Graves’ disease, an autoimmune disorder, is one of the most common causes of hyperthyroidism, affecting approximately 20 individuals per 100,000 per year.1 In patients with Graves’ disease the immune system produces thyroid-stimulating immunoglobulin (TSI), an autoantibody that attaches to the thyroid-stimulating hormone (TSH)-receptor. TSI mimics the action of TSH and stimulates the thyroid to overproduce and secrete thyroid hormones.2
If left untreated, Graves’ disease can cause severe thyrotoxicosis. A life-threatening thyrotoxic crisis (i.e. thyroid storm) can occur. Long-standing severe thyrotoxicosis leads to severe weight loss with catabolism of bone and muscle. Cardiac complications, and psychocognitive complications can cause significant morbidity. Graves’ disease is also associated with ophthalmopathy, dermopathy, and acropachy.3
Thyroid nodules are a common thyroid problem. Thyroid cancer (carcinoma) is one of the most important causes, but is responsible for less than 10% of thyroid nodules.4
Thyroid nodules/adenomas are usually benign neoplasms, which are often classified as colloid, follicular or papillary:5
The cause of benign thyroid nodules/cysts is largely unknown. In some instances these nodules/cysts can begin to autonomously produce and secrete thyroid hormones, leading to hyperthyroidism. If multiple nodules become overactive, the condition is known as multi-nodular goiter. This condition is more common in older patients, and can produce larger amounts of thyroid hormone compared with a single thyroid adenoma. Thyroid nodules may also be observed in patients with hypothyroidism, particularly if the cause of inflammation is Hashimoto’s thyroiditis.7
Worldwide, one of the most common causes of hypothyroidism is insufficient dietary intake of iodine, although this cause is rare in developed countries.8
Data from the USA suggest that Hashimoto’s thyroiditis is the most common cause of hypothyroidism in developed countries, with an incidence of approximately 3.5 per 1000 per year in women and 0.6 per 1000 per year in men.9,10
Hashimoto’s thyroiditis is a poorly understood autoimmune condition thought to be mediated by various cell- and antibody-mediated immune processes that gradually destroy the thyroid.
Although a small proportion of patients with Hashimoto’s thyroiditis may be antibody negative, many patients have antibodies to various thyroid antigens including:
It is thought that antibodies bind to the TSH receptor, further impairing thyroid function. If untreated for an extended period, Hashimoto’s thyroiditis may lead to muscle failure, including possible heart failure, and in rare cases patients may develop a brain disorder known as Hashimoto’s encephalopathy.12
Most patients with HIV display normal thyroid function.13 However, there is mounting evidence that patients receiving HAART are presenting with an unusually high proportion of symptoms linked to thyroid dysfunction.13 There is some evidence to suggest that hypothyroidism may be associated with protease inhibitor (PI) treatment and that hyperthyroidism may be associated with non-nucleoside reverse-transcriptase inhibitor (NNRTI) therapy13 (see drug-drug interactions).