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Item type:Publication, Beyond bones: Revisiting the role of vitamin D in chronic liver disease(Baishideng Publishing Group Inc., 2025) ;Guerrero-Guerrero, Rodrigo ;Méndez-Guerrero, Osvely ;Carranza-Carrasco, Anaisa; Ardon-López, AstridBeyond its traditional role in calcium and bone metabolism, vitamin D has emerged as a critical regulator of liver health. Its active form, calcitriol [1α,25(OH)2D], signals through the vitamin D receptor (VDR), which is expressed in hepatic stellate cells, Kupffer cells, and cholangiocytes. Through this pathway, vitamin D modulates fibrosis, inflammation, oxidative stress, bile acid homeostasis, and immune responses. This review explores the growing body of evidence linking vitamin D deficiency to chronic liver diseases, including autoimmune hepatitis, primary biliary cholangitis, alcoholic liver disease, viral hepatitis B and C, and metabolic-associated steatotic liver disease. Low vitamin D levels are frequently observed in these conditions and are associated with disease severity, complications (such as spontaneous bacterial peritonitis, sarcopenia, and hepatic encephalopathy), and increased mortality. Mechanistically, vitamin D-VDR signaling inhibits profibrotic TGF-β1/SMAD pathways, downregulates proinflammatory cytokines, enhances regulatory T cell differentiation, and improves insulin sensitivity. Although preclinical studies support its protective effects, clinical trials of vitamin D supplementation have produced mixed results. Overall, vitamin D appears to influence multiple pathways in liver disease pathophysiology, and correcting its deficiency may offer clinical benefits. However, its integration into clinical care will depend on identifying responsive patient subgroups and defining optimal dosing strategies to maximize therapeutic benefit. ©The authors ©Baishideng Publishing Group Inc. - Some of the metrics are blocked by yourconsent settings
Item type:Publication, Persistent Vitamin D Deficiency in Pediatric Patients with Cystic Fibrosis(MDPI AG, 2025) ;Reyes-Apodaca, Magali ;Lezana-Fernández, José L. ;Vázquez Frias, Rodrigo ;Rendón-Macías, Mario EnriqueGonzález-Molina, AlineBackground/Objectives: Cystic fibrosis (CF) is a multisystem disease caused by CFTR gene variants, with a high prevalence of vitamin D (VitD) deficiency despite the supplementation and schedules specifically developed for this population. Lower VitD levels have been associated with an increased risk of respiratory infections and pulmonary exacerbations in CF, with some pilot studies indicating the potential benefits of supplementation during acute episodes. This study aimed to describe the occurrence of VitD deficiency according to the supplemented dose in pediatric patients with CF. Methods: A cross-sectional analytical study was conducted to assess serum VitD levels in a pediatric population with cystic fibrosis. Clinical and biochemical data were collected, along with information on VitD intake and pancreatic enzyme dosage at the time of evaluation. Results: A total of 48 patients were included in the study. Normal VitD levels were observed in 41.7% of the patients, insufficiency in 31.3%, and deficiency in 27%. The median VitD intake was 2050 IU. A statistically significant difference was observed in patients with a daily intake exceeding 2000 IU. Only 10% of patients achieved levels above 30 ng/mL with a lower dose. No statistically significant association was identified between the pancreatic enzyme dosage and vitamin D levels. Conclusions: Vitamin D deficiency/insufficiency is a persistent problem in the pediatric CF population; the interventions targeting factors associated with this condition are required to refine supplementation schedules. These findings underscore the need for personalized strategies to optimize vitamin D status in PwCF. Ideally, these strategies should consider all associated factors, including genetic variants; however, with limited resources, our results suggest that a daily dose of 2000 IU of vitamin D may represent a reasonable and effective starting point for supplementation. © The authors © MDPI .
