Earlier, I posted about the beginning of this article. Now I’m finishing it up. This section talks about “antithyroid drugs of second choice”. These are drugs that don’t exactly “fix” the problem, but relieve some of the symptoms.
This drug is used if your hyperthyroidism is caused by eating too much iodine. It blocks the uptake of iodine by the thyroid. It has a pretty nasty side effect of possibly causing bone-marrow problems. Since this isn’t usually a problem for folks that read blogs, you can probably ignore this treatment.
β (Beta) Blockers
β blockers make you “feel” better by lowering some of the symptoms of Graves, including palpitations, anxiety, tremors and heat intolerance. They are also sometimes used as anti-anxiety pills by perfectly healthy folks. Two common β blockers are propranolol and atenolol. Propranolol can also help reduce the conversion of T4 to T3, which is helpful. Atenolol is used for people who have asthma, but doesn’t have the T4->T3 blocking effect. Many people are prescribed β blockers when they first get diagnosed as a way to feel better until their other treatments have time to take effect.
Inorganic iodide (and Lithium)
Suddenly eating a large amount of iodine will cause a temporary (~ 2 weeks) drop in thyroid hormone levels. However, because this is not a permanent fix, it is generally just used in specific situations such as prepping someone for thyroid surgery or if they are experiencing thyroid storm. Lithium has similar temporary effects and is sometimes used in similar, short-term situations.
This drug is used when the thyroid is inflamed (thyroiditis) and is a temporary treatment to bring down the inflammation. It does also prevent T4->T3 conversion. Steroids have multiple negative effects on the body and should be used only temporarily if possible, and the doses are usually tapered at the end (ie – you wean off of them).
This experimental treatment (ie, not yet available) is risky and currently is not considered better than the other treatments. RTX is sort of an anti-autoimmune drug. Basically, it is an antibody that fights the immune system’s over-reaction to the thyroid gland. By fighting your own immune system, though, there is a large potential for things to go awry. For example, out of only two clinical trials, patients developed all sorts of new autoimmune disorders such as allergic reactions, crohn’s disease, arthritis, psoriasis, and a demyelinating (degenerative nerve) disorder. Ick! The author’s take on this is that it “should not be considered as an option in uncomplicated Graves’ disease.” However, it does show promise in faster relief for Graves’ opthalmopathy, which might be a benefit in severe cases if it prevents the need for surgery.
Fumarola, A., A. Di Fiore, M. Dainelli, G. Grani, and A. Calvanese. “Medical Treatment of Hyperthyroidism: State of the Art.” Experimental and Clinical Endocrinology & Diabetes (5, 2010). http://www.thieme-connect.de/DOI/DOI?10.1055/s-0030-1253420.
Abstract Methimazole (MMI) and propylthiouracil (PTU) are the main antithyroid drugs used for hyper- thyroidism. They inhibit the synthesis of thyroid hormone at various levels and are used as the primary treatment for hyperthyroidism or as a preparation before radioiodine therapy or thy- roidectomy. MMI is the drug of choice because of its widespread availability, longer half-life and small number of severe side effects. Drugs of second choice are potassium perchlorate, beta blockers, iodine, lithium carbonate and gluco- corticoids. Rituximab, a monoclonal antibody directed against human CD20, was recently pro- posed as a biological therapy for cases of Graves’ disease unresponsive to traditional drugs.