الفهرس 
VITAMIN D METABOLISMOnly 14 pages are availabe for public view
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Abstract
T
his study aimed to assess the prevalence of vitamin D level among children with chronic liver disease, efficacy and safety of two suggested vitamin D regimes to correct and treat vitamin D deficiency and its sequalae, and to find out potential antifibrotic effect of vitamin D therapy that can potentially halt the progressive process of liver fibrosis or even reversing it.
Therefore, twenty-four age (4.5 – 11.5 years), sex (13 male and 11 female), and anthropometric matched children with CLD were randomly allocated in one of two groups and followed up for 6 months assessing clinical, laboratory, and imaging variables.
group A (n:12): who received stoss parenteral vitamin D therapy (200.000 IU) once followed by 600 IU/ day orally (equivalent to RDA as maintenance).
group B (n:12): who received 50.000 IU/ week for 4 weeks vitamin D orally followed by 600 IU/ day orally.
Both groups received calcium supplements on 50 mg/kg/day.
The aetiology of chronic liver disease was heterogenous with autoimmune hepatitis, Glycogen storage disease, or chronic hepatitis and hepatitis C affect the majority (75%). Others (25%) include congenital hepatic fibrosis, Budd Chiari disease, and Niemann pick disease. The majority are compensated with only 25% were complicated or have an overt vitamin D deficiency picture.
Following vitamin D supplementation, there were statistically significant increase of serum Ca level and vitamin D levels and statistically significant decrease of serum ALP level in both groups (P value <0.01) among deficient individuals. No difference could be detected on comparing both groups regarding their efficacy (P = 0.977 and 0.707 respectively).
However, there was no significant improvement in liver fibrosis evidenced by fibroscan in both groups with p value at 0.637 and 0.931 respectively.
A negative correlation could be detected between the age and vitamin D level change especially in group A, the older patients the lower vitamin D level. There is also weak positive correlation between serum Ca level and vitamin D changes especially in group A. Correlation between vitamin D changes in relation to fibroscan changes in both groups show no significant correlation. The same between vitamin D changes with Child Pugh scoring system or liver aetiology.
CONCLUSION
V
itamin D therapy using Stoss therapy or oral vitamin D therapy were equally safe and effective in improving the clinical and laboratory metabolic bone profile abnormalities. Vitamin D effect on liver fibrosis progression or reversion in children is still not understood and further studies are needed in this field taking in consideration the various causes of liver disease in children.
RECOMMENDATIONS
Regarding our findings, we recommend:
1. Measurement of vitamin D level in children with chronic liver disease as most patients with deficient levels are not evident clinically.
2. Supplementation of vitamin D to children with chronic liver disease as a preventive measure as most of these children have multifactorial vitamin D level deficiency.
3. Further studies are recommended to be done with longer duration, larger population, and with more homogenous groups to validate the findings with particular attention toward the potential antifibrotic effect of vitamin D.
4. Geographical factors, race, physical activities, dietary habits, and duration of daily sun exposure should also be considered in further studies as these are potential confounding factors that can alter the required exogenous source of vitamin D as supplement as well as curative regimes.