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SUPPLEMENTATION RESULTED IN LOWER PREVALENCE OF VITAMIN D DEFICIENCY IN INFANTS AND TODDLERS WITH CYSTIC FIBROSIS COMPARED TO THAT REPORTED FOR HEALTHY CHILDREN
Author(s) -
Chin Lyanne H,
Lai HuiChuan J,
Greer Frank R
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.800.1
Subject(s) - medicine , cystic fibrosis , pediatrics , vitamin d and neurology , malabsorption , vitamin d deficiency , population , vitamin , newborn screening , prospective cohort study , gastroenterology , environmental health
BACKGROUND Exocrine pancreatic insufficiency causes fat malabsorption in patients with cystic fibrosis (CF) and increases risks of vitamin D deficiency. Serum 25‐hydroxy vitamin D [25(OH)D] is the recommended biomarker for monitoring vitamin D status. The CF Foundation (CFF) recommends daily vitamin D supplementation, starting at 400–500IU/day of vitamin D 3 after diagnosis and 800–1000IU/day for children above 1 year old. The current Recommended Dietary Allowances (RDA) for vitamin D is 400IU/day for infants and 600IU/day for toddlers between 1 to 3 years old. The reported prevalence of suboptimal vitamin D status (<75nmol/L) in healthy infants and toddlers is approximately 40% (Arch Pediatr Adolesc Med 2008, 162:505–512). OBJECTIVE To evaluate 25(OH)D levels in the first 2 years of life in children with CF and its association with supplementation. METHODS The study population consists of infants enrolled in FIRST (Feeding Infants Right… from the STart), a multicenter prospective observational study initiated in 2012 at 6 CF centers (Madison, Milwaukee, Indianapolis, Salt Lake City, Boston, and Chicago) to identify optimal feeding for infants with CF. A total of 221 sera from 22 infants who have reached 1 year of age and 74 toddlers who have reached 2 years of age by 06/30/16 and were analyzed. Serum total 25(OH)D was measured at approximately age 4 months (n=73, 3.7 ± 0.2 months), 12 months (n=74, 12.6 ± 0.2 months), and 24 months (n=74, 22.9 ± 0.3 months). Vitamin D supplementation was assessed monthly prior to 6 months of age, bi‐monthly from 6–12 months, and every 3 months in the second year of life. RESULTS At around 4 months of age, only 5% had vitamin D deficiency (<50nmol/L) and 36% had vitamin D insufficiency (<75nmol/L). The prevalence of vitamin D deficiency and insufficiency decreased to 4% and 23% respectively at around 12 months of age. By 2 years of age, only 1% had vitamin D deficiency and 19% had vitamin D insufficiency. Serum 25(OH)D increases significantly with age, p<0.001. In toddlers who had serum 25(OH)D measured in both first and second year of life (n=70), 14% had persistent suboptimal vitamin D status. They were supplemented with at least 400IU/day in the first year of life (up to 2400IU/day) and a median dose of 800IU/day (up to 2800IU/day) in the second year of life. More than 60% of the toddlers had optimal vitamin D status (25(OH)D > 75nmol/L) throughout the first 2 years of life; half of them met CFF recommended supplementation dose in both years, 26% did not meet the recommended supplementation dose but still had adequate vitamin D status, and the remaining 24% met the recommended supplementation dose either in the first or second year. For the other 24% who had transient suboptimal vitamin D status in the first 2 years of life, the median supplement doses were 800IU in the first year and 1000IU in the second year. Serum 25(OH)D was found to be significantly associated with supplement intake for vitamin D (p=0.044), after adjusting for age. CONCLUSIONS Routine supplementation of vitamin D in infants with CF improved their vitamin D status. The prevalence of suboptimal vitamin D status decreases with age in the first 2 years of life. This prevalence is also lower than the reported prevalence for healthy infants, suggesting that vitamin D supplementation improve vitamin D status in infants and toddlers. Support or Funding Information NIH R01DK072126, UL1TR000427, CFFT‐LAI140A0