Serum Levels of Tumor Necrosis Factor-α, Soluble Intercellular Adhesion Molecule-1, Soluble Vascular Cell Adhesion Molecule-1, and Soluble Interleukin-1 Receptor Antagonist in Patients with Thyroid Eye Disease Undergoing Treatment with Somatostatin Analogues

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Abstract
The aim of this prospective, randomized study was to investigate the serum levels of tumor necrosis factor-α (TNF-α), soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), and soluble interleukin-1 receptor antagonist (sIL-1RA) in patients with thyroid eye disease (TED) before and 1 and 3 months after treatment with somatostatin analogues (SM-a). Thirty patients, all with signs and symptoms of TED, were studied. Twenty-two patients (13 females) had active eye disease with a clinical activity score (CAS) ≥ 4 (patients with active disease [PA]) and 8 patients (5 females) had inactive TED with CAS ≤ 3 (patients with inactive disease [PI]). All PA patients had a positive orbital octreoscan, whereas PI patients had a negative one. Fifteen patients from the PA group were selected randomly and received SM-a (PAS subgroup), while the remaining 7 patients were used as control subgroup (PA-C), received neither therapy, nor placebo. From the 15 patients who received SM-a (PA-S), 6 received octreotide (OCT) and 9 lanreotide (LRT). TED was reevaluated using the CAS 1 and 3 months after the initiation of SM-a treatment. Ten healthy individuals (6 females) were used as controls (group C). We found an increase in the basal levels of TNF-α (14.2 ± 7.1 pg/mL), sICAM-1 (809.1 ± 167.0 ng/mL), and sIL-1RA (542.1 ± 259.0 pg/mL) in PA patients as a total group compared with the PI (1.6 ± 1.9, 676.8 ± 73.4, 267.6 ± 152.8, respectively) group and C (1.9 ± 1.4, 598.0 ± 126.2, 258.6 ± 155.1, respectively). The basal levels of TNF-α (13.3 ± 8.3 pg/mL) and sIL-1RA (533.7 ± 308.9 pg/mL) in PA-S as well as in PA-C (16.0 ± 2.9, 560.2 ± 107.3, respectively) subgroups were also increased compared with PI patients and C (1.9 ± 1.4 and 258.6 ± 155.1, respectively). The same was true for sICAM-1 when baseline levels compared with C (817.1 ± 187.3 and 791.9 ± 123.5, respectively vs. 598.0 ± 126.2 ng/mL). After SM-a, serum levels of sICAM-1 and sVCAM-1 were decreased significantly 1 (781.2 ± 205.9, 1,193.5 ± 511.8 ng/mL) and 3 months (786.8 ± 199.6, 1,122.1 ± 225.3 ng/mL) after the initiation of treatment. In conclusion, serum levels of TNF-α, sICAM-1, and sIL-1RA were elevated in patients with active TED compared to controls. Furthermore, sICAM-1 and sVICAM-1 levels declined during the treatment with SM-a in patients with active TED.