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Thyroid Disease with Monoclonal (Immunoglobulin G ) Antibody to Triiodothyronine and Thyroxine^*

The Harry Webster Thorp Laboratories, Division of Clinical Immunology, and the Division of Endocrinology and Metabolism, McGill University Clinic, Royal Victoria Hospital, Montreal, Quebec, Canada

Address requests for reprints to: Dr. Leonard A. Moroz, Division of Clinical Immunology, Royal Victoria Hospital, 687 Pine Avenue West, Montreal, Quebec, Canada H3A 1A1.

A man with previous Graves' disease spontaneously developed hypothyroidism. He became euthyroid with T₄ therapy, but developed inappropriately elevated serum levels of T₃ and, to a lesser extent, T₄. Gel filtration analysis (Sephadex G-150) of serum trace-labeled with [¹²⁵I]T₃ revealed binding to a high molecular weight fraction, distinct from normal T₃-binding proteins. This abnormal activity cochromatographed with serum immunoglobulin G (IgG) by DEAE-cellulose chromatography and gel filtration, and was retained by the F(ab)₂ fragment of IgG, indicating its true antibody nature. By isoelectric focussing, there was restricted heterogeneity of the [¹²⁵I]T₃-antibody complex (pi 9.0–9.1), and the antibody was identified as an IgG () monoclonal Igby immune precipitation. Antigenic cross-reactivity with T₄ was demonstrated by inhibition of hapten binding. The affinity of the antibody for T₃ was high (K_a = 0.9 x 10⁹ liter mol^–1), and the T₃ binding capacity of the antibody in serum was estimated as 1132 ng/dl, equivalent to 1.39 mg T₃-specific IgG/liter (0.014% of the total serum IgG). This binding capacity was similar to the serum T₃ values (1100–1300 ng/dl) at which transition from hypothyroid to euthyroid states was observed, as judged by clinical examination and measurement of serum TSH levels. (J Clin Endocrinol Metab 56: 1009, 1983)

^* This work was supported by a grant from The Richard and Edith Strauss (Canada) Foundation.

Received May 25, 1982.

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