Abstract
During a six month period, six premature infants (gestation 28-31 wks, weight 790-1180 gm) developed cholestasis and severe metabolic bone disease while receiving parenteral alimentation. Spontaneous long bone fractures occurred in 3/6. Infants received PA amino acid solutions for a mean of 4.5 wks (range 1-9); 4/6 received Intralipid. Hepatic dysfunction (direct hyperbilirubinemia, elevated transaminases) was first noted at a mean of 29 d (range 6-65) after initiation of PA. Osteopenia was evident by x-ray in all. Photon absorptiometry bone mineral analysis (BMA) was decreased in 3/4 infants (Steichen, A.J. Roent. 126: 1283). 25-OH vitamin D (25-OHD) was markedly reduced, < 10 ng/ml in 6/6; normal 20-80 ng/ml (Belsey's). Serum Ca was normal in all and P was 3.1-5.9 mg/dl. One of six infants died of non-hepatic causes. The liver showed cholestasis with extramedullary hematopoesis, canalicular and hepatocellular stasis and minimal inflammation in two cases examined. Surviving infants were treated with 2500 units vit. D3 p.o. and Ca 100 mg/kg/d. Fractures healed in 3/3; serum 25-OHD levels normalized in 2/4; serial BMA showed continued poor mineralization in 3/4. Decreased serum 25-OHD may relate to decreased intake, absorption and hydroxylation of vitamin D and decreased enterohepatic circulation of 25-OHD. “Hepatic Rickets” can occur in premature infants who develop cholestasis while receiving parenteral alimentation and should be anticipated by serial measurement of serum 25-OH vitamin D.
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Farrell, M., Suchy, E., Tsang, R. et al. 421 NEONATAL “HEPATIC RICKETS” IN PREMATURE INFANTS RECEIVING PARENTERAL ALIMENTATION (PA). Pediatr Res 12 (Suppl 4), 434 (1978). https://doi.org/10.1203/00006450-197804001-00426
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DOI: https://doi.org/10.1203/00006450-197804001-00426