Viral hepatitis E

Introduction to hepatitis E virus Viral hepatitis (viral hepatitis type E, HE hepatitis E) is a self-limiting infectious disease, its mode of transmission, clinical manifestations and prognosis are similar to hepatitis A (hepatitis A), but the incidence of hepatitis E in children is low, pregnant women suffer Hepatitis E has a high mortality rate and is characterized by hepatitis. Its epidemic features also resemble hepatitis A. It is transmitted through the fecal-oral route and has obvious seasonality. It is more common in the rainy season or after the flood, without chronicity and good prognosis. basic knowledge The proportion of illness: 0.0035% Susceptible people: no specific population Mode of infection: digestive tract spread Complications: hepatic encephalopathy, hepatorenal syndrome

Cause of hepatitis E virus

(1) Causes of the disease

In 1983, Balayan et al first discovered HEV from the fecal samples of infected persons by immunoelectron microscopy. In 1989, Reyes et al. obtained molecular clones (HEV) cDNA clones and officially named the virus as hepatitis E virus (HEV). ).

HEV is a non-enveloped spherical granule with a diameter of 27-34 nm, protrusions and nicks on the surface, and uneven internal density. In 1989, Reyes et al first obtained the cloning of HEV gene. Studies have shown that the HEV genome is a single-stranded positive-strand DNA. The full length is 7.2 to 7.6 kb, encoding 2400 to 2533 amino acids, consisting of a 5' non-structural region (NS) and a 3' end structural region (S), and each of the 5' and 3' ends has a non-coding region (NC). The length is 28 bp and 68 bp, respectively. In addition, there is a polyadenylation (A) tail consisting of 150 to 300 adenosine residues at the 3' end. The virus is unstable and needs to be stored in liquid nitrogen for long-term storage. , magnesium or manganese ions help to maintain the integrity of the virus particles, sensitive to high salt, barium chloride and chloroform, relatively stable in an alkaline environment, the classification of HEV has not yet been finalized, originally attributed to microRNA virus It was found that its morphology and biological characteristics under electron microscopy were similar to those of sickle virus, so HEV was classified into a sickle virus, but it was recently found to be associated with a sickle virus when analyzing the nucleotide sequence homology of HEV genome. Different, comparative analysis of NS region genomic sequence revealed that it is associated with rubella virus Similar to beet necrotic yellow vein virus, it was suggested that the HEV virus belonging to the family of rubella viruses.

(two) pathogenesis

The exact pathogenesis of hepatitis E is still poorly known. From the results of primate experiments and the results of volunteer studies, it is speculated that the virus may be mainly infected by the mouth, and then enter the liver by the intestine, and then proliferate in the liver cells. After replication, it was discharged into the blood and bile, and finally excreted with the feces. The presence or absence of extrahepatic replication has not yet been concluded. The experiment also showed that the liver lesions mainly mediate the cellular immune response mediated by hepatocyte lysis.

The pathological changes of hepatitis E are similar to those of hepatitis A. It can be seen that there is neutral multinucleated cell infiltration in the portal area, hyperplasia of Kupffer cells, spotted necrosis in the lobules, balloon-like changes in hepatocytes, eosinophilic and eosinophils, and mild inflammation. The formation of intracranial cholestatic and capillary bile duct thrombus is more common. Most of the hepatic tissue pathological changes in patients with hepatitis E are moderately damaged, and even sub-macro or large necrosis can be seen.

Hepatitis E virus prevention

As with hepatitis A, it is mainly to take comprehensive measures to cut off the transmission route. To prevent water-borne transmission, it is mainly to protect water sources and prevent manure management. It is also important to pay attention to food hygiene, improve sanitation facilities and pay attention to personal hygiene. The prevention of hepatitis E by immunoglobulin and human placental immunoglobulin is largely ineffective, and ultimately depends on the vaccine. The success of HEV molecular cloning provides the basis for the development of vaccines.

Hepatitis E complication Complications, hepatic encephalopathy, hepatorenal syndrome

1. Hepatic encephalopathy.

2, bleeding.

3, liver and kidney syndrome.

4, secondary infection.

Hepatitis E virus symptoms common symptoms upper gastrointestinal bleeding massive liver cell necrosis appetite deficiency nasal congestion coma cold upper abdomen discomfort stool color lower extremity edema nausea

1. The incubation period has a long incubation period for hepatitis E. The current understanding is not uniform. The incubation period in Delhi in 1955 was 18-62 days, with an average of 40 days. The incubation period for volunteers in 1983 was 36 days. Azamgsn, Kashmir and China's Xinjiang survey for 10 to 49 days, an average of 15 days, Zhuang Hui comprehensive 3 times homologous hepatitis E epidemic, incubation period of 15 to 75 days, an average of 36 days, which is not completely similar to the epidemiological characteristics of each place Inconsistent statistical conditions, the number of viral infections and some differences in virus strains, comprehensive domestic and foreign reports, the consensus is that the latency of hepatitis E is slightly longer than that of hepatitis A, and shorter than that of hepatitis B, generally 2 to 9 weeks, with an average of 6 weeks.

2. Clinical manifestations Currently recognized clinical types include acute hepatitis, severe hepatitis and cholestatic hepatitis, and there is still controversy about chronic hepatitis.

(1) Acute hepatitis E: 86.5% to 90.0% of hepatitis E, including acute jaundice and acute jaundice, the ratio of which is about 1:5-10.

1 acute jaundice type: accounting for 75% of acute hepatitis E, clinical manifestations similar to hepatitis A, but its jaundice period is longer, the symptoms are more serious, A. jaundice early: mainly manifested as acute onset, can have chills at the onset, Fever, headache, sore throat, nasal congestion and other symptoms of upper respiratory tract infection (appearance rate of about 20%), joint pain (7% to 8%), fatigue and fatigue (60% to 70%), followed by loss of appetite (75% ~ 85%), nausea (60% to 80%), vomiting, upper abdominal discomfort, liver pain, bloating, diarrhea and other gastrointestinal symptoms, some patients showed mild hepatomegaly, accompanied by tenderness and snoring pain, this period continued Between a few days and a half months, at the end of the period, the urine color gradually deepens. For example, urinary bilirubin and urinary bile positive, blood bilirubin (Bil) and glutenase (ALT) increase, B. jaundice: The body temperature is normal, the jaundice is deepened, the urine is as deep as strong tea, the stool color is light, the skin is itchy (29%), and the digestive tract symptoms are heavy. It can be gradually relieved until the jaundice no longer rises. This period is generally 2 to 4 weeks. Individual cases can last for 8 weeks, and various liver function tests will also rise to the peak at this stage, and gradually ease later. C. Recovery period: symptoms, signs and tests comprehensively Turn, alleviate the symptoms disappeared on average to about 15 days, the liver and liver function normalization retraction average of about 27 days, this period is usually 2 to 3 weeks, a few up to 4 weeks.

2 acute jaundice-free type: clinical also has two phases of acute phase and recovery phase, but the performance is lighter than jaundice type, some patients have no clinical symptoms, sub-clinical, subclinical infection, adulthood is more clinically infected .

(2) heavy hepatitis E: about 5% of hepatitis E, more common than hepatitis A. Through the investigation of repeated epidemics of hepatitis E in the world in the past decade, it is unanimously recognized that there are more heavy women than men (2:1). ~ 5:1); pregnant women, severe hepatitis accounted for 60% to 70% of pregnant women, followed by the elderly and viral overlap infections, especially in patients with hepatitis B re-infection with HEV is prone to severe hepatitis, acute in severe hepatitis More heavy, the ratio of its subacute to heavy is about 17:1, the difference between the two can not be divided only by time, according to the majority of clinical reports in the epidemic of hepatitis E in Xinjiang, should also refer to the following characteristics.

1 acute heavy hepatitis E: more common in pregnant women (57% to 60%), especially in the third trimester of pregnancy (about 70%); the disease is developing rapidly, most pregnant women have a sharp change in normal or premature delivery; blood bilirubin In the mild or moderate elevation, a series of clinical manifestations of severe hepatitis can occur, and there is no separation of enzymes and bile; the dullness of the liver is half of the normal and half of the normal; all cases have hepatic encephalopathy, coma cases There are cerebral edema, the survival rate of coma above III degree is extremely low; the bleeding procedure is positively correlated with the depth of jaundice, and diffuse intravascular coagulation (DIC) occurs in individual cases; prognosis and depth of coma, degree of bleeding, morning and evening pregnancy and frequency of organ failure It was positively correlated and had no obvious relationship with the depth of Astragalus. Although the course of the survivors was longer, there was no manifestation of cirrhosis after hepatitis.

2 subacute severe hepatitis: in addition to pregnant women, also seen in the elderly and other viral infections, especially HBV; disease development is relatively slower than acute heavy; jaundice is deeper than acute severe hepatitis, duration is also long, enzyme biliary separation phenomenon is more common In most patients, the dullness of the liver does not shrink. In some cases, the liver and spleen are slightly enlarged. The latter occurs in patients with hepatitis B and HEV. In almost all cases, ascites, lower extremity edema and hypoproteinemia can occur. There are few hepatic encephalopathy; the course of disease is longer, and various complications can occur in the course of the disease; the mortality rate is closely related to the number of organ failure, and the frequency of organ failure is liver, coagulation system, central nervous system and kidney.

(3) Cholestatic hepatitis E: Xinjiang data is rare, accounting for only 0.1%. It has also been reported that cholestatic hepatitis E is more common, the incidence is higher than that of hepatitis A, which is about 7.5%. The clinical manifestations are similar to those of hepatitis A. The period is longer, but the prognosis is good.

(4) Chronic hepatitis E: The chronic hepatitis process of hepatitis E and the presence or absence of chronic viral carriers are not consistent. Japan reported that 58.2% of the cases developed chronic hepatitis during the epidemic period, and Zhao Suzhi had 500 cases of acute hepatitis E. After 3 to 28 months of follow-up, 12% of patients had symptoms, signs, liver function tests and biopsy tests that did not return to normal, and were consistent with chronic persistent hepatitis changes, but the case of secondary hepatitis E in eastern Xinjiang During the one-year systematic follow-up, no chronic cases were found. The observations of Zhuang Hui, Khroo et al. in India, and the development of acute hepatitis E were not found. The inconsistency of these results was related to the type of virus strain. The level of immunity, age and other social factors are relevant for further study.

(5) Clinical features of hepatitis E in different physiological stages:

1 Hepatitis E during pregnancy: not only the incidence is high, but also easy to develop into severe. In the 1985-1988 Xinjiang hepatic epidemic, the incidence of pregnant women accounted for 24%, in severe hepatitis, pregnant women accounted for 27%, non-pregnant women accounted for 4.6%, and the mortality rate was also High, multi-country reported in 10% to 20%, the highest 39%, the highest rate of mortality in the third trimester (20.96%), the second in the second (8.46%), early (1.5%) and the general women of childbearing age (1.4%), The disease develops rapidly, often when the jaundice has not reached the level of liver, that is, hepatic brain syndrome occurs, and the liver shrinks in half. The liver tissue pathological examination shows that the liver cells are mainly degenerative swelling, and the liver tissue after hemorrhage is also present with ischemia. Hypoxia changes, prone to miscarriage, premature delivery, stillbirth and postpartum infection, often in the postpartum condition, the main cause of death is cerebral edema, postpartum hemorrhage, hepatorenal syndrome, upper gastrointestinal bleeding and cerebral palsy, in the process of heavy development There were successive reductions in I, V, and VII factors. In most cases, platelets and fibrinogen were normal, and only DIC occurred.

2 children with hepatitis E: with the increase of age, the incidence rate is getting higher, there is no report of neonatal morbidity, 1 to 3 years old cases accounted for 22.2% of the incidence, 7 to 14 years old accounted for 77.8%, if compared with adults, children occur The rate is low. 3160 cases have been reported in Xinjiang. The children accounted for 9.11%, the mortality rate was 0.52%, and it was lower than that of adults. The onset was urgent and the symptoms were mild. There were more respiratory symptoms in the early stage of the disease (6.7%~20.3%). The proportion of splenomegaly (19.8%) was higher than that of adults (0.22%). Although the majority of jaundice cases (98.2%), the increase was not as large as that of adult jaundice, and the duration was long. The liver function changed with ALT. Mainly.

3 elderly hepatitis E: the incidence rate of about 3% to 10.9% of the total number of cases, lower than adults, higher than children, onset is more insidious, clinically also based on jaundice, cholestatic hepatitis accounted for a larger proportion , Huangqi deep, long duration, relatively long course of disease, slow recovery, hospitalization time is about 1 times longer than adult group, severe hepatitis is relatively more, higher than the adult group but lower than pregnant women, more complications, easy secondary infection The prognosis is good, the mortality rate is low, and no chronic report is found.

Examination of hepatitis E virus

Specific serum pathogens are the basis for diagnosis.

1. Enzyme-linked immunosorbent assay (ELISA) The detection of anti-HEV IgM in serum is an indicator for the diagnosis of acute hepatitis E. It is a recombinant or synthetic peptide as an antigen. Domestic application of this method to detect 111 cases of acute hepatitis E, anti-HEV The positive rate was 86.5%. In 32 patients with recovery period, the anti-HEV positive rate was 6.3%, suggesting that the duration of anti-HEV was shorter, and 63% of the patients were negative after 5 to 6 months.

2. Protein Blot (WB) This method is sensitive and specific to ELISA, but the method of operation is more complicated and the detection time is longer.

3. Polymerase chain reaction (PCR) is used to detect HEV-RNA in serum and feces of patients with hepatitis E. This method has high sensitivity and specificity, but it is prone to laboratory contamination during operation. Positive.

4. Immunoelectron microscopy (IEM) and immunofluorescence (IF) are used to detect HEV particles and HEV antigen (HEAg) in feces, bile and liver tissues of patients with hepatitis E, but both methods require special equipment and technology. Moreover, HEV has a shorter time in liver tissue, bile and feces, and the positive rate is lower, which is not suitable for routine examination.

Diagnosis and identification of viral hepatitis E

diagnosis

Comprehensive analysis should be carried out according to clinical manifestations and laboratory tests, combined with epidemiological conditions, according to the conditions of the "viral hepatitis prevention and treatment program" (hereinafter referred to as "the program") to determine whether the patient has liver disease, liver disease is secondary to other diseases or Viral hepatitis, according to the pathogen test results to determine whether it is hepatitis E, (due to anti-HEVIgM has a certain false positive rate, anti-HEVIgG in some patients can last a long time, it is best to detect both IgM and IgG, and Continuous detection, observation of dynamic changes, the significance of diagnosis is greater,) pathological diagnosis can increase the reliability of clinical diagnosis and classification, in the various clinical classifications listed in the "program", hepatitis E has no liver cirrhosis As for the presence or absence of chronic hepatitis E, it is highly controversial. It is now recognized that clinical types include acute hepatitis, severe hepatitis and cholestatic hepatitis.

Differential diagnosis

1. Upper respiratory tract infection.

2, digestive tract disease.

3, caused by other causes of jaundice.

4. Hepatitis caused by other causes.

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