Dr.Azad A Haleem AL.MezoriDCH, FIBMS

Lecturer University Of Duhok

Faculty of Medical ScienceSchool Of Medicine-Pediatrics Department

2015azad82d@gmail.com

Hepatitis in children

Hepatitis

Hepatitis• Definition: Acute hepatitis is defined as less than 6 months of liver

inflammation, and chronic hepatitis indicates an inflammatory process which has been present for 6 or more months.

Hepatitis• ETIOLOGY:• There are five primary hepatotropic viruses, which differ in their

virologic characteristics, transmission, severity, likelihood of persistence, and subsequent risk of hepatocellular carcinoma .

• HAV and hepatitis E virus (HEV) are transmitted by the fecal-oral route.

• HBV, HCV, and hepatitis D virus (HDV) are transmitted parenterally by IV drug use and sexual and perinatal modes.

• HDV, also known as the delta agent, is a defective virus that requires HBV for spread and causes either coinfection with HBV or superinfection in chronic HBsAg carriers.

• HBV, HCV, and HDV infections can result in chronic hepatitis, or a chronic carrier state, which facilitates spread.

• EPIDEMIOLOGY:• 70% to 80% of all new cases of viral hepatitis are related

to HAV, • 5% to 30% are related to HBV, • and 5% to 15% are related to HCV. • The major risk factors for HBV and HCV are injection drug

use, frequent exposure to blood products (hemophilia, organ transplants, chronic renal failure), and maternal infection.

• HBV and HCV cause chronic infection, which may lead to cirrhosis and is a significant risk factor for hepatocellular carcinoma and represents a persistent risk of transmission.

• CLINICAL MANIFESTATIONS :• There is considerable overlap in the characteristic clinical courses for

HAV, HBV, and HCV . • The preicteric phase, which lasts approximately 1 week, is

characterized by headache, anorexia, malaise, abdominal discomfort, nausea, and vomiting and usually precedes the onset of clinically detectable disease.

• Jaundice and tender hepatomegaly are the most common physical findings and are characteristic of the icteric phase. Prodromal symptoms, particularly in children, may abate during the icteric phase.

• Asymptomatic or mild, nonspecific illness without icterus is common with HAV, HBV, and HCV, especially in young children.

• Hepatitic enzymes may increase 15-fold to 20-fold. • Resolution of the hyperbilirubinemia and normalization of the

transaminases may take 6 to 8 weeks.

LABORATORY AND IMAGING STUDIES

• Alanine aminotransferase and aspartate aminotrans-ferase levels are elevated and generally reflect the degree of parenchymal inflammation.

• Alkaline phosphatase, 5'-nucleotidase, and total and direct (conjugated) bilirubin levels indicate the degree of cholestasis, which results from hepatocellular and bile duct damage.

• The prothrombin time is a good predictor of severe hepatocellular injury and progression to fulminant hepatic failure

• Hepatitis A : The diagnosis of viral hepatitis is confirmed by characteristic serologic testing .

• The presence of IgM-specific antibody to HAV with low or absent IgG antibody to HAV is presumptive evidence of HAV.

• There is no chronic carrier state of HAV.• Hepatitis C : • Serocon-version after HCV infection may occur 6 months after

infection. • A positive result of HCV ELISA should be confirmed with the

more specific recombinant immunoblot assay, which detects antibodies to multiple HCV antigens.

• Detection of HCV RNA by PCR is a sensitive marker for active infection, and results of this test may be positive 3 days after inoculation.

• Hepatitis B:• The presence of HBsAg signifies acute or chronic infection with HBV. • Antigenemia appears early in the illness and is usually transient, but also is

diagnostic of the carrier state. • Hepatitis B e antigen (HBeAg) appears in the serum with acute HBV. • The continued presence of HBsAg and HBeAg in the absence of antibody to e

antigen (anti-HBe) indicates high risk of transmissibility that is associated with ongoing viral replication.

• Clearance of HBsAg from the serum precedes a variable window period followed by the emergence of the antibody to surface antigen (anti-HBs), which indicates development of lifelong immunity.

• Antibody to core antigen (anti-HBc) a useful marker for recognizing HBV infection during the window phase (when HBsAg has disappeared, but before the appearance of anti-HBs).

• Anti-HBe is useful in predicting a low degree of infectivity during the carrier state.

Typical course of hepatitis B infection. After exposure to hepatitis B virus (HBV; arrow), the earliest detectable serum marker is a rise in HBsAg, which may appear at any time (weeks 1 to 10) postexposure; HBV DNA and HBAg follow closely. HBeAg is detectable 2 to 8 weeks before the onset of the symptomatic phase, which is heralded by an increase in alanine aminotransferase (ALT) levels, serum bilirubin concentrations, and constitutional signs. Clearance of HBsAg by immune aggregation with anti–hepatitis B core antigen (HBc) occurs by 6 to 8 months postinfection; those who fail to clear are termed HBsAg carriers. Anti-HBc, which appears just before the symptomatic phase, is the first detectable, host-induced immunologic marker of hepatitis B infection. Anti-HBc of the IgM class may be the only marker of HBV infection in serum after clearance of HBsAg and before a rise in anti-HBs. Anti-HBc is not a neutralizing antibody and therefore, in contrast to anti-HB, is not protective.

TREATMENT• The treatment of acute hepatitis is largely supportive and

involves rest, hydration, and adequate dietary intake. • Hospitalization is indicated for persons with severe

vomiting and dehydration, a prolonged prothrombin time, or signs of hepatic encephalopathy.

• When the diagnosis of viral hepatitis is established, attention should be directed toward preventing its spread to close contacts.

• For HAV, hygienic measures include hand washing and careful disposal of excreta, contaminated diapers or clothing, needles, and other blood-contaminated items.

• Chronic HBV infection may be treated with interferon alfa-2b or lamivudine,

• and HCV may be treated with interferon alfa alone or more often in combination with oral ribavirin.

TREATMENT

COMPLICATIONS

• A protracted or relapsing course may develop in 10% to 15% of cases of HAV in adults, lasting for 6 months with an undulating course before eventual clinical resolution.

• Fulminant hepatitis with hepatic encephalopathy, gastrointestinal bleeding from esophageal varices or coagulopathy, and profound jaundice is uncommon, but is associated with a high mortality rate.

PROGNOSIS• Most cases of acute viral hepatitis resolve without specific therapy, with

less than 0.1% of cases progressing to fulminant hepatic necrosis. • HBV, HCV, and HDV may persist as chronic infection with chronic

inflammation, fibrosis, and cirrhosis and the associated risk of hepatocellular carcinoma.

• Five percent to 10% of adults with HBV develop persistent infection, defined by persistence of HBsAg in the blood for more than 6 months compared with 90% of children who acquire HBV by perinatal transmission.

• Approximately 85% of persons infected with HCV remain chronically infected, which is characterized by fluctuating transaminase levels.

• Approximately 20% of persons with chronic infection develop cirrhosis, and approximately 25% of those develop hepatocellular carcinoma.

Prevention of hepatitis B

• Hepatitis B vaccine and hepatitis B immunoglobulin (HBIG) are available for prevention of HBV infection.

• Hepatitis B Immunoglobulin • HBIG is indicated only for specific postexposure

circumstances and provides only temporary protection (3-6 mo) . It plays a pivotal role in preventing perinatal transmission when administered within 12 h of birth.

• Two single antigen vaccines (Recombivax HB and Engerix-B) are approved for children and are the only preparations approved for infants <6 mo old.

• Three combination vaccines can be used for subsequent immunization dosing and enable integration of the HBV vaccine into the regular immunization schedule.

• Seropositivity is >95% with all vaccines, achieved after the 2nd dose in most patients. The 3rd dose serves as a booster and may have an effect on maintaining long-term immunity.

• In immunosuppressed patients and infants <2,000 g birthweight, a 4th dose is recommended, as is checking for seroconversion.

HbsAg-positive mothers?• To prevent perinatal transmission through improved maternal screening and

immunoprophylaxis of infants born to HbsAg-positive mothers, infants born to HBsAg-positive women should receive vaccine at birth, 1-2 mo, and 6 mo of age.

• The first dose should be accompanied by administration of 0.5 mL of HBIG as soon after delivery as possible (within 12 hr) because the effectiveness decreases rapidly with increased time after birth.

• Post-vaccination testing for HBsAg and anti-HBs should be done at 9-18 mo. • If the result is positive for anti-HBs, the child is immune to HBV. • If the result is positive for HBsAg only, the parent should be counseled and the

child evaluated by a pediatric gastroenterologist. • If the result is negative for both HBsAg and anti-HBs, a 2nd complete hepatitis B

vaccine series should be administered, followed by testing for anti-HBs to determine if subsequent doses are needed.