A 72-year-old woman presented to our medical center with an altered mental status having suffered a fall. She had a history of primary hypothyroidism for many years treated with a stable dose of levothyroxine 0.075 mg/d. She was clinically euthyroid without tremors, palpitations, tachycardia, or other findings suggesting thyrotoxicosis. A pathologic fracture of her right humerus eight years before had led to a diagnosis of multiple myeloma with an IgG kappa M spike paraprotein. She received chemotherapy and went into remission. However, a recent reexacerbation had occurred, and she was being considered for further therapy. Routine admission labs revealed hematocrit 20.9% (normal 38-47%), sodium 132 mmol/L (136-145), potassium 4.0 mmol/L (3.5-5.1), chloride 104 mmol/L (98-107), urea nitrogen 45 mmol/L (20-31), and creatinine 2.8 mg/dL (0.6-1.0). Oncologic studies were consistent with multiple myeloma with an M spike kappa IgG paraprotein: total protein 10.1 g/dL (5.7-8.2), albumin 1.8 g/dL (3.4-5.0), and serum albumin: globulin ratio: 0.22 (0.60-1.50). Serum protein electrophoresis revealed gamma globulin 5.8 g/dL (0.8-1.7), kappa chain 9270 mg/L (3.3-19.4), Lambda chain 9.3 mg/dL (5.7-26.3), K/L ratio 996.7 (0.26-1.65), and B2:macroglobulin: 17.9 mg/L (<or = 2.51).
Thyroid biochemistry (Table 1) on presentation performed with the Siemens Atellica chemiluminescent immunoassay kit reported a slightly high TSH of 6.27 uIU/mL (normal 0.55-4.78) with normal total T4 of 4.5 mug/dL (3.2-12.6) and free T4 1.22 ng/dL (0.89-1.76). However, total T3 was markedly elevated at >600 ng/dL (60-181). Tests for anti-ThyroPerOxidase (AntiTPO), anti-ThyroGlobulin (antiTG), Thyroid-Stimulating Immunoglobulin (TSI), and Human Anti-Mouse Antibodies (HAMA) were within normal limits at <1 IU/mL (<9), <1 IU/mL (<1), <89% (<140), and <56 ng/mL (<74), respectively. Assay for anti-T3 antibodies was negative using a proprietary chemiluminescent competitive immunoassay procedure performed by Quest/Nichols Laboratories. Repeat testing on the Siemens Atellica platform again reported an elevated TT3 >600 ng/dL. Reverse T3 (Thermo Aria platform) was normal at 21 ng/dL (8-25), while results for TSH, total T4, and free T4 were similar to those reported previously. Free T3 was low at 1.7 (2.3-4.2 pg/ml (Siemens Advia kit) consistent with Euthyroid Sick Syndrome. 14 months earlier, her thyroid biochemistry was reported to be normal using the Roche Cobas chemiluminescent immunoassay kit with total T3 82 ng/dL (80-200). Thyroid Hormone-Binding Protein (THBP) electrophoresis was normal: TBG 14.3 mcg T4/dL (10.3-24.9), albumin 16.6 mcg T4/dL (11.5-34.1), and transthyretin (prealbumin) 69 mg T4/dL (48.8-70.4). Follow-up testing on the Roche Cobas platform again reported normal total T3 47.4 ng/dL (Table 1). Polyethylene glycol (PEG) precipitation was planned, but the patient expired before it could be accomplished.
We conclude that the factitious elevation in TT3 was most likely due to assay interference from the documented multiple myeloma paraprotein as well as differences between the test platforms used.