Abstract
Primary adrenal insufficiency (Addison’s disease, AD) requires
lifelong steroid substitution. Excess exogenous glucocorticoids promote
abdominal obesity, insulin-glucose imbalance, and hypertension. Reliable
markers of the adequate glucocorticoid replacement are lacking. Visfatin is
a pro-inflammatory adipokine, with enzymatic activity of nicotinamide
phosphoribosyltransferase. It enhances leukocyte function and synthesis of
tumour necrosis factor α (TNFα) and interleukin-6 (IL-6).
Serum visfatin is elevated in autoimmunity, but also in obesity, insulin
resistance, and metabolic syndrome. This study was aimed to investigate
whether serum visfatin could guide the glucocorticoid substitution in AD.
Biochemical analyses were performed in 96 patients with AD (mean age
43.3±14.9 years) and 91 controls (43.5±12.5 years). Visfatin
level was significantly elevated in patients with AD compared to controls
(p<0.0001). Higher circulating IL-6 was also detected among subjects
with AD (p=0.006). In AD, visfatin level was positively correlated
with IL-6 (p=0.014), TNFα (p=0.001), body mass
(p=0.015), fasting insulin (p=0.001) and HOMA-IR
(p=0.001). No relationship was noticed with daily hydrocortisone
(p=0.096) and urinary free cortisol excretion (p=0.499).
Only the correlations with IL-6 and fasting insulin survived multiple
regression analysis (p=0.049 and p=0.005, respectively).
Additionally, positive correlation between visfatin and autoantibodies to
21-hydroxylase was noted (p=0.005). In the control group serum
visfatin was correlated with IL-6 (p=0.009) and TNFα
(p=0.0002). The current study reveals elevated serum visfatin in
autoimmune AD. Visfatin does not seem a useful marker of the glucocorticoid
replacement, although it correlates with fasting insulin and
pro-inflammatory molecules. Further functional analyses are warranted to
elucidate the role of visfatin in autoimmunity.
Key words
adrenal insufficiency - cytokine - glucocorticoid replacement - visfatin
