Case Report
A 32-year-old man with X-linked adrenomyeloneuropathy and chronic depression treated with hydrocortisone 10 mg bid, fampiridine 10 mg bid, paroxetine 20 mg once a day, and three capsules per day of an "investigational drug" consulted his general practitioner because of gradual-onset erectile dysfunction. The general practitioner ordered laboratory tests, which revealed hyperthyroidism with suppressed serum thyrotropin (TSH) (0.012 mIU/L) controlled at 0.017 (normal range, 0.27 to 4.2), elevated serum free thyroxine (fT4), and elevated free triiodothyronine at respectively 79.2 pmol/L (normal range, 12 to 2.9) and 11.5 pmol/L (normal range, 3.1 to 6.8). The general practitioner referred the patient to an endocrinologist, who found no signs of thyrotoxicosis on physical examination. Thyroid function tests repeated in the same laboratory confirmed the markedly elevated free triiodothyronine and fT4 and suppressed serum TSH levels. Positivity for anti-TSH receptor antibodies (>40 IU/L; normal, <1.75 IU/L) ( Table 1 ) established the diagnosis of Graves disease, and the patient was prescribed an antithyroid drug (carbimazole 40 mg/d).
Follow-up thyroid function tests performed five weeks after carbimazole initiation showed a slight improvement ( Table 1 ). Because his endocrinologist was on holiday, the patient was referred to our department to evaluate his treatment response. We were surprised by the lack of clinical signs of thyrotoxicosis despite the "frank and severe" biochemical hyperthyroidism. Noticing that all the patient's assays had been done at the same laboratory, which used the Roche Cobas e170 immunoassay platform, we suspected assay interference. We therefore repeated the thyroid function tests at our hospital laboratory, which uses a different assay platform. Surprisingly, all the results were normal: in particular, he tested negative for antithyroglobulin and antithyroid peroxidase antibodies, as well as for anti-TSH receptor antibodies ( Table 1 ).
When we questioned the patient about his medications, he drew our attention to an investigational "vitamin" therapy he was taking. We contacted the clinical research center and discovered that the investigational drug was in fact biotin, prescribed at a dose of 100 mg tid as part of a trial of high-dose biotin in X-linked adrenomyeloneuropathy (EudraCT Number: 2014-000698-38). This confirmed our suspicion that biotin had interfered in the hormone assays. Indeed, the first laboratory had used the streptavidin-biotin system, whereas our laboratory used a different platform. Carbimazole was thus stopped immediately.
J Endo Soc. 2017;1(5):431-435. © 2017 Endocrine Society
