GB 17011-1997 Diagnostic criteria and management principles for hepatitis E
Some standard content:
【GB170111997】
Diagnostic criteria and treatment principles for viral hepatitis E Preface
Viral hepatitis E is an enteric-transmitted disease caused by hepatitis E virus, characterized by inflammatory necrosis of hepatocytes. Patients are mainly adults, with a high mortality rate, especially in pregnant women in the last three months of pregnancy, when the mortality rate can reach 10% to 39%. Viral hepatitis E was first discovered in the Indian subcontinent, and there have been reports of large outbreaks in Central Asia, Southeast Asia, Africa, and the Indian subcontinent. Most outbreaks are waterborne. Reports of foodborne outbreaks have also been found in the literature. The infection rate of hepatitis E in the Chinese population is about 18%. Hepatitis E accounts for about 10% of acute sporadic hepatitis and is one of the Class B statutory infectious diseases in my country. Appendix A of this standard is the standard appendix.
Appendix B of this standard is the suggestive appendix.
This standard is proposed by the Ministry of Health of the People's Republic of China. This standard was drafted by the Institute of Virology, Chinese Academy of Preventive Medicine and Beijing Ditan Hospital.
The main drafters of this standard are Liu Chongbai and Xu Daozhen. The Chinese Academy of Preventive Medicine, the technical unit entrusted by the Ministry of Health, is responsible for the interpretation of this standard.
1 Scope
This standard specifies the diagnostic criteria and treatment principles of viral hepatitis E. This standard is applicable to medical and health epidemic prevention institutions at all levels as the basis for the diagnosis and prevention of viral hepatitis E.
2 Diagnostic criteria for viral hepatitis E
A comprehensive diagnosis is made based on epidemiological data, symptoms and signs, and laboratory tests. The diagnosis depends on pathogen serology or pathogen tests. 2.1 Acute hepatitis E and (jaundice type/non-jaundice type) 2.1.1 Epidemiological data: Contact with hepatitis patients or drinking water contaminated by feces and garbage or eating out within 2 to 6 weeks before the onset of the disease, or going to high-incidence or epidemic areas of hepatitis E. 2.1.2 Fatigue, loss of appetite or other gastrointestinal symptoms or hepatomegaly with tenderness or percussion pain for more than 1 week without other explanations. 2.1.3 Serum alanine aminotransferase (ALT) is significantly elevated. 2.1.4 Serological etiology excludes acute hepatitis A, B, C, and G. 2.1.5 Yellowing of skin and sclera, serum bilirubin BIL>17.1umol/L (>10mg/L) or positive urine bilirubin, and jaundice caused by other diseases is excluded. 2.1.6 Pathogen serological test, anti-HEV-IgM is positive or anti-HEV-IgG changes from negative to positive, or the titer changes from low to high, or from high to low by more than 4 times, clinical diagnosis: 2.1.2, 2.1.3 plus 2.1.4. Confirmed cases: 2.1.6.
Note: Those with 2.1.5 are jaundice type, and those without 2.1.5 are non-jaundice type. 2.2 Acute severe viral hepatitis E
2.2.1 Meets acute icteric hepatitis E (refer to 2.1). 2.2.2 Psychiatric and neurological symptoms (referring to hepatic encephalopathy) occur within 10 days after onset and other causes are excluded.
2.2.3 Jaundice rapidly deepens, serum bilirubin is greater than 171μmol/L. 2.2.4 Prothrombin time is prolonged, and prothrombin activity is less than 40%. Suspected cases: 2.2.1 plus 2.2.3.
Confirmed cases: Suspected cases plus 2.2.2 + 2.2.4. 2.3 Subacute severe viral hepatitis E
2.3.1 Meets acute hepatitis icteric type (refer to 2.1). 2.3. .2 The following conditions occur more than 10 days after onset: a) High strength and obvious loss of appetite or nausea and vomiting, yellowing of the skin and sclera, severe abdominal distension or ascites.
b) Serum bilirubin rises ≥171umol/L or the daily increase is greater than 17.1umol/L.
c) Serum prothrombin time is significantly prolonged, and prothrombin activity is less than 40%. d) Impairment of consciousness (referring to hepatic encephalopathy).
Suspected cases: 2.3.. 1 + 2.3.2a) and b). Diagnosed cases: Suspected cases plus 2.3.2c), refer to 2.3.2d). 3 Principles of treatment of hepatitis E
3.1 Principles of treatment of viral hepatitis E
3.1.1 Acute viral hepatitis E is a self-limiting disease that does not require special treatment. It is mainly supported by supportive therapy and symptomatic treatment.
3.1.2 Principles of treatment of severe hepatitis E: Strengthen the monitoring of patients and closely observe the condition. Take measures such as delaying the continued necrosis of liver cells, promoting liver cell regeneration, and improving liver microcirculation. Prevent and treat various complications, such as hepatic encephalopathy, cerebral edema, massive hemorrhage, renal insufficiency, secondary infection, electrolyte imbalance, ascites, hypoglycemia, etc., and strengthen supportive therapy. wwW.bzxz.Net
4 Prevention and epidemic management of hepatitis E (see Appendix A) 5 Pathogenic serological diagnostic reagents for hepatitis E (see Appendix B) Appendix A
(Standard Appendix)
Prevention and epidemic management of hepatitis E There is no specific active and passive immunization method for hepatitis E. Strengthening health education and cutting off the transmission route and managing the source of infection are the main measures to prevent hepatitis E. A1 Managing the source of infection and cutting off the transmission route A1.1 Medical personnel at all levels shall report cases in accordance with the Law of the People's Republic of China on the Prevention and Control of Infectious Diseases.
A1.2 Isolate patients for 3 weeks from the date of onset.
A1.3 Perform terminal disinfection on the patient's living and activity areas. A1.4 Observe contacts for 45 days and conduct ALT and urine bilirubin tests. AI.5 Patients with abnormal ALT, positive urine bilirubin, and positive anti-HEV-IgM are considered new cases and reported and isolated for treatment in accordance with the law. A1.6 Disinfect patient excreta including urine and feces and utensils that come into contact with urine according to Table A1.
Disinfection objects
1. Doors, windows, floors, furniture of houses
2. Vomit and excrement
3. Toilets and toilets
4. Food and nursing utensils
6. Clothes and bedding
7. Contaminated medical equipment
Types that can be sterilized under high pressure
Types that cannot be sterilized under high pressure
8. Drinking water
Disinfection method
0.5% Youlingjing spray
Add 2 parts of 10%~20% bleaching powder emulsion to 1 part of vomitus: Add 5 parts of bleaching powder to 1 part of vomitus without separation for 2h
Spray the supernatant of 3% bleaching powder on the toilet and soak it in the liquid for 1h2% peracetic acid, 2% bleaching powder or 3 parts of bleaching powder for 1h . Boil for 5~10min
0.2% ethyl peroxide bath or 0.2% eugenol bath for 2min
Environmental ethyl peroxide 0.4kg/m2 or formalin 100mL/m2, steam, airtight for 12~24h
High pressure fumigation 103425Pa: 15~39min: dry heat 160c1h or plain tape
Take 8ml of pentanediol (the original drug content is 25%), such as 0.3% sodium bicarbonate and water to 100mL. Make the pH to 7.7~8.3, slow soak for 1~~2h
The remaining rat protection is 0.3~1mg/L, or plain boil for 5min Appendix B
Take 0.5g of the original drug, add to 100ml
Take 3gc of bleaching powder, add a small amount of water to adjust and add water to 100mL.After the liquid is cleared, take the upper solution and use it in a sealed special sterilizer. (Appendix of the instructions) The pathogenic serological diagnostic reagents for hepatitis E cannot obtain viral antigens, chemically synthesized antigen peptides and cDNA recombinant antigens for diagnosis in tissue culture. The EIA reagents assembled from the two have similar sensitivity and specificity in detecting anti-HEV-IgG. The chemically synthesized oligopeptide antigen is composed of 42 amino acids of the B cell epitope determinant cluster at the 3' end of the second reading frame and 33 amino acids at the 3' end of the third reading frame: some amino acids of the RNA polymerase region dependent on RNA in the first reading frame are also synthesized. Among the three reading frames, the second and third reading frames are the dominant epitope determining groups, and the polymerase fragment of one frame is poor
B2CDNA recombinant antigen: The 3-end encoded polypeptides of the second and third reading frames expressed by prokaryotic cells are proved to have antigenicity and can be used as antigen materials for assembling diagnostic kits. The chimeric polypeptides can be obtained by chimeric expression of the B cell epitope determining group fragments of the second and third reading frames, which have antigenic reactions to the second and third reading frames, and the antigenicity is stronger than the peptides expressed separately. At present, EIA is used to detect hepatitis E at home and abroad. The basic principle is: the purified hepatitis E antigen is coated in the wells of the polystyrene plate under alkaline conditions, the unbound antigen is washed after saturated adsorption, the serum sample to be tested (1:20 dilution) is added and washed, and the anti-human IgG antibody labeled with horseradish peroxidase is added (if IgG is detected, the labeled anti-human IgG is added, if IgM type antibody is detected, the anti-human μ chain antibody is added). If the anti-HEV in the serum is positive, the labeled antibody can bind to the anti-HEV, incubate, wash, and add OPD substrate to show orange-yellow light absorption value (OD value) at a wavelength of 492nm. The greater the positive intensity, the colorless indicates a negative reaction. The positive judgment value is explained in the products of each manufacturer. The operation method and precautions are explained, so I will not elaborate on it here.
Anti-HEV-IgM appears in the early stage of the disease and can be used as an important judgment standard for the diagnosis of HEV pathogen typing. From the preliminary clinical test results, the reaction intensity of HEV-IgM is lower than that of hepatitis A, and the duration is also shorter. Therefore, blood samples should be collected immediately upon admission to the hospital for 1:5C dilution test of anti-HEV-IgM, and no later than half a month after the onset of the disease. Since the anti-HEV titer is low, rheumatoid factor should be tested for all anti-HEV-IgM positives. If the rheumatoid factor is positive and the anti-HEV-IgM is positive at the same time, the serum should be further diluted for verification. If the anti-HEV-IgM is still positive and the rheumatoid factor is negative, the diagnosis is established. Anti-human IgG can also be used to pre-neutralize the serum to be tested. If IgM can still be detected, it can be judged as anti-HEV-IgM positive. The indirect IgM detection method currently used has poorer specificity than the capture method and needs further improvement.
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