1. Graves’ disease accounts for 90% of cases of significant hyperthyroidism in Canada. The symptoms are obvious and well-known. Almost all patients appear to stare and roughly half will have other eye symptoms.

2. Graves’ affects about 1 Canadian in 100, with women overrepresented, and it seems to be getting more common. Some cases present with eye disease before they show thyroid dysfunction, but hyperthyroidism will almost invariably follow within 18 months. Most patients have anti-TSH receptor antibodies, often even before they develop frank hyperthyroidism. Remember, new symptomatic hyperthyroid patients should typically be on a beta-blocker until thyroid function is controlled.

3. In Canada, most cases of Graves’ are ultimately treated with radioiodine, though antithyroid drugs (methimazole or occasionally propylthiouracil) are generally tried first. Methimazole is cheaper, safer and easier in most patients. Drugs achieve lasting remission in about half of patients, less in the young. They may be withdrawn at about 18 months to see if improvement is lasting. If it’s not, radioiodine is used. This does its work over about 6 months, and methimazole is typically reinstated during this time.

4. Exceptions are the under 25s, and women who are pregnant, trying, or breastfeeding, in whom radioiodine is contraindicated. If young patients’ hyperthyroidism recurs after antithyroid drugs, they’re treated with thyroidectomy.

5. Radioiodine is the treatment most associated with deterioration of Graves’ ophthalmopathy, which can be exacerbated by both over- and undertreatment. Therefore, patients with significant eye disease may be treated with methimazole and levothyroxine instead. Alternatively, enteric coated prednisolone (about 30 mg daily) for 6 weeks can prevent worsening of ophthalmopathy if they do take radioiodine.

6. There’s no known reason why patients can’t be maintained on antithyroid drugs long-term. Adverse events such as urticarial rash or agranulocytosis tend to occur early or not at all. Risk of neutropenia is small and white cells don’t need monitoring.

7. “Block and replace” therapy involves using high-dose anti-thyroid drugs to stop thyroxine production completely, then replacing it with administered levothyroxine. This is helpful in Graves’, because it avoids fluctuating levels. Block and replace isn’t used in pregnancy, however, because more methimazole than levothyroxine crosses the placenta, risking fetal hypothyroidism.

8. Pregnancy usually requires changes in treatment. First, autoimmune disease tends to ameliorate during pregnancy so antithyroid doses can often be lowered. The TSH-receptor antibody that causes Graves’ can cross the placenta, so a
hyperthyroid mother will carry a hyperthyroid fetus. Luckily, antithyroid drugs also cross the placenta. They’re usually stopped for the last 4 weeks to avoid fetal hypothyroidism. Historically, propylthiouracil has been preferred in breastfeeding, as less of it enters the milk. But methimazole is now also considered safe.

9. Postpartum thyroiditis (PPT), is a very common transient autoimmune disease. But keep in mind, new-onset Graves’ disease may also crop up after pregnancy. Thyroid bruit, eye disease and positive anti-TSH receptor antibodies are the features that distinguish it from PPT. Patients who improve when retested after a month probably had PPT; those who don’t probably have Graves’ disease.

10. The downside of radioiodine and thyroidectomy, of course, is the very high chance of lifetime hypothyroidism. The best way to minimize this problem is to exclude cases of thyroiditis that will improve untreated. More on those conditions later.