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The present study describes a double antibody technique to evaluate antithyroglobulin autoantibodies in human serum. Rabbit anti-human γG is used to precipitate the immunocomplexes between labelled thyroglobulin and autoantibodies. Thyroglobulin has been labelled either in vivo, or chemically by electrolysis of iodide, a procedure which also produced substantial dissociation of the protein. The double antibody technique was compared with haemagglutination of sheep red blood cells coated with human thyroglobulin. A good correlation was established between the tanned red cell haemagglutination titre and the double antibody technique when ‘ in vivo’ labelled thyroglobulin was employed. The use of chemically iodinated thyroglobulin, purified after labelling, increased the sensitivity of the test 100 fold so that 38% of sera from patients with thyroid diseases having negative haemagglutination titres precipitate between 15% and 65% of the labelled antigen. The sensitivity and simplicity of this method provide a useful tool in clinical as well as in experimental work.

Conflicting results have been reported regarding serum lipoprotein(a) (Lp(a)) concentrations in patients with hypothyroidism. We addressed the question whether thyroid autoimmunity could be associated with elevated Lp(a) values independent of the thyroid status. Lp(a) was measured by ELISA in 30 males, 29 premenopausal and 30 postmenopausal females positive for thyroid peroxidase- and/ or thyroglobulin-antibody (T-Abs) and normolipidemic, screened out respectively from 428 male donors, 162 premenopausal donors and 108 postmenopausal females; they were compared with 65 males, 72 premenopausal and 48 postmenopausal females, negative for thyroid antibodies, normolipidemic and matched for age. T-Abs-positive male donors showed serum Lp(a) concentrations significantly increased compared with males without T-Abs (mean 19.7 +/- 15.9 vs 12.7 +/- 17.5 mg/dl; median 17.0 vs 4.0 mg/dl; Mann Whitney U test: P = 0.0000). In premenopausal females no difference could be found between T-Abs-positive and T-Abs-negative subjects (mean 13.2 +/- 16.1 vs 12.3 +/- 13.9 mg/dl; median 5.2 vs 8.7 mg/dl), suggesting an Lp(a) lowering effect of estrogens. The study was, therefore, extended to postmenopausal females. Significantly elevated Lp(a) levels were found in 30 postmenopausal females with T-Abs when compared with 48 postmenopausal females without T-Abs (40.0 +/- 34.2 mg/dl vs 20.7 +/- 19.3 mg/dl; median 32.0 vs 18.0 mg/dl; Mann Whitney U test: P = 0.0002). Finally, 21 postmenopausal, normolipidemic, autoimmune hypothyroid patients on L-thyroxine and euthyroid compared with 48 postmenopausal females without T-Abs also showed increased serum levels of Lp(a) (mean 27.0 +/- 16.8 mg/dl vs 20.7 +/- 19.3 mg/dl, median 25.0 vs 18 mg/dl; Mann Whitney U test: P = 0.0024). Thyrotropin levels in all subjects and patients were within the normal range. In conclusion, our results in males and postmenopausal females with T-Abs and euthyroid show an association between thyroid autoimmunity and increased levels of Lp(a), while the results obtained in premenopausal females suggest that estrogens might interfere with the Lp(a) increase related to thyroid autoimmunity.