GB 17010-1997 Diagnostic criteria and treatment principles for hepatitis A
Some standard content:
【GB17010—1997】
Diagnostic criteria and treatment principles for hepatitis A virus Preface
Hepatitis A virus (abbreviated as HAV) is a common gastrointestinal infectious disease caused by hepatitis A virus (HAV). The disease is mainly transmitted through fecal-oral route. It is not only sporadic throughout the year, but also often occurs in seasonal or food-borne outbreaks, thus endangering people's health. It is one of the Class B statutory infectious diseases in my country.
Appendix A, Appendix B, and Appendix C of this standard are all appendices to the standard. This standard was proposed by the Ministry of Health of the People's Republic of China. This standard was drafted by the Shanghai Infectious Diseases Hospital. The main drafters of this standard: Wu Shanming, Luo Chengyu, Jiang Weilun This standard is interpreted by the Chinese Academy of Preventive Medicine, the technical management unit entrusted by the Ministry of Health.
1 Scope
This standard specifies the diagnostic criteria and treatment principles for hepatitis A. This standard is applicable to medical institutions at all levels as the basis for the diagnosis and prevention of hepatitis A. 2 Diagnostic principles
Diagnosis is made based on epidemiological, clinical symptoms, signs, laboratory tests and other means, and comprehensive analysis of dynamic observation.
3 Diagnostic criteria
3.1 Acute hepatitis
3.1.1 Acute non-jaundiced hepatitis
3.1.1.1 Epidemiology: History of eating unclean food or drinking unclean raw water or close contact with acute hepatitis A patients within 45 days before onset. 3.1.1.2 Symptoms: Gastrointestinal symptoms such as fever, weakness and anorexia, nausea, and vomiting that have appeared in the past week or so without other explanations. 3.1.1.3 Signs: Enlarged liver, accompanied by tenderness or percussion pain. 3.1.1.4 Liver function test: Alanine aminotransferase (ALT) is obviously abnormal. 3.1.1.5 HAV marker test: serum anti-HAV-IgM positive or anti-HAV-IgG double serum with 4-fold increase (see Appendix A for details). Suspected cases: 3.1.1.2 + 3.1.1.4. wwW.bzxz.Net
Confirmed cases: suspected cases plus 3.1.1.5. 3.1.2 Acute icteric hepatitis
Anyone who meets the diagnostic conditions of acute non-icteric hepatitis, and whose serum bilirubin is greater than 17umO/L, urine bilirubin is positive, or clinically has sclera and skin jaundice and excludes jaundice caused by other diseases can be diagnosed
3.2 Cholestatic hepatitis
3.2.1 The onset is similar to acute icteric hepatitis, but the subjective symptoms are often milder. 3.2.2 Liver function test: serum bilirubin is significantly increased, mainly direct bilirubin, accompanied by significant increase in alkaline phosphatase, a-glutamyl transpeptidase, cholesterol, etc., and moderate increase in ALT.
3.2.3 Obstructive jaundice lasting for more than 3 weeks, and other causes of intrahepatic and extrahepatic obstructive jaundice can be excluded.
3.2.4 HAV marker detection: Same as 3.1.1.5. 3.2.5 Liver pathological characteristics: See Appendix B for details. Suspected cases: 3.2.1+3.2.2+3.2.3. Confirmed cases: Suspected cases plus 3.2.4 or 3.2.4 plus 3.2.5. 3.3 Severe hepatitis
3.3.1 Acute severe
3.3.1.1 Acute onset, severe gastrointestinal symptoms, and rapid onset of mental and neurological symptoms within 10 days after onset (hepatic encephalopathy of II° or above according to Smith classification), and other causes are excluded.
3.3.1.2 Physical signs: Rapid shrinkage of the liver. 3.3.1.3 Abnormal liver function, serum bilirubin greater than 171umol/L or daily increase greater than 17.1umol/L within a few days, prothrombin activity less than 40%. 3.3.1.4 HAV marker detection: Same as 3.1.1.5. 3.3.1.5 Liver pathological characteristics: See Appendix B for details. Suspected cases: 3.3.1.1+3.3.1.2+3.3.1.3. Confirmed cases: Suspected cases plus 3.3.1.4 or 3.3.1.2 plus 3.3.1.5. 3.3.2 Subacute severe
3.3.2.1 Onset with acute hepatitis, clinically there is extreme fatigue, severe loss of appetite, rapid deepening of jaundice, ascites and bleeding tendency. Progressive shrinkage of the liver. The course of the disease is more than 10 days and less than 8 weeks, and impaired consciousness occurs (hepatic encephalopathy of I° or above appears according to the Smith classification).
3.3.2.2 Significant liver function abnormalities, bile enzyme separation, albumin/globulin ratio inversion, decreased cholesterol, prothrombin activity less than 40%. 3.3.2.3 HAV marker detection; same as 3.1.1.5 3.3.2.4 Liver pathological characteristics: see Appendix B for details, suspected cases: 3.3.2.1 + 3.3.2.2. Confirmed cases: suspected cases plus 3.3.2.3 or 3.3.2.3 plus 3.3.2.4. 4 Treatment principles
See Appendix C for treatment principles.
4.1 Rest: In the early stage of acute hepatitis, patients should be hospitalized or isolated for treatment and rest. 4.2 Diet: Patients with acute hepatitis who have poor appetite should eat light and easily digestible food. Patients with obvious loss of appetite or vomiting can be given intravenous drip of 10% glucose solution. 4.3 Drug treatment: There is no significant difference in the efficacy of Chinese and Western medicines for the treatment of acute hepatitis. Local areas can choose appropriate western medicine or Chinese herbal medicine for treatment based on the source of medicine and local conditions. The types of medicines should not be too many, the time should not be too long, and the use of medicines should be simplified. The routine use of adrenocortical hormones to treat acute hepatitis is not advocated. 4.4 Severe hepatitis should be treated with enhanced care, close observation of changes in the condition, and comprehensive measures and supportive treatments such as blocking liver cell necrosis, promoting liver cell regeneration, and preventing and treating various complications should be adopted to prevent the disease from worsening
5 Principles of prevention
5.1 Strengthen health education and block fecal-oral transmission. 5.2
The catering industry should conscientiously implement the Food Hygiene Law. 5.3
Protect susceptible populations.
Appendix A
(Appendix to the standard)
Etiological diagnosis
A1 Serological examination for diagnosis of acute hepatitis A virus (HAV) infection This standard requires the use of MACELISA (IgM antibody capture enzyme-linked immunosorbent assay) to detect serum anti-HAV-IgM. The kit used should have a production document number approved by the Ministry of Health.
AI.1 Method for MACELISA detection of anti-HAV-IgM A1.1.1 Liquid preparation
A1.1.1 Coating solution (carbonate buffer pH 9.6) Sodium carbonate 0.16g, sodium bicarbonate 0.29g, distilled water to 100mL. A1.1.1.2 Washing solution (PBS-Tween-20 buffer pH 7.4) Sodium chloride 8g, potassium dihydrogen phosphate 0.2g, disodium hydrogen phosphate (12 crystal water) 2.9g Potassium chloride 0.2g, Tween-20 0.5mL, add distilled water to 1000mL A1.1.1.3 Dilution solution (10% calf serum PBS-Tween) Add calf serum 10mL to the above PBS-Tween-20 90mL. A1.1.1.4 Substrate solution
0.1mol/L disodium hydrogen phosphate 5.14mL, 0.05mol/L citric acid 4.86mL, o-phenylenediamine (OPD) 4mg, add 3% hydrogen peroxide, 0.05mL after dissolution (prepared before use). A1.1.1.5 Stop solution
2mol/LH2SO40
A1.1.2 Operation steps
A1.1.2.1 Coating: Dilute the pure anti-human IgM (μ chain specific) with the coating solution according to the determined multiple and add it to the plastic microwell reaction plate, 0.1mL per well, and place it at 4℃ overnight. Pour off the liquid, wash 3 times with detergent, and pat dry. A1.1.2.2 Sample addition: Dilute the serum sample with diluent at 1:1000, add 0.1mL to each well, and set up 3 negative control wells, 2 positive control wells, and 1 blank control well, place at 37℃, incubate for 4h, wash 3 times, and pat dry. A1.1.2.3 Add antigen: Add 0.05mL of HAV-Ag (cell culture proliferation) to each well and place it at 4℃ overnight. Wash 3 times and pat dry.
A1.1.2.4 Add enzyme conjugate: dilute anti-HAV-HRP with diluent according to the determined multiple, and add 0.1mL to each well (no addition to blank control wells). Incubate at 37℃ for 2h, wash 3 times, and pat dry.
A1.1.2.5 Color development: add freshly prepared substrate solution, 0.1mL to each well, color development at 37℃ for 15min, and add 0.05mL of stop solution to each well. A1.1.3 Result determination
Self-test method: color development is positive; colorless or very light yellow is negative. Colorimetric method: use an enzyme-labeled colorimeter with a wavelength of 492nm, calibrate the blank well to zero, read the optical density (OD) of each well, and calculate the cutoff value (COV). COV = average OD value of negative control × 2.1 (if the OD value of negative control is <0.05, calculate as 0.05). Any specimen with an OD value >COV is judged as positive, and the specimen OD value isCOV was judged to be negative, and the specimen was OD
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