Liver complications of pediatric parenteral nutrition - Epidemiology

被引:215
作者
Kelly, DA [1 ]
机构
[1] Childrens Hosp, NHS Trust, Liver Unit, Birmingham B16 8ET, W Midlands, England
关键词
D O I
10.1016/S0899-9007(97)00232-3
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Total parenteral nutrition (TPN)-induced liver disease develops in 40-60% of infants who require long-term TPN for intestinal failure. The clinical spectrum includes cholestasis, cholelithiasis, hepatic fibrosis with progression to biliary cirrhosis, and the development of portal hypertension and Liver failure in a significant number of children who are totally parenterally fed. The pathogenesis is multifactorial and is related to prematurity, low birth weight, and duration of TPN. The degree and severity of the liver disease is related to recurrent sepsis including catheter sepsis, bacterial translocation, and cholangitis. Lack of enteral feeding leading to reduced gut hormone secretion, reduction of bile flow, and biliary stasis may be important mechanisms in the development of cholestasis, biliary sludge, and cholelithiasis. Although it is unlikely that modern TPN solutions have a major role in the etiology of TPN liver disease, manganese toxicity recently has been recognized in children with hepatic dysfunction on TPN. Although there is a definite relationship with the degree of manganese toxicity and hepatic decompensation, it is not yet clear whether this is a primary mechanism or whether the high levels are related to reduced biliary excretion of manganese. The management strategies for the prevention of TPN-induced liver disease include early enteral feeding, a multidisciplinary approach to the management of parenteral nutrition, and aseptic catheter techniques to reduce sepsis. The administration of ursodeoxycholic acid may improve bile flow and reduce gall bladder and intestinal stasis. As survival from isolated intestinal transplantation improves, this therapeutic option should be considered before TPN liver disease becomes irreversible and combined liver and small bowel transplantation is required. (C) Elsevier Science Inc. 1998.
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收藏
页码:153 / 157
页数:5
相关论文
共 82 条
[1]   USE OF INTRAVENOUS LIPID AND HYPERBILIRUBINEMIA IN THE 1ST WEEK [J].
ADAMKIN, DH ;
RADMACHER, PG ;
KLINGBEIL, RL .
JOURNAL OF PEDIATRIC GASTROENTEROLOGY AND NUTRITION, 1992, 14 (02) :135-139
[2]   THE EFFECT OF GLUTAMINE-ENRICHED TPN ON GUT IMMUNE CELLULARITY [J].
ALVERDY, JA ;
AOYS, E ;
WEISSCARRINGTON, P ;
BURKE, DA .
JOURNAL OF SURGICAL RESEARCH, 1992, 52 (01) :34-38
[3]  
ALVERDY JC, 1988, SURGERY, V104, P185
[4]  
Baker A L, 1987, Am J Med, V82, P489, DOI 10.1016/0002-9343(87)90449-9
[5]   PATHOLOGIC VERSUS PHYSIOLOGIC CHOLESTASIS - ELEVATED SERUM CONCENTRATION OF A SECONDARY BILE-ACID IN THE PRESENCE OF HEPATOBILIARY DISEASE [J].
BALISTRERI, WF ;
SUCHY, FJ ;
FARRELL, MK ;
HEUBI, JE .
JOURNAL OF PEDIATRICS, 1981, 98 (03) :399-402
[6]  
Barbier J, 1992, Chirurgie, V118, P47
[7]  
BEALE EF, 1979, PEDIATRICS, V64, P342
[8]   Parenteral nutrition-related cholestasis in postsurgical neonates: Multivariate analysis of risk factors [J].
Beath, SV ;
Davies, P ;
Papadopoulou, A ;
Khan, AR ;
Buick, RG ;
Corkery, JJ ;
Gornall, P ;
Booth, IW .
JOURNAL OF PEDIATRIC SURGERY, 1996, 31 (04) :604-606
[9]   NUTRITIONAL CARE AND CANDIDATES FOR SMALL-BOWEL TRANSPLANTATION [J].
BEATH, SV ;
BOOTH, IW ;
MURPHY, MS ;
BUCKELS, JAC ;
MAYER, AD ;
MCKIERNAN, PJ ;
KELLY, DA .
ARCHIVES OF DISEASE IN CHILDHOOD, 1995, 73 (04) :348-350
[10]  
BEATH SV, 1997, J PEDIATR SURG, V32, P1