hepatitis B virus
Introduction
Introduction to hepatitis B Viral hepatitis (viral hepatitis type B, referred to as hepatitis B) is caused by hepatitis B virus (HBV), which is mainly caused by fatigue, loss of appetite, nausea, vomiting, anaesthesia, liver enlargement and abnormal liver function. Some cases have fever and jaundice; in a few cases, the course progresses to chronic, or develops into cirrhosis or even liver cancer; in severe cases, the disease progresses rapidly and can develop into severe hepatitis; other infected persons become asymptomatic carriers. basic knowledge The proportion of illness: 0.002% Susceptible people: no special people Mode of transmission: blood transmission, body fluid transmission, mother-to-child transmission Complications: fatty liver, liver cirrhosis, liver cancer
Cause
Cause of hepatitis B virus
Iatrogenic transmission (25%):
Infections caused by various unsterilized or incompletely sterilized syringes, needles, etc., or dental appliances and other invasive medical devices are not strictly sterilized. In addition, drug users may also cause infections due to the sharing of contaminated needles and syringes.
Mother-to-child transmission (20%):
Women of childbearing age who are suffering from acute hepatitis B and who are positive for hepatitis B virus surface antigen pass the hepatitis B virus to the newborn through pregnancy and childbirth. Mother-to-child transmission mainly refers to the infection of the baby in the embryo through the birth canal infection or intrauterine infection, and the infection is the same as the mother.
Sexual contact transmission (15%):
Individuals can cause infection through male semen and female vaginal secretions when they are in sexual contact or living in close contact with hepatitis B patients or viral carriers.
Blood transmission (20%):
Hepatitis B virus is transmitted through blood or blood products.
Pathogenesis
The pathogenesis of hepatitis B is very complicated, and there are many research data, but it has not been fully elucidated so far. It is believed that hepatocyte injury is not the result of HBV replication in hepatocytes, but is mediated by T cell cytotoxicity, human infection with HBV. After that, it can cause cellular and humoral immune responses, and stimulate autoimmune response and immune regulation dysfunction. These immune responses are important for the clinical manifestations and outcomes of hepatitis B.
I. Acute hepatitis
When the immune function is normally infected with HBV, its cytotoxic T cells (Tc cells) attack the infected liver cells, and the damaged hepatocytes release HBV into the blood, which is bound by specific antibodies, and the interferon production is more. The HBV was cleared and the condition improved.
2. Chronic active hepatitis
In patients with impaired immune function and immune regulation disorder, after HBV infection, Tc cell function is restricted due to abnormal function of Tc cells, or specific antibody blocks part of hepatocyte target antigen, resulting in partial hepatocyte damage and less interferon production. HBV continues to replicate, the formation of specific antibodies is insufficient, and hepatocytes are repeatedly invaded by HBV to form chronic infection. In addition, hepatocyte membrane-specific lipoprotein (Lsp) forms autoantigens due to HBV infection, and stimulates B cells to produce anti-Lsp (IgG type). In the case of decreased activity of inhibitory T cells (Ts cells), autoimmune ADCC effects cause progressive damage to hepatocytes.
3. Chronic persistent hepatitis and asymptomatic carriers of HBsAg
When the body's immune function is low, HBV infection can not produce an effective immune response, resulting in little or no hepatocyte damage, especially asymptomatic HBeAg carriers, lack of interferon, can not eliminate the virus, resulting in long-term carrying HBV.
4. Severe hepatitis
The occurrence of acute severe hepatitis, due to the body's immune response is too strong, short-term T-cell toxic response quickly destroys a large number of HBV-infected hepatocytes; or a large number of antigen-antibody complexes are formed in a short period of time, activation of complement, local hypersensitivity reaction (Arthus reaction) ), causing massive hepatocyte necrosis; absorption of intestinal endotoxin can cause Schwartzman reaction, causing ischemic necrosis of hepatocytes; adding -tumor necrosis factor (TNF-), IL-1 and leukotriene The cytokines are released by mononuclear macrophages and promote hepatocyte injury. The pathogenesis of subacute severe hepatitis is similar to that of acute severe hepatitis, but the progress is slow. The pathogenesis of chronic severe hepatitis is complicated and needs further study.
The most obvious liver lesions are scattered throughout the liver. The basic lesions are hepatocyte degeneration, necrosis, inflammatory cell infiltration, hepatocyte regeneration, and fibrous tissue hyperplasia.
Prevention
Hepatitis B prevention
1. Manage the source of infection
For patients with hepatitis B, the date of isolation may be determined. For hospitalized cases, as long as liver function is stable, they can be discharged. For HBsAg carriers during the recovery period, regular follow-up should be conducted. Those who are in direct contact with imported food should be regularly examined for health. In the acute phase, the patient will continue to be normal within half a year after recovery, and the HBsAg may be reverted to the original work. The chronic patients should be transferred away from direct contact with the imported food and childcare work. Before the suspected case is diagnosed, the original work should be suspended. Screening blood donors.
HBsAg carriers refer to HBsAg-positive, no signs of hepatitis symptoms, normal liver function tests, no change after half a year of observation, such personnel should not be treated according to current hepatitis patients, except for blood donation and direct contact with imported food and conservation Outside of work, you can work and study as usual, but to strengthen follow-up, carriers should pay attention to personal hygiene and industry hygiene, to prevent their own saliva, blood and other secretions from polluting the surrounding environment, utensils, shaving utensils, toothbrushes, toiletries should be used Separate from healthy people.
2. Cut off the route of transmission
Strengthen health education and management, prevent iatrogenic transmission, ensure disinfection by one person, one tube, one tube, one-time syringe, thoroughly disinfect and treat blood-contaminated items, and strengthen blood product management.
3. Susceptible population protection
Hepatitis B vaccine is highly effective and safe, and can be used according to the procedures of 0,1,6 months, deltoid muscle injection, blood source vaccine every 10~30g, recombinant vaccine 5~10g, and the anti-HBs titer produced is positively correlated with the protective effect. It is believed that >10U/L has protective effect. For hemodialysis patients and other immune-damaged patients, the dose or frequency of inoculation should be increased. Hepatitis B immunoglobulin (HBIg) is mainly used for newborns of HBeAg-positive mothers, and can be used with hepatitis B vaccine. In combination, the majority of domestically produced HBIg is U/ml, and the dosage should be 0.075 to 0.2 ml/kg.
Complication
Hepatitis B complications Complications fatty liver cirrhosis liver cancer
Hepatic diabetes
The clinical manifestations were similar to those of type II diabetes. The difference was that hepatic diabetes was significantly increased in fasting and the C-peptide was normal. After taking the sugar, the insulin was significantly increased and the C-peak was still slightly lower than normal because of the liver's ability to inactivate insulin. Decreased, promotes insulin elevation; in addition, glucagon inactivation in the liver is reduced, insulin receptors are reduced on hepatocytes, and resistance to insulin is produced, so that although insulin is elevated, blood sugar is still high; and C-peptide is less affected by liver. Therefore, the C peptide is not high, suggesting that the secretory function of cells is not abnormal. In order to distinguish it from type II diabetes, an insulin release test and a C-peptide release test can be used.
2. Fatty liver
The mechanism is still unclear, characterized by good general conditions, single ALT mild, moderately elevated, elevated blood lipids, B-mode ultrasound examination showed fatty liver waveform, confirmed according to liver biopsy pathological examination.
Cirrhosis
Chronic hepatitis develops into cirrhosis and is the result of liver fibrosis. The mechanism has not yet been fully elucidated. It is also seen in subacute, chronic severe hepatitis and asymptomatic HBsAg carriers with insidious onset.
4. Liver cancer
HBV, HCV infection is closely related to the disease. It is more common in patients with liver cancer and liver cirrhosis. It can also be seen that chronic HBV infection has not developed into liver cancer without liver cirrhosis. The mechanism of its occurrence is currently considered to be related to HBV-DNA integration. In particular, X gene integration, HBxAg transactivation of proto-oncogenes plays an important role, in addition to acacia and other carcinogens have a certain synergistic effect.
Symptom
Hepatitis B symptoms Common symptoms Hepatic liver qi stagnation hepatitis B surface antigen (... Hepatitis B e antigen (H... Intrahepatic HDAg only... Single ALT increases nausea and fatigue, nosebleed, body discomfort
Systemic symptoms
The liver affects the whole body. Due to impaired liver function, patients with hepatitis B often feel fatigue, physical weakness, lower limbs or systemic edema, fatigue, and can not afford mental, insomnia, dreams and other hepatitis B symptoms. A few people will have hepatitis B symptoms similar to a cold.
2. Gastrointestinal symptoms
The liver is an important digestive organ of the human body. Hepatitis B patients have reduced bile secretion, and often have obvious symptoms of hepatitis B such as loss of appetite, nausea, oil disability, upper abdominal discomfort, and abdominal distension.
3. Huang Wei
The liver is the center of bilirubin metabolism. The concentration of bilirubin in the blood of patients with hepatitis B is increased, jaundice will appear, the skin and urine will be yellow, and the urine will have symptoms such as strong brown color.
4. Liver pain
The liver generally does not feel pain, but there is a distribution of pain nerves on the liver capsule on the surface of the liver. When the hepatitis B deteriorates, hepatitis B patients have hepatitis B symptoms such as right upper quadrant, right quarter rib discomfort, and dull pain.
5. Hepatosplenomegaly
Hepatitis B patients often have hepatitis B symptoms such as liver enlargement due to inflammation, congestion, edema, and cholestasis.
6. Palm performance
Many patients with hepatitis B will have hepatitis B symptoms such as liver palm. The surface of the palm of the patient with hepatitis B will be congestive and red, and the palm of the second finger of the ring finger of both hands has obvious tenderness and other symptoms of hepatitis B.
7. Skin performance
Many patients with chronic hepatitis, especially those with cirrhosis, have dull or dark complexion, which is called liver disease. This may be due to hepatitis B symptoms caused by endocrine disorders. At the same time, spider mites appear on the skin of patients with hepatitis B.
Examine
Examination of hepatitis B virus
1. Liver function tests: including bilirubin, thymol turbidity test, AST, ALT, A/G, prothrombin time, serum protein electrophoresis, etc.
2. Specific serum pathogen examination: including HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HBc, anti-HBcIgM. Conditionally detect HBV-DNA, DNA-p, Pre-S1, Pre-S2, and the like. In situ hybridization was used to detect HBV-DNA in the liver.
3. Liver biopsy (liver biopsy).
Diagnosis
Diagnosis and identification of hepatitis B virus
diagnosis:
According to the clinical characteristics, reference to epidemiological data, exclude other related diseases, determine the diagnosis depends on the serological examination of the pathogen. For patients with atypical clinical manifestations, liver biopsy should be performed.
I. Pathogenic diagnosis
Because there are more carriers of asymptomatic HBsAg, these people are re-infected with hepatitis A, C, D, E virus or other hepatitis, because HBsAg positive is easily misdiagnosed as acute hepatitis B, so the diagnosis should be cautious.
Second, the diagnosis basis of acute hepatitis B
1HBsAg positive; 2HBeAg positive; 3 anti-HBcIgM positive, high titer (1:1000); 4HBV-DNA positive.
Differential diagnosis:
Drug-induced hepatitis
The characteristics are: 1 history of useful drugs, known to have a variety of drugs can cause different degrees of liver damage, such as isoniazid, rifampicin can cause similar clinical manifestations of viral hepatitis; long-term use of diacetate, methyl Dopa can cause slow-lived liver; chlorpromazine, methyltestosterone, arsenic, bismuth, ketoconazole, etc. can cause cholestatic hepatitis; 2 mild clinical symptoms, elevated ALT, eosinophils; 3 After the drug was stopped, the symptoms gradually improved and the ALT returned to normal.
2. Cholelithiasis
There was a history of biliary colic, high fever and chills, right upper abdominal pain, positive Morphy sign, increased white blood cells, and increased neutrophils.
3. Characteristics of primary single cirrhosis
1 middle-aged women are more common; 2 jaundice continues to be significant, itchy skin, often yellow tumor, hepatosplenomegaly, ALP is significantly elevated, most anti-mitochondrial antibodies are positive; 3 liver function damage is light; 4 hepatitis B marker negative .
4. Hepatolenticular degeneration (Wilson's disease)
Often family history, mostly manifested by large limbs, tremors, increased muscle tone, brown-green pigment ring (KF ring) at the edge of the cornea, reduced copper and ceruloplasmin, increased urinary copper, and slow-lived hepatic copper and The ceruloplasmin is markedly elevated.
5. Extrahepatic obstructive jaundice
Such as pancreatic cancer, common cholangiocarcinoma, chronic pancreatitis, etc. need to be identified.
