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The purpose of this study was to measure the nuclear DNA content of cells in three different areas of multinodular goiter from 15 patients. Diploid DNA was found in the cell samples from 12 patients; the biopsies from one patient contained a clear ipodiploid peak (61%, D.I. 0.75) and those from the remaining 2 had dubious ploidy. The calculation of the mitotic index, including cells in S + G2M phases, evidentiated a large variability between different samples from the same goiter, thus correlating with the cellular heterogeneous composition of the thyroid.

In the last ten years several experimental data have suggested that growth factors may play an important role in modulating thyroid growth and function. Epidermal Growth Factor (EGF) is present in large quantities in thyroid tissue, where it appears to stimulate DNA synthesis and inhibit cellular function. Insulin-like Growth Factors (IGFs), Interleukin I (IL-I) and Fibroblast Growth Factor (FGF) show the same stimulation on cell proliferation. On the contrary Transforming Growth Factor beta (TGF-beta) and somatostatin display inhibitory effects on follicular growth. Therefore it is likely that growth factors' altered production and/or their receptors abnormal expression on the thyroid cells surface might be involved in the development of multinodular goiter and some thyroid neoplasms.

This present review of the literature deals with the possible autoimmune genesis of the multinodular goiter. Some investigators have identified an immunoglobulin stimulating specifically the growth of the thyroid gland (TGI) in the sera of patients affected with sporadic goiter, quite different from TSI, involved in Graves' disease. Other authors report divergent results; however there are many methological differences in these studies that give rise to controversies about the evaluation of the data. At present, these studies have failed to demonstrate consistently an autoimmune genesis of multinodular goiter.

The authors consider the behaviour of TBII (TSH receptor binding inhibitory immunoglobulins) in multinodular goiter, in relation to the functional status of the thyroid classified on the basis of T3, FT4, TSH IRMA. The samples were collected from 53 patients with normal T3, FT4 and TSH; 14 patients with T3 and FT4 in normal range and TSH less than 0.15 milli U/l; 8 patients with T3 and/or FT4 above the superior limits of normal range and TSH less than 0.15 milli U/l and from a control group of 10 patients with Grave's disease. TBII was measured by radioreceptor assay and the index resulted less than 15% in all the patients with eufunctioning or hyperfunctioning multinodular goiter. Mean value in biochemically hyperthyroid patients was 6.25% and in euthyroid patients was 5.69%. The difference was statistically not significant. Moreover, significantly elevated levels of TBII were found in 60% of patients with Grave's disease.