Clinical Studies of Metabolic Bone Disease of Prematurity.
- Author:
Seung Yeon SUH
1
;
Eun Kyung LEE
;
Ran NAMGUNG
;
Hae Jung JOO
;
Min Soo PARK
;
Kook In PARK
;
Chul LEE
;
Dong Gwan HAN
;
Meung Jun KIM
;
Jin Suk SUH
Author Information
1. Department of Pediatrics, College of Medicine, Yonsei University, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
Metabolic bone disease;
Preterm infants
- MeSH:
Alkaline Phosphatase;
Birth Weight;
Bone Diseases, Metabolic*;
Diagnosis;
Enteral Nutrition;
Follow-Up Studies;
Gestational Age;
Humans;
Hypercalcemia;
Infant;
Infant, Newborn;
Infant, Premature;
Infant, Very Low Birth Weight;
Korea;
Malnutrition;
Metabolic Diseases;
Metabolism;
Nutritional Status;
Parenteral Nutrition;
Retrospective Studies;
Rickets;
Ventilation;
Vitamin D;
Vitamins
- From:Journal of the Korean Pediatric Society
1995;38(2):159-169
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
PURPOSE: Preterm formula used in Korea, theoretically does not supply the recommended mineral intake for optimal bone metabolism in very low birth weight infants(Formula 500-700 mg Ca/L, 300~370mg P/L, and 440IU of vitamin D/L). The purpose of this study is to identify th e possible etiologic factors and clinical course of rickets in these infants. METHODS: We recently identified radiographic rickets or osteopenia in 16 VLBW infants over a 30-month period from January 1990, to July 1992. We performed a retrospective case analysis to evaluate the clinical features, nutritional status, biochemical and radiological findings o f metabolic disease in preterm infants. RESULTS: Mean gestational age and birth weight were 29+/-2.1wks, and 1172+/-245gm. All infants received parenteral nutrition and 11 infants needed assisted ventilation. Enteral feeding w as started at a mean age of 9.4+/-11.0d and mean total calorie intakes were 62+/-16.2kcal/kg /d in the first 2wks and 111+/-26.9kcal/kg/d at 2-4 wks of age. Oral Ca/P intakes were severely restricted during the first month of life, and they were about 20% of recommended intakes of Ca /P for VLBW infants. At diagnosis of active rickets, serum Ca was high in 19% and serum P wa s low in 69% of infants. Serum alkaline phosphatase was increased in 56% and serum 25-hydroxyvitamin D was low in 67%. Active rickets was diagnosed at mean age of 38+/-14.7 d; 12 infants had overt rickets(grade 2), including 3 infants with fractures(grade 3). Healing rickets was diagnosed on follow-up at mean age of 67.3+/-22.0 days. Thus, metabolic bone disease of VLB W infants was associated with low mineral intakes compared to recommended intakes, and signs of P deficiency occurred at about 2 wks of age and persisted to 8 wks of age; hypercalcemia occurred initially, and these biochemical abnormalities precede the radiological abnormalities about 2 or 3 weeks. CONCLUSIONS: Many factors are related to the development of metabolic hone disease of prematurity; one of the most important factor in our study was nutritional deficiency, especially m ineral(phosphorus) and vitamin D. In preterm VLBW infants whose adequate enteral feeding is restricted, mineral(calcium and phosphorus) and vitamin D supplementation would be needed t o reduce the development of metabolic bone disease in preterm infants.
