ESPE Abstracts (2018) 89 P-P3-393

An Assay Led Astray: A Curious Case of Biotin-Induced Hyperthyroidism

Tashunka Taylor-Miller, Ashely Alexander, Tina Yen & Michele O’Connell


Royal Children’s Hospital, Melbourne, Australia


The third child to Burmese parents is born at term in good condition in a suburban hospital. The baby was breast fed from birth and had a normal physical examination without dysmorphic features or palpable liver edge. The parents have had two previous live male births at term, that developed severe jaundice and seizure in the first 24 hours of life; both passed away on day 3 of life. Due to concerns of possible metabolic condition, the baby was commenced on prophylactic phototherapy, oral pyridoxine, thiamine and biotin. The baby was transferred to a tertiary neonatal intensive care unit on day 2 of life. As part of the general diagnostic work up thyroid function tests were ordered on day 2 and 9 of life. [see Table 1]. Following these results, the baby was commenced on carbimazole and the breast-feeding mother was advised to avoid high iodine-containing foods. Discrepancy between clinical and biochemical picture, and absence of maternal hyperthyroidism, prompted literature review for possible cause. Concerns of possible biotin-streptavidin interaction prompted re-analysed, the results were completely normal [see Table 1]. Biotin was ceased and thyroid function normalised. Carbimazole was then ceased; 8 doses total were administered. Biotin has been shown to affect immunoassays that employ biotin-streptavidin bound to assay antibodies, such as the Roche immunoassays. The biochemical results suggesting thyrotoxicosis mislead clinicians with a clinically euthyroid patient. In cases where concerns of antibody-mediated thyroid disease are being considered, biotin may falsely elevated thyroid receptor antibodies, anti-thyroid peroxidase and anti-thyroglobulin antibodies, leading to further confusion regarding ‘confirmation’ of the diagnosis. Prophylactic metabolic supplements are prescribed often in neonates with suspected metabolic disorders. This case illustrates the seriousness of assay interference due to exogenous biotin which can mimic biochemical thyrotoxicosis.

Table 1 Biochemical thyroid function and immunoassay over time
AssayVitrosRocheRocheAbbottRocheRocheRoche
DOB is day 0Day 2Day 9 Day 10* Day 10*Day 12Day 16Day 23
TSH mIU/l0.21 (0.5–8.5)<0.05 (0.43 – 16.10)0.09 (0.43 – 16.10)3.81 (0.88–5.42)1.45 (0.43 –16.10)7.05 (0.43–8.05) 6.81 (0.43 – 8.05)
Free T4 pmol/l44.5 (18–27)>100 (8.5 – 39.8)>100 (8.5 – 39.8)19.4 (9.0-19.0)32.1 (8.5– 39.8)19.9 (8.5–39.8)17 (8.5 – 39.8)
T3 pmol/l9.3 (4.2–8.3)33.4 (3.1–6.8)19.3 (3.1–6.8)-9.2--
CBZ startedBiotin ceasedCBZ ceased
* same serum sample re-analysed

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