Total parenteral nutrition-associated cholestasis: Clinical and histopathologic correlation

Moss, Richard L.; Das, Jo; Raffensperger, John G.

doi:10.1016/s0022-3468(05)80311-2

Cited by 97 publications

(53 citation statements)

References 17 publications

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“…The severity of such as liver abscess or ascending cholangitis. Sepsisassociated cholestasis is more common with gram-negaillness appears to correlate with the duration of TPN therapy [15]. In addition, TPN-associated cholestasis is tive infections.…”

Section: Total Parenteral Nutrition Total Parenteral Nutrition (Tpn) mentioning

confidence: 99%

Intrahepatic Cholestatic Syndromes: Pathogenesis, Clinical Features and Management

Qureshi

1999

Dig Dis

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Intrahepatic cholestasis is characterized by a decrease in bile flow in the absence of overt bile duct obstruction, resulting in the accumulation of bile constituents in the liver and blood. Various etiological factors have been incriminated including drugs, total parenteral nutrition, sepsis, pregnancy, graft-versus-host disease and systemic disorders such as sarcoidosis, amyloidosis and Hodgkin’s disease. The pathogenesis of cholestasis is unclear and several mechanisms have been hypothesized, without convincing evidence that any of these play a role in clinical cholestasis. Despite the uncertainty about the pathophysiology of intrahepatic cholestasis, several forms of therapy have been employed. Ursodeoxycholic acid may relieve pruritus and lethargy, and in some cases may modify disease progression. If cholestasis persists, supportive therapy is important to maintain optimal physical and nutritional well-being. In patients with advanced liver disease associated with hepatocellular failure, liver transplantation is the only viable option.

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Section: Total Parenteral Nutrition Total Parenteral Nutrition (Tpn) mentioning

confidence: 99%

Intrahepatic Cholestatic Syndromes: Pathogenesis, Clinical Features and Management

Qureshi

1999

Dig Dis

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“…More specific, the hepatic uptake of fatty acids and triglycerides and their rates of synthesis, the secretion of these compounds via plasma or bile, or the hydrolysis of triglycerides or oxidation of fatty acids may be altered (21). These mechanisms may also be important in the development of hepatic steatosis as a result of the prolonged use of total parenteral nutrition, as some investigators have proposed that deficiencies or toxicities of the parenteral nutrition solution may lead to hepatic injury (22)(23)(24).…”

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confidence: 99%

Omega-3 Fatty Acid Supplementation Prevents Hepatic Steatosis in a Murine Model of Nonalcoholic Fatty Liver Disease

et al. 2005

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“…Finally, it is important to note that although the PELD includes the patient's bilirubin level as an indicator of liver injury and cholestasis, an elevated bilirubin level does not seem to correlate well with histologic evidence of liver injury (37)(38)(39).…”

Section: Discussionmentioning

confidence: 99%

900 13C-Methionine Breath Test to Assess Intestinal Failure Associated Liver Disease

Duro¹,

Fitzgibbons²,

Valim³

et al. 2009

Gastroenterology

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Oxidation of L[1-13 C]methionine ([ 13 C]-Met) in liver mitochondria can be quantified by measuring exhaled 13 CO 2 . We hypothesized that 13 CO 2 recovery after i.v. administered [ 13 C]-Met would provide a noninvasive measure of liver function in pediatric intestinal failure-associated liver disease (IFALD). After Institutional Review Board (IRB) approval, 27 patients underwent L[1-13 C]-Met breath tests ([ 13 C]-MBTs), five of whom underwent repeat testing after clinical changes in liver function. Sterile, pyrogen-free [ 13 C]-Met was given i.v. Six breath samples collected during 120 min were analyzed for 13 CO 2 enrichment using isotope ratio mass spectrometry. Pediatric end-stage liver disease (PELD) scores were recorded, and total carbon dioxide (CO 2 ) production was measured by indirect calorimetry. Twenty-seven patients (median age = 5.3 mo) underwent a total of 34 [ 13 C]-MBTs without adverse events. Fourteen patients had documented liver biopsies (five with cirrhosis and nine with cholestasis or fibrosis). The Intestinal failure (IF) is a clinical condition in which the body is incapable of supporting growth and/or fluid and electrolyte homeostasis because of inadequate functional intestinal surface area. In the neonatal population, recent reports estimate an incidence of up to 0.7% in very low birth weight infants, and up to 1.1% in extremely low birth weight infants. The associated mortality of IF in very low birth weight infants is thought to be as high as 20% (1).The mainstay of modern medical therapy for IF is parenteral nutrition (PN), but unfortunately, this therapy can be accompanied by liver injury that is termed intestinal failure-associated liver disease (IFALD). The etiology of IFALD can be multifactorial, and beyond its association with PN, IFALD has been linked with prematurity, number of infectious episodes, ability to tolerate enteral nutrition, number of laparotomies, number of days on antibiotics, and other yet to be identified factors (2). Although liver biopsy remains the gold standard for the evaluation of IFALD, the invasive nature of this test precludes its use as a frequent measure of disease progression or recovery. Conventional static biochemical liver tests (transaminase, bilirubin, alkaline phosphatase and albumin plasma levels, or prothrombin time) have been used to assess injury and function but vary widely in specificity and sensitivity (7-9). For example, patients with IFALD with normal or mildly elevated bilirubin can often have cirrhosis as determined by liver biopsy (10).In recognition of these deficiencies, the Child-Turcotte and Pugh (CTP) scoring system was initially developed in 1964 to assess the severity of chronic liver disease (11) and more recently, another widely used scoring system, the model for end-stage liver disease (MELD), was developed using serum creatinine, international normalized ratio (INR), and bilirubin to predict survival in adult patients with chronic liver disease (12). The pediatric end-stage liver disease (PELD) score is similar ...

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Total parenteral nutrition-associated cholestasis: Clinical and histopathologic correlation

Cited by 97 publications

References 17 publications

Intrahepatic Cholestatic Syndromes: Pathogenesis, Clinical Features and Management

Intrahepatic Cholestatic Syndromes: Pathogenesis, Clinical Features and Management

Omega-3 Fatty Acid Supplementation Prevents Hepatic Steatosis in a Murine Model of Nonalcoholic Fatty Liver Disease

900 13C-Methionine Breath Test to Assess Intestinal Failure Associated Liver Disease

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