Symptomatic and Pathophysiologic Predictors of Hepatitis C Virus Progression in Pediatric Patients

Biobehavioral Unit, Symptoms Management Branch, Intramural Research Program, National Institute of Nursing Research, National Institutes of Health, Bethesda, MD 20892, USA.
The Pediatric Infectious Disease Journal (Impact Factor: 2.72). 08/2009; 28(8):724-7. DOI: 10.1097/INF.0b013e31819f1f71
Source: PubMed


The slow progression of hepatitis C virus (HCV) infection could ultimately negatively impact pediatric patients during their lifespan. This study describes the symptomatic and pathophysiologic presentation of HCV infection in a cohort of pediatric outpatients.
HCV-positive patients were identified by diagnosis codes from outpatient visits. Demographic and pathophysiologic indicators (comorbidities, reported symptoms, alanine transaminase, aspartate transaminase, gamma glutamyl transpeptidase, HCV viral load, genotype, and liver biopsy results) were collected and analyzed.
We reviewed 62 patients with HCV infection who were from 3 months and 19 years of age (M +/- SD, 12.5 +/- 5.8 years). Sixty percent presented with clinical symptoms of fatigue, joint-abdominal pain, bruising/bleeding, or other non-specific symptoms. On liver biopsy (n = 35) 80% had evidence of inflammation, 57% had fibrosis, and 9% had steatosis. All patients with steatosis or cirrhosis reported symptoms. Males were significantly more likely than women to be symptomatic (58.3% vs. 41.7%, P = 0.04). Patients with symptoms were significantly older (M = 13.5 +/- 5.2 vs. 8.9 +/- 5.5 years, P = 0.003). There was a significant inverse relationship between viral load and symptoms (chi = 4.75, P = 0.03). Patients with low viral load (<2 million copies) were 5 times more likely to have symptoms than those with high viral loads (P = 0.03). Significance was also noted between HCV genotype and ALT levels (chi = 3.72, P = 0.05). There were no significant relationships between symptom status and race, comorbidities, alanine transaminase, aspartate transaminase, gamma glutamyl transpeptidase, HCV genotype, or liver histology.
Pediatric patients with HCV can have significant symptoms and physiologic liver changes related to HCV.

Download full-text


Available from: Wendy A Henderson,
22 Reads
  • The Pediatric Infectious Disease Journal 02/2010; 29(2):189-90; author reply 190. DOI:10.1097/INF.0b013e3181c11c27 · 2.72 Impact Factor
  • The Pediatric Infectious Disease Journal 02/2010; 29(2):190. DOI:10.1097/INF.0b013e3181c15dbc · 2.72 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: The outcome of patients with hepatitis C virus (HCV) infection acquired during childhood in the absence of antiviral therapy is not clear. The purpose of this study was to review the outcome of untreated HCV acquired in childhood. Only population-based studies were included, as referred cases would be predicted to have more severe disease. A systematic review of the literature was completed up to October 2010 to identify studies where a population was screened for HCV infection that was presumably acquired during childhood. Demographical and clinical data were collected on infected patients who had not been treated with an antiviral. Primary outcome was development of a severe adverse outcome (cirrhosis, hepatoma, need for a liver transplant or liver-related death). There were 25 studies reporting a total of 733 infected patients. Liver biopsy results were provided for 180 patients (25%), revealing cirrhosis in eight (1.0% of the total and 4.0% of those who had a biopsy). None of the other patients developed a severe adverse outcome. As a result of the small number of patients with a severe adverse outcome, risk factors for HCV progression could not be identified. Although HCV can lead to liver transplantation and death during childhood, the vast majority of patients with disease acquired during childhood have slowly progressive disease. There is no clear indication for antiviral therapy in the majority of children with HCV infection.
    Liver international: official journal of the International Association for the Study of the Liver 09/2011; 32(2):258-70. DOI:10.1111/j.1478-3231.2011.02633.x · 4.85 Impact Factor
Show more