"Daily vitamin D supplementation improves vitamin D deficiency in patients with chronic liver disease".
Journal of Pediatric Gastroenterology and Nutrition 2023 March 16
OBJECTIVE: To evaluate the response to 6,000 IU oral cholecalciferol (OC) treatment in children with chronic liver disease (CLD) and 25(OH)D deficiency.
METHODS: This historical cohort included non-transplanted CLD patients younger than 18 years old, which were analyzed for serum 25(OH)D, liver function, bone metabolism, Child-Pugh classification, and anthropometry. Patients with 25(OH)D deficiency (defined as 25(OH)D < 20 ng/mL) who received 6,000 IU/day of OC were analyzed pre- and post-intervention, and considered responders if 25(OH) D > 20 ng/mL after at least 60 days. We compared clinical and laboratory data from patients with and without 25(OH)D deficiency, responders and non-responders.
RESULTS: We studied 96 patients, of which 57.2% had biliary atresia. The prevalence of 25(OH)D deficiency was 67.7% (65/96). These patients were younger (p<0.001), had higher Child-Pugh scores (p<0.001), higher levels of total bilirubin (p<0.001), gamma-glutamyl transferase (p<0.001) and alkaline phosphatase (p=0.002), as well as lower levels of phosphorus (p=0.009) compared with patients without 25(OH)D deficiency. The median treatment length was 126 days (70-307 days). At the end of treatment, we observed a higher median of 25(OH)D (p<0.001), and lower median of parathyroid hormone (PTH) (p=0.023). Nine patients (29%) restored 25(OH)D to normal range; they had lower Child-Pugh score (p=0.001), lower total bilirubin levels (p=0.001) and higher level of phosphorus (p=0.003) after treatment.
CONCLUSION: Despite an increase in 25(OH)D and decrease in PTH levels, 6,000 IU/day of OC was not sufficient to restore 25(OH)D deficiency in most of the patients in this study.
METHODS: This historical cohort included non-transplanted CLD patients younger than 18 years old, which were analyzed for serum 25(OH)D, liver function, bone metabolism, Child-Pugh classification, and anthropometry. Patients with 25(OH)D deficiency (defined as 25(OH)D < 20 ng/mL) who received 6,000 IU/day of OC were analyzed pre- and post-intervention, and considered responders if 25(OH) D > 20 ng/mL after at least 60 days. We compared clinical and laboratory data from patients with and without 25(OH)D deficiency, responders and non-responders.
RESULTS: We studied 96 patients, of which 57.2% had biliary atresia. The prevalence of 25(OH)D deficiency was 67.7% (65/96). These patients were younger (p<0.001), had higher Child-Pugh scores (p<0.001), higher levels of total bilirubin (p<0.001), gamma-glutamyl transferase (p<0.001) and alkaline phosphatase (p=0.002), as well as lower levels of phosphorus (p=0.009) compared with patients without 25(OH)D deficiency. The median treatment length was 126 days (70-307 days). At the end of treatment, we observed a higher median of 25(OH)D (p<0.001), and lower median of parathyroid hormone (PTH) (p=0.023). Nine patients (29%) restored 25(OH)D to normal range; they had lower Child-Pugh score (p=0.001), lower total bilirubin levels (p=0.001) and higher level of phosphorus (p=0.003) after treatment.
CONCLUSION: Despite an increase in 25(OH)D and decrease in PTH levels, 6,000 IU/day of OC was not sufficient to restore 25(OH)D deficiency in most of the patients in this study.
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