
The diagnosis of Hashimoto’s thyroiditis is confirmed by finding high levels of antibodies in the blood. These work against the patient’s own thyroid proteins. The diagnosis can be firmly established by doing a thyroid biopsy but this is not usually done. To determine the function of the gland the level of TSH (thyroid stimulating hormone) is measured in the blood. TSH is the pituitary signal that controls thyroid function and growth (please refer to health guide 2). Women over 50 years of age should be periodically screened for thyroid dysfunction.
Treatment of Hashimoto’s thyroiditis consists of replacing the missing thyroid hormone, thyroxine. This is accomplished by taking a pill containing thyroxine (Euthyrox®, Synthroid®, Eltroxin®). If the dysfunction is mild, doses of 50 to 75 micrograms per day may be sufficient. The average replacement dose for more severe dysfunction is 1.6 micrograms/kg of body weight. If patients present with hypothyroidism and goitre, the goitre will usually shrink 6 to 18 months after replacement therapy has been introduced. Once the proper dose of thyroxine has been established, patients with Hashimoto’s thyroiditis should be seen by their family doctors at least once a year to ensure that the dose of thyroxine is still adequate.
Subacute Thyroiditis is about ten times less common than Hashimoto’s thyroiditis. It is a transient form of thyroiditis causing hyperthyroidism but not requiring treatment with radioactive iodine or by thyroidectomy. There is evidence that subacute thyroiditis is caused by a viral infection since most patients have had a throat infection a few weeks before the thyroiditis. The condition occurs in small epidemics, usually in association with known viral infections.
Subacute thyroïditis usually has three phases but some of them can go unnoticed because the symptoms are mild. There is an initial phase of hyperthyroidism, followed by hypothyroidism (because the thyroid hormone reserve has been depleted and the thyroid is recuperating) and then a return to normal thyroid function. In the beginning, the main symptoms are a painful swelling of the thyroid gland and symptoms of hyperthyroidism. These symptoms include heat intolerance, nervousness, palpitations and weakness. The hyperthyroidism is due to the leaking of thyroid hormones from the damaged thyroid cells as a result of the viral infection. On initial examination, the patient has a very tender, swollen thyroid gland and mild signs of hyperthyroidism.
The diagnosis of hyperthyroidism can be confirmed by showing high levels of blood thyroid hormones. The blood erythrocyte sedimentation rate (ESR), a very useful test for this condition, is very high (over 80) in the inflammatory phase. The radioactive iodine uptake test gives very low results. The normal range for this test is from 15-20%. In subacute thyroiditis the uptake is usually less than 1%. This is because the virus infected cells are “sick” and unable to take up iodine.
The treatment for milder forms of this condition is aspirin or non steroidal anti-inflammatory drugs, given for the inflammation, swelling and pain. Patients with severe symptoms may be given steroids (cortisone). Beta-blockers can also be given to help with the hyperthyroid symptoms. This type of medication is contra-indicated in people with asthma. In most cases, the patient recovers but in some it recurs. Some may require treatment with thyroxine during the temporary phase of hypothyroidism that follows the hyperthyroid phase.
Another cause of thyroiditis, which occurs about as frequently as subacute thyroiditis, is “silent” thyroiditis. This is so named because there are no symptoms or signs of thyroid inflammation. The patient is hyperthyroid at first and may have the same symptoms as patients with Graves’ hyperthyroidism, but then goes through a hypothyroid phase before full recovery. The presence of thyroid antibodies, similar to those seen in Hashimoto’s thyroiditis, is a risk factor for the persistence of hypothyroidism.
Postpartum thyroiditis occurs frequently in women with a past history of thyroid disease who have recently delivered a baby. In most respects, silent and postpartum thyroiditis resemble Hashimoto’s thyroiditis except that the gland tends to recover and thyroid hormone treatment need be given for only a few weeks. However, it does differ from subacute thyroiditis in that recurrences are common (10%) and progression to permanent hypothyroidism is more frequent (10%).
Updated in May 2010 by Hortensia Mircescu, MDFRCPC, Endocrinology Division, Centre Hospitalier de l’Université de Montréal, Assistant Clinical Professor, Faculty of Medicine, Université de Montréal from the original text written by: IrvingB.Rosen, MD., FRCS(C), FACS, Professor of Surgery, University of Toronto, Department of Surgery, Mount Sinai Hospital; Consultant in Surgery, Princess Margaret Hospital, Ontario Cancer Institute and Paul G. Walfish CM, MD, FRCP(C), FACP, FRSM., Professor of Medicine, Pediatrics and Otolaryngology, University of Toronto; Senior Consultant, Endocrinology and Metabolism and Head and Neck Oncology Program, Mount Sinai Hospital.