Inflammatory Markers Link Steroid Profiles to Bone Status in Patients with Autonomous Cortisol Secretion

Area of Science:

• Endocrinology
• Bone Metabolism
• Inflammation Biology

Background:

• Autonomous cortisol secretion (ACS) is a key cause of osteoporosis due to excess glucocorticoids.
• Cortisol excess alone doesn't fully explain bone status changes; androgen deficiency and inflammation may also play roles.

Purpose of the Study:

• To investigate associations between inflammatory markers, bone status, and steroid profiles in ACS.
• To explore the potential mediating role of inflammation in ACS-related bone changes.

Main Methods:

• Assessed inflammatory markers and bone status in 106 ACS patients and 95 controls (NFAT).
• Measured plasma steroid profiles using liquid chromatography-tandem mass spectrometry.
• Stratified analyses by sex and menopausal status to examine associations.

Main Results:

• ACS patients exhibited higher systemic immune-inflammation index (SII) and lower prognostic nutritional index (PNI) than controls.
• In premenopausal women with ACS, SII negatively correlated with trabecular bone score (TBS), while PNI positively correlated with TBS.
• Androsterone-glucuronide (AND-G) negatively correlated with SII and positively with PNI, mediating the association between AND-G and TBS via PNI.

Conclusions:

• Inflammatory markers correlate with reduced bone quality, especially in premenopausal women with ACS.
• Androgen deficiency is linked to inflammation, partially driving bone deterioration in ACS.
• PNI and AND-G levels are significant factors in bone health within the context of ACS.