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 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.

Figure 1

BMI percentile scores by steatosis category. The presence of steatosis was significantly associated with greater mean (±SE) BMI percentile scores (72^nd ± 5.8 vs. 58^th ± 3.5 percentile) F(1,101)=4.2, p=0.04). Diamonds represent 95% confidence intervals around the mean. Box plots represent subject to subject variation (box ends represent 25^th to 75^th percentiles).

Figure 2

BMI percentile scores by fibrosis stage. Mean (±SE) BMI percentile scores across the four categories of fibrosis were relatively constant (METAVIR 0 = 61^st ± 10.3, METAVIR 1 = 57^th ± 4.2, METAVIR 2 = 70^th ± 7.7, METAVIR 3-4 = 67^th ± 6.3), and not statistically different (F(3,98)=1.1, p =0.36). Diamonds represent 95% confidence intervals around the mean. Box plots represent subject to subject variation (box ends represent 25^th to 75^th percentiles).

Figure 3

BMI percentile scores by response to therapy. Mean (±SE) BMI percentile scores were higher for HCV treatment non-responders (NR) than for sustained virologic responders (SVR) (70^th (±7.4) versus 50^th (±6.5) respectively, p=0.04).

Figure 4

Logistic Response Curve for the Independent Effect of Baseline BMI Z-score on Sustained Virologic Response. Increasing baseline BMI Z score was independently associated with lower odds of response to therapy. One unit increase in baseline BMI Z score is associated with 12% decrease in response to therapy.