HBV Notes

21 09 2006

 I came across a couple of studies the other day and wanted to share this info with parents of HBV+ kids.  Here are my notes, with quite a bit of the text lifted from the reports:

Hepatitis B virus genotypes and how they might affect treatment and disease progression haven’t been studied much in kids and teens.  Stefan Wirth and colleagues investigated this question, studying a group of 249 children with an average age of 7 years. 

Ninety-six percent of the group had HBV genotypes A or D and the rest had genotypes B, C, E or F.  There seemed to be no significant difference in ALT levels (an enzyme released from liver cells, elevated numbers of which may indicate liver damage) or histological findings among the various genotypes.  (From PKIDs’ glossary, histology is sometimes called microscopic anatomy and focuses on the relationships of the minute structures of cells, tissue, and organs to their functions.)

However, children with HBV genotype D had very high hepatitis B virus DNA levels and tended to seroconvert to hepatitis B e antibody later than those with genotype A.

The scientists concluded that: children with HBV genotype D showed a significantly higher viral load as compared to patients with HBV genotype A.  Since children with vertical transmission and high viral replication respond significantly poorer to treatment, individuals with genotype D have to be monitored particularly careful.  Long-term studies need to clarify, whether these patients are prone to develop a more unfavorable outcome.

Maureen Jonas and colleagues at Boston Children’s reported on Histologic Features of Chronic Hepatitis B in Children.  They noted that chronic hepatitis B (CHB) is usually asymptomatic in children but may cause significant liver disease later in life.

Jonas evaluated liver biopsies from 76 children with CHB recorded between 1984 and 2004.  It’s unknown whether these children had other liver diseases at the time of the biopsy.  She looked at severity of inflammation, necroinflammatory activity and fibrosis. 

The report states that, at the time of biopsy, children were 1 to 19 years of age and 50 of the children were Asian, 15 Caucasian, six African or African American, and the race was not known in five.  All were seropositive for HBeAg.  Forty-two acquired HBV perinatally, four likely via blood transfusion, and the mode of acquisition was unknown in the rest.

All biopsies had evidence of chronic hepatitis.  Portal inflammation and necroinflammatory activity were generally mild.  All biopsies demonstrated some fibrosis. 

Portal plasma cells were present in 59 biopsies.  Two obese patients had coexisting steatohepatitis.  ALT values near the time of biopsy were available in 64 children.  The mean ALT was 154.2 IU/L

Weak positive associations between age and the stage of fibrosis and between ALT and fibrosis were seen.
The report concluded that children with CHB and abnormal ALT have a spectrum of hepatic histological findings.  Although most have mild inflammation and necroinflammatory activity, fibrosis is moderate to severe in more than half of children with CHB.  More than 35 percent of children in this review had either bridging fibrosis with lobular distortion or cirrhosis.  Older children and those with higher ALT tend to have greater degrees of fibrosis.

PKIDs’ note: A baseline biopsy, as is common for those infected with hepatitis C, may be warranted for children with CHB.

 

 


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14 02 2013
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