Hypothyroidism is a disorder that develops when there is not enough thyroid hormone in the body to meet the demands of the organs and tissues that are regulated by its activity. Different processes may contribute to a deficiency of thyroid hormone. Patients with Graves’ disease who have undergone treatment with radioactive iodine may develop a condition known as postablative hypothyroidism.
In the setting of Graves’ disease, the overall goal of treatment with radioactive iodine is to administer a dose of 131-Iodine that will deliver enough beta radiation to destroy most of the overactive follicular cells that produce and secrete excess amounts of thyroid hormone. If a dose of 131-Iodine is too low, it may not destroy enough of the overactive follicular cells. Patients who are treated with doses of 131-Iodine that are too low may continue to have persistent hyperthyroidism. If a dose of 131-Iodine is higher, it may destroy much of the remainder of the thyroid gland in addition to the overactive follicular cells. Over time, this destruction may lead to an overall deficiency of thyroid hormone. Postablative hypothyroidism is a fairly common condition. It may develop within the first year after treatment in up to 50% of all patients who treated with doses of 131-Iodine. In some respects, this condition may be considered to be a desirable goal of therapy. Patients who develop postablative hypothyroidism shift from an overactive state that may be difficult to monitor and control to an underactive state that is usually easy to manage with effective treatment.
What are the symptoms of postablative hypothyroidism?
Patients who develop postablative hypothyroidism may report a range of different symptoms that reflect an overall deficiency of thyroid hormone. These symptoms may become evident over the course of a few weeks, or they may gradually emerge over several months or years. Some patients may begin to notice that they are unable to tolerate cooler temperatures that feel perfectly comfortable to others around them. This symptom is called cold intolerance. Some patients may experience a substantial amount of weight gain due to changes in rates of energy consumption and metabolism. Some patients may feel tired and lethargic most of the time, sleeping for long periods of time without feeling energized or refreshed. Changes in behavior may be noted by friends, coworkers, or family members. Some patients may notice a decreased frequency of bowel movements.
What are the physical signs associated with postablative hypothyroidism?
Physical signs that may become apparent in patients who develop postablative hypothyroidism reflect the effects of an overall deficiency of thyroid hormone. Patients may be noted to have slow heart rates that reflect decreased stimulation of the cardiovascular system. If measurement of the pulse reveals that a patient's heart is beating at a rate that is less than 60 beats per minute, this condition is called bradycardia. Examination of patients who develop postablative hypothyroidism may reveal cool dry skin that is rough in texture. Characteristic skin changes may be related to decreased blood flow due to constriction of blood vessels in the tissue supporting the skin. Neurologic testing of patients who develop thyrotoxicosis may reveal characteristic findings related to decreased stimulation of the nervous system. Testing of the reflexes may reveal evidence of delayed relaxation of muscles when tendons in the arms, knees, and ankles are tapped with a reflex hammer.
How is postablative hypothyroidism diagnosed?
A diagnosis of postablative hypothyroidism can be made when blood tests reveal changes in thyroid hormone and TSH levels that are consistent with an overall deficiency of thyroid hormone. Doctors following patients with Graves’ disease who have undergone treatment with radioactive iodine are usually aware of the high likelihood that these patients may eventually develop postablative hypothyroidism. As such, these doctors usually make arrangements to check thyroid function tests on a regular basis to keep track of changes in thyroid hormone and TSH levels.
The actual thyroid function tests that are checked to monitor a patient's response to treatment with radioactive iodine may vary over time. While TSH levels usually provide the most sensitive indication of whether there is an adequate amount of thyroid hormone present in the body, they may not provide accurate information during the first few months after treatment with radioactive iodine. Long-term exposure to excess amounts of thyroid hormone may suppress the function of the cells that produce TSH in the pituitary gland to a point where it may take a period of several weeks for them to recover. During this period, TSH levels may remain suppressed, even after the amount of thyroid hormone in the body has returned to a normal level. For this reason, the amount of thyroid hormone in the body is usually measured directly during the first few months after treatment with radioactive iodine. This usually involves checking thyroid function tests that measure T4 levels, free T4 levels, or T3 levels. Serial thyroid function tests checked during this period may show a progressive decline in the amount of thyroid hormone present in the body as T4, free T4, and T3 fall below normal levels. If this decline is sustained, the pattern that emerges may be consistent with a diagnosis of postablative hypothyroidism.
Over time, as the cells that produce TSH in the pituitary gland gradually recover, they begin to secrete normal amounts of TSH that accurately reflect exposure to thyroid hormone. Once this recovery has occurred, TSH levels can be checked to monitor a patient's response to treatment. Serial thyroid function tests checked during this period may show a progressive increase in TSH levels that reflect a progressive decline in the amount of thyroid hormone present in the body. If this increase is sustained, the pattern that emerges may be consistent with a diagnosis of postablative hypothyroidism.
How is postablative hypothyroidism treated?
Postablative hypothyroidism is treated with thyroid hormone replacement therapy.