Cholestasis parenteral nutrition

San Luis VA, Btaiche IF. Ursodiol in patients with parenteral nutrition-associated cholestasis. Ann Pharma-cother2007 41(ll) 1867-72. 

Paraneoplastic syndrome Parasitic infections Parenteral nutrition Postoperative cholestasis Primary biliary cholangitis Primary sclerosing cholangitis Protoporphyria Right ventricular failure Sepsis... 

Forrest, E.H., Oien, K.A., Dickson, S., Galloway, D., Mills, P.R. Improvement in cholestasis associated with total parenteral nutrition after treatment with an antibody against tumour necrosis factor alpha. Liver 2002 22 317-320... 

Messing, B., Colombel, J.F., Heresbach, D., Chazouillres, O., Galian, A. Chronic cholestasis and macronutrient excess in patients treated with prolonged parenteral nutrition. Nutrition 1992 8 30-36... 

Moss, R.L., Das, J.B., Raffensperges, J.G. Total parenteral nutrition-associated cholestasis clinical and histopathologic correlation. J. Pediatr. Surg. 1993 28 1270-1275... 

Cholestasis from other causes can increase the accumulation of ciclosporin or its metabolites, which in turn worsens hepatic cholestasis. This mechanism has been suggested in patients with bowel diseases who experienced an aggravation of hyperbilirubinemia or an increased incidence of hepatotoxicity from the combination of total parenteral nutrition and ciclosporin (SEDA-19, 348) (288). 

Copper deficiency has been reported in a patient with Crohn s disease after removal of copper from the parenteral nutrition because of severe cholestasis (59). The patient developed pancytopenia with severely depressed serum copper concentrations after 8 weeks. Bone-marrow biopsy confirmed the cause as copper deficiency. Although intravenous replacement of copper improved the patient s anemia and other markers, he suddenly died of cardiac tamponade. 

When oral intake is precluded, the recommended daily parenteral supplementation of manganese is 0.15-0.8 mg. Manganese is mainly excreted in the bile during cholestasis serum manganese levels may rise, and manganese toxicity can result. Hjq)ermanganesemia after parenteral nutrition when first reported was linked to portosystemic encephalopathy. Patients with liver disease were particularly at risk. 

The possible hnk between hypermanganesemia and cholestasis has been investigated in patients receiving long-term parenteral nutrition (68). The authors concluded that cholestatic liver disease does not contribute to increased blood manganese concentrations in such patients, and that plasma concentrations reflect recent manganese exposure and impaired excretion when cholestasis is present. They also emphasized that serum concentrations are a poor marker and that erythrocyte manganese concentrations should be used instead. 

Intestinal transplantation is combined with liver transplantation in 46% of cases, because of terminal liver failure (93). Of 78 patients who had received parenteral nutrition for more than 2 years n — 66) and/ or had short bowel syndrome and could not be weaned from parenteral nutrition (n = 12), 58 developed chronic cholestasis and 37 developed one or more severe liver complication (serum bilirubin concentration 60 pmol/l, factor V (proaccelerin) 50%, portal hypertension, encephalopathy, ascites, bleeding from the gastrointestinal tract, or histological findings consisting of extensive fibrosis and cirrhosis) after 6 (3-132) months and 17 (2-155) months respectively. Liver disease was responsible for deaths in 6.5% of the patients (22% of deaths). 

In a prospective prevalence study of liver disease in 90 patients with permanent intestinal failure receiving parenteral nutrition hver biopsy was performed in 57 (95). Chronic cholestasis developed in 58 patients after a median of 6 (range 3-132) months, and 37 developed comphcated liver disease after a median of 17 (range 2-155) months. Chronic cholestasis was significantly associated with a risk of liver disease independent of parenteral nutrition, a bowel remnant shorter than 50 cm, and a lipid intake of 1 g/kg/day or more hver disease related to parenteral nutrition was significantly associated with chronic cholestasis and a parenteral hpid intake of 1 g/kg/day or more. The authors concluded that the prevalence of hver disease increased with the duration of parenteral nutrition and was one of the main causes of death in patients with permanent intestinal failure. Parenteral intake of long-chain hpid emulsion should be restricted to less than 1 g/kg/day. 

Several mechanisms have been proposed to explain the cholestasis that occurs during parenteral nutrition, but there is little direct evidence to support any of them. Nutrient deficiencies that may be critical for hepatic uptake, biotransformation, and secretion of bile may be involved. Deficiency of taurine, which is important for bile acid conjugation, may cause cholestasis in premature infants. Certain amino acids may act as toxins. Reduced... 

In a retrospective study of the incidence of cholestasis and liver failure in 42 patients with intestinal resection in the neonatal period who subsequently became dependent on parenteral nutrition support, the effect of various associated clinical factors on the incidence and severity of cholestasis was determined (103). Cholestasis developed in 28 while they were receiving parenteral nutrition. In 21 patients, the raised direct bilirubin concentration returned to normal while they continued to receive parenteral nutrition. Seven patients progressed to liver failure. Patients without cholestasis had been dependent on parenteral nutrition for longer than patients with cholestasis. It was clear from this study that cholestasis in neonates with intestinal resection is not simply a function of the duration of exposure to intravenous nutrition. 

The role of lipid emulsions in cholestasis associated with long-term parenteral nutrition has been investigated retrospectively in 10 children with a total of 23 episodes of cholestasis, associated with thrombocytopenia in 13 cases (104). Changes in lipid delivery, associated with increased daily amounts, preceded complications in more than half the cases, while temporary reduction in lipid administration led to normalization of bilirubin in 17 episodes. The authors concluded that lipid supply is one of the risk factors for cholestasis associated with parenteral nutrition. They recommended that when cholestasis occurs, lipid should be temporarily withdrawn, especially if there is associated thrombocytopenia. 

Taylor S, Manara AR. Manganese toxicity in a patient with cholestasis receiving total parenteral nutrition. Anaesthesia 1994 49(11) 1013. 

Teitelbaum DH. Parenteral nutrition-associated cholestasis. Curr Opin Pediatr 1997 9(3) 270-5. 

Drongowski RA, Coran AG. An analysis of factors contributing to the development of total parenteral nutrition-induced cholestasis. J Parenter Enteral Nutr 1989 13(6) 586-9. 

Iyer KR, Spitz L, Clayton P. BAPS prize lecture New insight into mechanisms of parenteral nutrition-associated cholestasis role of plant sterols. British Association of Paediatric Surgeons. J Pediatr Surg 1998 33(l) l-6. 

Sondheimer JM, Asturias E, Cadnapaphornchai M. Infection and cholestasis in neonates with intestinal resection and long-term parenteral nutrition. J Pediatr Gastroenterol Nutr 1998 27(2) 131-7. 

Colomb V, Jobert-Giraud A, Lacaille F, Goulet O, Fournet JC, Ricour C. Role of lipid emulsions in cholestasis associated with long-term parenteral nutrition in children. J Parenter Enteral Nutr 2000 24(6) 345-50. 

Reimund JM, Duclos B, Arondel Y, Baumann R. Persistent inflammation and immune activation contribute to cholestasis in patients receiving home parenteral nutrition. Nutrition 2001 17(4) 300-4. 

Levine A, Maayan A, Shamir R, Dinari G, Sulkes J, Sirotta L. Parenteral nutrition-associated cholestasis in preterm neonates evaluation of ursodeoxycholic acid treatment. J Pediatr Endocrinol Metab 1999 12(4) 549-53. 

Spagnuolo MI, lorio R, Vegnente A, Guarino A. Ursodeoxychohc acid for treatment of cholestasis in children on long-term total parenteral nutrition a pilot study. Gastroenterology 1996 111(3) 716-19. 

Yip YY, Lim AK, R J, Tan KL. A multivariate analysis of factors predictive of parenteral nutrition-related cholestasis (TPN cholestasis) in VLBW infants. J Singapore Paediatr Soc 1990 32(3-4) 144-8. 

Chou YH, Yau KI, Hsu HC, Chang MH. Total parenteral nutrition-associated cholestasis in infants clinical and liver histologic studies. Zhonghua Min Guo Xiao Er Ke Yi Xue Hui Za Zhi 1993 34(4) 264-71. 

Komura J, Yano H, Tanaka Y, Tsuru T. Increased incidence of cholestasis during total parenteral nutrition in children—factors affecting stone formation. Kurume Med J 1993 40(1) 7-11. 

Inflammatory conditions of the liver, in particular inflammatory hepatocellular cholestasis, are one of the most frequent causes of jaundice in the clinic. The major underlying denominator of this disorder is the inhibition of transporter expression and function by proinflammatory cytokines, which are either induced systemically or within the liver. Alcoholic hepatitis accounts for up to two-thirds of patients and is the most frequent trigger, followed by idiosyncratic drug reactions, sepsis or other extrahepatic bacterial infections, some variants of viral hepatitis, and total parenteral nutrition [95, 96]. 

R Cholestasis during parenteral nutrition a comparison of soybean oil and fish oils... 

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