Document Detail

Parenteral nutrition-induced hepatobiliary dysfunction in infants and prepubertal rabbits.
MedLine Citation:
PMID:  10525903     Owner:  NLM     Status:  MEDLINE    
We analyzed clinical, biochemical, and histo- logic parameters of ten infants with parenteral nutrition-induced hepatobiliary dysfunction. The data were compared with the results of a rabbit model. All infants were born prematurely with low birth weight. Their clinical diagnoses were necrotizing enterocolitis (6), gastroschisis (1), intrauterine volvulus (1), and lung hypoplasia (2). All required total (TPN) or partial parenteral nutrition for at least 8 weeks. All had repeated episodes of infections or sepsis. A rise in bilirubin and aminotransferase levels occurred after a minimum of 5 weeks; peak bilirubin levels ranged from 4 to 14 mg% and aminotransferases from 40 to 140 IU/l. One child later developed gallstones. Liver biopsies after 1 to 24 months showed fibrosis, bile-duct proliferation, cholestasis, and hydropic degeneration. All of the above-mentioned clinical factors have been accused of causing the observed biochemical and histologic changes. In our rabbit model we were able to produce almost identical symptoms by TPN alone: gallbladder distension, sludge, and stones developed after 1-4 weeks of TPN as well as uncharacteristic changes in aminotransferases and bilirubin after 4 weeks. Liver histology revealed severe hydropic degeneration of zone 3 as early as 1 week after beginning TPN. A rise of fibrosis and bile-duct proliferation after 1 to 4 weeks of infusion was statistically significant. Cholestasis, as was observed in the infants, could not be detected. In our model, all alterations observed could be attributed exclusively to TPN. We therefore assume that TPN was the true cause of the dysfunction. In a second experimental series infusions were reduced to 80% PN and free access to lab chow. These animals produced normal feces, indicating physiologic enteral stimulation. They developed the same degenerative and proliferative histologic changes, whereas gallbladder distension, sludge, and stones were not noted. We conclude that: (1) The TPN solution itself is responsible for the histologic changes in the liver, which is supported by the fact that hydropic degeneration of zone 3 is typical of a direct toxic effect; and (2) Complete enteral starvation with an absence of enteral stimulation causes disease of the lower biliary tract.
S Loff; B Kränzlin; M Moghadam; A Dzakovic; L Wessel; W Back; S Hosie; H Wirth; K L Waag
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Pediatric surgery international     Volume:  15     ISSN:  0179-0358     ISO Abbreviation:  Pediatr. Surg. Int.     Publication Date:  1999  
Date Detail:
Created Date:  1999-11-16     Completed Date:  1999-11-16     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8609169     Medline TA:  Pediatr Surg Int     Country:  GERMANY    
Other Details:
Languages:  eng     Pagination:  479-82     Citation Subset:  IM    
Kinderchirurgische Klinik, Klinikum Mannheim, Theodor-Kutzer-Ufer 1-4, D-68167 Mannheim, Germany.
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MeSH Terms
Biliary Tract Diseases / etiology*,  pathology
Bilirubin / blood
Infant, Low Birth Weight
Infant, Newborn
Infant, Premature*
Infant, Premature, Diseases / therapy*
Liver Diseases / etiology*,  pathology
Parenteral Nutrition / adverse effects*
Transaminases / blood
Reg. No./Substance:
635-65-4/Bilirubin; EC 2.6.1.-/Transaminases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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