Viral Hepatitis in the Elderly
Viral Hepatitis in the Elderly
As life expectancy continues to rise, elderly adults represent a rapidly growing proportion of the population. The likelihood of complications of acute and chronic liver disease and overall mortality are higher in elderly populations. Several physiological changes associated with aging, greater prevalence of co-morbid conditions, and cumulative exposure to hepatotropic viruses and environmental hepatotoxins may contribute to worse outcomes of viral hepatitis in the elderly. Although pharmacotherapy for hepatitis B and C continues to evolve, the efficacy, tolerability, and side effects of these agents have not been studied extensively in elderly adults. Immunization against hepatitis A and B in naïve elderly adults is an important public health intervention that needs to be revised and broadened.
Viral hepatitis has some unique clinical characteristics in older individuals who comprise an increasingly large segment of the US population. According to data from the US Census Bureau 12.7% of the US population is older than 65 years of age. The "Baby Boom" generation refers to individuals born between 1946 and 1964 and is the largest birth cohort in the US history, reflecting a marked increase in births following World War II. As the first Baby Boomers started turning 65 in 2011, the US Census Bureau projects that the elderly population will increase twofold by 2030 (72 million people) and will comprise ~20% of the US population. There are important differences in the epidemiology, clinical presentation, and management of viral hepatitis in the elderly compared with younger individuals. For example, acute hepatitis A is more clinically severe in older individuals and, although acute hepatitis B and C are most commonly recognized in young adults with high-risk behaviors, acute infection can also occur in the elderly. With the aging of the cohort of individuals chronically infected with hepatitis C, it is anticipated that there will be an increasing burden of decompensated cirrhosis and hepatocellular carcinoma (HCC) for the next two decades. It is also well established that elderly individuals with viral hepatitis have higher mortality rates than younger patients, reflecting in part a higher prevalence of co-morbid conditions. Furthermore, physiological changes associated with aging, such as diminished immune response ("immune senescence"), metabolic derangements, nutritional deficiencies, and greater cumulative exposure to environmental hepatotoxins may also contribute to worse outcomes of viral hepatitis in the elderly. Among the multiple age-related changes of the liver, significant reductions of up to 30–40% in parenchymal volume, liver blood flow, and perfusion have been noted. Although there are no age-specific alternations in serum bilirubin levels, aminotransferases, and fractionated alkaline phosphatase levels, the hepatic metabolism of multiple substances (i.e., hepatic nitrogen clearance and aminopyridine demethylation) may be significantly impaired (up to 50%) with advanced age. The age-related decline of liver regeneration has been described in animal models in which the mitogenic capacity of hepatocytes is reduced with aging (up to 70% lower than in younger animals). This finding has also been recently corroborated in humans with significant reductions in liver regeneration noted in individuals older than 50 years compared with younger adults undergoing living donor liver transplantation.
Abstract and Introduction
Abstract
As life expectancy continues to rise, elderly adults represent a rapidly growing proportion of the population. The likelihood of complications of acute and chronic liver disease and overall mortality are higher in elderly populations. Several physiological changes associated with aging, greater prevalence of co-morbid conditions, and cumulative exposure to hepatotropic viruses and environmental hepatotoxins may contribute to worse outcomes of viral hepatitis in the elderly. Although pharmacotherapy for hepatitis B and C continues to evolve, the efficacy, tolerability, and side effects of these agents have not been studied extensively in elderly adults. Immunization against hepatitis A and B in naïve elderly adults is an important public health intervention that needs to be revised and broadened.
Introduction
Viral hepatitis has some unique clinical characteristics in older individuals who comprise an increasingly large segment of the US population. According to data from the US Census Bureau 12.7% of the US population is older than 65 years of age. The "Baby Boom" generation refers to individuals born between 1946 and 1964 and is the largest birth cohort in the US history, reflecting a marked increase in births following World War II. As the first Baby Boomers started turning 65 in 2011, the US Census Bureau projects that the elderly population will increase twofold by 2030 (72 million people) and will comprise ~20% of the US population. There are important differences in the epidemiology, clinical presentation, and management of viral hepatitis in the elderly compared with younger individuals. For example, acute hepatitis A is more clinically severe in older individuals and, although acute hepatitis B and C are most commonly recognized in young adults with high-risk behaviors, acute infection can also occur in the elderly. With the aging of the cohort of individuals chronically infected with hepatitis C, it is anticipated that there will be an increasing burden of decompensated cirrhosis and hepatocellular carcinoma (HCC) for the next two decades. It is also well established that elderly individuals with viral hepatitis have higher mortality rates than younger patients, reflecting in part a higher prevalence of co-morbid conditions. Furthermore, physiological changes associated with aging, such as diminished immune response ("immune senescence"), metabolic derangements, nutritional deficiencies, and greater cumulative exposure to environmental hepatotoxins may also contribute to worse outcomes of viral hepatitis in the elderly. Among the multiple age-related changes of the liver, significant reductions of up to 30–40% in parenchymal volume, liver blood flow, and perfusion have been noted. Although there are no age-specific alternations in serum bilirubin levels, aminotransferases, and fractionated alkaline phosphatase levels, the hepatic metabolism of multiple substances (i.e., hepatic nitrogen clearance and aminopyridine demethylation) may be significantly impaired (up to 50%) with advanced age. The age-related decline of liver regeneration has been described in animal models in which the mitogenic capacity of hepatocytes is reduced with aging (up to 70% lower than in younger animals). This finding has also been recently corroborated in humans with significant reductions in liver regeneration noted in individuals older than 50 years compared with younger adults undergoing living donor liver transplantation.
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