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Glucocorticoids (GC) induce cardiometabolic risk while atherosclerosis is a chronic inflammation involving immunity. GC are immune suppressors, and the adrenocorticotrophic hormone (ACTH) has immune modulator activities. Both may act in atherothrombotic inflammation involving immune cells (IMNC). Aim . To investigate adhesion and activation surface cell markers (CDs) of peripheral IMNC in endogenous Cushing syndrome (CS) and the immune modulator role of ACTH. Material and Methods . 16 ACTH-dependent CS (ACTH-D), 10 ACTH-independent (ACTH-ID) CS, and 16 healthy controls (C) were included. Leukocytes (Leuc), monocytes (MN), lymphocytes (Lym), and neutrophils (N) were analyzed by flow cytometry for atherosclerosis previously associated with CDs. Results . Leuc, N, and MN correlated with CS (p0.05), WC (p0.001), WHR (p=0.003), BMI (p0.001), and hs-CRP (p0.001). CD14 ++ CD16 + (p=0.047); CD14 + CD16 ++ (p=0.053) MN; CD15 + (p=0.027); CD15 + CD16 + (p=0.008) N; and NK-Lym (p=0.019) were higher in CS. CD14 + CD16 ++ MN were higher in ACTH-ID (8.9 ± 3.5%) versus ACTH-D CS (4.2 ± 1.9%) versus C (4.9 ± 2.3%). NK-Lym correlated with c-LDL ( r = 0.433,p=0.039) and CD15 + N with hs-CRP ( r = 0.446,p=0.037). In multivariate analysis, Leuc, N, and MN depended on BMI (p=0.021), WC (p=0.002), and WHR (p=0.014), while CD15 + and CD15 + CD16 + N on hypercortisolism and CS (p=0.035). Conclusion . In CS, IMNC present changes in activation and adhesion CDs implicated in atherothrombotic inflammation. ACTH-IDCS presents a particular IMNC phenotype, possibly due to the absence of the immune modulator effect of ACTH.
Aranda et al. (Sun,) studied this question.