Chronic Hepatitis B in North American Children

As part of the Hepatitis B Research Network (HBRN), 343 children were enrolled in 7 U.S. and Canadian centers.  A recent study (KB Schwarz et al. J Pediatr 2015; 167: 1287-94) provides data on HBV epidemiology and a related commentary by Brian McMahon (1186-7) provides some useful advice on what is needed to further reduce HBV infection.

88 children were not enrolled.  More than half of these patients refused to participate, the other reasons included language barriers or inability to comply with follow-up.

Key findings:

  • 78% of the subjects in this study were Asian
  • 55% were adopted.  This high adoption rate likely skews some of the data because (according to the associated editorial) “children with HBV in the US..most are likely to be children of parents who immigrated to the US from endemic countries and not adoptees.”
  • 97% had international origins with either the child or a parent born abroad
  • HBV genotype B was most common (43%) followed by genotype C (32%), D (16%), A (5%), E (4%) or multiple (<1%).

In the editorial, Dr. McMahon notes that ascertaining the rate of a birth dose of HBV vaccine would be of interest.  In many countries, vaccination is started at ≥2 months and this is unlikely to prevent HBV transmission.  Two important public health issues for North America:

  • “First, all pregnant women, especially those foreign-born, need to be screened for HBsAg and if positive, their infants should receive HBV vaccine and hepatitis B immune globulin immediately after birth.”
  • “Second, all foreign-born children and adults who immigrate to the US or Canada should be tested for HBsAg.”

My take: This study provides an up-to-date snapshot of tertiary care for children with HBV in North America.  There are many opportunities to curtail (or hopefully eliminate) the impact of HBV in our communities and around the world.

AASLD Guideline (Nov 2015): Treatment of Chronic HBV 

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Revising the Textbooks on Isoniazid Hepatotoxicity

Previously, isoniazid (INH) hepatoxicity has generally been described as “idiosyncratic.”  New research shows that INH-induced hepatotoxicity is often associated with anti-INH and anti-cytochrome P450 antibodies (Hepatology 2014; 59: 1084-93, editorial 746-48).

Background: INH is a crucial treatment for tuberculosis.  About 10% of patients receiving monotherapy may develop mild elevations (<3-fold the upper limit of normal) of alanine aminotransferase.  However, 0.5-1% develop overt hepatitis and some develop acute liver failure (ALF).  Risk factors for ALF include female gender, age >35 years, cotreatment with other tuberculosis medications, INH dose >50 mg/kg, ethanol use, and slower metabolic pathways (slow acetylator N-acetyltransferase 2 or cytochrome (CYP) P450 2E1 genotype).

The authors utilized two patient groups: 19 from the ALF study group registry who had >50% likelihood of IHN toxicity and 20 control patients who were receiving INH prophylaxis.  In this control group, 15 had no liver injury and 5 had mild hepatitis. The authors utilized several immunoassays.

Key findings:

  • 15 of 19 cases of INH-associated ALF had detectable antibodies: 8 anti-INH and 11 had antiCYP2E1 Abs.
  • None of these antibodies were detected from INH-treated controls

Bottomline: from the authors of the study “Although the presence of these antibodies only in INH-induced liver failure suggests that INH-induced liver injury is immune mediated, there is no evidence that these Abs are actually responsible for the liver injury.”

In this same issue is a lengthy guideline on the “Evaluation for Liver Transplantation in Adults”:

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Liver toxicity -where to look online | gutsandgrowth