Retrospective cross-sectional study reveals vitamin D deficiency correlates with fibrosis stage but lacks independent association in MASLD, suggesting it marks overall disease burden.
Background Metabolic dysfunction–associated steatotic liver disease is the most common chronic liver disease worldwide, affecting approximately 25–30% of adults. Liver fibrosis is the principal determinant of disease progression and mortality in MASLD. Vitamin D deficiency is highly prevalent in individuals with metabolic disorders and has been implicated in hepatic inflammation and fibrogenesis. However, the relationship between vitamin D status and liver fibrosis in MASLD remains incompletely understood, particularly in Middle Eastern populations. Methods A retrospective cross‑sectional study was conducted at King’s College Hospital London, Dubai. Adult patients with MASLD who underwent vibration‑controlled transient elastography (FibroScan ® ) and had serum 25‑hydroxyvitamin D [25(OH)D] measurements within 90 days were included. Liver fibrosis was assessed using FibroScan-derived liver stiffness measurement. Hepatic steatosis was evaluated using both FibroScan-derived controlled attenuation parameter measurements and abdominal ultrasound findings where available. CAP was used as the quantitative measure of steatosis, while ultrasound grades were recorded for routine clinical assessment. Associations were evaluated using chi-square and non-parametric tests as appropriate. Multivariable logistic regression was performed to assess the independent association between vitamin D deficiency and clinically significant fibrosis. Results A total of 301 patients with MASLD were included (mean age 41.75 ± 8.90 years; 50.5% male). Vitamin D deficiency was observed in 69.76% of patients. Most patients had no to mild fibrosis (F0–F1, 80.83%), followed by significant fibrosis (F2, 14.98%), advanced fibrosis (F3, 3.48%), and cirrhosis (F4, 0.69%). Vitamin D deficiency was significantly associated with fibrosis stage ( p = 0.01) and hepatic steatosis severity ( p = 0.01). No significant associations were observed between vitamin D deficiency and BMI ( p = 0.20), diabetes/prediabetes ( p = 0.69), hypertension ( p = 0.92), or dyslipidaemia ( p = 0.71), while a significant association was noted with metabolic syndrome ( p < 0.01). Vitamin D deficiency was not independently associated with clinically significant fibrosis (aOR 0.89, 95% CI 0.44–1.80; p = 0.754). Increasing age (aOR 1.05, 95% CI 1.01–1.09; p = 0.018) and male sex (aOR 6.23, 95% CI 2.88–13.49; p < 0.001) were independently associated with clinically significant fibrosis. Conclusion Vitamin D deficiency is highly prevalent in this MASLD cohort and is significantly associated with greater fibrosis severity, suggesting that it may serve as a marker of disease burden. However, causality cannot be established, and prospective studies are required to determine whether vitamin D plays a causal role in disease progression. Clinical trial number Not applicable.
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