Viral Hepatitis in the Elderly

Andres F Carrion MD; Paul Martin MD; FACG

Disclosures

Am J Gastroenterol. 2012;107(5):691-697. 

In This Article

Hepatitis A

The age-specific incidence of hepatitis A virus (HAV) infection in children and adults in the United States declined rapidly following implementation of vaccination of children and individuals at risk.[11] Data from 2009 published by the Centers for Disease Control and Prevention demonstrate a low incidence of acute HAV infection of 0.6 per 100,000 people.[12] The seroprevalence of anti-HAV immunoglobulin (Ig) G, a marker of prior infection with HAV, increases proportionally with age reflecting a cumulative risk of HAV infection throughout life. Data from the third National Health and Nutrition Examination Survey (NHANES III) indicate that 31% of the overall US population had serological evidence of prior HAV infection (data collected before implementation of HAV vaccination): 9% of children aged 6–11 years, 19% of young adults aged 20–29 years, 33% of middle age adults aged 40–49 years, and 75% of those older than 70 years of age.[13]

Recovery from acute HAV infection is usually uneventful, especially in children and younger adults in whom the infection is often subclinical.[14] However, elderly individuals with acute HAV are likely to have more profound hepatocellular dysfunction with frequent jaundice and coagulopathy, as well as a higher incidence of complications such as prolonged cholestasis, pancreatitis, and ascites.[15,16] Multiple factors have been implicated in the greater severity of HAV infection in the elderly. Of these putative factors, an attenuated immune response due to age-related qualitative impairment of cell-mediated immune function has been postulated to be the most significant.[15] The more severe clinical course of HAV in the elderly is reflected in higher hospitalization rates and mortality. For example, during an outbreak of HAV infection in Memphis, TN, USA (1994–1995) 42% of individuals aged 70 years or older required hospitalization compared with 3–20% of adults aged 40–49 years.[17] Epidemiological data from the United Kingdom reveals mortality rates from HAV infection in individuals older than 75 years as high as 15%, which markedly contrasts with the very low mortality in adults aged 25–35 years (0.03–0.06%).[18] Case fatality rates due to HAV infection in the United States between 1983 and 1987 were lower than in the United Kingdom; however, age-related differences in outcomes were similar with 0.004% deaths in the 5–14 years of age group, and 2.7% in adults older than 49 years.[15,19] More recent data from the Centers for Disease Control and Prevention (2004–2007) show a downward trend in mortality from hepatitis A as the cause of death in all age groups. Importantly, the largest reduction in mortality associated with acute HAV infection (~50%) between 2004 and 2007 was observed in elderly adults aged ≥75 years. These data also confirm that mortality due to HAV increases with age with no fatalities reported in individuals younger than 34 years of age, 0.05 per 100,000 adults aged between 45–54 years, and 0.11 per 100,000 adults ≥75 years of age.[20] Higher mortality in elderly individuals was also noted during a HAV outbreak in Dallas County, TX, USA in 1999. Of the 232 reported cases of HAV, 25% occurred in individuals older than 60 years of age and the only two fatalities reported were in individuals older than 70 years.[15] Overall, the basis for worse outcomes in the elderly is thought to be multifactorial and influenced by higher prevalence of co-morbid conditions, decline in immune function, and reduced regenerative capacity of the liver with advanced age.[21] There are no specific data about age-related differences of the antibody-mediated response against HAV in the elderly; however, evidence suggests that older individuals have decreased antibody affinity against antigens in general.[22]

Although no formal recommendations from the Centers for Disease Control and Prevention for HAV vaccination in elderly adults have been issued, individuals without serological evidence of immunity to HAV should be considered candidates for immunization.[8] Data from the NHANES III indicate that the seroprevalence of anti-HAV IgG is >33% in adults older than 40 years of age in the United States; therefore, prevaccination screening for serological evidence of HAV immunity may be a cost-effective strategy.[13,23] In general, seroprotection from HAV vaccine is inversely related to age at the time of immunization. For example, 100% seroprotection has been reported in adults aged 18–45 years vs. 93% in adults older than 60 years of age based on the development of anti-HAV IgG antibodies following two doses of HAV vaccine.[21] In developed countries, HAV infection in adults has become less common; however, international travel, particularly to developing countries, remains a significant risk for acquisition. The median age of travelers from areas of low endemicity to areas of high endemicity is >40 years of age.[24] In addition, outbreaks of HAV infection continue to occur within the United States, most typically traced to an infected food handler or contaminated fruits or vegetables.[25,26] Thus, even in the absence of formal recommendations, there are cogent reasons to advise vaccination in HAV-naïve adults.

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