Hepatitis B

Introduction to hepatitis B Hepatitis B, also known as serum hepatitis and hepatitis B virus, is an infectious disease caused by hepatitis B virus (HBV). It is transmitted through blood and body fluids and has a chronic carrying state. Because it may be transmitted through sexual life, it is listed internationally as a sexually transmitted disease. Hepatitis B is widespread in China, and the infection rate is high. In some areas, the infection rate is more than 35%. Hepatitis B has diverse clinical manifestations and is prone to develop chronic hepatitis and cirrhosis. A small number of patients can be converted to primary liver cancer. The main treatment is antiviral therapy. The treatment of hepatitis should be based on the clinical type and different types of pathogens. The general principle is: take appropriate rest, reasonable nutrition, supplemented by selective use of drugs, avoid alcohol, prevent overwork and avoid The application of liver-damaging drugs should be simple and not suitable for use. Chronic hepatitis mainly includes antiviral replication and improves immune function. basic knowledge Sickness ratio: 1%-2% Susceptible people: good for infants, pregnant women, the elderly Mode of transmission: mother-to-child transmission of blood-borne transmission Complications: fatty liver, liver cirrhosis, liver cancer

Hepatitis B etiology

Sexual contact transmission (20%):

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. Sexual intercourse, homosexual contact and no protective measures.

Iatrogenic transmission (20%):

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 (10%):

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.

Blood transmission (30%):

Hepatitis B virus is transmitted through blood or blood products. The blood after blood donation in developed countries is checked for hepatitis virus, so the possibility of contracting hepatitis through blood in these areas is almost zero.

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 formed in a short period of time, activates complement, causing local hypersensitivity reaction (Arthus reaction) ), causing massive hepatocyte necrosis, absorption of intestinal endotoxin, can cause Schwartzman reaction, causing ischemic necrosis of hepatocytes, and adding -tumor necrosis factor (TNF-), IL-1 and leukotrienes 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.

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.

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. Therefore, although insulin is elevated and 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.

Hepatitis B symptoms Common symptoms Liver disease Rongda Sanyang core antibody (anti-H... Liver palm jaundice, alanine aminotransferase, high liver enlargement, nausea, abdominal distension, fatigue

The incubation period of this disease is 6 weeks to 6 months, usually 3 months. This period is called the incubation period from the invasion of the hepatitis virus to the initial clinical symptoms. The incubation period varies with the type, quantity, virulence, and immune status of the pathogen.

Whole body performance

Patients often feel weak, prone to fatigue, and may have mild fever. Insomnia, dreams, etc. may be related to this.

2. Digestive tract performance

In hepatitis, liver function is abnormal, bile secretion is reduced, and there is often loss of appetite, nausea, oiliness, upper abdominal discomfort, and abdominal distension.

3. Huang Wei

When the condition is severe, liver function is impaired, bilirubin intake, binding, secretion, excretion and other obstacles, blood bilirubin concentration increases. The bilirubin is discharged from the urine, and the color of the urine turns yellow, which is the earliest manifestation of jaundice. The concentration of bilirubin in the blood continues to increase, causing yellowing of the eyes and skin. Due to the discharge of bile acids, the concentration of bile acids in the blood is increased, and excessive bile acids are deposited on the skin, stimulating the peripheral nerves, which can cause itching.

4. Liver pain

Chronic hepatitis B generally does not have severe pain. Some patients may have upper right abdomen, right quarter rib discomfort, dull pain, tenderness or slap pain. If the liver area is severely painful, pay attention to the possibility of biliary disease, liver cancer, and gastrointestinal disease to avoid misdiagnosis.

5. Hepatosplenomegaly

Patients often have enlarged liver due to inflammation, congestion, edema, and cholestasis. In the late stage, a large number of liver cells are destroyed, fibrous tissue is contracted, and the liver can be shrunk. In the early stage of acute hepatitis or chronic hepatitis, the spleen has no obvious swelling. When the portal vein is high, the spleen is congested and can cause swelling of the spleen.

6. Extrahepatic manifestations

Chronic hepatitis B, especially in patients with cirrhosis, looks dull and dark, called liver disease. The palm of the hand and the small fish are obviously congested and called the liver palm. A cluster of radially expanding, capillary-like capillaries on the skin is called spider mites, and other parts can also appear. Males may have erectile dysfunction, symmetric or asymmetrical breast hyperplasia, swelling and breast development, and may be misdiagnosed as breast cancer; women may have menstrual disorders, amenorrhea, loss of libido and so on. This may be related to decreased liver function, decreased estrogen inactivation, and increased estrogen in the body.

7. Liver fibrosis

Chronic hepatitis B inflammation has long-term unhealed, repeated attacks, intrahepatic fibrous connective tissue hyperplasia, and its degradation activity is relatively or absolutely insufficient, a large number of extracellular matrix deposition to form liver fibrosis. If liver fibrosis is accompanied by destruction of the hepatic lobular structure (liver regeneration nodules), it is called cirrhosis. It is difficult to separate the two clinically. The chronic liver disease is a continuous development process from liver fibrosis to cirrhosis.

Hepatitis B checkup

1. Liver function test

Including bilirubin, thymol turbidity test, AST, ALT, A/G, prothrombin time, serum protein electrophoresis, etc.

2. Specific serum pathogen examination (hepatitis B 2 half check)

Including HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HBc, anti-HBcIgM, conditionally detectable HBV-DNA.

DNA-p, Pre-S1, Pre-S2, etc., in situ hybridization was used to detect HBV-DNA in the liver.

Blood picture

The total number of white blood cells is normal or slightly lower, the neutrophils can be reduced in the classification count, and the lymphocytes are relatively increased.

4. Urine

Patients with acute jaundice hepatitis can be positive for urinary bilirubin and urobilinogen before the onset of jaundice.

Hepatitis B diagnosis and identification

diagnosis

According to the clinical characteristics, reference to epidemiological data, to exclude other related diseases, to 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, hepatitis 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.

The characteristics of HBV infection are diversified clinical manifestations and long incubation period (about 45-160 days, average 60-90 days).

Acute hepatitis B

The onset is slower than hepatitis A.

(1) jaundice type: clinical can be divided into the first stage of jaundice, jaundice period and recovery period, the whole course of disease is 2 to 4 months, most of them have gastrointestinal symptoms in the early stage of jaundice, such as anaesthesia, loss of appetite, nausea, vomiting, bloating, Weakness, etc. Some patients have low fever or serum-like symptoms, such as joint pain, urticaria, angioedema, rash, etc., which are more common than hepatitis A. The progression and outcome of the disease are similar to those of hepatitis A, but a few patients The prolonged unhealed transition to chronic hepatitis.

(2) No jaundice type: The clinical symptoms are mild or asymptomatic. Most of them are found in physical examination or other diseases, and there is a single ALT elevation, which is easy to change to chronic.

2. Cholesterol

As with hepatitis A, it is characterized by longer-term intrahepatic obstructive jaundice, and the gastrointestinal symptoms are mild, the liver is enlarged, and the results of intrahepatic obstructive jaundice last for several months.

3. Chronic hepatitis B

The course of disease is more than 6 months.

(1) Chronic persistent hepatitis (slowly moving liver) has mild clinical symptoms, no jaundice or mild jaundice, mild hepatic swelling, spleen generally can not be touched, liver function damage is light, polynomial manifests as single ALT fluctuation, turbidity and There is no obvious abnormality in plasma protein, and there is generally no extrahepatic manifestation.

(2) Chronic active hepatitis (slow live liver) has severe clinical symptoms, persistent or recurring, and obvious signs, such as liver disease face, spider mites, liver palm, may have different degrees of jaundice, liver enlargement, medium-hard texture, Most splenomegaly, liver function damage is significant, ALT persists or repeatedly increases, turbidity is abnormal, plasma globulin is elevated, A/G ratio is decreased or inverted, and some patients have extrahepatic manifestations such as arthritis, nephritis, and dryness. Syndrome and nodular arteritis, such as anti-nuclear antibodies, anti-smooth muscle antibodies and anti-mitochondrial antibodies can be positive, can also be seen without jaundice and atypical, although the history is shorter, the symptoms are light, but chronic Signs of liver disease and liver function damage; or chronic prolonged hepatitis, but confirmed by liver tissue pathology as chronic active hepatitis.

In recent years, with the research progress of HBV-DNA pre-C gene mutation, existing scholars advocate that chronic hepatitis B can be divided into two types according to HBeAg and anti-HBe conditions: 1HBeAg-positive chronic hepatitis (typical chronic hepatitis B) from HBV wild The infection of the strain is caused by HBeAg-positive and anti-HBe-positive in the course of the disease. It is consistent with the previous view. HBeAg-positive is active in HBV replication in vivo, HBV-DNA positive in serum, liver function damage and liver tissue. Pathological changes, when HBeAg turned negative, anti-HBe turned positive, representing HBV replication weakened or stopped, serum HBV-DNA turned negative, liver function returned to normal, liver tissue lesions improved, 2 anti-HBe positive chronic hepatitis (atypical chronic Hepatitis B is thought to be caused by HBV pre-C gene mutant, HBeAg-negative in the serum, anti-HBe-positive, HBV-DNA in the body still replicates, liver shows progressive serious disease, easy to develop into severe hepatitis, cirrhosis And hepatocellular carcinoma.

4. Severe hepatitis B

(1) acute severe hepatitis (fullinant hepatitis): onset of acute jaundice-like hepatitis, but with high fatigue and significant gastrointestinal symptoms, such as severe loss of appetite, frequent nausea, vomiting, abdominal distension, hepatic encephalopathy within 10 days after onset Most of them are excited on the 3rd to 5th day after the illness, euphoric, multilingual, abnormal personality behavior, daytime sleepiness, no sleep at night, day and night inversion, unclear vision, unstable walking, etc., orientation and computational power obstacles, Further development into excitement, screaming and screaming, severe cases can be manifested as cerebral edema and increased intracranial pressure, such as increased blood pressure, conjunctival edema, and even larger pupils on both sides, cerebral palsy, so prevention and active treatment Cerebral edema, prevention of cerebral palsy, is of great significance for the rescue of patients, jaundice appears rapidly deepening, liver dullness area shrinks and obvious bleeding tendency, generally no ascites or late appearance, often died within 3 cerebral palsy, bleeding and other complications.

(2) Subacute severe hepatitis: the onset is the same as that of general acute jaundice hepatitis. The disease is aggravated after 10 days after the onset. It is characterized by high fatigue, abdominal distension, and no diet. The jaundice is deepened day by day, and the bleeding tendency is characteristic. Hepatorenal syndrome and hepatic encephalopathy appear, the course of disease is several weeks to several months, this type is easy to develop into cirrhosis after necrosis, and hepatic encephalopathy can be the first symptom after onset, but the medical history is over 10 days, other Similar to acute severe hepatitis.

(4) Asymptomatic HBsAg carriers: Most asymptomatic, HBsAg-positive at the time of physical examination, normal liver function or partial ALT elevation, less signs.

The clinical features of senile viral hepatitis are slow onset, mild symptoms and inconsistent severity, slow recovery, and chronicity. The incidence of severe hepatitis and slow-lived liver is higher, with subacute and chronic severe hepatitis. More common.

Differential diagnosis

Drug-induced hepatitis

The characteristics are: 1 history of useful medicine, 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 chronic liver, chlorpromazine, methyltestosterone, arsenic, expectorant, ketoconazole, etc. can cause cholestatic hepatitis. 2 clinical symptoms are mild, single ALT is elevated, and eosinophils are increased. 3 After the drug was stopped, the symptoms gradually improved and 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. Primary biliary cirrhosis

Features are more common in 1 middle-aged women. 2 Astragalus continued to be significant, itchy skin, often with yellow tumors, hepatosplenomegaly, ALP was significantly elevated, and most anti-mitochondrial antibodies were positive. 3 liver function damage is lighter. 4 Hepatitis B markers are negative.

4. Hepatolenticular degeneration (Wilson's disease)

There is often a family history, with extensive tremors of the limbs, increased muscle tone, a brown-green pigment ring at the edge of the cornea (KF ring), decreased copper and ceruloplasmin, increased urinary copper, and slow-lived hepatic copper and copper. Blue protein is significantly elevated.

5. Acute fatty liver during pregnancy

Most occur in the late pregnancy, the clinical features are: 1 early onset of acute severe abdominal pain, increased amylase, like acute pancreatitis. 2 Although jaundice is very heavy, serum direct bilirubin is increased, but urinary bilirubin is often negative. Domestic reports of this phenomenon can also be found in acute severe hepatitis for reference. 3 often before the onset of liver failure, severe bleeding and renal dysfunction, ALT increased, but turbidity is normal. 4B type ultrasound examination is a fatty liver waveform to help early diagnosis, confirmed by pathological examination, pathological features of the liver lobular to the middle of the cell enlargement, cytoplasm filled with fat vacuoles, no large hepatocyte necrosis.

6. Extrahepatic obstructive jaundice

Such as pancreatic cancer, total cholangiocarcinoma, chronic pancreatitis, etc. need to be identified.

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