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Graves' Disease Resource Page
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GRAVES' DISEASE TREATMENT OPTIONS
Antithyroid Drugs In the United States there are two drugs commonly given to people with hyperthyroidism to block the production of thyroid hormone. They are methimazole (brand name Tapazole) and propylthyrouricil (also known as PTU). In Europe, Carbimazole is commonly given. Antithyroid drugs don't cure the cause of the hyperthyroidism; but given in the right amounts, they keep thyroid levels normal, giving the patient a chance to go into remission--which occurs about 50% of the time. Generally after treatment with these drugs for 12-24 months, they are withdrawn to see if the patient is in remission. Of the 50% who are in remission, about 30% remain in remission indefinitely. The others become hyperthyroid again at some point. The best candidates for remission are usually people with mild hyperthyroidism and small goiters. Recent studies indicate that smokers have a significantly smaller chance of remission than nonsmokers do. While being treated with the antithyroid drugs, the patient needs to have his thyroid levels monitored regularly by his doctor. For some people, finding the right dose of antithyroid drug is fairly simple, and for others it's difficult to find a dose that will prevent hyperthyroidism without causing hypothyroidism. Approximately 30-40% of the time, antithyroid drugs cause some degree of hypothyroidism. It takes from 2-6 weeks after starting the drug for the patient to begin feeling better. There is a chance (less than 5%) of side effects from the drugs, ranging from mild (rash and itching) to a condition resulting in a low white blood count (1%), which in rare cases (0.02%) is severe and potentially fatal. Both methimazole and propylthiouricil are listed as carcinogenic to animals, and propylthiouricil is listed as a potential carcinogen for humans (while for methimazole, there is still insufficient evidence). Patients who are difficult to stabilize are sometimes put on a dose of antithyroid drugs large enough to block all thyroid function, and then given thyroid replacement hormone to normalize thyroid levels. This is sometimes known as "block and replace" therapy. The major drawback to this method is that the larger doses of antithyroid drugs necessary to block thyroid production are more likely to cause side effects. Many studies have shown that the block and replace method does not increase chance of remission, as once hoped.
Antithyroid
drugs are the only effective treatment for Graves' Disease that
preserves the thyroid. For this reason, many doctors
recommend this option for most people as a first-choice
treatment. Other doctors, discouraged by the high
percentage of relapse, recommend radioactive iodine (or
rarely, surgery) without trying antithyroid drugs first.
Regardless of
treatment choice, one of a
class of drugs known as beta-blockers is usually given to
hyperthyroid patients to relieve some of the symptoms of excess
thyroid hormone. Propranolol (Inderal) is one of the
more commonly used beta-blockers. Others include atenolol (Tenormin),
metoprolol (Lopressor), nadolol (Corgard), and timolol (Biocadren). Radioactive iodine (I-131) is the treatment recommended most often by doctors in the United States, mainly because it's usually a permanent control of hyperthyroidism and has few known adverse effects on the patient; except that it nearly always causes hypothyroidism--either in the first few months, or years down the road. Most doctors consider hypothyroidism to be easy to treat, and view it as a good trade-off for hyperthyroidism. (Not all patients experience it that way, however.) Studies done for more than 50 years have found an overall decrease in cancer deaths among people who've had radioactive iodine, rather than the increase that was expected. There is a slight increase of cancer of the thyroid, and cancer of the small bowel; but a decrease in smoking-related cancers. It hasn't been determined whether the increases in thyroid and small bowel cancer are related to the radioactive iodine or have more to do with the autoimmunity or other factors related to Graves' Disease. Cancer of the thyroid is virtually eliminated when ablative doses are given to the patient (doses large enough to destroy the thyroid quickly and more completely), but most doses of radioactive iodine given to Graves' Disease patients are small enough to damage part of the gland, leaving the patient with varying degrees of thyroid function (which continues to decline), and the possibility of avoiding immediate hypothyroidism. Take this link out to read a detailed description of problems associated with I-131 Therapy. For younger people considering RAI, this page discusses theoretical genetic damage to children born to mothers who have RAI therapy (although increases in birth defects have NOT been observed in current studies), and the increased chance of thyroid cancer in young people with I-131 thyroid damage, as observed after the Chernobyl nuclear accident. Many people choose RAI after being told by their doctors either that it will destroy the thyroid, or that it will "slow down" the thyroid gland. Both of these explanations are over-simplified and can lead to patient misconceptions. Radioactive iodine is generally given to Graves' Disease patients in MUCH smaller doses than is given to patients with thyroid cancer, for whom destroying the entire thyroid gland quickly is important. The doses given to Graves' Disease patients usually ranges from 5-15 millicuries, which isn't enough to destroy the entire thyroid immediately. Every patient responds differently, and so far there is no way to predict what dose will have the desired effect on a particular patient. There is an initial destructive effect of the radiation on the thyroid gland, affecting some thyroid tissue. In some patients this results in a temporary increase in hyperthyroidism, as the dying tissue releases its hormone. Production of thyroid hormone decreases over six weeks to six months, and many people become hypothyroid during this time and need to start on thyroid replacement hormone. A minority of patients remain hyperthyroid, and may need a second (and rarely, a third) RAI treatment to eliminate the over activity of the thyroid gland. For some people, thyroid function is slowed down enough that normal thyroid levels are achieved, without thyroid replacement hormone. Regardless of the outcome of the initial treatment, there is a continuing destruction of thyroid tissue (resulting in declining thyroid hormone output), both from continuing autoimmune factors and from premature aging of the radiation-damaged thyroid gland that remains. This results in hypothyroidism eventually for nearly everyone who had radioactive iodine treatment, usually by 5-10 years after the treatment. In time, most people end up with little or no thyroid output of their own, and are entirely dependent on thyroid replacement hormone. The time it takes for this to happen varies greatly from one person to another. When the decline in thyroid function is fairly rapid, the patient experiences a delay in feeling well following the RAI treatment that can go on for several years, because of the constantly changing thyroid levels and the need for increases in thyroid replacement hormone.
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(incomplete---to be continued as time permits in the near future) You
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