What caused this case of asymptomatic hyperthyroidism?
Everything pointed to an exogenous cause, but our patient denied taking anything. Only later did she mention a diet aid.
Iodide is an inorganic salt that is absorbed through the gastrointestinal mucosa and transported to the thyroid gland, where it is trapped and concentrated for thyroid hormone synthesis.3 Consuming large quantities of foods or other products that contain iodine—such as iodized salt, shellfish, cough syrups, multivitamins, or medications such as amiodarone and interferon alpha, as well as kelp—can cause hyperthyroidism.
What’s in that weight-loss aid?
Pu Erh, the dietary supplement Mary was taking, was not available for analysis; it was purchased in Poland and the patient had exhausted her supply by the time her physician told her to stop taking it. Each capsule contains 400 mg of red tea extract with 15 mcg chromium, according to the label.
Red tea and chromium. There are no reports associating red tea with thyroid dysfunction, but chromium is a popular weight-loss supplement whose efficacy and long-term safety are uncertain.4 It is unlikely that Mary’s hyperthyroidism was associated with chromium in-take, however, as multivitamins often contain 100 mcg of chromium—nearly 7 times the quantity in each Pu Erh capsule—with no reported thyroid side effects.
Did the supplement contain a thyroid extract? It’s possible, of course, that the supplement contained a thyroid extract, which would explain the resolution of symptoms after Mary stopped taking it. But without analysis of the product, we can’t be sure. Our suspicion, of course, is that it did.
Another possible, but unlikely, explanation. Theoretically, the fluctuating TSH could have been related to silent or subacute thyroiditis, in which T4 can remain elevated for 1 to 3 months. The fact that Mary had no history of cold or flu symptoms in the month preceding the initial TSH was inconsistent with this alternative diagnosis, however. Painless thyroiditis is also unlikely, as it is autoimmune in origin and the patient’s antithyroid antibodies were negative. The low thyroglobulin level supported an exogenous cause of hyperthyroidism.
Other supplements and thyroid dysfunction
Mary’s presentation is a single case indicating a possible link between a weight-loss supplement and asymptomatic hyperthyroidism—a clinically important condition that may be associated with disorders such as paroxysmal atrial fibrillation and osteoporosis. This is only one of a number of case reports of patients taking dietary supplements who have developed thyroid dysfunction.
Kelp. Long used as a dietary supplement, especially in Asia, kelp has been linked to thyroid dysfunction. One case report describes a 72-year-old woman with a history of thyroid disease having typical symptoms of hyperthyroidism while ingesting 4 to 6 kelp tablets daily for 1 year. Her TSH concentration was low, while total T3 and T4 levels were high. After discontinuing the kelp tablets, the hyperthyroidism resolved, and thyroid function tests returned to normal.5 Another report describes an instance of probable transient hyperthyroidism in a patient taking kelp in 2 different diet supplements.6
Tiratricol (Triac), a substance that has weak thyromimetic effects, resulted in a case of documented hyperthyroidism secondary to its use.1
Other reports. In Japan, the weight-reducing herbal medicines, Dream Shape and Ever Youth, became available in 2000. Twelve patients subsequently developed thyrotoxicosis after taking these herbal medicines, both of which were found to contain triiodothyronine and thyroxine.7
As early as 1986, researchers have described several patients who developed thyrotoxicosis from Enzo-Caps, a nonprescription diet aid manufactured in Peru. The product was touted as “a natural food product of papaya, garlic, and kelp” to assist with weight reduction. Researchers obtained the supplement for biochemical analysis and found that it had been adulterated with thyroid hormones, which led to thyrotoxicosis factitia.2
Patients in the report complained of palpitations, weakness, fatigue, headache, diaphoresis, irritability, and nervousness, and had elevated serum T3 and T4 levels. Thyroglobulin levels were not determined, but would have been useful in differentiating thyrotoxicosis factitia from hyperthyroxinemia (Graves’ disease, thyroiditis, nodular goiter).2
These reports, as well as our own experience, leave little doubt as to the importance of asking pointed questions about all prescription and nonprescription products a patient is taking. As we can attest, a little persistence goes a long way when it comes to identifying that agent your patient didn’t think was worth mentioning.
Correspondence
Taryn Taylor, MD, CCFP, Bruyere Family Medicine Center, University of Ottawa, 206 Monterey Drive, Ottawa, Ontario, Canada K2H 7A8; taryntaylor@hotmail.com
