The aim of the study was to compare the prevalence of autoimmune thyroid diseases (AITD) in patients with breast and colorectal cancer and controls and to evaluate the impact of AITD on the outcome of patients with breast cancer. Serum levels of TSH (thyroid-stimulating hormone), FT4 (free thyroxine), TPOAb (antibodies to thyroid peroxidase), TgAb (antibodies to thyroglobulin), selenium and prolactin were investigated in 210 randomly chosen women (89 with breast cancer and 72 with colorectal cancer after breast or abdominal surgery and 49 controls without oncological diseases). Eighty-four women with breast cancer were followed for a median of 136.0 months. The prevalence of positive titres of TPOAb (>60 kIU.l-1) was higher in the women with breast cancer as compared to positive titres in women with colorectal cancer and the controls (29.8 vs. 12.5 and 12.2%, respectively, P=0.016 and 0.036, respectively). Similarly, the prevalence of clinical, ultrasound and laboratory documented AITD was higher in women with breast cancer as compared to that in women with colorectal cancer and the controls (35.7 vs. 18.1 and 16.3%, respectively, P=0.014 and 0.029, respectively). We did not find any prognostic significance of FT4, TSH, TgAb, TPOAb, prolactin and the presence of AITD on relapse-free and overall survival among women with breast cancer. A negative prognostic significance of body mass index and serum levels of selenium on relapsefree survival was found. In conclusion, the prevalence of euthyroid AITD was higher in women with breast cancer as compared to euthyroid AITD in women with colorectal cancer and controls. The presence of AITD did not have an impact on the outcome of women with breast cancer.

SummaryInteractions between cytokines play an important role in the development of thyroid autoimmunity. Using enzyme-linked immunosorbent assay we investigated serum concentrations of soluble interleukin-2 receptor (sIL-2R), interferon-gamma, tumour necrosis factor (TNF)-a, interleukin (IL)-10, CD30, monokine induced by interferon-gamma (MIG), cytotoxic T lymphocyte antigen-4 and markers of apoptosis decoy receptor 3 and Bcl-2 in 28 patients with hyperthyroid Graves' disease (GD), 24 patients with untreated Hashimoto's thyroiditis (HT) and 15 healthy controls. TNF-a, IL-10 and sIL-2R were higher in GD compared with HT and controls (TNF-a: 8·79 in GD versus 2·54 pg/ml in HT, P = 0·01; IL-10: 10·00 versus 3·10 versus 3·10 pg/ ml, P1 < 0·001, P2 = 0·005; sIL-2R: 1·26 versus 0·64 versus 0·46 ng/ml, P < 0·001). MIG and CD30 were higher in HT compared with controls (649·22 Ϯ 262·55 versus 312·95 Ϯ 143·35 pg/ml, P = 0·037, 6·57 Ϯ 2·35 versus 3·03 Ϯ 1·04 U/ml, P = 0·036 respectively). In GD sIL-2R decreased when the euthyroid state was achieved (1·31 Ϯ 0·64 versus 0·260 Ϯ 0·11, n = 12, P < 0·001). sIL-2R correlated positively with free thyroxine (FT4) (R = 0·521, P = 0·000) and negatively with thyroid stimulating hormone (TSH) (R = -0·472, P = 0·00132). MIG correlated negatively with FT4 (R = -0·573, P = 0·00234) and positively with TSH (R = 0·462, P = 0·0179). The results suggest that serum concentrations of sIL-2R and MIG are related to thyroid function rather than to activation of autoimmunity.

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SummaryAutoantibodies against complement C1q (anti-C1q) have been well described in patients with systemic lupus erythematosus, where they correlate with the occurrence of severe lupus nephritis. However, data on anti-C1q in organspecific autoimmune diseases are scarce. In order to determine the prevalence of anti-C1q in patients with autoimmune thyroid disorders (AITD) and a possible association with thyroid function, we measured prospectively antiC1q in 23 patients with Graves' disease (GD) and 52 patients with Hashimoto's thyroiditis (HT). Anti-C1q levels were correlated with parameters of thyroid function and autoantibodies against thyroperoxidase, thyroglobulin and thyroid stimulating hormone (TSH) receptor. Twenty-one patients with multi-nodular goitre and 72 normal blood donors served as controls. We found elevated concentrations of anti-C1q more frequently in patients with AITD than in controls: seven of 23 (30%) patients with GD and 11 of 52 (21%) patients with HT, compared with one of 21 (5%) patients with multinodular goitre and six of 72 (8%) normal controls. Anti-C1q levels did not correlate with thyroid autoantibodies. However, in GD absolute levels of antiC1q correlated negatively with TSH and positively with free thyroxine (FT4) and triiodothyronine (FT3). In contrast, in HT, anti-C1q correlated positively with TSH levels. No correlation between TSH and thyroid autoantibodies was found. In conclusion, we found an increased prevalence of anti-C1q in patients with AITD and their levels correlated with the thyroid function in both GD and HT. This correlation seems to be independent of thyroid autoantibodies. Therefore, anti-C1q might point to a pathogenic mechanism involved in the development of AITD that is independent of classical thyroid autoantibodies.

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