Total parenteral nutrition

Peden, Virginia H.; Witzleben, C. L.; Skelton, M.A.

doi:10.1016/s0022-3476(71)80289-5

Cited by 246 publications

(55 citation statements)

References 2 publications

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“…Physiologic or toxic insults to the liver pose additional risks for immature enterohepatic circulation. 3 Parenteral nutrition-associated liver dysfunction was first described by Peden et al, 4 in 1971. Despite advances in the understanding of parenteral nutrition-associated liver dysfunction, there is still no specific test that will diagnose the liver injury that may occur following parenteral therapy.…”

Section: Introductionmentioning

confidence: 99%

Demographic and nutritional factors associated with prolonged cholestatic jaundice in the premature infant

et al. 2007

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Objective: The primary aim of this study was to determine if an association exists between amino-acid levels and development of cholestasis. The secondary aim of our amino-acid dose comparison trial was to identify factors associated with the development of prolonged cholestatic jaundice.Study Design: We compared demographic characteristics and amino-acid levels in neonates who developed cholestasis with those who did not. Parenteral-associated cholestatic liver disease was defined as a direct serum bilirubin above 5 mg per 100 ml any time during the first 28 days after birth in neonates with no history of biliary atresia or viral hepatitis. We obtained filter paper blood spots for amino acid and acylcarnitine measurements on the day of randomization and days 7 and 28 of age to identify a profile of values that could be used to identify neonates with evidence of abnormal liver function. Result:We enrolled 122 neonates in our study; 13 (10.7%) developed cholestasis. Neonates who developed cholestasis were more immature, had lower birth weight, were exposed to parenteral nutrition for a longer period, had a higher cumulative dose of amino acids, were less often on enteral nutrition by day 7 of age, more often had a patent ductus arteriosus and severe intraventricular hemorrhage and were more commonly treated with steroids by 28 days of age. Amino acid and acylcarnitine values were not different for the two groups on the day of randomization. On day 7 (parenteral phase of nutrition), blood urea nitrogen, citrulline, histidine, methionine and succinyl carnitine were higher, and serine, glutamate and thyroxine levels were lower in the neonates who developed cholestasis than in who did not. Conclusion:Cholestasis remains an important complication of parenteral nutrition, and several clinical and biochemical factors may be helpful in identifying high-risk patients.

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Section: Introductionmentioning

confidence: 99%

Demographic and nutritional factors associated with prolonged cholestatic jaundice in the premature infant

et al. 2007

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“…Following improvements in parenteral regimens including vitamins and trace elements and in catheter techniques to reduce the septic complications associated with TPN, TPN has been widely employed to provide complete nutritional support and therapeutic benefits in a variety of pathophysiological settings in which patients are unable to eat. However, TPN-induced hepatobiliary dysfunction, which was first described by Peden et al, 1) has been recognized as a cause of severe morbidity and a life-threatening complication of TPN, especially in neonates and infants. Hepatic dysfunction with steatosis is the most common complication associated with fat-free TPN in adults, and cholestasis is more common in infants.…”

Section: Introductionmentioning

confidence: 99%

Soybean Oil Fat Emulsion to Prevent TPN-Induced Liver Damage: Possible Molecular Mechanisms and Clinical Implications

Nishimura

Yamaguchi

Naito

et al. 2006

Biological & Pharmaceutical Bulletin

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INTRODUCTIONTotal parenteral nutrition (TPN), which is recognized as one method for parenteral hyperalimentation, has been found to be an effective and relatively safe method for supplying energy and nutrients to surgical patients. Following improvements in parenteral regimens including vitamins and trace elements and in catheter techniques to reduce the septic complications associated with TPN, TPN has been widely employed to provide complete nutritional support and therapeutic benefits in a variety of pathophysiological settings in which patients are unable to eat. However, TPN-induced hepatobiliary dysfunction, which was first described by Peden et al.,1) has been recognized as a cause of severe morbidity and a life-threatening complication of TPN, especially in neonates and infants. Hepatic dysfunction with steatosis is the most common complication associated with fat-free TPN in adults, and cholestasis is more common in infants.2,3) Recently, the 3-component infusion solution containing amino acids, glucose, and soybean oil emulsion, GA-1080 (MIXID ® , Otsuka Pharmaceutical Factory, Inc.; Tokushima, Japan), has been demonstrated to be effective in overcoming such hepatic morbidity in clinical studies.4) Intravenous fat emulsions, especially soybean oil, are now available as a source of essential fatty acids in patients receiving TPN, and the "three-in-one" solution GA-1080 has been found to be clinically safe, stable, and economical. However, the multifactorial pathogenesis of TPN-induced hepatic dysfunction remains unclear, and the molecular mechanisms by which GA-1080 prevents hepatic dysfunction have not yet been identified.We have recently developed an infant rat model of hepatobiliary dysfunction.5) Using this animal model, we have clearly demonstrated the metabolic complications in the liver that may occur due to the excessive administration of fat-free TPN in infant rats. Furthermore, we have shown that including fat in the TPN regimen is very important in preventing TPN-induced hepatic dysfunction. In this review, we describe the molecular mechanisms and the clinical implications of soybean oil in TPN solutions in avoiding the hepatic complications associated with parenteral nutrition. INFANT RAT TPN MODEL WITH HEPATOBILIARY DYSFUNCTIONSince the first studies of TPN in animal models conducted in 1968 by Dudrick et al.,6) it has been known that only a limited number of species (such as the dog, cat, rabbit, and guinea pig) can tolerate the surgical procedures required for TPN, and few studies have employed rats as an animal model for TPN. In 1981, Tashiro and Meng 7) were the first to report a technique for long-term TPN in unrestrained weanling or infant (3-week-old) rats, thus establishing an animal model for pediatric TPN. Numerous studies have focused on the optimal TPN composition in mature rats, but few have addressed this issue in infant rats.We have recently developed an infant rat model with hepatic dysfunction and steatosis induced by overdose of fatfree TPN. 5) After 30 infant (3-week-ol...

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“…Since its original description by Peden et al, 1 cholestasis has become a well-known complication of prolonged parenteral nutrition (PN) in neonates. Despite significant recent advances in the understanding of the physiology of bile formation, 2 the cause of parenteral nutrition-associated cholestasis (PNAC) remains unknown, and likely is multifactorial, involving a perpetuation of inflammatory and cholestatic conditions in a susceptible neonatal liver.…”

Section: Introductionmentioning

confidence: 99%

Increased Incidence of Parenteral Nutrition-Associated Cholestasis with Aminosyn PF Compared to Trophamine

et al. 2003

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OBJECTIVE:To compare the incidence of parenteral nutrition-associated cholestasis (PNAC) between two pediatric parenteral amino-acid formulations, Aminosyn PF (APF) and Trophamine (TA). RESULTS:No PNAC developed in any infant receiving parenteral nutrition (PN) for <3 weeks. Of 141 patients given PN for Z21 days, 24 were diagnosed with PNAC: Group I (TA, 10/78, 12.8%), Group II (APF, 9/27, 33.3%), and Group III (TA, 5/36, 13.9%). The incidence of PNAC was significantly higher in infants who received APF (p ¼ 0.043). Using logistic regression, only birth weight, duration of PN, and use of APF were significant risk factors for the development of PNAC. Despite an earlier initiation of enteral feedings, APF recipients developed PNAC sooner, had higher peak direct bilirubin levels, and remained jaundiced longer. CONCLUSIONS:The use of APF was temporally associated with a greater than two-fold increase in the incidence of PNAC compared to periods of exclusive TA use. In the absence of significant differences in parenteral nutrient or energy intake in neonates who developed PNAC, we speculate that possible differences between the amino-acid compositions of TA and APF may be responsible for the observed differences in the incidence of PNAC.

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Total parenteral nutrition

Cited by 246 publications

References 2 publications

Demographic and nutritional factors associated with prolonged cholestatic jaundice in the premature infant

Demographic and nutritional factors associated with prolonged cholestatic jaundice in the premature infant

Soybean Oil Fat Emulsion to Prevent TPN-Induced Liver Damage: Possible Molecular Mechanisms and Clinical Implications

Increased Incidence of Parenteral Nutrition-Associated Cholestasis with Aminosyn PF Compared to Trophamine

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