HBV and HCV superinfection

Introduction The overlap of HCV and HBV affects the prognosis of liver disease. HCV infection in patients with chronic liver disease, especially the double infection of HBV and HCV, may accelerate the progression of liver disease. Viral hepatitis (viral hepatitis) is a group of liver damage caused by a variety of different hepatitis viruses. According to the pathogen diagnosis, at least five kinds of hepatitis viruses, namely hepatitis A, B, C, D, and E, cause hepatitis A, B, C, D, E virus, respectively. Hepatitis A, hepatitis B, hepatitis C, hepatitis D, and hepatitis E. Another type is called hepatitis G virus, which is rare.

Cause

The pathogenesis of viral hepatitis is currently not fully elucidated.

Hepatitis A virus only causes slight damage to the liver and chest during the process of replication in hepatocytes. After a series of immune responses (including cellular immunity and humoral immunity) appear in the body, the liver has obvious lesions, which are manifested as hepatocyte necrosis and inflammatory reaction. . HAV is cleared by the body's immune response and, therefore, does not generally develop into chronic hepatitis, cirrhosis or viral portability.

Hepatitis B virus infects and replicates in hepatocytes, and is generally considered not to cause hepatocyte lesions directly, but the HBV gene is integrated into the liver cell chromosome of the host, which may have long-term consequences. The hepatocyte injury of hepatitis B is mainly caused by a series of immune responses, including cellular immunity. (HBcAg) and liver-specific lipoprotein expressed on the liver cell membrane are the main target antigens. The cytotoxic effect of sensitized T lymphocytes is the main mechanism of hepatocyte injury, while antibody-dependent cytotoxicity and lymphokines are single. The combined effects of nuclear factors and the like are also important, especially in the pathological mechanism of chronic active hepatitis, and the specific T-helper cell sustained damage plays an important role. The specific antibody binds to the corresponding antigen and viral particles in the circulation to form an immune complex and is cleared by phagocytic phagocytosis. Some immune complexes in the circulation can be deposited in the basement membrane of small blood vessels, in the joint cavity and in the small blood vessel wall of various organs, causing eclampsia, arthritis glomerulonephritis, nodular polyarteritis and other extrahepatic lesions. . The destruction of infected hepatocytes and the clearance of HBV by protective antibodies (anti-HBs, especially anti-pre-S2) can lead to termination of infection.

The strength of the body's immune response and whether the immune regulation function is normal is closely related to the clinical type and outcome of hepatitis B. In the body with normal immune response and immune regulation function, the infected liver cells are destroyed by the effector cells, causing the infection to terminate. The clinical manifestations are smooth acute hepatitis, and the liver cells are caused by the amount of virus and the virulence. The degree of damage varies with acute jaundice or acute jaundice-free hepatitis. If the body's specific humoral immunity and cellular immune function against HBV severely punish the defect or immunotolerance or immune paralysis, the infected liver cells are not subjected to immunological damage or only minor damage, and the virus fails to clear, it is manifested as asymptomatic chronic zone Poison. If the body's immune function (mainly the scavenging function) is low, the virus has not been completely removed, and the liver cells are continuously under mild damage, it is characterized by chronic persistent hepatitis and chronic active hepatitis. The pathogenesis of chronic active hepatitis is complicated. The body's specific immune function is low, and the virus in the circulating and infected liver cells cannot be fully removed. The virus continues to replicate in the liver cells, causing the liver cells to be immunely damaged. Insufficient quantity or function of suppressor T cells, and changes in the quality and quantity of immunoregulatory molecules formed in the liver caused by abnormal liver cell metabolism, leading to immunoregulatory dysfunction, resulting in TB cells and between T cell subpopulations Coordination dysfunction, increased autoantibody production, autoimmune liver damage through antibody-dependent cytotoxic effects or antibody-mediated complement-dependent cytolysis; or formation of large antigen-antibody complexes, resulting in hepatocytes and other organs Serious and lasting damage. The pathological damage mechanism of severe hepatitis is mainly due to the serious imbalance of the immune function of the body, the specific immune response is enhanced, and the autoimmune response is obvious. The hepatocyte mass necrosis is caused by the intrahepatic immune complex reaction and antibody-dependent cytotoxicity. In recent years, it has been considered that a large amount of tumor necrosis factor- (TNF) is released from endotoxemia, causing local microcirculation disturbance, which can lead to acute hemorrhagic necrosis and massive necrosis of the liver; and free radical changes are found in liver damage and hepatic It is related to the occurrence of encephalopathy.

Little is known about the pathogenesis of hepatitis C and hepatitis E. Some studies suggest that the pathogenesis of hepatitis C and hepatitis E is involved in the immune system, and liver cell damage is mainly mediated by immunity.

Animal studies on hepatitis D have shown that HDV and HBV overlap infection results in a large number of HDV replication, significantly more than the combination of HDV and HBV infection. HDV has direct pathogenicity to hepatocytes, and hepatitis B is associated with HDV infection, especially in patients with overlapping infections, liver cell damage is significantly aggravated.

There is no cross-immunization between various types of viral hepatitis. HDV and HBV combined infection or overlapping infection can aggravate the condition and easily develop into chronic hepatitis and severe hepatitis, especially those with HDV overlap in chronic hepatitis B. Overlapping infections with HAV or HBV also exacerbate the condition and can even progress to severe hepatitis.

an examination

Related inspection

Hepatitis C RNA liver function examination ultrasound diagnosis of liver disease

(1) Clinical diagnosis

Acute hepatitis

(1) Acute jaundice-free hepatitis: Symptoms and liver function damage are relatively mild, and comprehensive analysis of epidemiological data, symptoms, signs and chemical examinations must be performed. The diagnosis is based on the following.

1 Epidemiological data: Whether there is close contact with patients with confirmed viral hepatitis within half a year, especially the presence or absence of hepatitis in the family has important reference value. Whether there is a history of blood transfusion or blood products, or a history of injection or acupuncture that is not strictly disinfected within half a year. There are no water sources, food contamination history, etc.

2 Symptoms: fatigue, loss of appetite, anaesthesia, bloating, sputum and liver pain that have occurred for more than a few days in the near future.

3 signs: In the near future, the liver is swollen and tender, and it hurts. May be accompanied by mild swelling of the spleen.

4 assay: mainly for ALT activity increased. Positive pathogen test (see pathogen diagnosis for details).

Any test that is positive, and two of the other three are positive, or the test and symptoms or laboratory and physical signs are significantly positive, and can exclude other diseases, can be diagnosed as acute jaundice-free hepatitis.

Any single ALT increase, or only symptom, physical signs or only epidemiological data and one of the other three are suspected patients. Suspected patients can be diagnosed if the pathogen diagnosis is positive and other diseases are excluded.

(2) Acute jaundice hepatitis

According to the acute onset of acute hepatitis symptoms, abnormal physical examination, and serum bilirubin above 17mol / L, urinary bilirubin positive, and exclude other causes of jaundice, can make a diagnosis.

2. Chronic hepatitis

(1) Chronic persistent hepatitis

There is a history of confirmed or suspected acute hepatitis. There are still mild symptoms in the course of more than half a year, accompanied by elevated serum ALT or other mild liver damage. Or liver biopsy is consistent with the diagnosis of prolonged hepatitis.

(2) Chronic active hepatitis

There is a history of hepatitis, or the course of acute hepatitis has been delayed for more than half a year, but there are more obvious symptoms of hepatitis at present; hepatomegaly, moderate to moderate hardness may be accompanied by spider mites, dull complexion, liver palm and splenomegaly; serum ALT activity Continuous increase or repeated fluctuations, long-term or repeated increase in serum bilirubin, accompanied by albumin reduction, elevated globulin, abnormal ratio of white and globulin, or increased gamma globulin; autoantibody or extrahepatic damage may occur. Or liver biopsy meets the histological changes of chronic hepatitis.

3. Severe hepatitis

Patients with acute, chronic hepatitis or cirrhosis have high fever, extreme fatigue, severe gastrointestinal symptoms, deepening of jaundice, bleeding tendency, neuropsychiatric symptoms, progressive liver shrinkage, marked damage to liver cells, and prolonged prothrombin time. Both should be considered as severe hepatitis.

4. Cholestatic hepatitis

Acute onset, symptoms and signs of intrahepatic obstructive jaundice lasting more than 3 weeks, hepatitis symptoms are mild, liver enlargement is more obvious; liver function tests are mainly manifested as test results of obstructive jaundice; and other livers can be excluded , external obstructive jaundice, can be diagnosed as acute cholestatic hepatitis. Those with the above manifestations based on chronic hepatitis can be diagnosed as chronic cholestatic hepatitis.

(2) Pathogenic diagnosis

1. Hepatitis A: 1 acute phase serum anti-HAVIgM positive. 2 The serum anti-HAV total antibody titer in the acute phase and the recovery phase increased by more than 4 times. 3 Acute early fecal immunoelectron microscopy of HAV particles. 4 HAAg was found in acute early feces. Any positive of any of the above can be diagnosed as a recent infection with HAV. 5 HAV RNA was detected in serum or feces.

2. Hepatitis B:

(1) Current HBV infection: Diagnosis can be made by any of the following. 1 serum HBsAg positive. 2 serum HBV DNA positive or HBV DNA polymerase positive. 3 serum anti-HBc-IgM positive. 4 Intrahepatic HVcAg positive and / or HBsAg positive, or HBV DNA positive.

(2) Acute hepatitis B: It can be diagnosed if it has one of the following dynamic indicators. The 1HBsAg titer was from high to low, and the anti-HBs turned positive after disappearing. 2 The acute phase serum anti-HBc-IgM showed a high titer, while anti-Hbc IgG (a) or low titer.

(3) Chronic hepatitis B: clinically consistent with chronic hepatitis, and there are more than one positive indicator of HBV infection.

(4) Chronic HBsAg carriers: no clinical symptoms or signs, normal liver function, serum HBsAg test continued positive for more than 6 months.

3. Hepatitis C

(1) Exclusion diagnosis: Anyone who does not meet the diagnostic criteria for viral hepatitis A, B, and E, and excludes Epstein-Barr virus, acute infection with cytomegalovirus (negative IgM antibody negative) and other known causes of hepatitis, such as Drug-induced hepatitis, alcoholic hepatitis, etc., epidemiological indications for non-oral infection, can be diagnosed as hepatitis C.

(2) Specific diagnosis: serum anti-HCV or HCV RNA positive.

4. Hepatitis D: simultaneous or overlapping infection with HBV.

(1) Anti-HD-IgM is positive in serum, or anti-HD positive, or HDAg positive.

(2) HDV RNA positive in serum.

(3) HDAg positive in liver tissue.

5. Hepatitis E

(1) Exclusion diagnosis: Any hepatitis that meets the acute infections of type A, B, C, D, cytomegalovirus, EBV and other known causes, epidemiological evidence that oral infection can be diagnosed as Hepatitis.

(2) Specific diagnosis: acute anti-HEV-IgM positive in the acute phase, or HEV granules in the acute phase of fecal immunoelectron microscopy, or negative anti-HEV in the acute phase and positive recovery in the recovery phase.

Differential diagnosis

(1) Acute jaundice hepatitis

1. Early stage of jaundice: should be differentiated from upper respiratory tract infection, infectious mononucleosis, rheumatic fever and gastroenteritis.

2. Astragalus stage: should be differentiated from other diseases that can cause jaundice, such as drug-induced hepatitis, leptospirosis, infectious mononucleosis, cholecystitis, cholelithiasis.

(2) No jaundice hepatitis and chronic hepatitis: should be differentiated from other diseases that can cause liver (spleen) enlargement and liver function damage, such as chronic schistosomiasis, clonorchiasis, drug-induced or toxic hepatitis, fat Liver and so on.

(C) chronic hepatitis jaundice lasts longer: must be differentiated from liver cancer, cholangiocarcinoma, pancreatic head cancer.

(4) Severe hepatitis: It should be differentiated from severe liver damage caused by other causes, such as drug poisoning and fulminant fatty liver. In addition, in the case of acute severe hepatitis clinical jaundice is not obvious, should pay attention to other causes of gastrointestinal bleeding, coma, neuropsychiatric symptoms.

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