Viral hepatitis A

Introduction to viral hepatitis A Viral hepatitis (viralhepatitis A, referred to as hepatitis A) is an acute liver inflammation caused by hepatitis A virus (HAV), which is mainly transmitted through the fecal-oral route. It occurs in children and adolescents, mainly due to loss of appetite and nausea. Vomiting, fatigue, hepatomegaly and abnormal liver function, often have fever at the beginning of the disease, clinically often self-limiting, the vast majority of patients can return to normal within a few weeks. basic knowledge The proportion of illness: 15% Susceptible people: good for children and adolescents Mode of transmission: spread through the fecal-oral route Complications: cholecystitis, pericarditis, nodular polyarteritis

Cause of hepatitis A virus

Epidemiology

a source of infection: hepatitis A patients and asymptomatic infections are the source of infection. Hepatitis A patients only discharge pathogens from the feces. The blood HAV mainly occurs 14-21 days before the onset of jaundice. In this period, the patient's blood is infected. Sexuality has been reported to be transmitted through blood transfusions, but the blood of patients is usually not contagious after jaundice. Most of the patients with hepatitis A are acute, and the cases without jaundice account for 50%-90% of the total number of cases, especially in children. The patient discharged the most amount of HAV from the feces 2 weeks before the onset and 1 week after the onset, and the infection was the strongest at this time. However, a small percentage of patients discharged HAV from the feces up to 30 days after the onset of illness.

b Transmission route: Hepatitis A takes the faecal-oral route as the main route of transmission, and the way of faecal-oral transmission is diverse. Under normal circumstances, contact with daily life is the main mode of transmission of sporadic morbidity, so in collective units such as child care institutions The incidence of hepatitis A in schools and troops is high. The spread of water and food, especially aquatic shellfish such as edulis, is the main mode of transmission of hepatitis A outbreaks. In 1988, Shanghai suffered the largest epidemic of hepatitis A since the founding of the country due to the consumption of edema contaminated by feces, with a total of 310,000 cases in 4 months.

c Susceptibility and immunity: People who are not injected with hepatitis A vaccine are generally susceptible to HAV. In China, children and adolescents under the age of 15 are most likely to develop hepatitis A, because they have acquired long-lasting immunity, and by adulthood, The number of people with hepatitis A is reduced, and the number of elderly people is less. People who have been infected with hepatitis A or have been infected with the hepatitis A virus can gain long-lasting immunity.

Pathogenesis

After entering the body, the HAV enters the bloodstream through the intestines, causing viremia. It reaches the liver after about one week, and then passes through the bile into the intestines and appears in the feces. Defecation can be maintained for 1-2 weeks. The main organ that the virus invades is the liver, and the pharynx and tonsils may be the site of extrahepatic reproduction of HAV. The mechanism of HAV-induced hepatocyte injury is not clear. It is generally believed that HAV does not directly cause hepatocyte lesions, which are caused by immunopathological responses of HAV-infected hepatocytes.

Hepatitis A prevention

1. Control the source of infection

Acute patients should be separated according to the digestive tract to 3 weeks after the illness. Patients in the child care institution should be isolated to normal liver function, the pathogen marker is negative, the patient's feces and excretion should be strictly disinfected, and the food and beverage personnel should be checked regularly.

2. Cut off the route of transmission

Do a good job in environmental sanitation, strengthen water and manure management, develop good hygiene habits, and not eat semi-ripe aquatic products.

3. Protect susceptible populations

The gamma globulin preparation contains a relatively high-priced anti-HAV, which can be effectively prevented by injection within 7 to 14 days after contact with the patient. In recent years, the hepatitis A vaccine has been widely used, and it has safety and immunogenicity, and can produce energy. To prevent and stop the neutralizing antibodies of infection, the live attenuated hepatitis A vaccine was produced in Zhejiang, Shanghai, Kunming, Changchun and other places in China. From the vaccination situation of primary school students and some children, the reaction was light and safe, and Shike and Merck were killed. Live vaccines also have good antigenicity, and the genetically engineered vaccine currently under development is an ideal vaccine for preventing high purity and high titer of hepatitis A.

Hepatitis A complications Complications cholecystitis pericarditis nodular polyarteritis

Complications of acute hepatitis are less, of which more common cholecystitis, occasionally pericarditis, nodular polyarteritis.

Symptoms of viral hepatitis A common symptoms collateral circulation of the portal body dysfunction, fainting, coma, reflexes, upper abdomen, discomfort, dysfunction, abdominal distension, flapping tremor, oliguria

Acute jaundice

(1) Early stage of jaundice: The incubation period of infected people after 15 to 45 days (average 30 days), most of the acute onset, chills, fever, fatigue, muscle aches, lack of appetite, nausea and oil, vomiting and upper abdominal discomfort, etc. For several days to 2 weeks, a small number of patients have no obvious symptoms. The main signs are tenderness and suffocation in the liver area. The total number of peripheral white blood cells is normal or slightly lower. The lymphocytes are increased. Abnormal lymphocytes, urinary bilirubin positive, ALT are seen. Increased, anti-HAV IgM positive.

(2) jaundice period: about 1 week after the onset, fever subsides, urinary yellow like strong tea, sclera, yellow skin staining, jaundice peak in 1 to 2 weeks, liver, tenderness and sputum pain, some patients have Mild splenomegaly, elevated ALT, serum bilirubin over 17.1mol / L, lasting 2 to 6 weeks.

(3) recovery period: jaundice subsided, symptoms disappeared, liver function returned to normal, lasting 2 weeks to 4 months, a few for up to 6 months.

2. Acute jaundice-free type

Generally mild, short course, easy to ignore, only manifested as fatigue, loss of appetite, abdominal distension and liver pain, some patients have no clinical symptoms (subclinical), may have hepatomegaly, anti-HAV IgM positive and elevated ALT The total bilirubin is below 17.1 mol/L.

3. Acute cholestatic hepatitis A

Acute onset, digestive tract symptoms are not obvious, dark urine color, sclera, skin yellow staining, gray and white itching, serum bilirubin increased significantly, direct bilirubin, serum transpeptidase Alkaline phosphatase, cholesterol, etc. were significantly elevated, ALT was moderately elevated, jaundice lasted for more than 3 weeks, a few for more than 3 months, and other extrahepatic obstructive jaundice were excluded.

4. Heavy hepatitis A

Acute severe onset is rapid, rapid development, the course of disease is within 10 days, jaundice is rapidly deepened, frequent nausea and vomiting, high abdominal distension, extreme fatigue, bleeding tendency, and rapid neuropsychiatric symptoms, major signs of conscious disturbance, flapping tremor, and liver dullness The narrowing of the boundary, serum total bilirubin 171mol / L or more, prothrombin time is significantly prolonged, activity is less than 40%, cholinesterase activity, C3, serum cholesterol and cholesterol lipids are significantly reduced, but there are also jaundice Those with obvious or no jaundice and first psychiatric symptoms, those with a course of more than 10 days are subacute severe hepatitis, and the clinical manifestations are the same as acute severe. The main complications of severe hepatitis are as follows.

(1) Hepatic encephalopathy: common, classified according to the degree of clinical manifestations, grade IV, grade I: sleep disorders, mental disorders, behavioral disorders, apathy or excitement; Level II: insanity, disorientation, computational power Decreased, hyperreflexia, increased muscle tone, flapping tremor and convulsions, Babinski sign positive, EEG changes; Grade III: stunned, callable, slow, unresponsive, painful presence Increased muscle tone, flapping tremor, positive pyramidal tract sign, abnormal EEG; Grade IV: coma, no response, no response to various stimuli, decreased muscle tone, severe changes in EEG.

(2) cerebral edema: more common, manifested as headache, vomiting, blurred vision, disturbance of consciousness, irritability, elevated blood pressure, conjunctival edema, pupillary changes (smaller, moderately large, large and small, ranging from Large) and respiratory changes, even respiratory arrest, etc., often coexist with hepatic encephalopathy.

(3) Bleeding: manifested as skin mucosal ecchymosis, nasal cavity, oral cavity, gum bleeding, some patients may have hemoptysis, hematemesis, blood in the stool or hematuria, and even upper gastrointestinal bleeding.

(4) Hepatorenal syndrome: In liver failure, renal blood flow decreases and glomerular filtration rate decreases, and small blood vessels in the kidney are highly paralyzed, showing oliguria or no urine.

Examination of hepatitis A virus

1. Detection of HAV and HAV antigens: The feces of patients before and 2 days after the disease were taken, and the HAV or HAV antigen particles were detected by immunoelectron microscopy. The HAV RNA in feces and serum was detected by polymerase chain reaction (PCR). The HAV or HAV antigen in the liver tissue of the patient can be detected by immunofluorescence, immunoelectron microscopy or radioimmunoassay.

2. Detection of specific antibodies: Anti-HAV IgM is detected by enzyme-linked immunosorbent assay (ELISA), which has high specificity and is significantly elevated in the early stage of the disease. It can be used as an indicator of recent infection of HAV, and anti-HAV IgG is protective. The antibody can be detected in January after the disease, and reaches a peak after 3 months. It is maintained for 2 to 10 years. Anti-HAV IgG positive is a marker of past HAV infection and immunity of the body, and can be used for epidemiological investigation.

There were abnormal changes in liver ultrasound and electrocardiogram.

Diagnosis and identification of viral hepatitis A

Diagnostic criteria

1. Epidemiological history

There is a history of water or food contaminated with feces from patients with hepatitis A, especially contaminated buttercups, cockroaches and other semi-cooked foods, or a close history of contact with patients.

2. Clinical manifestations

Acute onset, after fever subsides, there are no other reasons to explain the lack of fatigue, loss of appetite, nausea, oil, jaundice, liver and other clinical manifestations.

3. Liver function test

Serum total bilirubin began to increase in the early stage of jaundice, reaching a peak in 2 weeks, and the heavy and cholestatic type could reach 171mol/L or more; serum ALT began to rise in the late incubation period, AST also increased, and severe prothrombin time Significantly prolonged, the degree of activity declined progressively.

4. Specific immunological detection

Detection of anti-HAV IgM by enzyme-linked immunosorbent assay (ELISA) is the most reliable method for the diagnosis of acute hepatitis A, maintaining a high titer within 8 weeks after the onset and continuing until the early recovery.

Differential diagnosis

Acute hepatitis A and hepatitis B, hepatitis C identification is not difficult, hepatitis A is generally epidemic or outbreaks, more common in preschool children and young adults, acute onset, often fever, suspicious and unclean diet before illness History, and B, hepatitis C is mostly distributed, mainly adult, no fever, hepatitis A and hepatitis E are sometimes difficult to identify, hepatitis E is also a pandemic or outbreak, there is also a history of unclean diet, but the incidence The age is more than 15 to 39 years old, and the proportion of cholestatic type is higher, and the main basis for differential diagnosis is virus-specific immunological detection. In addition, acute severe hepatitis A must be associated with toxic and drug-induced hepatitis. Identification, mainly based on pre-dose toxic or medication history, acute hepatitis A must be differentiated from EBV infection, the latter has a longer fever, often angina, lymphadenopathy, atypical lymphocytosis, phagocytosis Immune agglutination test positive, anti-HAV IgM positive, etc., in the differential diagnosis, should also consider the systemic infectious diseases such as typhoid, sepsis and other liver, jaundice, liver function abnormalities, such as patients with pregnant women still need to be acute with pregnancy Identification of fatty liver, the disease is seen in primipara, in the late pregnancy, there are deep jaundice, acute abdominal pain, bleeding tendency, liver and kidney syndrome and coma and other clinical manifestations, urinary bilirubin negative, ultrasound is a typical fatty liver waveform.

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