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More Than IL-6 in Graves’ Disease?¹

Hacettepe University Institute of Oncology Sihhiye-Ankara, Turkey 06100

We read with great interest the remarkable report by Salvi et al. (August 1996 JCEM) delineating the soluble interleukin-6 (IL-6) receptor (sIL6-R) profile of Graves’ disease (GD) (1). By commenting to our trial (2) in their article, they confirmed the increased IL-6 concentrations in GD with an additional, novel finding of elevated sIL6-R in the hyperthyroid phase. sIL6-R returned to normal in the euthyroid state achieved by methimazole, but IL-6 levels did not. The latter finding seems paradoxical in that, according to their results, the median euthyroid IL-6 level (49.2 fmol/L), though low in comparison to the controls (55 fmol/L), did not reach a statistical significance when compared with the hyperthyroid level (69 fmol/L). If this was the case, it would be difficult to rationalize a steady state IL-6 level despite a lowered sIL6-R where the measured serum IL-6 is a total of free IL-6 plus the fraction bound to the soluble receptor. As a reasonable explanation, type II (ß) error, a limitation of nonparametric tests in smaller groups might be responsible for the undetectable significance.

In our trial, lowered IL-6 concentrations in the euthyroid state compared with the hyperthyroid levels were documented in both toxic multinodular goiter (TMNG) and in GD patients. Only GD subjects exhibited an elevated level of serum tumor necrosis factor-alpha (TNF-), which was not reversed by propylthiouracil, with TNF- levels being normal in TMNG or simple diffuse goiter patients and in controls (2). Thus, being the first to hypothesize TNF- to predict the autoimmune process of GD, we reconfirmed IL-6 to be a nonspecific but reversible marker of thyroid inflammation (3).

As currently described by Salvi et al., not only IL-6 but also sIL-6R failed to discriminate the state of remission or relapse in GD. Regarding the complex interactions of intrathyroidal cytokine network to initiate and/or perpetuate the autoimmune process, the serum cytokine profile of GD deserves further research, perhaps with a particular emphasis on the TNF- receptor status.

Footnotes

¹ Address correspondence to: Ismail Çelik, Department of Medical Oncology, Hacettepe University Institute of Oncology, Sihhiye-Ankara 06100.

Received November 13, 1996.

References

1. Salvi M, Girasole G, Pedrazzoni M, et al. 1996 Increased serum concentrations of interleukin-6 (IL-6) and soluble IL-6 receptor in patients with Graves’ disease. J Clin Endocrinol Metab. 81:2976–2979.[Abstract]
2. Çelik I, Akalin S, Erba T. 1995 Serum levels of interleukin 6 and tumor necrosis factor- in hyperthyroid patients before and after propylthiouracil treatment. Eur J Endocrinol. 132:668–672.[Abstract/Free Full Text]
3. Bartalena L, Brogioni S, Grasso L, Martino E. 1993 Increased serum interleukin-6 concentration in patients with subacute thyroiditis: relationship with concomitant changes in serum T₄-binding globulin concentration. J Endocrinol Invest. 16:213–218.[Medline]

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