Severe Sarcopenia and Increased Fat Stores in Pediatric Patients With Liver, Kidney, or Intestine Failure

Richard Mangus, Weston J. Bush, Chandrashekhar A. Kubal, Christina Miller

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

OBJECTIVES:: Malnutrition and wasting predict clinical outcomes in children with severe chronic illness. Objectively calculated malnutrition in children with end-stage organ failure has not been well studied. This analysis compares children with kidney, liver or intestine failure to healthy controls to quantitate the disparity in muscle and fat stores. METHODS:: Children younger than age 19 with end stage liver, kidney or intestine failure and with pre-transplant computed tomography (CT) imaging were selected from the transplant database. Age and gender-matched healthy controls were selected from the trauma database. Measures of nutrition status included a scaled scoring of core muscle mass, and visceral and subcutaneous fat stores. Analysis was conducted using the pooled and individually matched subject-control differences. RESULTS:: There were 81 subjects included in the final analysis (liver (n?=?35), kidney (n?=?20) and intestine (n?=?26)). Children with end-stage liver disease had a 23% reduction in muscle mass, a 69% increase in visceral fat and a 29% increase in subcutaneous fat. End-stage renal disease patients had a 19% reduction in muscle mass and a 258% increase in subcutaneous fat. Intestine failure patients had a 24% reduction in muscle mass, a 30% increase in visceral fat and a 46% increase in subcutaneous fat. CONCLUSIONS:: These results demonstrate significant sarcopenia and increased fat stores in end-stage organ failure patients which supports the idea of an active physiologic mechanism to store fat while losing muscle mass. Sarcopenia may be related to total protein loss from a catabolic state, or from decreased synthesis (liver), wasting (kidney) or malabsorption (intestine).

Original languageEnglish (US)
JournalJournal of Pediatric Gastroenterology and Nutrition
DOIs
StateAccepted/In press - Jun 9 2017

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Sarcopenia
Intestines
Subcutaneous Fat
Fats
Pediatrics
Kidney
Muscles
Intra-Abdominal Fat
Liver
Child Nutrition Disorders
Databases
Transplants
End Stage Liver Disease
Nutritional Status
Malnutrition
Chronic Kidney Failure
Chronic Disease
Tomography
Wounds and Injuries

ASJC Scopus subject areas

  • Pediatrics, Perinatology, and Child Health
  • Gastroenterology

Cite this

Severe Sarcopenia and Increased Fat Stores in Pediatric Patients With Liver, Kidney, or Intestine Failure. / Mangus, Richard; Bush, Weston J.; Kubal, Chandrashekhar A.; Miller, Christina.

In: Journal of Pediatric Gastroenterology and Nutrition, 09.06.2017.

Research output: Contribution to journalArticle

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abstract = "OBJECTIVES:: Malnutrition and wasting predict clinical outcomes in children with severe chronic illness. Objectively calculated malnutrition in children with end-stage organ failure has not been well studied. This analysis compares children with kidney, liver or intestine failure to healthy controls to quantitate the disparity in muscle and fat stores. METHODS:: Children younger than age 19 with end stage liver, kidney or intestine failure and with pre-transplant computed tomography (CT) imaging were selected from the transplant database. Age and gender-matched healthy controls were selected from the trauma database. Measures of nutrition status included a scaled scoring of core muscle mass, and visceral and subcutaneous fat stores. Analysis was conducted using the pooled and individually matched subject-control differences. RESULTS:: There were 81 subjects included in the final analysis (liver (n?=?35), kidney (n?=?20) and intestine (n?=?26)). Children with end-stage liver disease had a 23{\%} reduction in muscle mass, a 69{\%} increase in visceral fat and a 29{\%} increase in subcutaneous fat. End-stage renal disease patients had a 19{\%} reduction in muscle mass and a 258{\%} increase in subcutaneous fat. Intestine failure patients had a 24{\%} reduction in muscle mass, a 30{\%} increase in visceral fat and a 46{\%} increase in subcutaneous fat. CONCLUSIONS:: These results demonstrate significant sarcopenia and increased fat stores in end-stage organ failure patients which supports the idea of an active physiologic mechanism to store fat while losing muscle mass. Sarcopenia may be related to total protein loss from a catabolic state, or from decreased synthesis (liver), wasting (kidney) or malabsorption (intestine).",
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N2 - OBJECTIVES:: Malnutrition and wasting predict clinical outcomes in children with severe chronic illness. Objectively calculated malnutrition in children with end-stage organ failure has not been well studied. This analysis compares children with kidney, liver or intestine failure to healthy controls to quantitate the disparity in muscle and fat stores. METHODS:: Children younger than age 19 with end stage liver, kidney or intestine failure and with pre-transplant computed tomography (CT) imaging were selected from the transplant database. Age and gender-matched healthy controls were selected from the trauma database. Measures of nutrition status included a scaled scoring of core muscle mass, and visceral and subcutaneous fat stores. Analysis was conducted using the pooled and individually matched subject-control differences. RESULTS:: There were 81 subjects included in the final analysis (liver (n?=?35), kidney (n?=?20) and intestine (n?=?26)). Children with end-stage liver disease had a 23% reduction in muscle mass, a 69% increase in visceral fat and a 29% increase in subcutaneous fat. End-stage renal disease patients had a 19% reduction in muscle mass and a 258% increase in subcutaneous fat. Intestine failure patients had a 24% reduction in muscle mass, a 30% increase in visceral fat and a 46% increase in subcutaneous fat. CONCLUSIONS:: These results demonstrate significant sarcopenia and increased fat stores in end-stage organ failure patients which supports the idea of an active physiologic mechanism to store fat while losing muscle mass. Sarcopenia may be related to total protein loss from a catabolic state, or from decreased synthesis (liver), wasting (kidney) or malabsorption (intestine).

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