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FERRITIN PREDICTS LIVER FIBROSIS IN STEATOSIS: A READILY AVAILABLE, UNDERUSED MARKER BEYOND INFLAMMATION

Youness Dendane 1, Mouhssine Benderrou 1, Ouiam Elmqaddem 1, Hajar Koulali 1, Zazour Abdelkrim 1, Zahi Ismaili 1, Ghizlane Kharrasse 1

Affiliations

1 Faculty of Medicine and Pharmacy/University Hospital Center Mohammed VI, Oujda, Morocco

Summary

AI Generated

In a retrospective study of 99 adults with hepatic steatosis, serum ferritin above 90 ng/mL independently predicted significant fibrosis (FIB-4 ≥1.0) after adjusting for age, CRP, and metabolic comorbidities.

Hyperferritinemia (ferritin >90 ng/mL) was present in 48.5% of patients and independently associated with fibrosis (OR 2.9, 95% CI 1.2–7.3, p=0.021), while CRP levels did not differ between fibrotic and non-fibrotic groups (p=0.78).
Ferritin demonstrated discriminative performance with AUC 0.72 overall, strongest in patients under 50 years (AUC 0.78), and remained significant across both sexes (men AUC 0.75, women AUC 0.69).
Combining ferritin with FIB-4 increased discriminative performance to AUC 0.76, suggesting complementary utility in risk stratification.
The authors propose that ferritin may serve as a pragmatic, inexpensive biomarker for fibrosis screening in primary care or resource-limited settings, pending multicentric prospective validation.
This material is relevant to clinicians managing metabolic liver disease who seek accessible biomarkers for early fibrosis detection where elastography is unavailable.

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This summary was generated by an AI large language model based on the content transcript. It is for informational purposes only and should not be considered a substitute for clinical judgment. Always rely on your professional expertise and the full clinical context when making clinical decisions.

Abstract

Introduction

With the global rise in metabolic liver disease, there is an urgent need for scalable and affordable tools to detect liver fibrosis early—particularly in settings where elastography is unavailable. Ferritin is widely available and routinely tested, yet its potential role in liver fibrogenesis remains under-recognized. We hypothesized that in patients with hepatic steatosis, elevated ferritin reflects fibrotic remodeling independently of systemic inflammation or metabolic comorbidities.

Aims & Methods

To determine whether hyperferritinemia independently predicts significant fibrosis in steatotic patients, beyond inflammatory and metabolic factors, and to assess the consistency of this association across age and sex subgroups. This retrospective monocentric study included adults diagnosed with hepatic steatosis by ultrasound between January 2020 and December 2024.

Exclusion criteria: secondary causes of liver disease (alcohol >20 g/day, viral hepatitis, drug-induced steatosis), and factors affecting ferritin (active infection, malignancy, recent transfusion).
Significant fibrosis: FIB-4 ≥1.0, per AASLD and EASL guidelines for early detection.
Hyperferritinemia: serum ferritin >90 ng/mL, based on internal cut-offs linked to early fibrotic progression.
Demographic, metabolic, and inflammatory data—including CRP—were collected. Subgroup analyses were conducted by age (<50 vs. ≥50) and sex. ROC curves and multivariate logistic regression were used to assess predictive value.

Results

Ninety-nine patients were included (mean age 51.9 ± 13.2 years; 74% female; mean BMI 30.8 kg/m²). Metabolic comorbidities included diabetes (38%), hypertension (23%), and dyslipidemia (18%). Hyperferritinemia was found in 48.5%, associated with older age (p=0.027), but similar BMI and metabolic profile. Significant fibrosis (FIB-4 ≥1.0) was more frequent in this group (77% vs. 42%, p<0.001). Mean ferritin levels were higher in fibrotic patients (127 vs. 82 ng/mL, p=0.003), while CRP levels did not differ (p=0.78). In multivariate analysis, age (OR=1.04 per year, p=0.005), CRP (p=0.011), and ferritin >90 ng/mL (OR=2.9, 95% CI [1.2–7.3], p=0.021) were independently associated with fibrosis. Ferritin alone had an AUC of 0.72; its predictive value remained significant in both men (AUC=0.75) and women (AUC=0.69), and was strongest in patients <50 years (AUC=0.78). Combining ferritin with FIB-4 increased discriminative performance (AUC=0.76), suggesting complementary utility.

Conclusion

In hepatic steatosis, serum ferritin >90 ng/mL independently predicts significant liver fibrosis, even after adjusting for CRP and metabolic comorbidities. Ferritin—an inexpensive and underused biomarker—may serve as a pragmatic fibrosis signal in primary care or resource-limited hepatology settings. Its discriminative power in younger patients highlights its potential for early risk stratification. These findings support the integration of ferritin into composite non-invasive scoring systems and pave the way for multicentric prospective validation. Incorporating ferritin into fibrosis screening workflows, including telemedicine triage, may reduce underdiagnosis and optimize care pathways in steatotic liver disease.

Conference

UEG Week Berlin 2025

Topics

Hepatobiliary

Submission format

Abstract

Session

LIVER (Posters)

Citation

United European Gastroenterology Journal 2025; 13 (Supplement 8)

Published

2025

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