Neonatal hepatitis B

Introduction to neonatal hepatitis B Hepatitis B is caused by hepatitis B virus infection, and hepatitis virus infection in the neonatal period mainly refers to HBV infection. Most of them are chronic, often unsustainable, and become chronic carriers or chronic hepatitis, which seriously affects children's health. The relationship between this disease and chronic liver failure has gradually attracted people's attention. China is a high-risk area of hepatitis B. It is estimated that about 100 million people in the country are infected with hepatitis B. basic knowledge The proportion of sickness: 0.01% Susceptible people: children Mode of transmission: blood transmission mother-to-child transmission Complications: chronic hepatitis, liver cirrhosis, hepatic encephalopathy

Neonatal hepatitis B cause

(1) Causes of the disease

Neonatal infection with HBV is mainly caused by vertical transmission and horizontal transmission of mother and child.

1. Mother-to-child transmission: The vertical transmission of mother and baby includes:

(1) Transplacental transmission: The mother may be infected with HBV during pregnancy or a chronic HBV carrier, and the virus may be transmitted to the fetus.

(2) Infection through the birth canal: When the newborn is delivered, it is infected by swallowing vaginal fluid with HBV.

(3) Infection by breast milk: Newborns are infected with breast milk of HBsAg-positive mothers and are infected.

(4) Close contact after birth: Infected with infected mother's saliva, colostrum, sweat, bloody secretions, and infected.

The chance of infection in children is closely related to the viral infectivity of the mother during childbirth. For example, the pregnant mother delivers in the acute phase of hepatitis B, and the fetus and 60% to 70% of the infants within 2 months after delivery are infected, and the mother is HBsAg positive. The incidence of mother-to-child transmission in HBV carriers with or without symptoms is very low in Europe and North America, while in Asia it is as high as 40% to 50%. The mother is carrier and the e antigen (HBe) is positive. % to 85% of babies are infected.

2. Horizontal transmission: mainly injecting and infusion of blood products and living in close contact with the spread. In addition, after the newborn is born, it can also be infected by the contact and ingestion of surrounding patients, carriers, and viral contaminants. Whether the baby is a carrier of hepatitis B virus, Rosendaht believes that it depends on the baby's race, and may be different from different races.

(two) pathogenesis

It is generally believed that HBV has no direct damage to liver cells. The pathological changes of hepatocytes are mainly caused by the body's immune response to infected liver cells. In HBV infection, viral antigens are taken up by mononuclear macrophages, processed and presented to Th cells. Th cells activate and proliferate and release interleukin-2 (IL-2). IL-2 stimulates the clonal proliferation of Tc cells sensitized by HBV antigen, forming a large number of effector T cells and attacking hepatocytes infected with HBV. Degeneration and necrosis of hepatocytes, target antigens attacked by Tc cells, mainly HBcAg and HBeAg on hepatocyte membrane, only hepatocytes expressing both target antigen and MHC class I antigen are recognized, attacked and destroyed by Tc cells, interference Both can enhance the expression of MHC class I antigen in hepatocytes, the recognition and binding of Tc cells to target hepatocytes, and the involvement of adhesion molecules. Fas antigen is expressed on the surface of infected liver cells, while FasL is expressed on the surface of activated Tc cells.

When the two are combined, the hepatocyte nuclear program-killing gene is initiated to cause apoptosis, and HBV infection can denature the hepatocyte membrane-specific lipoprotein (LSP) to form a "self antigen", which stimulates B cells to produce corresponding IgG antibodies, IgG antibodies The Fab end binds to the hepatocyte membrane LSP, and its Fc end binds to the killer cell (K cell) Fc receptor, which activates K cells to kill hepatocytes, ie, antibody-dependent cell-mediated cytotoxicity (ADCC), which is an autoimmune response. The onset of various types of hepatitis depends on the immune status of the body and the relationship between the growth and decline of hepatitis B virus. It is generally believed that after normal HBV infection, functional Tc cells attack infected liver cells, and specific antibodies are cleared from the lysed liver. The HBV released by the cells, the virus is cleared, the infection is terminated, and the clinical manifestation is acute hepatitis; the hyperthyroidism, due to the premature and anti-HBs production, rapidly destroys a large number of hepatocytes, forming an immune complex with excess antibody, leading to local allergic necrosis. Reacts to cause acute or subacute hepatitis; when immunity is low, due to insufficient production of anti-HBs, HBV cannot be effectively eliminated, making HBV follow Violations of new liver cells, slow the formation of hepatitis or chronic HBV carrier status, children are mostly due to the immune system is not yet mature, and often become chronic hepatitis B and chronic HBV carriers.

Neonatal hepatitis B prevention

Blocking mother-to-child transmission is a key measure to reduce and ultimately eliminate the chronic carryover of HBsAg, including active and passive immunization.

1. Passive immunization: Hepatitis B vaccine is given at the end of 1 month and at the end of 6 months. The dose is determined according to different products. The anti-HBs produced can last for more than 3 years, and will be strengthened once every 5 years. Infants born in the acute or concomitant phase of hepatitis B (regardless of e antigen positive or negative), regardless of whether HBsAg is measured or not, the use of specific high-potency immunoglobulin (hepatitis B human immune serum globulin, HBIG) can make infant hepatitis B virus The carrying rate is greatly reduced. The method is as follows: within 4 hours of birth, 3 months, and 6 months, each time 0.5 to 1 ml/kg (containing more than 100 U/ml of anti-HBs), when the passive immune antibody disappears quickly. Later, it became a susceptible person, but the carrying rate was significantly reduced. In 1983, China reported that the protective rate of hepatitis B immunoglobulin developed by Changhai Institute of Biological Products to block mother-to-child transmission was 61.2%, and HBsAg positive carriers. It is not advisable to give breast milk, and the newborn should be isolated and observed. Passive immunization should be used first.

2. Active immunization: Hepatitis B immunoglobulin (HBIG) is a passive immunization with rapid protection. HBeAg or HbsAg-positive mothers should be injected with HBIG 1ml immediately after birth (no later than 24h), at 1, 2, 3 Hepatitis B vaccine was given once a month.

For the application of hepatitis B vaccine, there are currently blood-borne and genetically recombined (half-half) hepatitis B vaccines prepared from human blood, HBsAg-positive newborns born with HBeAg-positive or HBV-DNA-positive mothers, if no special Preventive measures, 80% to 96% of children can become HBsAg positive 3 to 6 months after birth, HBsAg-only, especially when the HBsAg titer is low or hepatitis B e antibody is positive, its contagiousness is very low, or even not contagious. Hepatitis B vaccine vaccination has been carried out in some areas of China. The method is for children born to HBsAg-positive and/or HBeAg-positive mothers within 24 hours (or 7 days), 1 month, and 6 months after birth. Vaccination 1 time, each time 20 ~ 30g, foreign authors reported that each time with 5g or 2g vaccination, the same immune response, injection of local over-excited no other side effects, occasional allergic reactions.

If only vaccination is used, the protection rate is about 70%. In particular, at least 30% of infants with HBeAg-positive mothers will become carriers of HBsAg. The automatic immune response from HBIG-interfering vaccine is not obvious. Currently, the method of co-injection with hepatitis B vaccine and HBIG is preferred. For example, infants with HBeAg-positive mothers can protect 95% of the infants by the above-mentioned combined injections. The comparison of various regimens in Beijing is best with 3 hepatitis B vaccines and 3 HBIG combined injections, but there are also reports that passive - Active or active vaccination has similar effects, so more observations and summaries are needed.

The currently recommended methods are:

(1) HBIG 0.5 ml intramuscular injection within 24 hours after birth.

(2) Hepatitis B vaccine 0.5ml (10g) and HBIG at the same time or within 7 days after birth, intramuscular injection on the other side, and then once every 1 and 6 months, this method can make 85% to 93% of infants get Protection, hepatitis B surface antigen antibody titer is still high in 1 to 2 years old, anti-HBs can last for 3 to 5 years, so a dose of 10g booster vaccination in 3 to 5 years is meaningful to prevent HBV level transmission in children, immunization HBsAg positive in the last 6 months showed immunological failure. If the baby was positive for 15 months, the infant was chronic carriers. For example, HBsAg-negative anti-HBe positive infants were protected for 15 months.

Neonatal hepatitis B complications Complications chronic hepatitis cirrhosis hepatic encephalopathy

Often complicated by vitamin A, D deficiency, a small number of patients have a tendency to develop chronic hepatitis, cirrhosis, or complicated with hepatic encephalopathy, liver failure, etc., it should be diagnosed and treated early.

Newborn hepatitis B symptoms Common symptoms Skin yellow jaundice sclera yellow stained large liver cell necrosis small Sanyang splenomegaly gray white stool poor appetite liver swelling yellow urine like strong tea

Once infected, there are several weeks to 6 months of incubation, and most infected infants exhibit a subclinical process.

The onset is slow and the newborn is asymptomatic at birth. Chronic antigenemia and transaminase persistence in 1 to 6 months, mildly elevated, sometimes HBsAg antibodies were detected at 6 to 12 months, and neonatal hepatitis B was mainly characterized by jaundice. Can be expressed as a delay in the disappearance of jaundice after birth, or recurs, or gradually deepen, some cases of clinical symptoms, such as jaundice (early obstructive jaundice), fever, liver, poor appetite, and then recover or present Chronic hepatitis, also manifested as persistent obstructive jaundice, sclera and skin yellow staining, urine darkening such as brown, stool color decreased or terracotta color, liver, splenomegaly, mainly liver enlargement, weight loss The urine color is deep. Most patients have no other clinical symptoms at birth, and generally do not affect fetal development, nor teratogenic, or even liver function and serological changes.

A small number of fulminant passes, jaundice appears rapidly increased, short-term development of hepatic encephalopathy, hemorrhage and other symptoms of liver failure, rapid death, poor prognosis, if you can survive, liver tissue can be restored to normal.

Examination of neonatal hepatitis B

1. Liver function test: Liver function may be normal or only mild abnormality in neonatal hepatitis, serum alanine aminotransferase (ALT, GPT) begins to rise in the early stage of jaundice, peak in serum bilirubin peak Previously, it continued until a few weeks after the jaundice subsided. Serum bilirubin began to increase at the end of the jaundice. Most of the whitening tests were biphasic positive. The urinary bilirubin and urinary bilirubin at the end of the jaundice began to show a positive reaction. An important basis for early diagnosis.

2. Hepatitis B serum marker detection: HBsAg can be positive.

B-ultrasound examination has hepatosplenomegaly, mainly liver, mostly moderately large.

Diagnosis and diagnosis of neonatal hepatitis B

diagnosis

It is important that severe chronic liver disease can occur in patients with no clinical symptoms and only HBsAg-positive.

1. History and clinical manifestations: In high-incidence areas of hepatitis B, infants with HBsAg and/or HBeAg-positive mothers and/or poor appetite after birth, fever, jaundice, liver enlargement, etc. should be considered disease.

2. Laboratory examination and auxiliary diagnosis: It is the most important basis. In addition to the increase of serum enzyme and bilirubin, the determination of antigen and antibody should be carried out. Currently, radioimmunoassay and enzyme-linked immunoassay are the most sensitive, followed by reverse. Passive hemagglutination and immunoadhesive hemagglutination, immune diffusion and convective electrophoresis are not very sensitive, but still widely used in China, three antigens, antibody systems, to detect HBsAg most useful.

Differential diagnosis

1. Biliary atresia: It is mainly caused by the occurrence of jaundice and pathological jaundice in neonatal period. Hepatitis B is hepatic jaundice, and serum bilirubin is biphasic, but it is blocked first in the early neonatal period due to hepatocyte excretion function. What appears is obstructive jaundice, so the most important is the identification of biliary atresia, because the latter must strive for a diagnosis after 3 months of birth, the two can be identified from the following aspects:

(1) Medical history: The general condition and stomach anorexia of hepatitis B patients may be fluctuating, the degree of jaundice may fluctuate, the color of white clay soil is also fluctuating, the degree of hepatosplenomegaly is not significant, and the early transaminase is high.

(2) serum fetal globulin: hepatitis B is significantly increased, often greater than 1600ng / ml.

(3) iodine rose red excretion test: after taking phenobarbital or cholestyramine in hepatitis B, 131I rose red excretion increased and there was no change in biliary atresia.

(4) Vitamin E absorption test: Hepatitis B can reduce the hemolysis effect of hydrogen peroxide after oral administration of vitamin E, and the biliary atresia can not be improved.

(5) Lipoprotein X measurement: Hepatitis B was negative for lipoprotein X and positive for biliary atresia.

(6) Others: such as 99mTc-IDA imaging examination, B-mode ultrasound examination, percutaneous liver biopsy, duodenal fluid biliary pigmentation examination is more meaningful for the diagnosis of biliary atresia.

2. Metabolic deficiency diseases such as galactosemia, 1-antitrypsin deficiency, etc. The mother of this disease suffers from hepatitis B and is directly transmitted to the fetus by the mother. The incidence of neonatal is high, and laboratory tests are helpful for differential diagnosis.

The material in this site is intended to be of general informational use and is not intended to constitute medical advice, probable diagnosis, or recommended treatments.