Hepatitis B antigenemia

Introduction to hepatitis B antigenemia Hepatitis B antigenemia: Hepatitis B patients can have a variety of skin manifestations, and acute skin manifestations are associated with immune complexes formed by antibodies to HBsAg and anti-HBsAg. Immunological fluorimetry can be used to detect immune complexes and complement in the blood vessels of lesions. basic knowledge The proportion of illness: 10% Susceptible people: no special people Mode of infection: non-infectious Complications: pancreatic head cancer primary liver cancer

Causes of hepatitis B antigenemia

Cause:

It is caused by hepatitis B virus whose surface antigen is ayw subtype.

Pathogenesis

There are many studies at home and abroad, but there are still many problems to be further studied.

1. Mechanism of hepatocyte injury

It is believed that hepatitis B virus itself does not cause obvious liver cell damage. Hepatocyte damage is mainly caused by immunopathology, that is, the body's immune response causes liver cell damage during the process of clearing HBV. Whether HBV itself can cause liver lesions, Chisari It has been found in transgenic mice that accumulation of large amounts of pre-S1 large proteins in hepatocytes can cause hepatocyte necrosis and even cirrhosis and liver cancer, which is due to the large expression of this large protein by transgenic mice under the control of a strong promoter. At the same time, due to the lack of complete genes, it can not be assembled into a complete virus and cause hepatocyte damage, which is completely different from the natural infection of human HBV, and may be similar to some variants, such as the cleavage site of P25e large protein. Mutation occurs, large proteins can not be digested to form e antigens and excreted outside the cells. Large amounts of large proteins accumulating in cells can also cause liver cell damage.

The mechanism of immunopathology causing liver cell damage can be roughly divided into two types.

(1) Liver damage caused by specific immunity:

1 cytotoxic T cell (CTL)-induced liver injury: This damage needs to be recognized by double recognition, that is, CTL recognizes both the target antigen and the homologous HLA on the hepatocyte membrane that binds to the target antigen (antigen peptide: MHC molecule complex) HLA expression is rare on normal liver cell membranes, and HLA expression is increased during hepatitis. Some drugs such as interferon can increase the expression of HLA on the hepatocyte membrane, so there is an effect of enhancing CTL. Introduction to target antigens, effector cells and regulatory factors as follows:

Target antigen: In acute hepatitis B, the target antigen may be mainly HBsAg. Some people have previously detected the cellular immunity against pre-S2, HBcAg and HBsAg before the onset of acute hepatitis B, and found that the cellular immunity to HBsAg is closest to the incidence of acute hepatitis B. The target antigen in chronic hepatitis B may be mainly HBcAg (including HBeAg, because the antigenicity of the two is very close), which is mainly based on the results of the in vitro killing test: cytotoxicity can occur when the patient's lymphocytes are incubated with autologous hepatocytes. However, when autologous hepatocytes are incubated with anti-HBs or anti-HBc in advance, only anti-HBc has the effect of blocking cytotoxicity. In addition, many pathologists also support the view that HBcAg is a target antigen for chronic hepatitis B. Whether HBsAg is also a target antigen has different opinions. The above autocytotoxicity test does not seem to support the view that HBsAg is a target antigen, but some pathologists believe that coarse-grained and serosal HBsAg may be target antigens, and transgenic mice are tested ( See also) support this view.

Effector cells: CTL is the main effector cell. CTL recognizes the antigen peptide: MHC complex, then adheres to the liver cell membrane. After extensive contact with the cell membrane of both cells, CTL secretes perforin and granzyme ( Granzyme) causes membrane lysis of the target cell. In addition, Fas antigen is expressed on the hepatocyte membrane, and FasL expression is expressed on the CTL membrane, so hepatocyte apoptosis can also be induced by the action of Fas-FasL.

Regulatory factors: The killing effect of CTL is regulated by many factors, firstly inhibitory T cells and helper T cells, followed by various cytokines (interleukins, interferons, tumor necrosis factors, etc.), serum factors (E rose) Some inhibitory factors, serum immunosuppressive factors, etc.), in addition, certain substances produced after the destruction of hepatocytes can also affect cellular immune function.

2 Liver damage caused by autoimmunity: There are at least two kinds of hepatocyte serosal antigens, one is hepatocyte membrane antigen (LMAg), the immune response to it is mainly found in autoimmune hepatitis, and the other is hepatocyte membrane-specific lipoprotein. (LSP), may be associated with viral hepatitis.

Anti-LSP can be found in various types of hepatitis. We have used ELlSA method to detect: the positive rate of acute hepatitis is 45.5%, that of chronic persistent hepatitis is 22.86%, that of chronic active hepatitis is 75%, and that of acute severe hepatitis is 4/4. Scholars have similar reports, all patients with hepatitis also have a cellular immune response compared to LSP, this reaction may be caused by antibody-dependent cytotoxicity (ADCC) to kill, domestic patients with serum and rabbit liver Cells, healthy human lymphocytes were incubated together, found acute hepatitis 53.7%, chronic active hepatitis 85.3%, severe hepatitis 10/10 ADCC phenomenon, if the patient's serum is first absorbed by LSP, it can significantly reduce the rabbit liver cells Killing, other scholars have similar reports.

To clarify whether anti-LSP is unique to hepatitis B and its role in pathogenesis, we compared the anti-LSP positive rates of acute hepatitis A with acute hepatitis B and found 79% and 88%, respectively. , P>0.05, which means: A. Anti-LSP is not specific to hepatitis B; B. Anti-LSP is not related to chronic hepatitis B, because hepatitis A is not chronic and the positive rate of anti-LSP is also high.

These results suggest that anti-LSP is likely to be a consequence of hepatocyte injury. In vitro experiments have shown that anti-LSP can cause liver cell damage through ADCC, but the role in human hepatitis needs further study, it is likely that in acute hepatitis it It is only the consequence of liver cell damage. In chronic hepatitis, especially when it has autoimmune tendency, it may also play a role, and further proof is needed.

(2) Non-specific liver damage caused by cytokines: such as TNF, IL-1, etc. It has been found that in vitro culture, TNF only causes necrosis of HBV-transfected hepatocytes, and Chinese scholars have also found that TNF is injected into rats alone. Does not cause liver lesions, but TNF can aggravate liver damage caused by D-galactosamine, and anti-TNF monoclonal antibody can significantly alleviate this damage. Duck hepatitis test also proves that anti-TNF monoclonal antibody can prevent duck hepatitis virus Hepatocyte necrosis caused by endotoxin, the above materials all indicate that TNF plays an important role in hepatic necrosis, and its mechanism may be related to the activation of lysosomal activity in hepatocytes, mainly chymotrypsin, using chymotrypsin inhibitor APNE. To prevent TNF-induced cell necrosis, it has also been shown that TNF can activate serine protease, phospholipase A2 and directly destroy the liver cell membrane. In addition, it has also been found that TNF and IL-1 have a synergistic effect in liver necrosis.

(3) Other factors: microcirculatory disorders, such as hepatic sinus capillary vascularization, capillary blood flow disorders, etc. also play a role in chronic hepatitis liver injury, lymphokine activated killer cells (LAKC) also have a certain infection of HBV hepatocytes The killing effect.

2. Pathogenesis of different clinical manifestations

(1) Acute hepatitis: often occurs in patients with normal immune function. HBV infection causes normal cellular and humoral immune responses, destroying a certain number of hepatocytes during the process of clearing the virus (heavy jaundice occurs), and healed after removing the virus.

(2) Chronic hepatitis: mainly related to immune tolerance, specific immune function, virus mutation, etc. (see Chraging Mechanism for details).

(3) Severe hepatitis: HBV-induced severe hepatitis, especially the mechanism of acute severe hepatitis, has been studied more, but it has not been fully conclusive. It is currently considered that the possibility of two injury theory is the greatest, that is, primary injury plus succession Primary injury, primary injury is caused by excessive immunopathology. Immunopathology is caused by excessive cellular immunity, that is, killer T cells kill more hepatocytes expressing HBV antigen. On the other hand, caused by excessive humoral immunity, that is, the patient's humoral immune response is too strong, so the anti-HBs produced by the spleen are early and large, and after entering the hepatic sinus, hepatocytes are released (hepatocytes). HBsAg, which is activated by sensitized T cells, forms an immune complex that stimulates type III hypersensitivity in the liver (Arthus reaction): the immune complex deposits on the surface of the hepatic sinusoidal endothelium, binds and fixes, activates complement, attracts Neutrophil and platelet aggregation cause a large number of hepatocytes to undergo ischemic necrosis. The clinically seen fulminant hepatitis B is often negative for HBsAg and anti-HBs at admission, and later anti-HBs , Sometimes it appears positive anti -HBs admission, seems to support this view.

As for why there is a strong immunopathology, it is still not clear, and the virus may also play a role. For example, double or multiple viral infections may be more likely to cause severe hepatitis, and some variant strains may also have a certain relationship, such as Hasegawa et al (Hepatology, 1995, 22:26) transfected transgenic mice with full-length HBV DNA (replacement of four amino acids in the envelope) compared to wild-type strains in patients with fulminant hepatitis, enabling C3H mice High titers of anti-HBs are produced, while transfection of wild-type strains does not produce anti-HBs. As described above, excessive pre-HBs production may cause Arthus reaction in the liver.

Secondary injury is mainly caused by tumor necrosis factor alpha (TNF-). TNF- itself does not cause liver necrosis, but TNF- can cause massive hepatocyte necrosis on the basis of liver damage. Injection of TNF- into normal animals does not cause hepatocyte necrosis, but injection of duck hepatitis B virus into normal animals and then injection of TNF- can cause massive hepatocyte necrosis. The source of TNF- is mainly From endotoxin stimulation of mononuclear cells and macrophages produced by the liver, on the basis of primary liver injury, due to impaired liver barrier function, especially the function of liver macrophages, the bacterial endotoxin from the intestine Can not be cleared, and form enterogenous endotoxemia, which induces TNF-, endotoxin can not only induce TNF- but also induce a large number of other cytokines, such as IL-1, IL-6, IL-8, thromboxane, platelet activating factor, leukotriene, transforming growth factor 1, endothelin, reactive oxygen intermediate, etc., these factors can also synergistic, auxiliary and potentiating effects on TNF-.

The mechanism of TNF--induced hepatocyte necrosis can be divided into direct and indirect effects. The direct effect is to destroy the lipid membrane structure and DNA of hepatocytes through complex biochemical processes. The indirect effect is mainly to damage the sinusoidal endothelial cells and promote hepatic sinusoids. Internal fibrin deposition, microthrombus formation and microcirculatory disorders lead to a large number of hepatocytes hypoxic necrosis, which is less clear for the pathogenesis of subacute severe hepatitis and chronic severe hepatitis.

(4) Cholestatic hepatitis: pathogenesis refers to hepatitis E.

(5) The chronic HBsAg carriers are described below (chronic mechanism).

3. Mechanism of extrahepatic injury HBV infection has more extrahepatic manifestations, such as nephritis, nodular polyarteritis, etc., which may be mainly related to the deposition of hepatitis B antigen-antibody complex in these tissues.

4. Chronic mechanism HBV can not be cleared from the human body to form a chronic HBV infection, chronic can be manifested as chronic carriers of HBV, can also be manifested as chronic hepatitis, showing complete immune tolerance to HBV, showing chronic carriers, HBV immune function is low, that is, the HBV antigen has certain recognition and clearance ability, which leads to certain liver cell damage, but can not completely eliminate the virus, it is manifested as chronic hepatitis, and the cause of immune tolerance and immune function to HBV may be low. There are two factors of virus and organism.

(1) Virus factors:

1HBV mutates to produce an immune escape strain;

2HBV DNA is integrated with hepatocyte DNA, and the body cannot remove it;

3 combined with other chronic infections, such as HDV, HCV, etc.

(2) Body factors:

1 The immune system is not yet mature, and the fetal immune system is still in the developmental stage. At this time, if HBV is infected, the thymus is negatively selected, and the T cells that respond to HBV are lacking, central immune tolerance can be produced. This tolerance is often difficult. Disappeared, the immune system in the neonatal period is still not fully mature. At this time, HBV infection can occur in the peripheral T cells (T cells leaving the thymus). Later, as the age increases, the chance of tolerance becomes less and less. In adulthood, the immune system is mature. At this time, if there is no immunodeficiency, it will be acute hepatitis after infection with HBV and heal itself.

2 The immune system has low function, which can be characterized by low T cell function, low B cell function, and low function of antigen presenting cells (such as dendritic cells), resulting in low immune function, in addition to some known factors that can affect immunity ( In addition to AIDS, hemodialysis, application of immunosuppressive agents, etc., there may be many unknowns. For example, does HBV infection of various immune cells directly affect their function? Many reports have confirmed that HBV can infect mononuclear giants. Phagocytes, which may affect antigen presentation and affect cellular and humoral immunity. The effect of this effect on strong antigens is less affected by weak antigens. In HBV infection, HBcAg is more antigenic, so anti-HBc is often Positive, HBsAg antigenicity is weak, so often can not induce anti-HBs, HBV infection of T cells have also been reported, which will directly affect the clearance of HBV by T cells, immunoregulatory factors will also have an important impact on cellular and humoral immunity. Many authors have found that chronic hepatitis B often has helper T cell function, inhibited T cell function, interferon alpha, interferon gamma, IL-2 hypoxia, TNF, IL-4, IL-6 increase, rosette formation inhibitory factor, increased serum inhibitory factor, etc. The reasons for these regulatory factors are not clear, some may be the consequences of HBV infection, and some may be the consequences of liver damage, but This in turn affects the body's immune response to HBV, which is a very complex immune network system that requires more systematic and further research.

5. The mechanism of the removal of hepatitis B virus has always been believed that the removal of hepatitis B virus is mainly through the cell destruction mechanism, that is, CTL destroys the liver cells, releases the hepatitis B virus in the cells, and then removes it, but in recent years, it has been found in acute hepatitis. The clearance of hepatitis B virus in hepatocytes is mainly through non-cell destructive mechanisms, ie more than 90% of intracellular viruses, including HBV covalently closed circular DNA (cDNA), before hepatocyte destruction (elevated serum transaminase) And before hepatocytes appear to have been cleared, this clearance is mainly achieved by the cytokines TNF- and IFN-, because transgenic mice have shown that blocking antibodies can be blocked by antibodies against these cytokines. The scavenging effect of transgenic mice also demonstrated that chronic HBV infection due to immune tolerance can also clear hepatitis B virus in liver cells through a non-cell destructive mechanism.

6. The pathology of acute hepatitis is seen in hepatitis A.

7. The pathology of cholestatic hepatitis is seen in hepatitis E.

8. Pathology of chronic hepatitis Since 1968, chronic hepatitis has been classified into chronic persistent hepatitis (CPH) and chronic active hepatitis (CAH) at home and abroad. In recent years, it has been found that this diagnostic method is easy to misunderstand CPH and CAH. It is two different disease states, or even two different diseases. In fact, there is no essential difference between the two. They are only different in weight and can be converted. In order to avoid misunderstanding, some foreign experts recommend abolishing the CPH and CAH names. The degree of inflammation and the degree of fibrosis in the liver were scored separately. Domestic scholars agreed with this opinion. According to this opinion, two new national pathological criteria were formulated at the 1995 and 2000 national academic conferences. The principle is: according to severe liver disease The degree is divided into light, medium and heavy three degrees, and then divided into 0 to 4 (G) according to the degree of inflammation, according to the degree of fibrosis is divided into 0 to 4 (S), such as mild chronic hepatitis, Gl, S2; severe Chronic hepatitis, G4, S3.

Indexing criteria:

(1) Mild chronic hepatitis is equivalent to the original CPH and light CAH:

1 hepatocyte degeneration, point, focal necrosis, eosinophils;

2 There is (no) inflammatory cell infiltration in the portal area, which is enlarged, and mild degeneration and necrosis can be seen;

3 leaflet structure is complete.

(2) Moderate chronic hepatitis is equivalent to the original medium CAH:

1 Inflammation is obvious in the portal area with moderate degeneration and necrosis;

2 lobular inflammation is heavy, with bridging necrosis;

3 fiber spacing is formed, and the lobular structure is mostly preserved.

(3) Severe chronic hepatitis is equivalent to the original heavy CAH:

1 Inflammation of the portal area is severe or with severe debris-like necrosis;

2 bridging necrosis has a wide range, involving most of the lobules;

3 Most of the interfiber septal lobular structure disorder, or the formation of early cirrhosis.

9. Pathology of severe hepatitis

(1) Acute severe hepatitis: According to the lesion, it can be divided into the following two types.

1 acute edema type: manifested as severe diffuse hepatocyte swelling, liver cells squeeze into each other into a polygon, lobular structure deformation, which there are scattered and varying sizes of necrotic lesions.

2 acute necrosis: characterized by extensive hepatocyte necrosis, necrosis of whole lobules or multiple lobules, extreme expansion of the hepatic sinus, with extensive hemorrhage, infiltration of lymphocytes and histiocytes in the portal area, the mesh stent does not collapse.

(2) Subacute severe hepatitis: liver tissue is new and old sub-macro necrosis (necrosis area <50%), necrotic area mesh stent collapses, there is obvious convergence of the portal area, and agglomerated hepatocytes appear around the leaflet Hyperplasia, small bile duct hyperplasia around the portal area, with cholestasis.

(3) Chronic severe hepatitis: the clinical manifestation is chronic severe hepatitis, there is still no unified change in pathology, which may be severe chronic hepatitis, or may appear massive (full leaflet) or sub-large on the basis of other chronic hepatitis or cirrhosis Block of fresh liver parenchymal necrosis.

10. Pathology of hepatitis cirrhosis The liver has pseudolobule formation, and then it is divided into active cirrhosis and resting cirrhosis according to the presence or absence of obvious inflammation.

Hepatitis B antigenemia prevention

Comprehensive preventive measures based on hepatitis B vaccination should be adopted.

1. Vaccine and hepatitis B immunoglobulin (HBIG) vaccination

(1) Newborn vaccination can be as follows:

1 The mother is a newborn with HBsAg and HBeAg double positive: it is best to use hepatitis B vaccine and HBIG in combination. According to the report of Beijing Epidemic Prevention Station in 1990, 2 times of HBIG is used for this newborn (immediately after birth and 1 month after birth) One regimen, one each, 200 IU each, and three blood-borne hepatitis B vaccines (one in each of 2, 3, and 5 months after birth, 20 g/time), the protection rate for HBV infection can reach 97.13. %, take 1 injection of HBIG (1 injection immediately after birth) and 3 blood-borne hepatitis B vaccines (immediately after birth, 1 month after birth, 1 time in June, 30 g/time), the protection rate can also be Up to 91.98%, the vaccine was administered only 3 times of blood-borne hepatitis B vaccine (immediately after birth, 1 month after birth, 1 time in June, 30 g/time), and the protection rate was only 86.65%. The Shanghai Medical University Pediatric Hospital also has A similar report: the newborns who received HBIG three times and the three hepatitis B vaccines had a chronic carrier rate of 3.4% at the age of 2, and the newborns who received the three hepatitis B vaccines alone had a chronic carrier rate of 11.1% at the age of 2 years. However, some people believe that if the quality of hepatitis B vaccine is good, the HBsAg content is high, the first injection time is very early, and the hepatitis B vaccine alone can reach 9 With a blocking effect of about 0%, the Ministry of Health has officially stipulated that the production and sale of blood-borne hepatitis B vaccine should be stopped at the end of 1999. The genetic recombinant HBsAg vaccination has been included in the planned immunization management, and the newborn born to the double-positive mother is recommended at birth. Immediately inject HBIG 1ml (200U/ml), and inject the same amount of HBIG once a month; 2, 3, 6 months of injection of recombinant hepatitis B vaccine 10g intramuscular injection (upper arm deltoid), the protection rate can reach more than 95%, If the recombinant vaccine (0, 1, 6 months) is injected with 10 g each of 3 needles, the protection rate can reach 85%.

2 The mother is HBsAg-positive, HBeAg-negative newborn: the hepatitis B vaccine alone can achieve better results. The Beijing Epidemic Prevention Station reported in 1990 that three times of blood-borne hepatitis B vaccine was used (30 g immediately after birth, 1 month later) 20g, 10g in June after birth, followed up for 1 year, no HBsAg persistent positive, so the application of recombinant hepatitis B vaccine at birth, 1 month and 6 months after birth, each 10g, intramuscular injection, have the same protection rate.

3 mother HBsAg-negative neonates: hepatitis B vaccine alone can achieve better results, Beijing Municipal Epidemic Prevention Station materials believe that the first needle of blood-borne hepatitis B vaccine 20g, the last two needles each 10g (0,1,6 months) The effect is better than 10 needles of 10 g. The former has an anti-HBs positive conversion rate of 96.6% and the latter is 88.3%. The recombinant hepatitis B vaccine can be used at birth, 1 month and 6 months after birth. 5 g was injected with the same protection rate.

However, even if the best method is applied, there are always a few newborns who become carriers of chronic HBV after birth. These carriers are considered to be intrauterine communicators. There are two ways to prevent intrauterine transmission: one is in pregnancy. In the next 3 months, pregnant women will be given 200 U of hepatitis B immunoglobulin every month. After the newborn is born, it will be routinely prevented. It is believed that the intrauterine transmission can be reduced. However, whether this method has a curative effect remains to be proved. Another method is before pregnancy. That is, lamivudine is applied until after delivery, which may be useful for lamivudine, but whether lamivudine has no effect on pregnancy, further proof is needed.

(2) Inoculation for children and adults: Preschool children who have not been vaccinated against hepatitis B should be replanted. HBVM may be checked before or after replanting, depending on the local conditions at the time. It is generally believed that even if vaccinated It has been HBsAg or anti-HBs positive before, and there is no adverse effect after vaccination with hepatitis B vaccine. The dose can be adjusted with 5g×3 (0, l, 6 months) of recombinant hepatitis B vaccine. The risk group in adults (the spouse of HBsAg positive person) Hepatitis B vaccine should also be given to people who are in close contact with blood, medical staff, hemodialysis patients, etc. Because there are only a few susceptible persons in adults, it is best to test HBsAg and anti-HBs first, and both are negative. For vaccination, the dose can be adjusted with a recombinant hepatitis B vaccine 10 g × 3 (0, 1, 6 months).

(3) Inoculation of accidental infected persons: Accidental infection refers to needle sticks accidentally contaminated by HBsAg-positive blood or splashed by HBsAg-positive blood in the conjunctiva or oral mucosa or HBsAg-positive blood. If the recipient is known to be HBsAg-positive or anti-HBs-positive, it can be left untreated. If you don't know if it is positive, you should immediately take blood to check HBsAg and anti-HBs, and then immediately (the sooner the better) intramuscular injection of HBIG The dosage can be such that the blood anti-HBs can reach >10mU/ml. Therefore, if HBIG contains anti-HBs 200U/ml, it can be injected 0.05-0.07ml/kg; if the content is low, it should be increased accordingly. Dosage, the dose of HBIG in the transfusion recipient should be increased, at least the anti-HBs in the blood should be more than 20mU / ml, and then different treatment according to the test results: for non-transfusion recipients, if HBsAg or anti-HBs are positive Can no longer be treated, if both are negative, then three injections of recombinant hepatitis B vaccine should be injected 5g×3 (0,1,6 months). For transfusion recipients, three injections of recombinant hepatitis B vaccine should be injected regardless of the test results. 10g × 3 (0, 1, 6 months), because after HBsAg-positive blood Detection of HBsAg is unreliable. Although anti-HBs positive indicates that immunity is present, the amount of disease contained in the blood transfusion is too large. It is better for injecting vaccines.

At present, genetically engineered hepatitis B vaccine has been used in China, one of which is yeast vaccine, which has strong immunogenicity, 5g can be equivalent to 10g of blood source vaccine, and the other is CHO (Chinese hamster egg cell) vaccine, its immunogen Similar to the blood source vaccine, the hepatitis B vaccine is safe. Even if it is a blood source vaccine, it will not infect other diseases because of strict inactivation measures. The side effects of hepatitis B vaccine are very light, mostly local pain, occasionally redness and swelling. , induration, systemic response to fever, >38 °C accounted for about 1.8%, followed by fatigue, upper respiratory symptoms, gastrointestinal symptoms, rare Guillain-Barre syndrome, disabled for formaldehyde or thimerosal allergy, can Inoculation with other vaccines, no mutual interference was observed.

2. Prevention of iatrogenic transmission

Disposable syringes should be vigorously promoted. All kinds of medical and preventive injections should be one-on-one, one-piece, one-piece, various medical instruments and utensils (blood needles, acupuncture needles, surgical instruments, scratch needles, probes, endoscopes, dental drills, etc.) All should be disinfected one by one, the disinfection and isolation system of medical and health units at all levels should be improved, and the disinfection of body fluids such as blood should be strictly enforced, and the management of blood donors and blood products should be strengthened.

Hepatitis B antigenic complications Complications, pancreatic head cancer, primary liver cancer

It occurs in the limbs and face, and it does not itch papular dermatitis. The rash can last for many years and fluctuates with the change of hepatitis. May be associated with superficial lymphadenopathy.

In severe cases, abdominal wall edema may occur, and skin tension may appear.

The skin is yellow-stained and progressively deepened, mostly pancreatic cancer, biliary system cancer or primary liver cancer.

Hepatitis B antigenic symptoms Common symptoms Dasanyang mouth sticky hepatitis B surface antigen (... Hepatitis B e antigen (H... Single ALT increased bleeding tendency bloating papules liver splenomegaly nodules

Acute hepatitis B may have serum-like symptoms 2 weeks before onset, 10% to 20% of patients develop urticaria, and a small number of patients may develop erythema, maculopapular rash, polymorphous erythema, scarlet fever-like erythema, leukocyte rupture vasculitis , erythroderma, allergic purpura and cryoglobulinemia, patients with facial butterfly erythema, may be associated with joint pain and arthritis, HBsAg-Ab complex can be measured in serum and joint fluid.

Chronic active hepatitis can occur in the trunk, inflammatory papules in the extremities, central suppuration, scarring, atrophy, and the formation of characteristic acne-like scars. This rash can last for many years and fluctuates with changes in hepatitis conditions. In addition, it can occur Common skin manifestations of liver disease, such as erythema, acne, lupus-like changes, localized scleroderma, swelling, purpura, subarachnoid and nail hemorrhage, and nodular polyarteritis.

Examination of hepatitis B antigenemia

Serum transaminase can be elevated frequently in chronic hepatitis, often with decreased serum albumin, elevated globulin, abnormal serum bilirubin, often mildly decreased white blood cells, and often reduced prothrombin activity. White blood cells can be normal or mildly elevated, the most important is prothrombin activity <40%, hepatitis cirrhosis often has a marked decrease in white blood cells and platelets, inversion of globulin.

Histopathology: pathological changes in multiple line allergic vasculitis.

Diagnosis and identification of hepatitis B antigenemia

diagnosis

Acute hepatitis B

The clinical diagnosis is basically the same as that of hepatitis A, but there is no more jaundice type. The pathogen diagnosis is mainly based on HBsAg(), but HBsAg-positive acute hepatitis is not necessarily true acute hepatitis B or chronic HBV infection (HBsAg). Acute exacerbation of patients with carriers or asymptomatic mild chronic hepatitis B or concurrent acute hepatitis (hepatitis D, hepatitis E, drug-induced hepatitis, etc.), especially acute exacerbations of chronic HBV infection, is clinically difficult Acute hepatitis B identification, and the prognosis and treatment principles of the two are very different. For identification, anti-HBcIgM and anti-HBcIgG can be detected simultaneously, such as IgG strong positive, IgM negative or low titer is chronic HBV infection. Acute attacks, such as IgM strong positive, IgG negative or low titer is acute hepatitis B, liver biopsy sometimes helps to identify, in addition, such as acute HBsAg positive, recovery period HBsAg negative, anti-HBs turn yang It can be diagnosed as acute hepatitis B. In addition, if acute hepatitis patients are admitted to the hospital, HBV DNA has turned negative or HBV DNA titer drops rapidly during the course of the disease or e system conversion is indicated as true acute B. Hepatitis.

2. Diagnosis of chronic hepatitis B

The diagnosis of chronic hepatitis B should include three parts: pathogenic diagnosis, pathological diagnosis and clinical diagnosis.

(1) Pathogenic diagnosis: Chronic hepatitis B mainly depends on HBsAg ( ). In rare cases, HBsAg-negative slow hepatitis B may also occur. This may be due to HBV variation or HBsAg expression is too low. This HBsAg-negative Slow hepatitis B, other serum indicators (such as e system or anti-HBc) can be positive, negative, or all negative, but HBV DNA is generally positive, in rare cases, all markers of hepatitis B are negative, even anti-HBs Positive, while HBsAg or (and) HBcAg in liver biopsy tissue can still be positive.

(2) Clinical diagnosis: Where the course of acute hepatitis has not recovered for more than 1 year, or the date of onset is unknown, the patient has signs of chronic hepatitis (liver disease face, liver palm, spider mites, splenomegaly) or (and) test at the time of diagnosis. (A / G inverted, gamma globulin is very high) or (and) imaging test positive, can be diagnosed as chronic hepatitis, and then according to the indexing criteria for light, medium, heavy indexing, or according to various laboratory indicators The degree of inflammatory activity, degree of liver damage and degree of fibrosis [detection of hyaluronic acid (HA), procollagen III peptide (PCIII), type IV collagen, etc.].

For a long time, clinically, pathological diagnostic criteria have been used to distinguish chronic hepatitis into CAH and CPH. Recently, many pathologists believe that in order to avoid confusion, these two terms should be abolished, which is supported from a clinical perspective because of clinical It is difficult to distinguish the two from each other. In theory, the clinical diagnosis of chronic hepatitis should include three parts:

1 degree of inflammation activity

2 degree of liver damage

3 The degree of fibrosis and the speed of progression, these indicators are important for determining prognosis and guiding treatment, but because the current indicators of liver fibrosis are still immature, this diagnosis method cannot be used, so in 1995, 2000 The diagnostic criteria for chronic hepatitis developed by the national academic conference are only light, medium and heavy:

1 mild (equivalent to the original CPH or light CAH): the condition is mild, the symptoms are not obvious or although there are symptoms, but the biochemical indicators are only one or two mild abnormalities;

2 moderate (equivalent to the original medium-sized CAH): the severity of the disease is between mild and severe;

3 severe (equivalent to the original heavy CAH): there are more obvious or persistent hepatitis symptoms, can be associated with liver disease face, liver palm, spider mites or hepatosplenomegaly and exclude other causes, laboratory tests in addition to serum transaminase repeated or continuous In addition, there is a significant decrease in albumin (32g/L) or (and) bilirubin (>85.5mol/L), or (and) prothrombin activity is significantly reduced (40%-60) %), or (and) cholinesterase <41.7mol·S-1/L (2500U/L), B-ultrasound also contributes to the diagnosis of chronic hepatitis, but this method of indexing is not satisfactory, For example, whether the severity refers to heavy inflammation, or whether the liver function damage is heavy, or whether the fibrosis is heavy? It is unclear. In the future, as the understanding of chronic hepatitis continues to deepen, there will be better and better clinical classification. Standard research is coming out.

3. The diagnosis of severe hepatitis should also include clinical diagnosis and pathogenic diagnosis.

(1) Clinical diagnosis: mainly based on clinical manifestations, where there is no previous history of hepatitis, and clinical manifestations of acute or subacute severe hepatitis, prothrombin activity <40% can be diagnosed, the difference between acute or subacute is mainly The order of occurrence of various symptoms, in the early (14 days), mental and neurological symptoms (hepatic encephalopathy), after the emergence of obvious jaundice, bleeding tendency, high abdominal distension, etc. should be considered as acute heavy liver, where the first height of fatigue, Highly gastrointestinal symptoms, high abdominal distension, high bleeding tendency, ascites, and then (hepatic encephalopathy only after 14 days) should be considered as subacute severe liver. In addition, due to vitamin K deficiency, prothrombin activity can be reduced. Therefore, it should be treated with vitamin K for 3 days, and then the activity is reliable.

Patients with a history of chronic hepatitis or cirrhosis and a subhepatic liver should be considered as chronic severe hepatitis.

(2) Pathogenic diagnosis: basically the same as acute hepatitis, but it must be noted.

1 In acute hepatic and subacute severe liver, if the patient is admitted to the hospital earlier, sometimes the antibody has not formed to the detectable level, so the antibody negative can not be excluded from the diagnosis and should be retested during the recovery period.

2 When acute hepatitis B is admitted to hospital, HBsAg can also be negative, and it can be re-positive or anti-HBs in the recovery period. This is because the acute phase HBsAg may form an immune complex with anti-HBs, so it cannot be detected until the recovery period. If the virus has been cleared, anti-HBs may be positive, and if it is not cleared, HBsAg may be positive (rare).

4. Diagnosis of acute type B cholestatic hepatitis: clinical diagnosis sees hepatitis E, and pathogenic diagnosis sees acute hepatitis B.

5. Diagnosis of hepatitis cirrhosis

Early cirrhosis is difficult to diagnose by clinical data alone and must rely on pathological diagnosis. Imaging (B-ultrasound, CT) and laparoscopy are also helpful in diagnosis. Advanced cirrhosis, or clinical cirrhosis, can be diagnosed according to clinical conditions. Patients with chronic hepatitis have evidence of affective portal hypertension (abdominal wall, esophageal or gastric varices or hematemesis, obvious ascites, except for other causes) can be diagnosed as hepatitis cirrhosis, and then classified as active or static according to inflammatory activity; According to the degree of compensation, it is classified as compensatory or decompensated.

Regarding pathogenic diagnosis, it is mainly based on HBsAg positive. In a few cases, anti-HBs-positive quiescent cirrhosis can be diagnosed if it can exclude other causes. This is because HBsAg may be positive in the early stage, but the virus has been cirrhotic. It was cleared and turned into anti-HBS positive.

Differential diagnosis

The differential diagnosis of acute hepatitis B and acute cholestatic hepatitis B can be seen in hepatitis A and hepatitis E. Chronic hepatitis should be associated with chronic hepatitis C and other causes (alcohol, drugs, parasites, fatty liver, autoimmunity, metabolism). Identification of chronic liver disease caused by abnormalities, etc., severe hepatitis should be differentiated from severe hepatitis caused by other hepatitis viruses, drugs, poisoning, etc., as well as fatty liver of pregnancy.

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.