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Thyroid Peroxidase Activity-Inhibiting Immunoglobulins in Patients with Autoimmune Thyroid Disease

Second Department of Internal Medicine, Osaka City University Medical School, Abeno-ku Osaka 545, Japan
Ito Thyroid Clinic and Hospital (H.S., J.N., K.I.), Shibuya-ku Tokyo 150, Japan

Address all correspondence and requests for reprints to: Noboru Hamada, M.D., Second Department of Internal Medicine, Osaka City University Medical School, 1-5-7 Asahimachi, Abeno-ku, Osaka 545, Japan.

The thyroid microsomal antibody (M-Ab) has been found to be an antibody against thyroid peroxidase (TPO), and such antibodies have been reported not only to bind TPO but also to directly inhibit TPO activity. In this study we investigated the relationship between TPO activity-inhibiting immunoglobulin (TPII) and thyroid function in 55 untreated patients with hyperthyroidism due to Graves’ disease and 35 untreated patients with Hashimoto’s disease. TPO partially purified from the microsomal fraction of Graves’ thyroid tissue by Sephacryl S-300 gel filtration was incubated with immunoglobulin (Ig) fractions of serum prepared by precipitation with 15% polyethylene glycol. At the end of incubation, TPO activity was measured by a guaiacol assay. The TPII level was expressed as the TPII index, defined as the inhibition of TPO activity by patient Ig divided by inhibition produced by a known positive Ig. We also measured serum free T₄, free T₃, and TSH concentrations and anti-M-Ab titers, the latter by a microenzymelinked immunosorbent assay.

When a positive TPII index was defined as more than the mean + 2 SD of the TPII index (0.38) for 15 normal subjects, 13 patients with Graves’ disease and 14 patients with Hashimoto’s disease had positive TPII index values. There was a positive correlation between the TPII index values and the M-Ab titers in patients with either Graves’ disease (r = 0.38; P < 0.01) or Hashimoto’s disease (r = 0.52; P < 0.01). The mean TPII index in patients with Hashimoto’s disease was significantly higher than that in patients with Graves’ disease [0.38 ± 0.42 (±SD) vs. 0.19 ± 0.41; P < 0.05]. The slope of the regression line between the TPII index values and the M-Ab titers for patients with Hashimoto’s disease was steeper than that for patients with Graves’ disease. The mean serum free T₄ concentration was significantly lower in those patients with Hashimoto’s disease who had positive TPII index values than in those with negative TPII index values (14.0 ± 5.0 vs. 9.6 ± 3.7 pmol/L; P < 0.01). There was no significant difference in thyroid function between the patients with Graves’ disease with positive and negative TPII index values.

TPII appears to inhibit thyroid function in some patients, but no simple relationship between TPII and thyroid function in autoimmune thyroid disease was demonstrated. Understanding the factors that control access of anti-TPO antibody to its antigen may help to elucidate the significance of circulating anti-TPO antibody.

Received July 5, 1988.

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