eMedicine Specialties > Pediatrics: General Medicine > Infectious Disease

Hepatitis C

Author: Nicholas John Bennett, MBBCh, PhD, Staff Physician, Department of Pediatrics, State University of New York Upstate Medical University
Coauthor(s): Joseph Domachowske, MD, Professor of Pediatrics, Microbiology and Immunology, Department of Pediatrics, Division of Infectious Diseases, State University of New York-Upstate Medical University; Donald K Strickland, MD, National Liaison, Avastin, Genentech BioOncology
Contributor Information and Disclosures

Updated: Aug 12, 2008

Introduction

Background

Hepatitis C virus (HCV) is one of 6 viruses (along with hepatitis A, B, D, E, and G viruses) that cause viral hepatitis. Prior to identification of the virus, it was termed non-A/non-B hepatitis to distinguish it from the viral causes of nonalcoholic hepatitis that were known at the time.

Several distinct genotypes of hepatitis C virus have been identified, and genotyping has proven to be a useful clinical tool because the response to therapy and prognosis is influenced by the viral genotype. Genotype 1 is less than half as likely as other genotypes to respond to therapy, and the combination therapy regimens vary depending on the different genotypes (see Medication).

Unfortunately, most patients have chronic infection and are at risk for progressive liver disease. Furthermore, diagnosis primarily relies on identifying the risk factors of transmission because infected individuals typically have few or no symptoms. Once hepatitis C virus infection is diagnosed, current treatment options for eradication are limited and often result in significant adverse effects.

Although hepatitis C virus infection is uncommon in the pediatric population, the caregiver should be familiar with the basic concepts. For example, patients transfused as recently as July 1992 may have been exposed to the virus. Furthermore, vertical transmission of hepatitis C virus is possible. Most studies performed to further delineate the natural history have involved adult cohorts; therefore, further research on the ultimate outcome of infection during childhood is clearly needed.

Pathophysiology

Hepatitis C virus is a member of the Flaviviridae family of RNA-containing viruses; thus, it is not integrated into the host genome. Although the liver is the primary target of infection, studies to better define the steps of hepatitis C virus infection are greatly hampered by the lack of a suitable animal model for such studies (the only animal known to be susceptible to hepatitis C virus is the chimpanzee). A tissue-culture system using recombinant DNA technology was recently developed and has advanced the scientific knowledge base considerably, including early forays into vaccine development.

The primary immune response to hepatitis C virus is mounted by cytotoxic T lymphocytes. Unfortunately, this process fails to eradicate infection in most people; in fact, it may contribute to liver inflammation and, ultimately, tissue necrosis. The ability of hepatitis C virus to escape immune surveillance is the subject of much speculation. One likely means of viral persistence relies on the presence of closely related but heterogeneous populations of viral genomes. Further studies of these quasi-species enable classification of several genotypes and subtypes, which may have clinical implications.

Frequency

United States

An estimated 30,000 new infections occur annually, although only 25-30% are diagnosed. Since the 1980s, acute infections have declined by more than 80%. Nearly 4 million Americans, or about 2% of the US population, are infected with hepatitis C virus.

International

Although the worldwide prevalence varies considerably by geographic region, more than 3% of the global population is infected.

Mortality/Morbidity

• Acute fulminate infection is rare. More than 80% of acutely infected patients have chronic hepatitis C virus. Annually, it accounts for 8,000-10,000 deaths in the United States.
• In more than 20% of adults with chronic infection, progression to cirrhosis occurs an average of 20 years after initial infection. Patients with this condition have a secondary risk of portal hypertension, liver failure, and other complications. Hepatitis C is now the leading reason for liver transplantation in the United States.
• In 1-5% of patients, most of whom have underlying cirrhosis, hepatocellular carcinoma (HCC) is diagnosed an average of 30 years after initial hepatitis C virus infection.

Race

• With respect to the frequency of infection worldwide, significant racial differences are observed.
• In the United States, infection is more common among members of minority populations than in other groups.
• The effect of ethnic background on the risk of significant liver disease is undefined.

Sex

• Hepatitis C virus infection is far more common in males than in females.
• Females have been reported to have a higher rate of infection from blood product transfusions and a lower rate of intravenous drug and alcohol abuse compared with males.
• Females may have less evidence of liver damage (liver enzyme levels, fibrosis) and high rates of spontaneous viral clearance.¹

Age

• In the United States, the highest incidence is among individuals aged 20-39 years, and the highest prevalence is among those aged 30-49 years.
• The age at time of initial infection likely has important implications on the natural history of infection because individuals who are infected at a younger age tend to have a decreased risk of progression to cirrhosis and HCC.

Clinical

History

• The incubation period widely varies, with a mean of 7-10 weeks and a range of 2-20 weeks.
• Infections are often inapparent or subclinical. Only 25-35% of patients have nonspecific symptoms such as weakness, malaise, and anorexia; likewise, patients with chronic hepatitis C virus (HCV) often have few or no symptoms. Fatigue is reported most often.

Physical

• Approximately 25% of patients with acute infection have jaundice, whereas less than one third have hepatomegaly.
• Some patients with chronic infection have findings consistent with chronic liver disease; these include hepatomegaly, ascites, splenomegaly, and spider nevi.

Causes

• Direct percutaneous exposure is the primary means of transmission.
• Blood transfusions are another means of transmission.
  • Historically, most hepatitis C virus infections result from blood transfusions.
  • The risk of transfusion-borne hepatitis C virus began to decline in 1986, when surrogate-marker screening of blood donors started.
  • Further declines were noted after the introduction of hepatitis C virus–directed antibody screening in 1990 (first generation) and 1992 (second generation).
  • The current risk of transfusion-derived hepatitis C virus is estimated to be 1 case in every 100,000 units transfused.
• Currently, the use of injected drugs is the most important epidemiologic risk factor, probably accounting for around 50% of both acute and chronic infections.
• Other parenteral routes may be involved.
  • Hemodialysis is a possible cause of hepatitis C virus infection.
  • Health care employees may be accidentally exposed.
  • Tattooing, body piercing, and acupuncture with unsterile equipment are possible routes of infection.
• The risk of sexual transmission appears to be low, even among individuals with multiple sex partners; however, the presence of coexisting sexually transmitted diseases (eg, human immunodeficiency virus [HIV] infection) appears to increase the risk.
• Vertical transmission may occur.
  • Perinatal transmission is possible and affects an estimated 5% of babies born to mothers with hepatitis C virus infection.
  • The risk is higher for babies born to mothers who are co-infected with hepatitis C virus and HIV.
  • Breastfeeding is not contraindicated for mothers with hepatitis C virus infection.
• Approximately 10% of adults with hepatitis C virus infection have no identified risk factor for infection; this frequency is probably higher among pediatric patients.

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