Introduction
Two years after the Delphi consensus-proposed revolution in the nomenclature and diagnosis of Steatotic Liver Disease (SLD), the potential benefits of adopting Metabolic dysfunction-associated steatotic liver disease (MASLD) rather than Metabolic dysfunction-associated fatty liver disease (MAFLD) diagnostic criteria in defining the disease progression risk of SLD patients have never been systematically and longitudinally evaluated in real-life.
Aims & Methods
The present study aimed to compare MASLD and MAFLD criteria in estimating the 3-year risk of advanced fibrosis (AF) progression and Acute Cardiovascular Event (ACE) occurrence in not-lean (NL) and lean (L) SLD patients.
For this purpose, we retrospectively analyzed the anthropometrical, biochemical, clinical, and Liver Stiffness Measurement (LSM - FibroScan) data stored in the University Hospital (UH)-official Health Documents Digitization Archive of 931 SLD patients admitted to UH “Luigi Vanvitelli” (between January 2016 and May 2021), and followed up for 3 years. Based on baseline Body Mass Index (BMI), patients were subdivided into “L” (BMI <25 kg/m2) (n:134) and “NL” (n:797) and, subsequently, by applying MAFLD and MASLD criteria, in NL-MASLD (n:206), NL-MASLD/MAFLD (n:481), NL-MAFLD (n:110), and L-MASLD (n:39), L-MASLD/MAFLD (n:68), L-MAFLD (n:27). The following validated LSM cut-offs were used to identify the different liver fibrosis stages according to the Metavir score: (a) F0-F2 ≤ 9.6 kPa; (b) F3: 9.7 - 13.5 kPa; (c) F4 ≥ 13.6 kPa. AF (F3-F4) was defined by LSM values > 9.7 kPa. The transition from F0-F2 to F3-F4 defined AF progression. Retrospectively collected and documented ACEs were: (1) Acute Myocardial Infarction (IMA), (2) Acute Coronary Syndrome (ACS), (3) Ictus cerebri (IC), and (4) Transient Ischemic Attack (TIA).
Results
MASLD and MAFLD criteria similarly estimated [MASLD: OR: 2.334, C.I.95%: 1.878 - 3.028, MAFLD: OR: 2.469, C.I.95%: 1.892 - 3.668, p < 0.0001; positive predictive value (PPV), MASLD: 0.800, C.I. 95%: 0.641-0.89 vs MAFLD: 0.785, C.I. 95%: 0.604-0.897, p: 0.076)] the overall 3-year risk of AF progression in NL-SLD, whereas in L-SLD, MAFLD criteria better estimated the overall 3-year risk of AF progression [PPV, MASLD: 0.571, C.I. 95%: 0.405-0.841 vs MAFLD: 0.714, C.I. 95%: 0.558-0.794, p: 0.006].
Compared to MASLD, MAFLD diagnostic criteria better estimated the 3-year risk of ACEs occurrence in NL [HR: 1.104, C.I..95%: 0.024-1.293, p:0.025], and not in L [HR: 1.260, C.I..95%: 0.665-2.101, p:0.071] patients. Multivariate competing risk analysis (adjusted for sex, age, diabetes, steatosis, and fibrosis severity) revealed diabetes (aHR: 2.113, C.I. 95%: 1.981-2.434, p:0.001), high-sensitivity-C-reactive protein (aHR: 1.441; C.I. 95%: 1.232-1.775; p:0.02) and Homeostatic-model-assessment-for-insulin-resistance (aHR: 1.228; C.I. 95%: 1.152-1.893; p:0.03) as associated with ACE occurrence in NL-MAFLD patients.
Conclusion
MAFLD criteria better estimate the 3-year AF progression and the ACE occurrence risk in L-SLD and NL-SLD patients, respectively.
References
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