Premium
Soluble interleukin‐1 receptor antagonist concentration in patients with Graves' ophthalmopathy is neither related to cigarette smoking nor predictive of subsequent response to glucocorticoids
Author(s) -
Bartalena Luigi,
Manetti Luca,
Tanda Maria Laura,
Dell'Unto Enrica,
Mazzi Barbara,
Rocchi Roberto,
Barbesino Giuseppe,
Pinchera Aldo,
Marcocci Claudio
Publication year - 2000
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1046/j.1365-2265.2000.00988.x
Subject(s) - interleukin 1 receptor antagonist , glucocorticoid , medicine , endocrinology , basal (medicine) , receptor antagonist , glucocorticoid receptor , antagonist , cigarette smoking , antiglucocorticoid , receptor , insulin
OBJECTIVE The aim of the present study was to evaluate serum soluble interleukin‐1 receptor antagonist (sIL‐1RA) concentration and its relationship with the degree of cigarette smoking in patients with Graves' ophthalmopathy (GO). DESIGN AND SUBJECTS Twenty‐two consecutive GO patients (20 women, two men; age range 25–68 years, mean 48 years; 12 smokers, 10 non‐smokers) submitted to IV glucocorticoid pulses over a 3‐month period. MEASUREMENTS sIL‐1RA levels were measured by an immunoenzymatic assay (sensitivity, 4 ng/l; normal range, 50–290 ng/l) before glucocorticoid treatment, after two months of therapy, and 3 months after drug withdrawal. RESULTS Thirteen patients responded to treatment (59%; five smokers and eight non‐smokers), nine were non‐responders (41%; seven smokers and two non‐smokers). Baseline median sIL‐1RA concentration did not differ in smokers and non‐smokers (222 and 173 ng/l, respectively; P = 0.69). Likewise, no significant differences were found between the two groups during treatment (537 and 389 ng/l, respectively; P = 0.28); sIL‐1RA concentration after treatment was higher in smokers (258 vs . 94 ng/l; P = 0.02). There was no correlation between basal sIL‐1RA levels and the degree of cigarette smoking. Likewise, there was no difference in sIL‐1RA levels in responders and non‐responders, either at baseline (186 vs . 216 ng/l; P = 0.83), during or after treatment. CONCLUSION Our study suggests that circulating soluble interleukin‐1 receptor antagonist levels, both at baseline and during glucocorticoid treatment, are neither influenced by cigarette smoking nor predictive of subsequent response to glucocorticoid treatment.