Hepatitis E in children

　　1, Etiology

　　Hepatitis E virus (hepatitis Evirus, HEV) belongs to the Caliciviridae family, has no envelope, and its nucleic acid is single-stranded positive-sense RNA. It has two genotypes: Myanmar strain (B) and Mexico strain (M). The Chinese strain belongs to the same subtype as the former. The virus is unstable in vitro and sensitive to high salt, cesium chloride, chloroform, etc. Cell culture has not been established, and various non-human primates can be infected with HEV.

　　2, Pathogenesis

　　HEV mainly invades the liver, causing liver cell inflammation and necrosis through direct pathogenic effect and/or immune injury. Liver pathological changes include liver cell degeneration, focal necrosis, infiltration of lymphocytes, mononuclear macrophages, and NK cells in the portal area. More than half of acute icteric type patients show cholestasis and bile thrombus formation.

　　A few cases can present as acute or subacute severe hepatitis, or chronic hepatitis. Severe complications such as hepatic encephalopathy, hepatorenal syndrome, secondary infection, hemorrhage, electrolyte disorder, primary peritonitis, etc.

　　I, Acute icteric type

　　Occupying 86.5% of overt infections, the clinical course of the three phases is similar to that of hepatitis A, and the prodromal symptoms can last until the 4th to 5th day after the appearance of jaundice. Cholestasis is common, and the total course of the disease is 4 to 6 weeks.

　　II, Acute nonicteric type

　　The manifestations are similar to those of hepatitis A.

　　III, Cholestasis type

　　Common, the course of the disease can last for more than 2 months.

　　IV, Severe

　　Accounting for about 5%, high-risk factors include:

　　1, Pregnant women;

　　2, Elderly and weak individuals;

　　3, Concurrent HBV infection, mostly acute severe.

　　V, Mixed infection with other viruses

　　1, Simultaneous or sequential infection with HEV and HAV: It does not worsen the condition.

　　2, Co-infection with HEV and HBV: Patients with HBV often have active replication, HEV is not easily cleared, the condition is prone to persistence or recurrence, the condition is severe, and there are many severe cases. India reported that 80.7% of acute severe and 75.5% of subacute severe cases were caused by HBsAg carriers co-infected with HEV.

　　Since patients with this disease have already excreted a large amount of virus in the late incubation period before symptoms appear, they are highly contagious and difficult to detect and take isolation measures in time. As there is currently no active or passive immunization preparation available for prevention, the prevention strategy for hepatitis E is a comprehensive preventive measure mainly focusing on cutting off the transmission routes.

　　Most outbreaks of hepatitis E are transmitted through water. Ensuring water safety, widely publicizing the drinking of boiled water, not drinking unboiled water, improving environmental and personal hygiene, and vigorously carrying out health education are important. Good management of water sources, feces, food, and patients should be carried out, and the mass health campaign should be actively carried out, especially paying attention to collective units and child care institutions to prevent outbreaks and reduce the number of cases.

　　The current gamma globulin cannot prevent this disease. The recombinant vaccine for HEV is still under development. Using HEV gene peptides containing the ORF3 HEV cDNA fragment, the eukaryotic expression plasmid (pSVL) is inserted to construct the HEV cDNA vaccine, which is inoculated into experimental mice. The serum of these mice can be detected with positive anti-HEV, providing feasibility for the development of HEV gene vaccines. The main measures are to protect water sources, strengthen food hygiene management, pay attention to personal hygiene, and improve the environmental hygiene. Human gamma globulin has no significant preventive effect on this disease. Recombinant vaccines and nucleic acid vaccines are under research.

　　1. Viral particle and antigen examination

　　During the end of latency to the early acute phase, feces should be collected for the detection of viral particles by immunoelectron microscopy or detection of viral antigens by enzyme immunoassay. The detection rate is 100% 1-4 days before the onset of the disease, and decreases to 70% 1-3 days after the onset, 60% 4-6 days after the onset, and 25% 7-9 days after the onset. It cannot be detected after 2 weeks, and the latter is prone to false positives.

　　2. Serological examination

　　Acute phase specific IgM positivity has clinical diagnostic value. The detection rate of specific IgG is 72.7% within 2-3 weeks after onset, and 84.9% within 4-8 weeks. The EIA method established using the complete ORF2 protein as an antigen has high sensitivity and specificity.

　　3. Viral gene examination

　　HEV RNA can be detected in serum and feces by RT-PCR. Abdominal ultrasound should be performed to understand the liver and spleen conditions, etc.

　　Patients with hepatitis E should pay attention to their diet:

　　Patients with hepatitis E must strictly control the entry of the disease through the mouth, pay attention to food hygiene, wash hands before and after meals, choose restaurants with good hygiene when eating out, implement a separate meal system during group meals as much as possible, regularly disinfect tableware and utensils, wash vegetables and fruits thoroughly before eating them raw, do not eat food that has been stored for a long time or is not fresh, and do not drink unboiled water, etc.

　　Sufficient high-quality protein can improve the body's immune function, increase liver glycogen storage, and is beneficial to the repair of liver cells and the recovery of liver function. However, due to the increase in blood ammonia caused by the increase of protein in the diet, it is necessary to eat more protein foods with low ammonia production, such as dairy products.

　　Diet should be suitable for the patient's taste, easy to digest, and light food. It should contain a variety of vitamins, have sufficient calories and appropriate amounts of protein, and fat should not be restricted too strictly.

　　I. Treatment

　　There is no specific antiviral drug. Comprehensive symptomatic measures are similar to those for hepatitis A.

　　1. General treatment

　　Avoid strenuous exercise, take adequate rest, and must rest in bed when fever, vomiting, and fatigue occur. Have a reasonable diet, and provide intravenous fluid replacement for those who cannot eat.

　　2. Drug treatment

　　To prevent the development of severe hepatitis, in addition to close monitoring, protective western medicine or Chinese herbal medicine for clearing the liver and benefiting the gallbladder can be appropriately selected according to the drug source and local conditions.

　　3. Severe hepatitis

　　Patients should be hospitalized for isolation treatment, rest in bed absolutely, strengthen nursing, perform monitoring, closely observe the condition, take comprehensive measures, such as preventing further necrosis of liver cells, promoting liver cell regeneration, reducing serum bilirubin, improving liver microcirculation, preventing and treating complications such as hepatic encephalopathy, hepatorenal syndrome, secondary infection, hemorrhage, electrolyte disorder, primary peritonitis, etc., to promote the recovery of liver function.

　　4. Cholestatic hepatitis

　　This type of jaundice is relatively deep, lasts for a long time, and the treatment effect is not ideal, but the prognosis is good.

　　(1) Aspartate Potassium Magnesium: 0.2-0.4ml/kg of aspartate potassium magnesium can be administered each time, once/d, added to an appropriate amount of 5%-10% glucose injection, administered by intravenous infusion.

　　(2) Yinzhu Huang: Yinzhu Huang injection 2-6ml, added to 5%-10% glucose solution 50-100ml, 1-2 times/d, administered by intravenous infusion.

　　(3) Anisodamine (654-2): Anisodamine (654-2) injection 0.1-0.2mg/(kg·time), added to 5%-10% glucose 20-40ml, administered by intravenous infusion, 1-2 times/d.

　　(4) Prednisolone (Prednisolone): If necessary, use prednisolone (Prednisolone) 1-2mg/(kg·d), administered twice by intravenous infusion, and gradually reduce the dose and discontinue the drug once jaundice begins to fade.

　　II. Prognosis

　　The mortality rate of this disease is 2.5%; the mortality rate of pregnant patients is 10% to 20%, up to 39%, and increases with gestational age.