Influence of Body Mass Index on Outcome of Pediatric Chronic Hepatitis C Virus Infection

ABSTRACT Background and Aims: Evidence demonstrates that obesity is associated with progression of chronic hepatitis C virus (HCV) infection and poor response to interferon therapy among HCV‐infected adults. However, this evidence has been confounded by multiple comorbidities present in adult cohort...

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Published inJournal of pediatric gastroenterology and nutrition Vol. 51; no. 2; pp. 191 - 197
Main Authors Delgado‐Borrego, Aymin, Healey, David, Negre, Betania, Christofi, Marielle, Sabharwal, Sabina, Ludwig, David A, Chung, Raymond T, Jonas, Maureen M
Format Journal Article
LanguageEnglish
Published Hagerstown, MD Copyright by ESPGHAN and NASPGHAN 01.08.2010
Lippincott Williams & Wilkins
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Abstract ABSTRACT Background and Aims: Evidence demonstrates that obesity is associated with progression of chronic hepatitis C virus (HCV) infection and poor response to interferon therapy among HCV‐infected adults. However, this evidence has been confounded by multiple comorbidities present in adult cohorts and the use of single adult doses. Patients and Methods: We performed a retrospective investigation to evaluate the role of body mass index (BMI) in chronic HCV progression and response to therapy in the children. One hundred twenty‐three children and teenagers studied at Children's Hospital Boston for HCV infection between 1998 and 2007 were included. Patients' weight and height at the time of liver biopsy or before and after HCV therapy were obtained and BMI was calculated. Results: The presence of steatosis was statistically associated with higher mean (±SE) BMI percentiles (72nd ± 5.8 vs 58th ± 3.5) percentile; F(1,101) = 4.2, P = 0.04. Nonresponders to treatment had a higher mean (±SE) BMI percentile (70th ± 7.4) when compared with responders (50th ± 6.5) in univariate and multivariate analyses (P = 0.04, P = 0.02, respectively). Using a multivariate model, it was calculated that 1 standard deviation (1 z‐score unit) increase in baseline BMI z score is associated with a 12% decrease in the probability of sustained virologic response. Conclusions: Overweight adversely affects the progression of chronic HCV liver disease and is associated with diminished response to antiviral therapy using weight‐based dosing in a cohort with minimal comorbidities.
AbstractList ABSTRACT Background and Aims: Evidence demonstrates that obesity is associated with progression of chronic hepatitis C virus (HCV) infection and poor response to interferon therapy among HCV‐infected adults. However, this evidence has been confounded by multiple comorbidities present in adult cohorts and the use of single adult doses. Patients and Methods: We performed a retrospective investigation to evaluate the role of body mass index (BMI) in chronic HCV progression and response to therapy in the children. One hundred twenty‐three children and teenagers studied at Children's Hospital Boston for HCV infection between 1998 and 2007 were included. Patients' weight and height at the time of liver biopsy or before and after HCV therapy were obtained and BMI was calculated. Results: The presence of steatosis was statistically associated with higher mean (±SE) BMI percentiles (72nd ± 5.8 vs 58th ± 3.5) percentile; F(1,101) = 4.2, P = 0.04. Nonresponders to treatment had a higher mean (±SE) BMI percentile (70th ± 7.4) when compared with responders (50th ± 6.5) in univariate and multivariate analyses (P = 0.04, P = 0.02, respectively). Using a multivariate model, it was calculated that 1 standard deviation (1 z‐score unit) increase in baseline BMI z score is associated with a 12% decrease in the probability of sustained virologic response. Conclusions: Overweight adversely affects the progression of chronic HCV liver disease and is associated with diminished response to antiviral therapy using weight‐based dosing in a cohort with minimal comorbidities.
BACKGROUND AND AIMS:Evidence demonstrates that obesity is associated with progression of chronic hepatitis C virus (HCV) infection and poor response to interferon therapy among HCV-infected adults. However, this evidence has been confounded by multiple comorbidities present in adult cohorts and the use of single adult doses. PATIENTS AND METHODS:We performed a retrospective investigation to evaluate the role of body mass index (BMI) in chronic HCV progression and response to therapy in the children. One hundred twenty-three children and teenagers studied at Childrenʼs Hospital Boston for HCV infection between 1998 and 2007 were included. Patientsʼ weight and height at the time of liver biopsy or before and after HCV therapy were obtained and BMI was calculated. RESULTS:The presence of steatosis was statistically associated with higher mean (±SE) BMI percentiles (72nd ± 5.8 vs 58th ± 3.5) percentile; F(1,101) = 4.2, P = 0.04. Nonresponders to treatment had a higher mean (±SE) BMI percentile (70th ± 7.4) when compared with responders (50th ± 6.5) in univariate and multivariate analyses (P = 0.04, P = 0.02, respectively). Using a multivariate model, it was calculated that 1 standard deviation (1 z-score unit) increase in baseline BMI z score is associated with a 12% decrease in the probability of sustained virologic response. CONCLUSIONS:Overweight adversely affects the progression of chronic HCV liver disease and is associated with diminished response to antiviral therapy using weight-based dosing in a cohort with minimal comorbidities.
Evidence demonstrates that obesity is associated with progression of chronic hepatitis C virus (HCV) infection and poor response to interferon therapy among HCV-infected adults. However, this evidence has been confounded by multiple comorbidities present in adult cohorts and the use of single adult doses. We performed a retrospective investigation to evaluate the role of body mass index (BMI) in chronic HCV progression and response to therapy in the children. One hundred twenty-three children and teenagers studied at Children's Hospital Boston for HCV infection between 1998 and 2007 were included. Patients' weight and height at the time of liver biopsy or before and after HCV therapy were obtained and BMI was calculated. The presence of steatosis was statistically associated with higher mean (+/-SE) BMI percentiles (72nd +/- 5.8 vs 58th +/- 3.5) percentile; F(1,101) = 4.2, P = 0.04. Nonresponders to treatment had a higher mean (+/-SE) BMI percentile (70th +/- 7.4) when compared with responders (50th +/- 6.5) in univariate and multivariate analyses (P = 0.04, P = 0.02, respectively). Using a multivariate model, it was calculated that 1 standard deviation (1 z-score unit) increase in baseline BMI z score is associated with a 12% decrease in the probability of sustained virologic response. Overweight adversely affects the progression of chronic HCV liver disease and is associated with diminished response to antiviral therapy using weight-based dosing in a cohort with minimal comorbidities.
Author Negre, Betania
Ludwig, David A
Delgado‐Borrego, Aymin
Christofi, Marielle
Chung, Raymond T
Jonas, Maureen M
Sabharwal, Sabina
Healey, David
AuthorAffiliation Division of Clinical Research and Division of Gastroenterology, Department of Pediatrics, Batchelor Childrenʼs Research Institute, University of Miami, Miami, FL, USA †Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Childrenʼs Hospital Boston, Boston, USA ‡Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
AuthorAffiliation_xml – name: Division of Clinical Research and Division of Gastroenterology, Department of Pediatrics, Batchelor Childrenʼs Research Institute, University of Miami, Miami, FL, USA †Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Childrenʼs Hospital Boston, Boston, USA ‡Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, Boston, MA, USA
– name: b Division of Gastroenterology, Hepatology and Nutrition, Department of Pediatrics, Children's Hospital Boston, 300 Longwood Avenue, Boston, MA 02115
– name: c Gastrointestinal Unit, Department of Medicine, Massachusetts General Hospital, 55 Fruit Street, Boston, MA 02114
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Keywords Human
Obesity
Pediatrics
Prognosis
Cytokine
Nutrition disorder
Hepatic disease
Metabolic diseases
Steatosis
pediatric
Infection
Body mass index
Viral disease
Fibrosis
Gastroenterology
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Notes This work was supported by NIH DK070022 (A.D.B.), DK78772 (RTC), and the Robert Wood Johnson Foundation (A.D.B.).
Drs Chung and Jonas are co‐senior authors.
The authors report no conflicts of interest.
Co-senior authors
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Snippet ABSTRACT Background and Aims: Evidence demonstrates that obesity is associated with progression of chronic hepatitis C virus (HCV) infection and poor response...
BACKGROUND AND AIMS:Evidence demonstrates that obesity is associated with progression of chronic hepatitis C virus (HCV) infection and poor response to...
Evidence demonstrates that obesity is associated with progression of chronic hepatitis C virus (HCV) infection and poor response to interferon therapy among...
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pascalfrancis
wolterskluwer
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SourceType Open Access Repository
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StartPage 191
SubjectTerms Adolescent
Antiviral Agents - pharmacology
Antiviral Agents - therapeutic use
Biological and medical sciences
Body Mass Index
Child
Disease Progression
Drug Resistance, Viral
Fatty Liver - drug therapy
Fatty Liver - etiology
Fatty Liver - virology
Feeding. Feeding behavior
Female
fibrosis
Fundamental and applied biological sciences. Psychology
Hepacivirus - drug effects
Hepatitis C, Chronic - complications
Hepatitis C, Chronic - drug therapy
Hepatitis C, Chronic - virology
Human viral diseases
Humans
Infectious diseases
interferon
Male
Medical sciences
Metabolic diseases
Models, Statistical
Multivariate Analysis
Obesity
Obesity - complications
pediatric
Retrospective Studies
steatosis
Vertebrates: anatomy and physiology, studies on body, several organs or systems
Viral diseases
Viral hepatitis
Title Influence of Body Mass Index on Outcome of Pediatric Chronic Hepatitis C Virus Infection
URI https://onlinelibrary.wiley.com/doi/abs/10.1097%2FMPG.0b013e3181d32756
https://www.ncbi.nlm.nih.gov/pubmed/20531022
https://pubmed.ncbi.nlm.nih.gov/PMC2910782
Volume 51
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