Over 27 million Americans have overactive or underactive thyroid glands, but more than half remain undiagnosed.
In-Depth Report on Hypothyroidism
Hypothyroidism occurs when thyroxine (T4) levels drop so low that body processes begin to slow down. Hypothyroidism was first diagnosed in the late nineteenth century when doctors observed that surgical removal of the thyroid resulted in the swelling of the hands, face, feet, and tissues around the eyes. They named this syndrome myxedema and correctly concluded that it was the outcome of the absence of substances, thyroid hormones, normally produced by the thyroid gland. Hypothyroidism is usually progressive and irreversible. Treatment, however, is nearly always completely successful and allows a patient to live a fully normal life.
Subclinical hypothyroidism (mildly underactive thyroid), also called early-stage hypothyroidism, is a condition in which thyrotropin (TSH) levels have started to increase in response to an early decline in T4 levels in the thyroid. However, blood tests for T4 are still normal. The patient may have mild symptoms (usually slight fatigue) or none at all. Mildly underactive thyroid is very common (affecting about 10 million Americans) and is a topic of considerable debate among professionals because it is not clear how to manage this condition.
For instance, mildly underactive thyroid does not progress to the full-blown disorder in most people. Experts estimate that each year approximately 2 – 5% of people with mildly underactive thyroid will go on to develop overt hypothyroidism. Other factors associated with a higher risk include being an older woman (up to 20% of women over age 60 have subclinical hypothyroidism), having a goiter (enlarged thyroid gland) or thyroid antibodies, or harboring immune factors that suggest an autoimmune condition.
Mildly underactive thyroid is determined on the basis of the TSH laboratory blood tests. According to a 2004 consensus statement from the American Thyroid Association, the American Association of Clinical Endocrinologists, and the Endocrine Society, the normal range of TSH concentration falls between 0.45 and 4.5 mU/L. Patients with mildly underactive thyroid have TSH levels between 4.5 mU/L and 10mU/L. Patients with levels greater than 10mU/L are considered to have overt hypothyroidism and should be treated with medication.
For patients in the mildly underactive thyroid range, treatment decisions are less clear. The consensus committee recommended against routine treatment for patients with mildly underactive thyroid , but did suggest repeat screenings of thyroid function every 6 – 12 months to detect any changes in TSH levels. However, these are general guidelines, and individual cases and risk factors may differ. Patients should discuss with their doctor the course of action that is most appropriate for them.
Many permanent or temporary conditions can reduce thyroid hormone secretion and cause hypothyroidism. About 95% of hypothyroidism cases occur from problems that originate in the thyroid gland. In such cases, the disorder is called primary hypothyroidism. (Secondary hypothyroidism is caused by disorders of the pituitary gland. Tertiary hypothyroidism is caused by disorders of the hypothalamus.)
The two most common causes of primary hypothyroidism are:
Hashimoto’s thyroiditis. This is an autoimmune condition in which the body’s immune system attacks its own cells.
Overtreatment of hyperthyroidism (an overactive thyroid).
Thyroid Autoimmunity (Hashimoto’s Thyroiditis and Others)
Hashimoto’s thyroiditis, atrophic thyroiditis, and postpartum thyroiditis are all autoimmune diseases of the thyroid. An autoimmune disease occurs when the immune system mistakenly attacks the body’s own healthy cells. In the case of autoimmune thyroiditis, a common form of primary hypothyroid disease, the cells under attack are in the thyroid gland.
All forms of thyroid autoimmunity typically start with T and B cells:
Important immune factors called T and B cells infiltrate the thyroid gland in equal numbers. These white blood cells are the primary infection-fighting immune cells. T cells identify invasive molecules, such as viral proteins, and help B cells to produce antibodies that are designed specifically to attack these invaders.
In cases of autoimmunity, T cells are tricked into classifying molecules on the body’s own cells as invaders. In such cases, B cells then produce antibodies, called autoantibodies, which attack those cells.
In most cases of thyroid autoimmunity, the autoantibodies launch an attack on a thyroid protein called thyroid peroxidase; this attack appears to destroy thyroid cells.
Experts do not know why the immune system starts the process that injures the thyroid. Some theories follow:
One theory starts with a virus that has a protein resembling a thyroid protein. During an infection, T cells induce B cells to secrete specific antibodies that attack the invasive viral protein. Unfortunately, the T cells are also tricked into inducing a B-cell attack on the similar thyroid protein.
Genetic factors most likely play some role in autoimmune thyroiditis. For example, many patients with Hashimoto’s thyroiditis express a gene called the Fas gene, which interacts with thyroid cells and triggers a process called apoptosis, in which the cells begin to self-destruct. The Fas gene is linked to genes that regulate tumor necrosis factors, which are products of the immune system that trigger a damaging inflammatory response in cells.
In some women, thyroid autoimmunity may have developed while they were pregnant. In such cases, some evidence suggests that fetal cells accumulated in the mother’s thyroid gland, triggering an immune attack.
In some cases of Hashimoto’s thyroiditis, antibodies block a receptor on thyroid cells that bind to thyrotropin (TSH). This effect is more likely to be involved in worsening the disorder, but does not explain initial destruction.
Some evidence suggests that excess iodine intake triggers the process leading to Hashimoto’s thyroiditis.
The most common form of hypothyroidism in the U.S. is Hashimoto’s thyroiditis, a genetic disease named after the Japanese doctor who first described thyroid inflammation. It occurs in about 0.3 – 5 people per 1,000 per year, and women are 15 – 20 times more likely than men to develop this disease.
An enlargement of the thyroid gland, called a goiter, is almost always present and may appear as a cyst-like or fibrous growth in the neck. Hashimoto’s thyroiditis is permanent and requires lifelong treatment. Both genetic and environmental factors appear to play a role in its development.
One theory proposes that Hashimoto’s thyroiditis and Graves’ disease (a form of hyperthyroidism) are caused by a similar immunologic dysfunction. Similar immune system substances called antibodies are present in both diseases, and some experts believe that the predominance of one or another antibody determines which of the diseases become manifest. The two diseases, then, are essentially two sides of a single coin.
Atrophic thyroiditis is similar to Hashimoto’s thyroiditis, except a goiter is not present.
Riedel’s Thyroiditis. Riedel’s thyroiditis is a rare autoimmune disorder, in which scar tissue progresses in the thyroid until it produces a hard stony mass that suggests cancer. Hypothyroidism develops as the scar tissue replaces healthy tissue. Surgery is usually required, although early stages may be treated with tamoxifen, corticosteroids, or other immunosuppressive drugs.
Autoimmune Thyroiditis Due to Pregnancy. Hypothyroidism may also occur in women who develop antibodies to their own thyroid during pregnancy, causing an inflammation of the thyroid after delivery.
Subacute thyroiditis is a temporary condition that passes through three phases: hyperthyroidism, hypothyroidism, and a return to normal thyroid levels. Patients may exhibit symptoms of both hyperthyroidism and hypothyroidism (rapid heartbeat, nervousness, weight loss), and they can feel extremely sick. Symptoms last about 6 – 8 weeks and then resolve in most patients, although each form carries some risk for becoming chronic. Experts estimate that subacute thyroiditis is responsible for 10% of all cases of hypothyroidism.
The three forms of subacute thyroiditis follow a similar course:
Painless Postpartum Subacute Thyroiditis
Postpartum thyroiditis is an autoimmune condition that occurs in up to 10% of pregnant women and tends to develop between 4 – 12 months after delivery. In most cases, a woman develops a small, painless goiter. Although 80% of women with this condition have normal thyroid function within a year, some evidence suggests that half of women with this condition develop permanent hypothyroidism within 7 years. Women who have had recurrent episodes after previous pregnancies and women who have other autoimmune disorders are at higher risk for this form of subacute thyroiditis. It is generally self-limiting and requires no therapy unless the hypothyroid phase is prolonged. In such cases, therapy may be thyroxine replacement for a few months. A doctor will prescribe beta blockers if the hyperthyroid phase requires treatment.
Painless Sporadic, or Silent, Thyroiditis
This painless condition is very similar to postpartum thyroiditis except it can occur in both men and women and at any age. About 20% of patients with silent thyroiditis may develop chronic hypothyroidism. Treatment considerations are the same as for postpartum subacute thyroiditis.
Painful, or Granulomatous, Thyroiditis
This condition comes on suddenly with flu-like symptoms and severe neck pain and swelling. It generally occurs in the summer and is five times more common in women. It recurs in about 2% of patients. Hypothyroidism persists in about 5%. Treatments typically include pain reli