Abstract

Adrenal incidentalomas (AIs), particularly subclinical hypercortisolism (SH), are related to an increased risk of atherosclerosis. The anti-oxidative enzyme paraoxonase-1 (PON1) and the acute phase reactant serum amyloid A (SAA) are transported by highdensity lipoprotein and reciprocally regulated in acute inflammatory response. Our aim was to investigate serum SAA, PON1, and apolipoprotein levels as indicators of subclinical atherosclerosis in patients with nonfunctioning AI (NFAI) and SH. The study group consisted of 60 controls, 14 SH, and 86 NFAI subjects. Serum amyloid A (SAA), PON1 activity, lipid profiles, apoA and B, lipoprotein A (LpA), hsCRP, and HOMA-IR levels were compared in all groups. Serum insulin, triglyceride, SAA, SAA/PON1 ratio, LpA, apoB, hsCRP, and morning cortisol levels were found to be higher while PON1 and apoAI levels were lower in the SH and NFAI groups compared with the controls, and these parameters were found to be more impaired in SH group than NFAI group (p <0.001). HOMA-IR was higher and DHEAS was lower in the SH group than in the other groups. The SAA/PON1 ratio was positively correlated with LpA (r=0.460; p <0.001), apoB (r=0.515; p <0.001), insulin (r=0.275; p=0.026), triglyceride (r=0.248; p=0.002), morning cortisol (r=0.259; p=0.045), and UFC (r=0.274; p <0.001) and negatively correlated with apoAI (r=0.329; p <0.001), ACTH (r=-0.384; p <0.001), and DHEAS (r=-0.521, p <0.001) levels. The cut-off value of the SAA/PON1 ratio for NFAI was >0.23, and for SH it was >1.33. The serum SAA/PON1 ratio was high in both the NFAI and SH groups and also exhibited higher levels in SH group. An increased SAA/PON1 ratio and low DHEAS could be attributable to subclinical atherosclerosis risk in SH patients.

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