Nutritional deficiencies have become a common problem among patients with chronic liver disease (CLD) and may easily be underestimated by clinical appearance alone; they negatively impact the neurocognitive development and growth. CLD is defined as the process of long-term progressive destruction and regeneration of liver parenchyma leading to fibrosis and cirrhosis. Children with CLD are more at risk than adults for severe malnutrition and feature lower reserves. In the United States, the overall incidence of liver disease in neonates is approximately 1 in every 2500 live births with extra hepatic biliary atresia (BA), metabolic disorders, and neonatal hepatitis being the most common causes of CLD in neonates, whereas metabolic disorders, chronic intrahepatic cholestasis, obesity-related steatohepatitis, drug and toxin-induced disorders, and viral hepatitis are common causes in older children.
Approximately 25% of children diagnosed with CLD worldwide are undernourished, with a higher incidence observed in developing countries. Malnourishment is considered a predictor of poorer outcomes in liver transplantation and is often associated with increased risks for morbidity and mortality. The development of malnutrition in children with CLD is complex and multifactorial, involving a decreased dietary intake, malabsorption, increased energy expenditure, and disordered substrate synthesis and metabolism. CLD affects absorption, metabolism, and storage of fat-soluble vitamins (FSVs). VDD is the major cause of hepatic osteodystrophy
However, limited knowledge can explain about the prevalence of VDD and metabolic bone disease in children with CLD from tropical setting with abundant sunlight. Recent studies demonstrated that VDD was prevalent in children with CLD despite vitamin D supplementation. Overall, 28% of the subjects were either vitamin D deficient or insufficient. In addition, more than 1 in 5 children with CLD presents at least one physical symptom of VDD. General guidelines have been developed for nutritional management in adult patients with CLD. However, the ideal dose of vitamin D and minerals in children with CLD to prevent and treat hepatic osteodystrophy is not well defined. Routine vitamin supplementation within recommended daily allowances has been considered to be a reasonable approach. In a study, no adverse events or overdose effects were detected among the patients receiving standard daily dose of FSVs for 3 months. The rates of vitamins A, D, and E deficiency in the patients receiving FSVs decreased from 80.0%, 100%, and 100%, 70.0%, 60.0%, and 60.0% respectively after 3 months of oral supplementation.
In conclusion, malnutrition commonly occurs in children with CLD, may easily be underestimated and requires aggressive and appropriate management. The clinicians should maintain alertness and evaluate the children with CLD to determine the possibilities of nutritional deficiencies. Clinical and laboratory assessment of FSV levels should be undertaken periodically to detect deficiency and to monitor response to any supplementation. A better nutritional status is associated with better survival before and after liver transplantation for advanced liver diseases. Thus, aggressive nutritional management is an important part of the care of these children, and close monitoring of various serum nutrient levels and routine oral vitamin supplementation in all Pediatric patients with CLD are mandatory.
