Pediatric hepatitis D

Introduction to pediatric hepatitis B virus Viral hepatitis (viralhepatitis type D) is an acute and chronic hepatic inflammatory disease caused by hepatitis D virus (HDV), a defective virus that can only be present in HBV-infected humans and certain hepadnavirus surface antigens. Among the positive animals, there is very little HDV infection alone, and the clinical manifestations of hepatitis D depend to some extent on the accompanying HBV infection status. basic knowledge The proportion of illness: 0.0006% Susceptible people: children Mode of transmission: blood transmission, contact transmission Complications: chronic hepatitis

The cause of pediatric hepatitis B virus

(1) Causes of the disease

The intact HDV particles are spherical, 35-37 nm in diameter, containing HDV RNA and HDAg, and the outer shell is HBsAg. HDV RNA is the genome of HDV, consisting of 1679-1683 nucleotides, which is single-stranded, circular, and Folded into a non-branched rod-like structure, HDV-RNA has 9 coding regions (ORF), ORF5 encodes HDAg, HDAg is a nuclear protein that enables the body to induce anti-HDIgM and anti-HDIgG, anti-HDIgM Earlier, it is usually positive in the early stage of acute HDV infection, and the recovery period gradually disappears. The high titer of anti-HDIgM indicates chronic disease, and anti-HD IgG appears later, and it can be maintained for many years after 3 to 8 weeks after onset. Low titer positive, anti-HDIgG increased when the disease activity, the current infection often showed anti-HDIgM positive, the previous infection was anti-HDIgM negative, and anti-HDIgG positive, anti-HD is not neutralizing antibody, still positive It can be contagious.

HDV infection can significantly inhibit the synthesis of HBV DNA. Serological tests show that HDAg is consistent with the decrease of HBV DNA in serum. When HDAg expression is increased, HBV DNA is decreased. When HDAg expression is at a peak, HBV DNA often disappears, but with With the appearance of HDAg-negative and anti-HD, HBV DNA returned to its original level. It was previously thought that the assembly of HDV relied on the synthesis of HBsAg, and its replication and expression also required the assistance of HBV or other hepadnaviruses. The replication of HDV-RNA and the expression of HDAg do not require the help of hepadnavirus. HDV itself can be done independently, but in the formation of intact HDV, it must be provided by a hepadna virus.

(two) pathogenesis

The pathogenesis of hepatitis D has not yet been clarified, and it is likely that both the direct pathogenic effect of HDV and the host immune response are mediated.

HDV may be similar to the same mechanism of HBV. It is infected with hepatocyte receptors by the presence of HBsAg-containing Pre-S1 protein and Pre-S2 protein, and most of the HDAg-positive hepatocytes have different degrees of lesions. Hybridization showed that HDV RNA in hepatocytes was distributed in areas with obvious hepatocyte lesions; human hepatoblastoma HepG cell line was transfected with HDAg recombinant plasmid for culture, and a large amount of HDAg expression was observed in a short period of time, followed by transfected cell line. Necrosis occurs. These experimental results indicate that HDV has a strong direct cytotoxic effect, and clinical data show that there are asymptomatic carriers with no obvious liver lesions when HDV and HBV overlap infection; liver tissue with liver pathological HDV infection, sink Inflammation cells can be seen in the tube area, lymphocyte infiltration in the liver parenchyma and lymphocyte pseudopods protruding into the liver cells. HDAg may be the target antigen for immune response attack, which is related to the immune response.

Pediatric viral hepatitis prevention

At present, there is no hepatitis D vaccination. Because hepatitis D virus is a defective virus, it must rely on hepatitis B virus to replicate. It can protect against HBV infection by preventing hepatitis B virus infection. It is an effective means to control HDV infection and is widely vaccinated by susceptible people. Hepatitis B vaccine can achieve the purpose of preventing HDV infection. For HBsAg-positive people to re-infect HDV, it is necessary to minimize blood transfusion, no or less blood products, strict screening of blood donors and medical equipment disinfection management can reduce HDV transmission, with The research on new vaccines will improve the existing hepatitis B gene vaccine to prevent both HBV infection and HDV infection. The nucleic acid vaccine against HDV will be vaccinated in the near future.

Pediatric viral hepatitis complications Complications chronic hepatitis

Development of chronic hepatitis, prone to acute or subacute severe hepatitis, leading to liver failure.

Children with viral hepatitis symptoms common symptoms

1. HDV and HBV simultaneous infection (co-infection) incubation period of 6 to 12 weeks, mostly manifested as acute jaundice, ALT can be bimodal, due to the two viruses mutually restricting, the condition is often self-limiting, good prognosis.

2. HDV and HBV overlap infection (superinfection) The incubation period is 3 to 4 weeks. The clinical manifestations are related to the original HBV infection status. The general trend is that the original liver disease is aggravated. The original asymptomatic HBsAg carriers are mostly acute hepatitis or Developed into chronic hepatitis; the original chronic hepatitis is exacerbated, prone to acute or subacute severe hepatitis.

Examination of pediatric hepatitis B virus

Etiology check:

1. HDV Ag examination serum HDV Ag positive is the direct evidence for the diagnosis of acute infection. In acute hepatitis, the duration of antigenemia lasts an average of 21 days. The positive rate is 87% and 100% by ELISA and RIA, respectively. The antigen persists, but it is mostly in the form of immune complexes. It needs to be analyzed by immunoblotting. The detection of HDV Ag in the liver is more direct diagnostic value.

2. Anti-HDV determination Anti-HDV IgM occurs in the early stage of acute phase, and the chronic infection period is persistently high. Once the virus is eliminated, the antibody decreases rapidly, and the anti-HDV IgG is lower than the 3-8 weeks after the onset; the chronic infection continues to be high. concentration.

3. HDV RNA examination can detect HDV RNA in serum or liver tissue by dot blot hybridization or RT-PCR, which is a reliable indicator for the diagnosis of HDV infection.

Regular abdominal B ultrasound, understand the liver and other conditions.

Diagnosis and diagnosis of pediatric hepatitis B virus

diagnosis

For patients with hepatitis B, when HBsAg carriers are significantly fluctuating or progressively worsening, and patients with severe hepatitis should consider the possibility of simultaneous or overlapping HDV infection, the diagnosis depends on laboratory tests.

1. Patients with acute HDV/HBV infection at the same time, except for acute HBV infection markers, serum anti-HDIgM positive, anti-HDIgG low titer positive; or serum and/or intrahepatic HDAg, HDV-RNA positive.

2. HDV/HBV overlap infection in patients with chronic hepatitis B or chronic HBsAg carriers, serum HDV-RNA and/or HDAg-positive; or anti-HDIgM and anti-HD IgG high titer positive; or intrahepatic HDV-RNA and Or) HDAg positive.

Differential diagnosis

There are many causes of liver damage in childhood, which may be caused by infectious diseases, or due to non-infectious causes and genetic metabolic diseases. The key is to detect the existence of hepatitis B virus or other antigens.

1. Cytomegalovirus hepatitis is the most common pathogen in infant hepatitis syndrome, which can be acute onset, jaundice, hepatomegaly, liver function damage and prolonged unhealed. When CMV infection is manifested as liver damage, clinically and B Hepatitis is more difficult to identify, but CMV hepatitis is more obvious than hepatitis B, and more often accompanied by splenomegaly. When the spleen enlarges or even exceeds the liver, it is mostly non-B hepatitis. The serum CMV DNA is positive or anti-CMV. IgM is positive.

2. Toxic hepatitis and liver abscess caused by bacterial infection of toxic hepatitis and liver abscess are mainly caused by symptoms of infection, such as high fever, poisoned face, symptoms of toxemia or sepsis, peripheral blood leukocyte count >20×109 /L, the classification is mainly neutrophils, blood culture is easy to grow to pathogenic bacteria.

3. Kawasaki disease liver damage can occur jaundice, and jaundice can also be very deep, liver enlargement, liver function damage and gastrointestinal reactions, difficult to distinguish from acute hepatitis B early severe disease, the disease usually fever continues to retreat, with the ball Combined with membrane congestion, lip flushing, strawberry tongue, pharyngeal congestion, hard edema of the hands and feet, erythema of the palm of the hand, membrane-like desquamation of the nails, and shallow lymph node enlargement, although serum albumin is low, but often There is an increase in platelets.

4. Liver type - hepatolenticular degeneration disease This type is mainly liver damage, showing hepatosplenomegaly, liver area tenderness, gastrointestinal reactions can be nausea, vomiting, jaundice is deepening, may have bleeding tendency, can be presented Subacute severe hepatitis, severe liver failure, pediatric clinical severe liver damage need routine detection of serum ceruloplasmin, the disease content is significantly lower than 200mg / L, once low, then detect serum copper oxidase activity, also shows low 24h urinary copper, the child can be as high as 100 ~ 1000g, the children around the cornea have copper particles deposited, ring-shaped, called KF ring, observed under the ophthalmic slit lamp can be diagnosed.

5. common biliary obstruction in children because of common bile duct stricture and common bile duct stones, more common in children to preschool children, once encountered a child due to jaundice, liver damage, hospitalized for viral hepatitis, not detected The pathogen, due to jaundice subsided, liver function returned to hospital, and due to fever, abdominal pain, jaundice, mild liver enlargement and re-admitted to hospital, jaundice is deep, accompanied by fever, with the infection control jaundice subsided faster, by B-mode ultrasound examination found Gallbladder enlargement and extrahepatic bile duct obstruction, in addition to 99Tc radionuclide scan, showed the presence of nuclear retention and obstruction, confirmed by laparotomy and radical.

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