Anti-tumour necrosis factor antibody treatment does not change serum levels of cortisol binding globulin in patients with rheumatoid arthritis but it increases androstenedione relative to cortisol

Abstract

Background: Cortisol binding globulin (CBG) is produced by liver cells and is inhibited by proinflammatory cytokines such as interleukin (IL) 6. CBG serum levels are typically low during prolonged inflammatory processes. Thus, observed changes of cortisol during anti-tumour necrosis factor (TNF) treatment may be related to changes of CBG in rheumatoid arthritis (RA).

Objective: To investigate the course of CBG during anti-TNF treatment in RA.

Methods: 13 patients with longstanding RA, without prior prednisolone treatment, were included in this longitudinal study with subcutaneous adalimumab.

Results: Treatment with anti-TNF markedly decreased clinical markers of inflammation and serum IL6. Serum levels of cortisol, CBG, and the ratio of cortisol/CBG did not change markedly, whereas the ratio of serum CBG/IL6 increased (p = 0.004). In parallel, levels of adrenocorticotropic hormone decreased during the observation period. The ratio serum androstenedione/serum cortisol increased during the study (p = 0.036).

Conclusions: During anti-TNF treatment relatively normal levels of CBG and a normal ratio of CBG/cortisol are found. Changes of cortisol in relation to IL6 during anti-TNF treatment, seen previously, may not be related to changes of CBG.

Figure 1

Course of serum cortisol binding globulin (CBG) and androstenedione (ASD) in relation to cortisol during 12 weeks of anti-TNF antibody treatment in patients with RA. Baseline values are given as time point 0. The graph depicts serum CBG (A), the ratio serum cortisol/CBG (B), the ratio serum CBG/IL6 (C), serum ASD (D), and the ratio serum ASD/cortisol (E). The data are given as means (SEM). The p value according to Friedman's test is given.