Ruchi Mathur, MD, FRCP(C)
Ruchi Mathur, MD, FRCP(C)
Ruchi Mathur, MD, FRCP(C) is an Attending Physician with the Division of Endocrinology, Diabetes and Metabolism and Associate Director of Clinical Research, Recruitment and Phenotyping with the Center for Androgen Related Disorders, Department of Obstetrics and Gynecology at Cedars-Sinai Medical Center.
William C. Shiel Jr., MD, FACP, FACR
William C. Shiel Jr., MD, FACP, FACR
Dr. Shiel received a Bachelor of Science degree with honors from the University of Notre Dame. There he was involved in research in radiation biology and received the Huisking Scholarship. After graduating from St. Louis University School of Medicine, he completed his Internal Medicine residency and Rheumatology fellowship at the University of California, Irvine. He is board-certified in Internal Medicine and Rheumatology.
In this Article
Thyroid hormone regulation- the chain of command
The thyroid itself is regulated by another gland that is located in the brain, called the pituitary. In turn, the pituitary is regulated in part by the thyroid (via a "feedback" effect of thyroid hormone on the pituitary gland) and by another gland called the hypothalamus.
The hypothalamus releases a hormone called thyrotropin releasing hormone (TRH), which sends a signal to the pituitary to release thyroid stimulating hormone (TSH). In turn, TSH sends a signal to the thyroid to release thyroid hormones. If a disruption occurs at any of these levels, a defect in thyroid hormone production may result in a deficiency of thyroid hormone (hypothyroidism).
Hypothalamus - TRH
The rate of thyroid hormone production is controlled by the pituitary gland. If there is an insufficient amount of thyroid hormone circulating in the body to allow for normal functioning, the release of TSH is increased by the pituitary gland in an attempt to stimulate more thyroid hormone production. In contrast, when there is an excessive amount of circulating thyroid hormone, TSH levels fall as the pituitary attempts to decrease the production of thyroid hormone. In persons with hypothyroidism, there is a persistent low level of circulating thyroid hormones.
What causes hypothyroidism?
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Hypothyroidism is a very common condition. It is estimated that 3% to 5% of the population has some form of hypothyroidism. The condition is more common in women than in men, and its incidence increases with age.
Below is a list of some of the common causes of hypothyroidism in adults followed by a discussion of these conditions.
The most common cause of hypothyroidism in the United States is an inherited condition called Hashimoto's thyroiditis. This condition is named after Dr. Hakaru Hashimoto who first described it in 1912. In this condition, the thyroid gland is usually enlarged (goiter) and has a decreased ability to make thyroid hormones. Hashimoto's is an autoimmune disease in which the body's immune system inappropriately attacks the thyroid tissue. In part, this condition is believed to have a genetic basis. This means that the tendency toward developing Hashimoto's thyroiditis can run in families. Hashimoto's is 5 to 10 times more common in women than in men. Blood samples drawn from patients with this disease reveal an increased number of antibodies to the enzyme, thyroid peroxidase (anti-TPO antibodies). Since the basis for autoimmune diseases may have a common origin, it is not unusual to find that a patient with Hashimoto's thyroiditis has one or more other autoimmune diseases such as diabetes or pernicious anemia ( B12 deficiency). Hashimoto's can be identified by detecting anti-TPO antibodies in the blood and/or by performing a thyroid scan.
Lymphocytic thyroiditis following hyperthyroidism
Thyroiditis refers to inflammation of the thyroid gland. When the inflammation is caused by a particular type of white blood cell known as a lymphocyte, the condition is referred to as lymphocytic thyroiditis. This condition is particularly common after pregnancy and can actually affect up to 8% of women after they deliver. In these cases, there is usually a hyperthyroid phase (in which excessive amounts of thyroid hormone leak out of the inflamed gland), which is followed by a hypothyroid phase that can last for up to six months. The majority of affected women eventually return to a state of normal thyroid function, although there is a possibility of remaining hypothyroid.
Thyroid destruction econdary to radioactive iodine or surgery
Patients who have been treated for a hyperthyroid condition (such as Graves' disease) and received radioactive iodine may be left with little or no functioning thyroid tissue after treatment. The likelihood of this depends on a number of factors including the dose of iodine given, along with the size and the activity of the thyroid gland. If there is no significant activity of the thyroid gland six months after the radioactive iodine treatment, it is usually assumed that the thyroid will no longer function adequately. The result is hypothyroidism. Similarly, removal of the thyroid gland during surgery will be followed by hypothyroidism.
Pituitary or Hypothalamic disease
If for some reason the pituitary gland or the hypothalamus are unable to signal the thyroid and instruct it to produce thyroid hormones, a decreased level of circulating T4 and T3 may result, even if the thyroid gland itself is normal. If this defect is caused by pituitary disease, the condition is called "secondary hypothyroidism." If the defect is due to hypothalamic disease, it is called "tertiary hypothyroidism."
A pituitary injury may result after brain surgery or if there has been a decrease of blood supply to the area. In these cases of pituitary injury, the TSH that is produced by the pituitary gland is deficient and blood levels of TSH are low. Hypothyroidism results because the thyroid gland is no longer stimulated by the pituitary TSH. This form of hypothyroidism can, therefore, be distinguished from hypothyroidism that is caused by thyroid gland disease, in which the TSH level becomes elevated as the pituitary gland attempts to encourage thyroid hormone production by stimulating the thyroid gland with more TSH. Usually, hypothyroidism from pituitary gland injury occurs in conjunction with other hormone deficiencies, since the pituitary regulates other processes such as growth, reproduction, and adrenal function.
Medications that are used to treat an over-active thyroid (hyperthyroidism) may actually cause hypothyroidism. These drugs include methimazole (Tapazole) and propylthiouracil (PTU). The psychiatric medication, lithium (Eskalith, Lithobid), is also known to alter thyroid function and cause hypothyroidism. Interestingly, drugs containing a large amount of iodine such as amiodarone (Cordarone), potassium iodide (SSKI, Pima), and Lugol's solution can cause changes in thyroid function, which may result in low blood levels of thyroid hormone.
Severe iodine deficiency
In areas of the world where there is an iodine deficiency in the diet, severe hypothyroidism can be seen in 5% to 15% of the population. Examples of these areas include Zaire, Ecuador, India, and Chile. Severe iodine deficiency is also seen in remote mountain areas such as the Andes and the Himalayas. Since the addition of iodine to table salt and to bread, iodine deficiency is rarely seen in the United States.
Medically Reviewed by a Doctor on 10/9/2013
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