High Levels of Serum Soluble Interleukin-2 Receptors in Hyperthyroid Patients: Correlation with Serum Thyroid Hormones and Independence from the Etiology of the Hyperthyroidism

Abstract

The serum levels of soluble interleukin-2 receptors (s-IL-2R) and soluble CD8 antigens (s-CD8) were measured in 33 patients with Graves' disease (GD), 29 with toxic nodular goiter (TNG), 6 with toxic adenoma (TA), and 12 with hypothyroidism, as well as in 11 patients with infectious mononucleosis (known to have high s-IL-2R and s-CD8 levels) and 34 normal controls. Serum levels of T3 and T4, both total and free, and of TSH were simultaneously determined. s-IL-2R levels were significantly higher in all patients with hyperthyroidism (mean +/- SD, 3276 +/- 1273 U/mL for GD, 4183 +/- 1832 for TNG, and 1671 +/- 648 for TA) compared to normal control values (P less than 0.001 for GD and TNG and P less than 0.01 for TA), while in the euthyroid state they were within the normal range (535 +/- 240 U/mL). Hypothyroid patients had significantly lower s-IL-2R levels compared to normal controls (P less than 0.05). A positive correlation (P less than 0.001) between serum s-IL-2R levels and total/free T3-T4 levels was found in these groups of patients, while no correlation between s-CD8 levels and s-IL-2R/T3/T4 was found. These findings suggest an association between hyperthyroxinaemia and activation of human lymphocytes in vivo.

A case of thyroid storm with a markedly elevated level of circulating soluble interleukin-2 receptor complicated by multiple organ failure and disseminated intravascular coagulation syndrome

“…Multiple imaging studies and the clinical course definitely ruled out a complication by hematological malignancies. An increase in circulating sIL-2R levels has previously been correlated with thyroid hormone levels in untreated Graves' disease and other thyrotoxic disorders [8][9][10]. However, FT3 and FT4 levels in this case were similar to those in TS cases reported in the nationwide survey, and were indistinguishable from those in non-storm Graves' disease patients [2].…”

“…Mild elevations in serum sIL-2R levels have also been reported in non-immunogenic thyroid disorders including toxic nodular goiter and toxic adenoma. In contrast, circulating sIL-2R levels were shown to be significantly lower in hypothyroid patients than in normal subjects [8][9][10]. Taken together, the production and/or release of sIL-2R in these thyroid disorders has been considered to be positively regulated by thyroid hormones rather than reflecting the autoimmune process.…”

“…A mild elevation in sIL2-R has also been observed in several autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis, and could reflect disease activities [5,7]. Circulating sIL-2R levels have also been reported to mildly increase in autoimmune Graves' disease and were positively correlated with thyroid hormone levels, but not with anti-thyroid autoantibodies [8][9][10]. Mild elevations in serum sIL-2R levels have also been reported in non-immunogenic thyroid disorders including toxic nodular goiter and toxic adenoma.…”

Low T3 Syndrome in Head-Injured Patients is Associated with Prolonged Suppression of Markers of Cell-Mediated Immune Response

“…Recently, it has become clear that T 3 exerts pleiotropic effects on the thymus by inducing thymocyte proliferation and release from thymic nurse cells [37]. Strong evidence also exists for a modulation of serum sIL-2R levels by thyroid hormones [23,24]. An action of thyroid hormones on thymic function in head-injured patients was suggested by the observation that low T 3 levels correlated with decreased thymulin concentrations [38].…”

“…Drugs were not administered on a routine prophylactic regimen f This patient suffered from Pseudomonas sepsis g patient without low T 3 syndrome lected a group of pro-and anti-inflammatory cytokines, some of which have been investigated in previous studies although using serum samples only [4][5][6]. Since T-lymphocyte-derived sIL-2R has been shown to correlate with the extent of low T 3 syndrome [5,22] and due to the fact that thyroid hormones themselves influence cellular immune functions [23,24], we measured further lymphocyte counts and mononuclear cell activation markers (i.e., neopterin, β 2 -microglobulin [β2m)). Neopterin is synthesized by stimulated monocytes/macrophages [25], and β2m is released by activated lymphocytes and neutrophils [26,27].…”