Misdiagnosis of Graves' hyperthyroidism due to therapeutic biotin intervention.

BACKGROUND: Lately, high dose of biotin is often given orally to patients with a primary progressive multiple sclerosis (PPMS). However, the molecule biotin is also a principle compound in various analytic immunoassays. CLINICAL CASE: An asymptomatic 60-year-old woman with PPMS on high dose of biotin therapy (3 × 100 mg/d) displayed abnormal thyroid function tests (TSH 0.02 mU/l, fT4 > 103 pmol/l, and fT3 > 46 pmol/l). TSH was determined by a homogeneous sandwich chemiluminescent immunoassay and fT4 and fT3 were both determined by a homogeneous, sequential, chemiluminescent immunoassay. TSH receptor antibodies were found to be markedly elevated (>40 IU/l) using a electrochemiluminescence immunoassay, suggestive for Graves' hyperthyroidism. Due to inconsistency between clinical presentation and laboratory results, thyroid function tests have been repeated with two other immunoassays. A direct, labeled antibody, competitive immunoassay to determine TSH and a luminescent immunometric immunoassay to determine fT4 and fT3 showed a subclinical hyperthyroidism (TSH < 0.02 mU/l, fT4 15.9 pmol/l, and fT3 4.7 pmol/l). Normal thyroid function tests (TSH 1.66 mU/l, fT4 15.3 pmol/l, and fT3 4.7 pmol/l) were obtained by a chemiluminescent microparticle immunoassay. All abnormal levels of TSH, fT4, fT3, and TSH-R-Ab were observed in immunoassays using biotin as a reagent. CONCLUSION: Abnormal thyroid function tests in this euthyroid patient were found to be false due to significant interference of supraphysiological levels of plasma biotin. Laboratory tests applying immunoassays using a biotin-containing reagent should be interpreted with caution in patients on biotin substitution.

Patients with the metabolic syndrome and a disturbed cortisol balance display more microalbuminuria.

The objective of this study was to investigate whether patients with the metabolic syndrome (MetS) and an imbalance in cortisol metabolism express increased urinary albumin excretion compared to those patients with metabolic syndrome alone. Seventy-four patients with MetS were evaluated using a low-dose dexamethasone suppression test (LDDST) to identify disturbed cortisol balance (cortisol levels > 50 nmol/L after LDDST). The level of albumin in the urine was also evaluated. Disturbed cortisol balance was found in 8% of all evaluated patients with MetS. Microalbuminuria was present significantly more often (p<0.01) in those patients with MetS and an imbalance in cortisol metabolism compared with patients suffering MetS alone (urine albumin: 210 mg/L vs. 26 mg/L, respectively, p<0.01). A substantial percentage of patients with MetS had inappropriate cortisol homeostasis. Of importance, excretion of urinary albumin was increased in these patients. This observation may indicate that this subgroup within the MetS population has a higher cardiovascular risk and possible increased endothelial dysfunction, with a subsequent need for stricter control to prevent cardiovascular morbidity and mortality.