Observational analysis assesses liver fibrosis and steatosis in patients with Cushing syndrome and MACS, suggesting non-invasive markers.
Background/Introduction Cushing syndrome (CS) and mild autonomous cortisol secretion (MACS) are associated with an increased prevalence of steatotic liver disease (SLD), which if not treated may lead to liver fibrosis (LF). The prevalence of SLD and LF in hypercortisolemia varies in different studies. To the best of our knowledge there are no studies assessing liver impairment in endogenous hypercortisolemia using Shear Wave Elastography (SWE). Purpose To assess LF and SLD among CS and MACS patients in (SWE). Methods 38 patients with endogenous hypercortisolemia(52+/-15year old; 82%women;26 pituitary[pCS],2adrenal[aCS],2 ectopic[eCS], 8 MACS).Liver stiffness (LF>8.27kPa) and steatosis (SLD>228db/m) values measured in SWE were compared with hypercortisolemia markers, liver enzymes and serum inflammation based scores (SIBS) calculated from complete blood count. Analysis:Statistica 13.3, p<0.05. Results LF: Mean stiffness value 6.6 +/- 1.16kPa (CS 6.4+/-1.15; MACS: 7.5+/-1.4). LF:2/30 CS and 3/8 MACS. Negative correlation with late night salivary cortisol (LNSC) and platelet/lyphocyte rate (PLR) (r= -0.36, r= -0.36, p<0.05). Positive correlation with ALT and AST (r=0.36, r=0.45, p<0.05). SLD: Mean steatosis values 238+/-39.7db/m (CS 234.6+/-38.7; MACS: 254.2+/-39.4). SLD:16/30 CS (5mild,6moderate,5severe) and 5/8 MACS (3moderate,2severe). Positive correlation with ALT, AST and GGTP (r=0.5, r=0.44, r=0.56, p<0.05). Conclusion(s) LF prevalence in CS was 6.7% and 37.5% in MACS. SLD prevalence in CS was 53% and 62.5% in MACS. LNSC and PLR may be potential candidates for non-invasive LF markers. We plan to extend the study group, add a control group and reassess the elastography after hypercortisolemia treatment.
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Minasyan et al. (2025) studied this question.
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