Abstract
A unique 16-year old female patient presented after acute Epstein-Barr virus (EBV) infection with severe primary hypothyroidism. Her thyroid test results were thyrotropin level (TSH) of 198 mU/L (normal, 0.4-4 mU/L), free thyroxine [FT4], 2.5 pmol/L (normal, 10-25 pmol/L), total triiodothyronine (TT3) > 19.5 nmol/L (normal, 1.3-2.7 nmol/L), and free triiodothyronine (FT3), 0.77 pmol/L (normal, 3.3-6.3 pmol/L). She had high titers of thyroglobulin and thyroid peroxidase autoantibodies. In vitro triiodothyronine (T3)-binding measured by radioimmunoprecipitation was 86% (normal, up to 8.5%) and thyroxine (T4)-binding 8.2% (normal, 6.4%). Serum immunoglobulin G (IgG) absorption, achieved by protein-G Sepharose beads, decreased TT3 toward normal. Levothyroxine treatment normalized the low baseline FT4 and FT3 values, and suppressed TSH to normal. However, TT3 remained highly elevated and returned to normal after 20 months, while T3 binding gradually decreased. Thus, her severe hypothyroidism was masked by this unusual phenomenon. Thirty-four patients with EBV infection (15 with acute disease and 19 with previous infection) were tested for thyroid hormone levels. EBV antibodies (early antigen immunoglobulin M [IgM] and IgG and anti-Epstein-Barr virus nuclear antigen [EBNA] IgG) were measured by enzyme-linked immunosorbent assay (ELISA). In 15 patients with acute EBV the mean TT3 level was 2.47 ± 0.39 nmol/L (5 had TT3 values above normal) compared to a mean TT3 of 1.70± 0.53 nmol/L in 19 subjects with previous infection (p < 0.0005; only 1 had a TT3 result above normal), with no differences in FT4 and TSH concentrations between the two groups. Acute EBV infection may be associated with transient mild to severe TT3 elevation as a result of assay interference by anti-T3 autoantibodies.
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