Pediatric Hepatitis C

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 (see Treatment).

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. Clinicians may also need to be aware of how to counsel parents of children exposed to HCV in utero. Even though most of these children will remain uninfected or clear their infection, considerable anxiety may be involved.

Most studies performed to further delineate the natural history of HCV have involved adult cohorts; therefore, further research on the ultimate outcome of infection during childhood is clearly needed.

See also Pediatric Hepatitis A and Pediatric Hepatitis B.

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.

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 or hepatitis B virus. ^[1]

Density of viral infection with hepatitis C virus affects the likelihood of transmission from mother to child in utero. While density of approximately 100 particles per milliliter produced no vertical transmission to the baby, 1 million particles per milliliter resulted in a transmission rate of 36%. ^[2] Overall, transmission to babies was 6% in mothers who were hepatitis C virus antibody–positive and 10% in mothers who were hepatitis C virus RNA–positive. 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.

An estimated 30,000 new hepatitis C infections occur annually in the United States, 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. Although the worldwide prevalence varies considerably by geographic region, more than 3% of the global population is infected.

Race-, sex-, and age-related demographics

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, but patients of African descent do not respond as well to therapy.

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 from 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. ^[3]

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 hepatocellular carcinoma.

Acute fulminant hepatitis C virus infection is rare, but more than 80% of acutely infected individuals develop chronic hepatitis. Most patients chronically infected with hepatitis C virus remain asymptomatic and do not have significant liver disease. The prognosis is guarded for those who have hepatitis C virus–related complications such as hepatocellular carcinoma and liver failure.

In more than 20% of adults with chronic infection, progression to cirrhosis occurs an average of 20 years after initial infection. Cirrhosis poses 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. Annually, hepatitis C virus infection accounts for 8,000-10,000 deaths in the United States.

Instruct the patient to avoid all alcohol use. Inform the infected patient about the health practices listed in Deterrence/Prevention. The patient and other household members should be vaccinated against hepatitis A and B viruses.

For patient education information, see the Hepatitis Center and Liver, Gallbladder, and Pancreas Center, as well as Hepatitis C.