HEPATOLOGY WATCH®

Editorial Board: Emmet B. Keeffe, MD (Chair);

M. Eric Gershwin, MD; Ira S. Goldman, MD;

John L. Gollan, MD, PhD; Kris V. Kowdley, MD;

Paul Martin, MD; Marion G. Peters, MD

 

MAY 2005

HEPATITIS B VIRUS (HBV) VACCINATION

Protection after 15 years of follow-up.  Alaska Natives have a high prevalence of chronic HBV infection that is primarily acquired during early childhood.  Brian McMahon and colleagues report data on persistence of anti-HBs and protection afforded by HBV vaccination of an Alaska Native population after 15 years of follow-up.  Between November 1981 and May 1982, 1,578 Alaska Natives aged 6 months or older residing in 15 villages received 3 doses of plasma-derived hepatitis B vaccine. This cohort was followed annually for the first 11 years, and 841 of the participants (53%) were tested at 15 years.  Mean plasma levels of anti-HBs decreased from 822 mIU/mL after vaccination to 27 mIU/mL at 15 years.  A longitudinal linear mixed model identified initial anti-HBs level, age >4 years at vaccination, and male sex to be associated with the persistence of higher anti-HBs levels at 15 years.  Asymptomatic breakthrough infection developed in only 16 participants and occurred more frequently in vaccination nonresponders than responders (P=0.01); serum HBV DNA was detected in 6 of these participants. Two persons were infected with wild-type HBsAg, and 4 persons were infected with both wild-type HBsAg and HBsAg variants. These data demonstrated that HBV vaccination provided good protection against infection for at least 15 years.  Antibody levels in persons immunized at 4 years of age or younger were found to decrease the most in this population. ♦ In an editorial, D.S. Chen observed that this long-term follow-up study confirms the preliminary results of studies conducted in highly populous settings elsewhere. It is not clear whether the decrease in serum anti-HBs levels seen in children vaccinated in early childhood indicates that booster immunization is necessary.  (McMahon BJ, et al. Ann Intern Med. 2005;142:333–341; Chen DS. Ann Intern Med. 2005;142:384–385)

 

PRIMARY BILIARY CIRRHOSIS (PBC)

Prevalence of isotype-specific antinuclear antibodies (ANAs).  E.I. Rigopoulou and coworkers from the King's College Hospital in London assessed the prevalence of PBC-specific ANAs (rim-like/membranous or multiple-nuclear dot patterns) in 90 patients with PBC from Greece and Spain.  PBC-specific ANA reactivity was observed in 14 patients (15.6%) when tested with an anti-IgG (total) antiserum.  However, 58 patients (64.4%) were found to be ANA positive when specific antisera to each of the 4 IgG isotypes were used. Significantly more severe biochemical and histologic disease was present in patients with PBC-specific ANA positivity than in those who were seronegative. This analysis showed that specific ANAs were found in the majority of PBC patients and were associated with a more severe clinical course.  (Rigopoulou EI, et al. Gut. 2005;54:528–532)

 

LIVER FAILURE

Prophylaxis of variceal bleeding: endoscopic variceal ligation (EVL) plus nadolol vs EVL alone. Joaquin de la Pena and others conducted a study in which 80 patients with cirrhosis who were hospitalized for acute variceal bleeding were randomized after primary therapy to receive prophylactic treatment with EVL plus nadolol or EVL alone.  EVL sessions were repeated every 10 to 12 days until all varices were eradicated. After a median follow-up of 16 months (range, 1–24 months), the variceal bleeding recurrence rate was 14% for patients treated with EVL plus nadolol, compared with 38% for patients treated with EVL alone (P= 0.006). Mortality was similar in both groups (5 vs 4 deaths). Adverse events related to nadolol occurred in 11% of patients. These results showed that the addition of nadolol to EVL reduced the incidence of variceal rebleeding but did not improve survival.
(de la Pena J, et al. Hepatology. 2005;41:572–578)

 

CHRONIC HEPATITIS C VIRUS (HCV) INFECTION

Insulin resistance impairs sustained virologic response (SVR) rate.  Experimental and clinical studies support a role for HCV infection in the development of insulin resistance.  Manuel Romero-Gomez and colleagues evaluated the effect of insulin resistance and other factors on SVR in 159 HCV patients treated with peginterferon plus ribavirin. SVR was achieved in 43.4% of patients.  Multivariate regression analysis identified genotype, insulin resistance index, and fibrosis to be independent factors related to SVR following combination peginterferon and ribavirin therapy. (Romero-Gomez M, et al. Gastroenterology. 2005;128:636–641)

 

Peginterferon α-2b monotherapy in acute HCV.  Teresa Santantonio and colleagues utilized peginterferon α-2b (1.5 mg/kg once weekly for 24 weeks) in 16 patients with acute HCV infection who remained viremic after 12 weeks of observation. At the end of 24 weeks of treatment, HCV RNA was undetectable in 15 patients, and ALT had normalized in 14 patients. After 6 and 12 months of follow-up, 15 patients (94%) had ongoing virologic and biochemical responses. These results, demonstrating that delayed antiviral therapy is effective, provide a rationale for delaying treatment for 12 weeks in order to target therapy to only those patients who fail to spontaneously clear HCV. ♦ Amany Zekry and others highlight several issues in the treatment of acute HCV infection in an accompanying editorial.  (Santantonio T, et al. J Hepatol. 2005;42:329–333; Zekry A, et al. J Hepatol. 2005;42:293–296)

 

NEW SECTION: DID YOU KNOW?

PBC is 8 times more common in British Columbia's First Nation peoples than in the non-native population. Genetic and environmental factors are being investigated in this unique population. (Arbour L, et al. Int J Circumpolar Health. 2004;63(suppl 2):185–188). Wilson disease (WD) has recently been reported in 2 septuagenarian siblings.  Although WD usually presents in the first decades of life, the diagnosis of WD should be considered at all ages in patients with hepatic disease, neurologic disease, and psychiatric symptoms.  (Ala A, et al. Hepatology. 2005;41:668–670)

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