Endocrine Abstracts

Introduction: Thyroid function tests are crucial in diagnosing and managing endocrine disorders, but their reliability can be compromised by analytical interference. Rare but important cause is heterophile antibody interference where endogenous antibodies bind to assay antibodies resulting in abnormal results. This can mimic thyroid disease leading to unnecessary investigations or treatments. Correlating laboratory data with patient’s clinical status and working closely with biochemistry colleagues will help in identifying this promptly.

Case report: A 72-year-old gentleman with type 2 diabetes mellitus on insulin and a background of left renal cell carcinoma was admitted with biliary sepsis and an obstructed femoral hernia requiring surgical repair. During admission, routine thyroid function tests performed on the Roche platform showed a markedly elevated free thyroxine (FT4) (70.9 mU/l) and with an inappropriately normal thyroid stimulating hormone (TSH) (4.58 pmol/l). Free triiodothyronine (FT3) was also elevated (9.2 pmol/l). Thyroid antibodies were negative. The patient was asymptomatic and clinically euthyroid, He was receiving unfractionated heparin for venous thromboembolism prophylaxis, raising a suspicion of heparin-induced displacement of T4 from binding proteins. Heparin was withheld for 24 hours but repeat thyroid functions remained unchanged. Given the discordance between biochemical and clinical findings, the case was discussed with biochemists and targeted interference studies were undertaken. Dilution studies demonstrated non-linear FT4 and FT3 values; however, this was also seen in control samples and therefore reflected assay characteristics rather than interference. Polyethylene glycol (PEG) precipitation produced a marked reduction in free hormone concentrations in the patient’s sample but not in controls, consistent with the presence of a large protein such as a heterophile antibody. To confirm the finding, samples were tested on the Abbott platform, showing normal results (TSH 3.41 mU/l, FT4 16.2 pmol/l, FT3 3.09 pmol/l). A sample was also sent for assessment of total T4 levels which confirmed calculated FT4 was slightly lower than measured FT4, consistent with displacement. The overall picture confirmed heterophile antibody interference as the key explanation for the abnormal thyroid profile with heparin effect being a possible confounding factor. No thyroid-specific treatment or further investigations were needed.

Conclusion: This case demonstrates that marked biochemical abnormalities in a euthyroid patient should raise suspicion of assay interference. Heterophile antibody interference can be identified with PEG precipitation and cross-platform testing. Close clinician–laboratory collaboration prevents unnecessary investigations, treatment, and potential patient harm.