ACTH as the liver fibrosis predictor in non-cushing syndrome population

Mari Minasyan; Wiktoria Suchy; Joanna Kokoszka; Alicja Hubalewska-Dydejczyk; Elena Valassi; Aleksandra Gilis-Januszewska

doi:10.1530/endoabs.110.EP875

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Endocrine Abstracts (2025) 110 EP875 | DOI: 10.1530/endoabs.110.EP875

ECEESPE2025 ePoster Presentations Metabolism, Nutrition and Obesity (164 abstracts)

ACTH as the liver fibrosis predictor in non-cushing syndrome population

Mari Minasyan ¹ , Wiktoria Suchy ² , Joanna Kokoszka ³ , Alicja Hubalewska-Dydejczyk ¹ , Elena Valassi ^4,5 & Aleksandra Gilis-Januszewska ¹

Author affiliations

¹Department of Endocrinology, Jagiellonian University Medical College, Kraków, Poland; ²Students’ Scientific Group of Endocrinology, Department of Endocrinology, Jagiellonian University Medical College, Kraków, Poland., Kraków, Poland; ³Department of Endocrinology, Oncological Endocrinology and Nuclear Medicine, University Hospital, Kraków, Poland; ⁴Endocrinology Department, Hospital Germans Trias i Pujol, Badalona (Barcelona), Spain, Barcelona, Spain; ⁵Universitat Internacional de Catalunya (UIC), Barcelona, Spain

JOINT3070

Introduction: The data on the impact of adrenocorticotropic hormone (ACTH) and cortisol on liver function are scarce and conflicting. To the best of our knowledge there are no studies evaluating cortisol and ACTH as liver fibrosis (LF) biomarker in non-Cushing syndrome (CS).

Objectives: To evaluate the role of ACTH and cortisol in LF among non-CS.

Materials and Methods: We analyzed retrospectively 350 consecutive patients (66%female, median age 65 [56-70]) with non-secretive adrenal adenomas. CS was excluded on 1 mg dexamethasone suppression test (C-DST [morning cortisol <1.8 mg/dL]). FIB4 (Age×AST/PLT×ALT 1/2) was used as a LF predictor (<1.3 low risk [LR-LF], 1.3-2.67 intermediate risk [IR-LF], >2.67 high risk [HR-LF]). Multimodal logistic regression analyses were performed (RStudio version 4.2.2, P <0.05). Age, gender, bmi diabetes mellitus and hypercholesterolemia were included as co-variates to account for its potential influence on FIB-4.

Results: For every 1, 2, 10 and 30pg/ml ACTH rise, the odds for IR-LF rise by 3%, 6%, 16%, 35% and 148% (P = 0.039) and for HR-LF increase by 6%, 13%, 35%, 83% and 517% P = 0.006). The OR for the association between LF and cortisol (morning, midnight, C-DST) was statistically non-significant.

Conclusions: ACTH may have an impact on LF in non-CS population. Further studies examining the relation between ACTH, cortisol and liver fibrosis are needed.