Cardiometabolic index fails to discriminate the histological status of metabolic dysfunction-associated steatotic liver disease patients: A report from biopsy-proven Turkish metabolic dysfunction-associated steatotic liver disease cohort


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Fakih S., Kaya E., Kirik A., Keklikkiran C., Yilmaz Y.

HEPATOLOGY FORUM, cilt.7, sa.4, ss.329-336, 2026 (ESCI, Scopus, TRDizin)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 7 Sayı: 4
  • Basım Tarihi: 2026
  • Doi Numarası: 10.14744/hf.2026.48815
  • Dergi Adı: HEPATOLOGY FORUM
  • Derginin Tarandığı İndeksler: Emerging Sources Citation Index (ESCI), Scopus, Central & Eastern European Academic Source (CEEAS), TR DİZİN (ULAKBİM), Health Research Premium Collection (ProQuest)
  • Sayfa Sayıları: ss.329-336
  • Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
  • Recep Tayyip Erdoğan Üniversitesi Adresli: Evet

Özet

Background and Aim: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a major global health challenge, and cardiovascular mortality has been shown to be significantly associated with the cardiometabolic index (CMI). However, data linking CMI with histological severity in MASLD are lacking. In this study, we aimed to investigate the association between CMI and histological parameters and to evaluate its discriminatory performance for clinically relevant fibrosis stages in a biopsy-proven MASLD cohort. Material and Methods: A total of 617 biopsy-proven MASLD patients from the Turkish MASLD Biobank were included in the analysis. Histological assessments were performed according to the steatosis, activity, fibrosis (SAF) fatty liver inhibition of progression algorithm. The CMI was calculated as follows: Triglyceride (TG) to high-density lipoprotein (HDL) multiplied by waist-to-height ratio. Results: The median age was 48 (18-71) years, and 329 participants were male (53.3%). Neither CMI nor the TG/HDL ratio showed a significant monotonic trend across SAF fibrosis, activity, or steatosis grades (all p>0.05). Across clinically relevant fibrosis thresholds, neither marker differed significantly, except for a lower TG/HDL ratio in patients with cirrhosis (Holm-adjusted p=0.036). The AUROCs of CMI were 0.530 (95% CI: 0.483-0.577) for significant fibrosis and 0.475 (95% CI: 0.418-0.532) for advanced fibrosis, whereas fibrosis-4 index demonstrated better discrimination, with corresponding AUROCs of 0.688 (95% CI: 0.645-0.731) and 0.755 (95% CI: 0.708-0.803). In an exploratory analysis of cirrhosis (n=26), lower TG/HDL values showed inverse discrimination for cirrhosis, with an AUROC of 0.651 (95% CI: 0.544-0.757). Conclusion: CMI was not significantly associated with histological fibrosis severity and showed poor discriminatory performance across clinically relevant fibrosis thresholds. These findings do not support the use of CMI as a non-invasive marker of histological fibrosis severity in MASLD.