title: Clinical correlates of histopathology in pediatric nonalcoholic steatohepatitis.
abstract: OBJECTIVE
  Nonalcoholic fatty liver disease (NAFLD) is the most prevalent liver disease in American children. Noninvasive means to discriminate between NAFLD and nonalcoholic steatohepatitis (NASH) might diminish the requirement for liver biopsy or predict those at increased risk for progression.
  
  
  METHODS
  Data obtained prospectively from children (age, 6-17 y) enrolled in the NASH Clinical Research Network were analyzed to identify clinical-pathologic correlates of pediatric NAFLD. All participants underwent liver biopsy within 6 months of clinical data that were reviewed by a central pathology committee.
  
  
  RESULTS
  A total of 176 children (mean age, 12.4 y; 77% male) were eligible for inclusion. By using ordinal logistic regression analysis, increasing aspartate aminotransferase (AST) level (odds ratio [OR], 1.017 per U/L; 95% confidence interval [CI], 1.004-1.031) and gamma-glutamyltransferase level (OR, 1.016 per U/L; 95% CI, 1.000-1.033) were associated independently with increasing severity of NASH. Increasing AST level (OR, 1.015 per U/L; 95% CI, 1.006-1.024), increasing white blood cell count (OR, 1.22 per 1000/mm(3); 95% CI, 1.07-1.38), and decreasing hematocrit (OR, 0.87 per %; 95% CI, 0.79-0.96) were associated independently with increasing severity of fibrosis. Area under the receiver operator characteristic curve for a model with AST and alanine aminotransferase was 0.75 (95% CI, 0.66-0.84) and 0.74 (95% CI, 0.63-0.85) for distinguishing steatosis from more advanced forms of NASH and bridging fibrosis from lesser degrees of fibrosis, respectively.
  
  
  CONCLUSIONS
  Certain components of routine laboratory tests are predictive of NAFLD pattern and fibrosis severity, but do not have adequate discriminate power to replace liver biopsy in evaluating pediatric NAFLD.
authors.affiliation: Division of Gastroenterology, University of California, San Diego, San Diego, California 92103, USA.
authors.forename: Heather M
authors.initials: HM
authors.lastname: Patton
authors.forename: Joel E
authors.initials: JE
authors.lastname: Lavine
authors.forename: Mark L
authors.initials: ML
authors.lastname: Van Natta
authors.forename: Jeffrey B
authors.initials: JB
authors.lastname: Schwimmer
authors.forename: David
authors.initials: D
authors.lastname: Kleiner
authors.forename: Jean
authors.initials: J
authors.lastname: Molleston
mesh_terms: D000293:Adolescent; D000410:Alanine Transaminase / Q000097:blood; D000975:Antioxidants / Q000627:therapeutic use; D001219:Aspartate Aminotransferases / Q000097:blood; D001706:Biopsy; D002648:Child; D004359:Drug Therapy, Combination; D005234:Fatty Liver / Q000188:drug therapy / Q000201:enzymology / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D006400:Hematocrit; D006801:Humans; D007004:Hypoglycemic Agents / Q000627:therapeutic use; D007958:Leukocyte Count; D008099:Liver / Q000473:pathology*; D008297:Male; D008687:Metformin / Q000627:therapeutic use*; D011237:Predictive Value of Tests; D015995:Prevalence; D011379:Prognosis; D011446:Prospective Studies; D012372:ROC Curve; D012720:Severity of Illness Index; D014810:Vitamin E / Q000627:therapeutic use*
chemical_list: D000975:Antioxidants; D007004:Hypoglycemic Agents; D014810:Vitamin E; D008687:Metformin; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase