This standard specifies the diagnostic criteria and treatment principles for hepatitis B virus (HBV). This standard is applicable to medical institutions at all levels as a basis for the diagnosis and treatment of HBV patients. GB 15990-1995 Diagnostic criteria and treatment principles for hepatitis B virus GB15990-1995 Standard download decompression password: www.bzxz.net

GB15990--1995
Hepatitis B (abbreviated as HBV) is an infectious disease caused by the hepatitis B virus (HBV). This disease is widely prevalent in my country, with a high infection rate among the population. It is one of the most common infectious diseases that endangers people's health. Appendix A and Appendix B of this standard are both appendices to the standard. This standard is proposed by the Ministry of Health of the People's Republic of China. The drafting units of this standard are: Beijing Ditan Hospital, Beijing You'an Hospital, and the Infectious Diseases Teaching and Research Group of Beijing Medical University. The main drafters of this standard are: Lin Xiuyu, Xu Daozhen, and Wang Qinhuan. This standard is interpreted by the Office of Infectious Disease Supervision and Management of the Ministry of Health, the technical unit entrusted by the Ministry of Health. 329
1 Scope
National Standard of the People's Republic of China
Diagnostic criteria and principle of management of hepatitis B This standard specifies the diagnostic criteria and management principles of hepatitis B (abbreviated as HBV). This standard is applicable to medical institutions at all levels as a basis for the diagnosis and treatment of hepatitis B patients. 2 Reference standards
GB15990—1995
The provisions contained in the following standards constitute the provisions of this standard by being cited in this standard. The versions shown are valid when this standard is published. All standards will be revised, and the parties using this standard should explore the possibility of using the latest version of the following standards. (B15982-1995 Hospital Disinfection and Hygiene Standard 3 Diagnostic criteria and treatment principles of type B viral hepatitis 3.1 Diagnostic principles
Based on epidemiology, clinical symptoms, signs, laboratory tests and/or liver biopsy, etc., comprehensive analysis and dynamic observation are carried out to make a diagnosis.
3.2 Diagnostic criteria
3.2.1 Acute hepatitis
3.2.1.1 Acute non-jaundice hepatitis
a) Epidemiological data: Those who have received blood and blood products within six months or have had other medical-related infections, close contact in life, especially those who did not use condoms before sexual contact.
h) Symptoms: refers to the recent onset of obvious fatigue and digestive tract symptoms that have lasted for more than one week without any other explanation. ℃) Signs: mainly refers to liver enlargement, accompanied by tenderness or percussion pain. d) Liver function test: alanine aminotransferase (ALT) is significantly elevated. C) HBV marker detection: meets the pathogenic signs of acute hepatitis B, see A2 in Appendix A (Standard Appendix) for details. f) Pathological histological characteristics: if differential diagnosis requires, liver biopsy can be performed if conditions permit, see Appendix B for details. Among the above items, pathogenic indicators, symptoms and abnormal liver function are necessary conditions, and epidemiological data and signs are reference conditions. Suspected case: meets the above items b) + d). Confirmed case: suspected case + e).
3.2.1.2 Acute icteric hepatitis
a) 3.2.1.1.a).
b) refers to the recent onset of obvious fatigue, digestive tract symptoms and yellow urine that have lasted for more than one week without any other explanation. C) Physical signs: yellowing of skin and sclera, hepatomegaly, accompanied by tenderness or throbbing pain. d) Liver function test: ALT elevation, serum bilirubin (Bil) greater than 17.1μmol/1 (greater than 1mg/dL) and/or positive urine bilirubin and exclusion of jaundice caused by other diseases.
Approved by the State Administration of Technical Supervision on December 15, 1995 330
Implementation on July 1, 1996
GB15990-1995
() HBV marker detection: in line with the etiological indicators of acute hepatitis B, see Appendix A (Standard Appendix) A2 for details,) Pathological histological characteristics: if differential diagnosis is required, liver biopsy can be performed if conditions permit, see Appendix B for details. Suspected cases: b)+c)+d).
Confirmed cases: Suspected cases e).
3.2.1.3 Chronic persistent hepatitis (abbreviated as chronic persistent hepatitis)) Patients with acute hepatitis B for more than half a year and not yet cured, if there is no history of acute hepatitis B, the hepatitis course has not been cured for more than half a year, and the condition is too mild to be diagnosed as chronic active hepatitis.
h) Liver function test, ALT continuous or intermittent abnormalities. () HBV marker detection: meet the etiological indicators of chronic hepatitis B. See A3 in Appendix A (Standard Appendix) for details. d) Liver pathological histological characteristics: See Appendix B for details. Suspected case: a) + h) + c).
Confirmed case: Suspected case + d) or c) + d). 3.2.1.4 Chronic active hepatitis (abbreviated as chronic active hepatitis) a) There are obvious symptoms of hepatitis.
h) Physical signs: There may be liver disease face, liver palms, spider nevi, splenomegaly or jaundice (excluding other causes). ) Functional examination: AI.T is repeatedly and/or persistently elevated, plasma albumin is decreased, A/G protein ratio is abnormal, Y-globulin is elevated and/or bilirubin is abnormal for a long time or repeatedly.
d) IV marker test: in line with the etiological indicators of chronic hepatitis B, see A3 in Appendix A (Standard Appendix). () Pathological histological characteristics of the liver: see Appendix B for details. Clinically, it is difficult to distinguish between mild chronic active liver and chronic metastatic liver. The diagnosis must be made by combining pathological histological characteristics with clinical manifestations. Suspected case: a)+b)+c)+d).
Confirmed case: Suspected case+e) or d)+e). 3.2.1.5 Severe hepatitis
) Acute severe
1) No history of hepatitis B. The onset is acute jaundice hepatitis, and mental and neurological symptoms (hepatic encephalopathy of more than Ⅱ months) appear quickly within 10 days after onset, and other causes are excluded. In addition, jaundice rapidly deepens and severe gastrointestinal symptoms. 2) Physical signs; liver dullness rapidly narrows, etc. 3) Abnormal liver function, especially prolonged prothrombin time and prothrombin activity less than 40%. 4) HBV marker detection: in line with the etiological indicators of acute hepatitis B. See A2 in Appendix A (Standard Appendix). However, HBsAg may be negative while anti-HBs and anti-HBe may be positive during pregnancy. 5) Pathological histological characteristics of the liver: liver biopsy can be performed if conditions permit, see Appendix B for details. Suspected cases: 1) + 2) + 3).
Confirmed cases: suspected cases + 4) or suspected cases + 4) + 5). b) Subacute severe
1) Onset with acute jaundice hepatitis, the course of the disease is more than 10 days and less than 8 weeks, and impaired consciousness (hepatic encephalopathy above 1°). At the same time, jaundice rapidly increases and there is a tendency to bleed. 2) Laboratory examination: liver function is completely damaged, serum bilirubin is greater than 171tmol/l. or rises by more than 17.1umol/l every day. Alcohol tolerance is reduced. Prothrombin activity is less than 40%. 3) HBV marker detection: meet the etiological indicators of acute hepatitis B. See A2 in Appendix A (Standard Appendix) for details. J) Pathological histological characteristics of liver: see Appendix B for details. Similar cases: 1) 2).
Confirmed cases: suspected cases + 3) or suspected cases + 3) + 4). c) Chronic severe
GB15990-1995
Occurs on the basis of chronic active liver or post-hepatitis B cirrhosis, clinical manifestations and liver function changes are basically the same as subacute severe hepatitis. 3.2.1.6 Cholestatic hepatitis
a) Onset of acute jaundice hepatitis, jaundice lasts for 2 to 4 months or longer. b) Clinical manifestations are intrahepatic obstructive jaundice, and other causes of intrahepatic and extrahepatic obstructive jaundice can be excluded. C) Laboratory examination: Elevated serum bilirubin, mainly direct bilirubin, and significantly elevated alkaline phosphatase, Y-GT, and cholesterol. d) HBV marker detection: Meets the etiological indicators of acute hepatitis B. See A2 in Appendix A (Standard Appendix) for details. () Liver pathological histological characteristics: Liver biopsy can be performed if necessary, see Appendix B for details. Suspected case: a) + b) + c).
Confirmed case: Suspected case + d) or suspected case + d) + e). 3.2.1.7 Post-hepatitis B cirrhosis
a) Active cirrhosis
1) Has clinical manifestations of slow-acting liver. There are signs of portal hypertension and significant splenomegaly and hypersplenism (except portal hypertension caused by other reasons),
2) Laboratory examination: ALT increased, serum bilirubin increased, serum albumin decreased, A/G ratio inverted, beta-globulin increased. Thrombocytopenia and leukocytopenia. bZxz.net
3) Liver pathological histological characteristics: Do it when necessary, see Appendix B for details. b) Cirrhosis quiescent stage: Same as cirrhosis active stage, but ALT remains normal. 4 Principles of treatment of hepatitis B
4.1 Implement the hepatitis B vaccine immunization program for newborns. Carry out prenatal examinations, especially for infants born to mothers who are HBsAg positive and accompanied by HBeAg positive, use hepatitis B vaccine combined with hepatitis B high-titer immunoglobulin injection to block mother-to-child vertical transmission. The specific plan shall be implemented in accordance with relevant regulations.
4.2. Screening of blood donors
Blood donors must test serum transaminase (ALT) and HBsAg by sensitive method (EIISA) before each blood donation. Those who are positive for any of the two items are not allowed to donate blood
4.3 Carefully carry out health publicity and education to improve the knowledge of the whole people on the prevention and treatment of HBV infection; do a good job in premarital examinations, and the spouses who are positive and other high-risk groups exposed to HBV should also be vaccinated with hepatitis B vaccine. 4.4 Preventing medical transmission
Medical and health units at all levels should strictly implement one needle and one tube per person, and various medical and health supplies and equipment should be implemented in accordance with the relevant provisions of GB15982.
4.5 Management and follow-up of chronic HBsAg carriers Those who are positive for HBsAg in the blood but have no symptoms and signs, normal liver function, and no changes after half a year of follow-up are chronic HBsAg carriers. 4.5.1 Those who cannot donate blood can work and study as usual. 4.5.2 Pay attention to personal hygiene, menstrual hygiene, and industrial hygiene. The razors, shaving utensils, toothbrushes, and toiletries used should be used separately. 5 Principles of treatment of hepatitis B
Hepatitis B has various clinical manifestations and should be treated differently according to different types and stages of the disease. 5.1 Rest
In the early stage of acute hepatitis B, bed rest is recommended. Chronic hepatitis B should be properly rested. When the condition improves, pay attention to the combination of movement and rest. During the recovery period, gradually increase activities, but avoid overwork.
5.2 Diet
In the acute stage of acute hepatitis B, it is advisable to eat a light diet that is easy to digest and rich in vitamins. If chronic hepatitis B is not cured after repeated symptoms, it is advisable to eat a high-protein diet. 5.3 Drug treatment
5.3.1 Acute hepatitis B
GB15990—1995
Most cases are self-limiting. Localities should take appropriate measures and use local materials to select Chinese and Western medicines for symptomatic treatment and jaundice and bile-removing treatment. 5.3.2 Chronic hepatitis
The clinical manifestations are complex. Antiviral, immune adjustment, liver cell protection, liver fibrosis prevention, liver function improvement, liver microcirculation improvement and other therapies should be adopted according to the specific conditions of the patient. There are many kinds of drugs, and 1-2 kinds can be selected at the same time as appropriate. The course of treatment should be no less than three months. 5.3.3 Severe hepatitis
The condition is serious and should be treated with enhanced care, monitoring, and close observation of changes in the condition. On the basis of active supportive therapy, comprehensive measures should be taken to block progressive necrosis of liver cells, promote liver cell regeneration, improve liver function, and prevent and treat various complications (such as hepatic encephalopathy, cerebral edema, hemorrhage, renal insufficiency, secondary infection, electrolyte disorders, ascites, etc.) to prevent the condition from worsening and improve the cure rate. 333
Standard for the diagnosis of hepatitis B etiology GB15990-1995
Appendix A
(Appendix to the standard)
Methods for etiological examination
This standard requires the detection of HBV markers by ELISA, and requires the use of kits that meet the quality control standards. The specific operating steps are as follows:HBsAg
EL.ISA double antibody sandwich method operating steps: 1. Anti-HBs pure product is coated on the polystyrene plate wells, 0.1mL per well. 4'C overnight. 2. Wash 4 times with washing solution.
3. Add serum to be tested, 0.1mL per well, place at 37℃ for 2h or 43℃ for 1h. Add washing solution and wash 4 times.
5. Add anti-HBs enzyme marker, 0.1mL per well, place at 37℃ for 2h or 43℃ for 1h. 6. Wash 4~5 times with washing solution and pat dry.
7. Add substrate, 0.1mL per well, place at room temperature and avoid light for 15~30min, add 2mol/L sulfuric acid 30μL to terminate the reaction. 8. Result judgment:
Visual inspection:
Positive is colorimetric; negative is colorless.
Use microplate reader to read OD value:
Specimen OD value is greater than or equal to 2.1 times the negative control OD value is positive. Specimen OD value is less than 2.1 times the negative control OD value is negative. Anti-HBS
EIISA double antigen sandwich method operation steps:
1. HBsAg pure product is coated on the polystyrene plate wells, 0.1mL per well, overnight at 4C. 2. . Wash the plate 4 times with washing solution.
3. Add the serum to be tested, 0.1mL per well, 37C2h or 43C1h. 4. Wash the plate 4 times with washing solution.
5. Add HBsAg enzyme marker, 0.1mL per well, 37C2h or 43C1h. 6. Wash the plate 4~5 times with washing solution and pat dry.
7. Add substrate, 0.1mL per well, place at room temperature and avoid light for 15~30min, add 2mol/L sulfuric acid 30μul to terminate the reaction. 8. Result judgment:
Visual inspection:
Positive is color; negative is colorless.
Use microplate reader to measure OD value:
Specimen OD value is greater than or equal to 2.1 times of negative control OD value, which is positive. Sample OD value is less than 2.1 times of negative control OD value, which is negative. HBeAg
EI.ISA double antibody sandwich method operation steps: 334
GB15990
1. Anti-HBe pure product is coated on polystyrene plate wells, 0.1mL per well, 4C overnight. 2. Wash 4 times with washing solution.
3. Add serum to be tested, 0.1ml per well, 37℃2h or 43C1h. 4. Wash 4 times with washing solution.
5. Add anti-HBe enzyme marker, 0.1mL per well, 37C2h or 43C1h. 6. Wash 4-5 times with washing solution. Pat dry.
7. Add substrate, 0.1mL per well, place at room temperature and avoid light for 15-30min, add 30uL of 2mol/L sulfuric acid to terminate the reaction. 8. Result judgment:
Daily test:
Positive is colored; negative is colorless.
Use microplate reader to measure OD value:
Specimen ()D) value is greater than or equal to 2.1 times the negative control ()D value is positive. Sample (OD value is less than 2.1 times the OD value of the negative control is negative. Anti-HBe
EIISA neutralization test steps:
1. Anti-HBe pure product is coated on the polystyrene plate wells. 0.1mL per well, 4C overnight. 2. Wash with washing solution 4 times.
3. Add 0.05mL of the sample to be tested to each well, add 0.05mlL of neutralizing reagent (HBeAg) to the neutralization plate, and place at 37C2h or 43'C1h. 1. Add HBeAg pure product, 0.1mL per well, and place at 37C2h or 43'C1h. 5. Wash with washing solution 4 times
6. Add anti-HBe enzyme marker and serum to be tested, 0.1ml to each well, incubate at 37C for 2h or 43C for 1h. 7. Wash with washing solution 4~5 times, pat dry.
8. Add substrate, 0.1mL to each well, incubate at room temperature away from light for 15~30min, add 30μL of 2mol/L sulfuric acid to terminate the reaction. 9. Result judgment:
National test:
Positive is colorless; negative is colorimetric.
Use microplate reader to read (OD value, calculate inhibition rate: inhibition rate (%) = negative control OnFu = serum to be tested OD Value × 100 negative control OD value
Inhibition rate greater than or equal to 50% is positive.
Inhibition rate less than 50% is negative.
Anti-HBc
EI.ISA competitive method detection steps:
1. HBcAg pure product is coated on the polystyrene plate wells, 0.1ml per well, 4C overnight 2. Wash with washing solution 4 times.
3. Add the serum to be tested and the anti-HBc enzyme marker, each well 0.05mL, put 37C2h or 43C1h1. Wash 4~5 times with washing solution, tap on
5. Add substrate, 0.1mL per well, room temperature and dark for 15~30min, add 2mol/L sulfuric acid 30μL to terminate the reaction. 6. Result determination:
Visual inspection:
Positive is colorless; negative is color.
(AI)
Use microplate reader to read ()D value:
GB 15990—1995
Specimens (D value greater than or equal to 2.1 times the positive control OD value are negative. Specimens (D value less than 2.1 times the positive control OD value are positive. Spectrophotometer measures OD value (492nm)
Inhibition rate greater than or equal to 50% is positive (ten). Inhibition rate less than 50% is negative (one).
Inhibition rate (%) minus negative control OD is calculated as replacement serum OD value × 100 negative control OD value
Anti-HBcIgM
1. Anti-μ serum is coated on the polystyrene plate wells, 0.1mL per well, 4C overnight. 2. Wash with washing solution 4 times.
3. Add serum to be tested, 0.1mL per well, and place at 37C for 2h or 43C for 1h. 4. Wash with washing solution 4 times.
5. Add HBeAg, 0.1ml per well. Place at 37C for 2h or 43C for 1h. 6. Wash with washing solution 4 times.
7. Add anti-HBc enzyme-labeled antibody, 0.1mL, place at 372h or 43C1h. 8. Wash 4 times with washing solution and pat dry.
9. Add substrate, 0.1mL per well, place at room temperature and avoid light for 15~～30min, add 2mol/L sulfuric acid for 30min to terminate the reaction. 10. Result judgment:
National test:
Positive is colorimetric; negative is colorless.
Use microplate reader to read OD value:
Specimen ()I) value is greater than or equal to 2.1 times the negative control OD value is positive. Specimen (ID) value is less than 2.1 times the negative control OD value is negative. Anti-HBcIgG
1. Antiserum is coated on the polystyrene plate wells, 0.1mL per well, 4C overnight. 2. Wash 4 times with washing solution.
3. Add serum to be tested, 0.1mL per well. Place at 37℃ for 2h or 43C1h. 1. Wash 4 times with washing solution and pat dry.
5. Add HBcAg, 0.1ml per well. Place 37C2h or 43C1h. 6. Wash 4 times with washing solution and pat dry.
7. Add anti-HBc enzyme-labeled antibody, 0.1mL per well, place 37C2h or 43C1h. 8. Wash 4 times with washing solution and pat dry.
9. Add substrate, 0.1mL per well, place at room temperature and avoid light for 15-30min, add 2mol/L sulfuric acid for 30min to terminate the reaction. 10. Result determination:
Visual inspection:
Positive is colorimetric; negative is colorless.
Use an enzyme reader to read the OD value:
The sample OD value is greater than or equal to 2.1 times the negative control OD value for positive. The OD value of the specimen is less than 2.1 times that of the negative control (OD value is negative. Criteria for determining markers of HBV infection
(1) Serum HBsAg positive
GB15990—1995
(2) Serum HBVDNA positive (dot hybridization method), or HBVDNA polymerase positive, or HBeAg positive (HBeAg positive alone·Need to undergo a neutralization test to exclude false positives)·Serum anti-HBcIgG positive (positive alone, need to undergo a neutralization test to exclude false positives)
(3) Intrahepatic HBcAg positive and/or HBsAg positive, or HBVDNA positive. Patients with any of the above positive items can be diagnosed with HBV infection. A2 Diagnostic criteria for acute HBV infection markers
(1) During the course of the disease, H13sAg changes from positive to negative, or HBsAg changes from positive to negative and anti-HBs Positive conversion. (2) Anti-HBcIgM titer is high, while anti-HBcIgG is negative or low. A3 Diagnostic criteria for chronic HBV infection markers
Anti-HBcIgM titer is not high or negative, but either serum HBsAg or HBV DNA is positive and the course of disease lasts for more than half a year. Appendix B
(Standard Appendix)
Diagnostic criteria for pathological histology of viral hepatitis B1 Basic histological changes of viral hepatitis B1.1 Inflammatory changes: Main infiltrating cells such as lymphocytes, monocytes, plasma cells and tissue cells. B1.1.1 Interstitial inflammation: Inflammatory cells are present in the portal area or the newly formed fibrous septum, and a large number of lymphocytes infiltrate. Lymphoid follicles may sometimes be formed.
B1.1.2 Inflammation in the parenchyma: Inflammatory cells of varying numbers can be seen in the necrotic focus, and lymphocytes can be seen in close contact with hepatocytes, and even entering the hepatocytes.
B1.2 Necrotic changes
B1.2.1 Necrosis of a single hepatocyte: The cells undergo coagulative necrosis, and finally form eosinophilic bodies. B1.2.2 Focal necrosis: Small groups of hepatocytes undergo lytic necrosis, with infiltration of mononuclear and lymphocytes, with or without reticular scaffolds. Collapse, followed by Kupffer cell proliferation and phagocytosis of cell fragments. B1.2.3 Piecewise necrosis: Hepatocyte necrosis occurs at the junction of liver parenchyma and interstitium. When necrosis occurs in the portal area, accompanied by destruction of the boundary plate, it is called periportal piecewise necrosis. If necrosis occurs at the interface of the newly formed septum and liver parenchyma, it is called periseptal piecewise necrosis. In the necrotic focus, the liver cells are fragmented or dissociated from each other, inflammatory cells can invade the liver cells, and the liver cells can be seen surrounded by lymphocytes. Separated from each other. Such isolated and surviving hepatocytes sometimes form glandular structures, which are surrounded by collagen fibers. B1.2.4 Bridge necrosis: When two fragmentary necrotic foci fuse with each other, or when fragmentary necrotic foci fuse with the central necrotic foci of a lobule, it is called bridge necrosis.
B1.2.5 Multilobular necrosis: The necrosis range involves multiple lobules. B1.3 Other changes in liver parenchyma
B1.3.1 Edema, looseness, ballooning and eosinophilic changes of hepatocytes. B1.3.2 Bile stasis in hepatocytes and bile duct capillaries. B1.3.3 Hepatocyte regeneration, manifested by different sizes of hepatocytes and nuclei, the appearance of binucleated and multinucleated cells and the formation of double-layered hepatocyte cords. B1.3.4 Ground glass cells: There are lightly stained homogeneous structures in the cytoplasm, which are diffuse, and the inclusion or membrane distribution is more common in chronic hepatitis and HBsAg carriers.
B1.4 Biliary changes: regeneration of small bile ducts, occasional swelling and ballooning of bile duct epithelium. 337
B1.5 Fibrosis and septal formation
GB15990-1995
B1.5.1 Active septa: after fragmentary necrosis, fibrous tissue proliferates and extends into the lobule, forming a wedge shape, accompanied by infiltration of a large number of inflammatory cells.
B1.5.2 Passive septa: formed due to hepatocyte necrosis, collapse of reticular scaffold and fibrosis, with very mild inflammatory infiltration, and clear boundaries between septa and liver parenchyma.
B2 Histological diagnostic criteria for viral hepatitis
B2.1 Acute hepatitis
B2.1.1 Acute icteric hepatitis: hepatocyte swelling, ballooning, pale cytoplasmic staining, nuclear condensation, eosinophilic degeneration, eosinophilic body formation, nuclear vacuolar degeneration, or nuclear dissolution, focal necrosis and regeneration of hepatocytes. Infiltration of large mononuclear and lymphocytes in the portal area. Proliferation of Kuffer cells in the wall of the hepatic sinusoids.
B2.1.2 Acute non-icteric hepatitis; the lesions are similar to those of the acute icteric type, but the degree is milder. B2.2 Chronic hepatitis
B2.2.1' Chronic persistent hepatitis is divided into three categories: a) Chronic lobular hepatitis
Mainly inflammation in the liver lobules and degeneration and necrosis of hepatocytes, and the changes in the portal area are not obvious. b) Chronic interstitial hepatitis
The inflammatory reaction and degeneration and necrosis in the lobule are mild. There are fibroblasts in the portal area extending into the lobule to form septa. There are few inflammatory cells in the septa and no pseudolobule is formed.
c) Chronic portal hepatitis
The degeneration and necrosis of the liver parenchyma are mild. There are a few punctate necrosis. Occasionally, eosinophilic bodies are seen. There are a large number of inflammatory cells infiltrating the portal area, causing the portal area to enlarge, but there is no destruction of the boundary plate or fragmentary necrosis. B2.2.2 Chronic active hepatitis
Fragmentary necrosis is the main feature, and the lesions in the lobule include punctate and (or) focal necrosis, or even focal fusion necrosis, as well as degeneration and inflammatory reaction.
Chronic active hepatitis is divided into three categories:
a) Mild chronic active hepatitis
Meets the basic characteristics of this type, but the lesions are milder. b) Moderate chronic active hepatitis
There is extensive fragmentary necrosis and active septation formation, severe degeneration and necrosis of the liver parenchyma, bridge necrosis and passive septation formation can be seen, but most lobular structures can still be identified. c) Severe chronic active hepatitis
Bridge necrosis is more extensive, involving most lobules and destroying the integrity of the lobules. B2.3 Cholestatic hepatitis
The pathological histology is similar to acute icteric hepatitis, and there is bile thrombus formation in the bile duct capillaries, bile pigment retention in the cells, small dot-like particles appear in the hepatocytes, and small bile duct dilatation and neutrophil infiltration in the portal area. B2.4 Cirrhosis
B2.4.1 Active cirrhosis
Cirrhosis is accompanied by fragmentary necrosis, which can exist around the portal area and at the junction of the fibrous septum and the liver parenchyma. The hepatocytes have degeneration, necrosis and inflammatory reactions.
B2.4.2 Silent cirrhosis
There are few inflammatory cells in the fibrous septa around the pseudolobules, and the boundary between the interstitium and the substance is very clear. B2.5 Severe hepatitis
B2.5.1 Acute severe hepatitis
a) Acute edematous severe hepatitis
GB15990 ---1995
Severe diffuse swelling of hepatocytes, obvious cell membrane, lightly stained or nearly transparent cytoplasm, cells squeezed against each other to form polygons, similar to plant cells. The lobule structure is disordered, and there are many necrotic foci of varying sizes in the lobules. There is obvious bile duct congestion between the swollen hepatocytes. b) Acute necrotizing severe hepatitis
There is extensive hepatocyte necrosis, the hepatocytes in this area disappear, and the reticular scaffold is left. The hepatic sinusoids are congested, with infiltration of neutrophils, monocytes, lymphocytes and a large number of phagocytes, and small bile duct congestion can be seen in some of the remaining reticular structures. B2.5.2 Subacute severe hepatitis
Large necrosis and bridge-shaped necrosis of varying ages can be seen, reticular stent collapse, obvious portal area concentration, a large number of proliferating bile ducts and cholestasis can be seen, and the remaining hepatocytes proliferate into clusters, presenting a pseudolobular structure. B2.5.3 Chronic severe hepatitis
Large or sub-massive necrosis can be seen on the background of chronic liver lesions (i.e., fresh large or sub-massive necrosis on the background of chronic old lesions, such as chronic active liver and cirrhosis).
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