Post-blood transfusion hepatitis

　　How is hepatitis B after blood transfusion caused? Briefly describe the following three types of hepatitis after blood transfusion:

　　One, Hepatitis B after blood transfusion

　　HBsAg is the most common and most important marker of hepatitis B virus, and the detection of HBsAg is one of the routine projects for screening blood donors in China. Currently, enzyme immunoassay (EIA) is used, which has greatly reduced the occurrence of hepatitis B after blood transfusion, but it is still impossible to prevent it completely. The reason is:

　　1, Acute hepatitis is in the incubation period, HBsAg has not appeared or the concentration is low;

　　2, Chronic hepatitis carriers may have HBsAg levels below the detection level;

　　Gene mutation of hepatitis B virus (HBV);

　　Technical errors in detection;

　　Non-blood transfusion routes of transmission;

　　The infectivity is strong, 0.00004ml of blood containing HBV is enough to cause infection.

　　Whether the recipient of HBV (+) blood is infected depends on the amount of virus infected and the immune level of the recipient. In a survey in the 1980s, it was found that the HBV infection rate of recipients with HBsAg (+) was 50.0%, and only one case developed post-transfusion hepatitis, which was an explosive hepatitis. 21.4% of recipients received blood from donors with HbcAb (+) and 5.9% received blood from donors with HbsAg (-)/HbcAb (-), and both developed transient asymptomatic infections without overt hepatitis. It is possible that the virus content in HBsAg (-) blood is low, and such transmission is rarely detected clinically.

　　Manifest post-transfusion hepatitis B is often acute. Due to the large amount of virus infected through blood transfusion, many cases of post-transfusion hepatitis present an explosive course; approximately 1/4 of explosive hepatitis B is due to blood transfusion, of which 45%-60% is caused by HBV.

　　Post-transfusion hepatitis C

　　In September 1989, at the International Non-A, Non-B Hepatitis Conference held in Tokyo, Japan, NANBH was officially divided into HC and HE. It is reported that 90% of post-transfusion hepatitis (PTH) is PTH-C type, of which 50%-60% can develop into chronic hepatitis. Among chronic hepatitis, 20% develop into cirrhosis and primary liver cancer. Early studies in the United States reported a PTH-C incidence of 21%, which has now decreased to 1%-4%. The positive rate of anti-HCV in the normal Chinese population is 1.35%, while the reported positive rate of blood donors varies from place to place.

　　The incubation period of acute hepatitis C virus (HCV) infection is 2-26 weeks, with an average of 7-4 weeks. 40%-75% of cases are asymptomatic, and HCV RNA in serum is detected only when alanine aminotransferase (ALT) levels are elevated. Symptoms are generally mild if present. Studies on the natural course of chronic hepatitis C show that about 50% (30%-60%) of acute HCV infections will evolve into a persistent carrier state. Due to the presence of viremia, it can become an important source of infection. Chronic hepatitis C includes chronic persistent hepatitis and chronic active hepatitis, which can evolve from acute hepatitis or occur covertly. Compared to hepatitis B, hepatitis C has a stronger tendency towards chronicity, with about 20% of chronic hepatitis C patients developing cirrhosis within 20-30 years, and these patients may develop liver cancer within the next 10 years. The incidence and mortality rates of severe hepatitis are lower than those of hepatitis B.

　　Post-transfusion hepatitis G

　　The hepatitis G virus is a suspected hepatitis virus isolated from two patients with hepatitis using modern molecular virology techniques, respectively named GBV-C and HGV. Sequence analysis shows that the homology at the nucleotide and amino acid levels is 85% and 95%, respectively. Therefore, GBV-C and HGV are different strains of the same virus, and have similar structural genes to HCV.

　　The transmission route has been confirmed to be transmitted through blood transfusion, susceptible groups include those receiving hemodialysis, as well as medical personnel in contact with blood sources; in addition, intravenous drug use is another important route. The detection rate of hepatitis G virus RNA in serum of patients with intravenous drug use reaches 11.6%; pregnant women infected with hepatitis G virus have the highest mother-to-child transmission rate up to 33%. It can be seen that the focus of prevention and control of hepatitis G is to strictly control blood transfusion, early detection, and early treatment.

　　About 50% (30%-60%) of acuteHepatitis C virus (. HCV) infectors will evolve into a persistent carrier state of the virus. Due to the presence of viremia, it can become an important source of infection. Chronic hepatitis C includes chronic persistent hepatitis and chronic active hepatitis, which can evolve from acute hepatitis or occur covertly. Compared with hepatitis B, hepatitis C has a stronger tendency to chronicity, and about 20% of chronic hepatitis C patients will develop liver cirrhosis within 20-30 years, and these patients may develop liver cancer within the next 10 years.

　　Hepatitis G can be co-infected with other hepatitis viruses, among which the co-infection withHepatitis B virus (. HBV), HCV infectors are the majority. According to statistics, 10%-20% of patients with hepatitis B and C simultaneously infected with GBV-C/HGV. In China, surveys have shown that the infection rates of GBV-C/HGV in clinical hepatitis B, C, and non-A, non-E hepatitis are 9%, 10%, and 17%, respectively. Although GBV-C/HGV can cause chronic infection and viremia, it rarely causes inflammation of liver cells, and most infected individuals do not have symptoms.Alanine aminotransferase (. ALT levels are usually normal.

　　Common symptoms of post-transfusion hepatitis include: general fatigue, loss of appetite, fever, nausea, vomiting, fear of eating greasy foods, discomfort or fullness in the upper abdomen, and明显 yellow urine. After suffering from hepatitis, due to the impact on the function of liver cells, the ability to excrete bilirubin decreases, causing bile to fail to be excreted into the small intestine through the normal pathway, resulting in an increase of bilirubin in the blood. Therefore, hepatitis patients often experience jaundice and yellow urine. Due to the inflammation and swelling of the liver, the liver capsule on the liver surface becomes too tense, causing the patient to experience pain in the liver area.

　　Patients with chronic hepatitis and liver cirrhosis often show signs of decreased sexual function. For example, male patients may experience a decrease or loss of libido, thinning and shedding of pubic and armpit hair, atrophy and shrinkage of the testicles, impotence, infertility, breast enlargement, and the occurrence of liver palms, spider nevi, and other symptoms; female patients may experience menstrual irregularities, such as irregular menstrual periods, excessive or insufficient menstrual flow, amenorrhea, dysmenorrhea, and other symptoms. These phenomena are due to the decline in the liver's regulatory function of sex hormones, leading to a disorder of sex hormones. Severe hepatitis and liver cirrhosis patients may develop edema or ascites due to reasons such as increased portal vein pressure.

　　Common signs of hepatitis patients include:

　　1. Liver enlargement.Most patients will have varying degrees of liver enlargement, usually 1 to 3 centimeters below the costal arch, but severe hepatitis patients, due to massive necrosis of liver cells, the liver not only does not enlarge, but often shrinks to varying degrees.

　　2. Liver tenderness and percussion pain.Liver enlargement with tenderness and percussion pain is the most important and most common sign of hepatitis.

　　3. Jaundice.Mild jaundice often only involves the yellowing of the white of the eyes (sclera); severe jaundice can cause明显 jaundice of the entire body.

　　4. Splenomegaly.Acute hepatitis patients generally have varying degrees of splenomegaly.

　　5. Liver palms and spider angiomas.

　　6. Pale complexion.Patients with chronic hepatitis and liver cirrhosis often have a pale, lackluster, or dark complexion.

　　How to prevent post-transfusion hepatitis? It is generally believed that the occurrence of the disease is related to the source of blood, the inactivation treatment of blood products, and the preparation methods. Generally speaking, if not screened, the blood of professional blood donors is often more likely to cause post-transfusion hepatitis than that of real voluntary donors; blood products not treated with inactivation are more likely to cause post-transfusion hepatitis than those treated with inactivation; mixed plasma is more likely to cause post-transfusion hepatitis than single-unit plasma. This is because the cultural and health level of professional blood donors is often lower, especially after repeated blood donation, the chance of infection is greater: especially among blood donors who donate plasma and red blood cells, the positive rate of anti-HCV can reach more than 50%. Therefore, it is easy to develop post-transfusion hepatitis when blood from unscreened donors is transfused. If the inactivation treatment of blood products is not strict or not treated with inactivation, there is a greater possibility of hepatitis virus. After transfusing such blood, the possibility of developing post-transfusion hepatitis is also greater. As long as there is one positive HCV in the mixed plasma, the entire plasma can be contaminated, of course, the risk of mixed plasma is greater than that of single-unit plasma.

　　In addition to the above factors, post-transfusion hepatitis is also related to the body's resistance of the recipient, the number of blood transfusions, and the amount of blood transfusion. The lower the body's resistance of the recipient, the more frequent and the greater the amount of blood transfusion, the higher the incidence of post-transfusion hepatitis. Therefore, it is very important to inactivate blood products, screen blood donors, improve the preparation methods of blood products, advocate component transfusion, strictly control the indications for blood transfusion, and not to abuse blood products to prevent post-transfusion hepatitis.

　　What should be checked for post-transfusion hepatitis? A brief description is as follows:

　　1. Blood count

　　The total white blood cell count is normal or slightly low, with a relative increase in lymphocytes, and occasionally abnormal lymphocytes may appear. The total white blood cell count and neutrophils in severe hepatitis patients can increase. In some chronic hepatitis patients, there is a decrease in platelets.

　　2. Liver function tests

　　There are many types of liver function tests, and they should be selected according to the specific situation.

　　1. Jaundice index and bilirubin quantitative test. The above indicators of jaundice hepatitis can all increase. Urinalysis shows an increase in bilirubin, urobilinogen, and urobilin.

　　2. Determination of serum enzymes. The commonly used ones are alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Serum transaminases can increase during the incubation period, early onset, and asymptomatic infection of hepatitis, so they are helpful for early diagnosis. It has been confirmed that there are two types of AST, one is ASTs, which exist in the cytoplasm of liver cells, and the other is ASTm, which exists in the shallow mitochondria of liver cells. When there is extensive necrosis of liver cells, the level of ASTm in the serum increases, so in severe hepatitis, the increase of ASTm is mainly observed. Since the half-life of ASTm is shorter than that of ASTs, recovery is also earlier. When ASTm is persistently elevated in acute hepatitis, there is a possibility of becoming chronic hepatitis. In chronic hepatitis, a persistently increased ASTm should be considered as chronic active hepatitis. Glutathione S-transferase (GST) increases earliest in severe hepatitis and is helpful for early diagnosis. Fructose 1,6-bisphosphatase is one of the glycogen synthesis enzymes, and its serum content is significantly increased in all types of chronic hepatitis. Serum guanylate kinase (GDA) has the same activity as ALT and has organ specificity.

　　3. Determination of cholesterol, cholesterol esters, and cholesteryl esterase. When liver cells are damaged, the total cholesterol in the blood decreases, and when there is obstructive jaundice, cholesterol increases. In patients with severe hepatitis, cholesterol, cholesterol esters, and cholesteryl esterase can all significantly decrease, indicating a poor prognosis.

　　4. Determination of serum proteins and amino acids. In chronic active hepatitis, the electrophoresis of proteins shows that gamma globulin is often >26%; in liver cirrhosis, gamma globulin can be >30%. However, in schistosomiasis cirrhosis, autoimmune diseases, myeloma, sarcoidosis, and other conditions, the percentage of gamma globulin can be increased.

　　5. Determination of serum procollagen III (PⅢP). An increased level of serum PⅢP suggests the formation of fibrosis in the liver, and the sensitivity reported in the literature may be 31.4%, with a specificity of 75.0%, the normal value of PⅢP is

　　Three, serum immunological examination

　　1. Hepatitis A: The determination of anti-HAV-IgM is valuable for early diagnosis; to judge the presence of hepatitis B infection: HBV markers (HBsAg, HBeAg, HBCAg and anti-HBs, anti-HBe, anti-HBc); to determine whether there is HBV replication in the body of patients with hepatitis B: HBV-DNA, DNA-P and PHSA receptor determination; diagnosis of acute hepatitis B: high titer anti-HBc-IgM positivity. The localization of pre-S antigen in the liver cells of patients with acute and chronic hepatitis B: tissue chemistry and solid-phase radioimmunoassay can be used to study; anti-pre-S1 positivity can be used as an early diagnostic indicator of acute hepatitis B, and anti-pre-S2 can be used as an indicator of hepatitis recovery.

　　2. Hepatitis C is often diagnosed by ruling out hepatitis A, B, E, and other viruses (CMV, EBV), and the positivity of serum anti-HCV-IgM or/and HCV-RNA can confirm the diagnosis.

　　3. The serological diagnosis of hepatitis D depends on the positivity of serum anti-HDV-IgM, or HDAg or HDVcDNA hybridization; the positivity of HDAg in liver cells or HDVcDNA hybridization can confirm the diagnosis.

　　4. The diagnosis of hepatitis E depends on the positivity of serum anti-HEV-IgM or the presence of 30-32nm virus particles in the stool observed by immunoelectron microscopy.

　　Polymerase chain reaction (PCR) is a new method with high specificity and sensitivity for detecting viral hepatitis. PCR is a polymerase chain reaction of specific DNA in the tube under the action of primers, which can synthesize millions of the same type of DNA in a few hours, greatly increasing the sensitivity and specificity of the test. In the case of viral hepatitis, due to the low content of viruses in serum, the current detection methods are not sensitive enough and are prone to missed diagnosis. However, PCR can detect a positive reaction when the virus content in serum is as low as 10^4/ml, greatly improving the sensitivity of the detection. PCR was initially applied to the diagnosis of hepatitis B, and is now also used to detect and confirm hepatitis C.

　　Four, liver biopsy pathological examination

　　The diagnosis of various types of hepatitis has great value. Through the use of electron microscopy of liver tissue, immunohistochemical detection, and observation with the Knodell HAI scoring system, correct data on the etiology, etiology, degree of inflammation activity, and degree of fibrosis of chronic hepatitis are obtained, which is conducive to clinical diagnosis and differential diagnosis.

　　The diet for patients with post-transfusion hepatitis should be light, easy to digest, and to the patient's taste, containing a variety of vitamins, sufficient calories, and an appropriate amount of protein. The protein intake should aim to reach 1-1.5g/kg per day, and appropriate supplements of vitamin B complex and C should be taken. When the intake is too low, intravenous glucose and vitamin C can be supplemented. There is no emphasis on high sugar and low-fat diets.

　　1. Provide an appropriate amount of calories.

　　2. Adequate protein supply can maintain nitrogen balance, improve liver function, and is conducive to the repair and regeneration of liver cell damage.

　　3. Provide an appropriate amount of carbohydrates. Carbohydrates should provide 50-70% of the total calories. An appropriate amount of carbohydrates can not only ensure the supply of total calories for patients with chronic hepatitis but also reduce the decomposition of body tissue proteins, promote the liver's utilization of amino acids, increase liver glycogen reserves, and enhance the detoxification ability of liver cells.

　　4. Appropriate restriction of fat intake. Fat is one of the three major nutritional elements, and the unsaturated fatty acids it provides are essential nutrients for the body, which cannot be replaced by other foods, so it is not necessary to restrict it excessively. In addition, the intake of an appropriate amount of fat is beneficial for the absorption of fat-soluble vitamins (such as vitamin A, E, K, etc.). Due to the decreased appetite in patients with chronic hepatitis, they often have gallbladder diseases, and fat intake is often insufficient. Patients with chronic hepatitis need to consume an appropriate amount of fat-containing foods, but excessive restriction of fat is not appropriate. The daily fat supply should generally be 40-60g, or about 25% of the total daily energy intake. For patients with chronic hepatitis complicated with fatty liver, hyperlipidemia, or acute attack of cholecystitis, fat should be restricted.

　　5. Supplement adequate amounts of vitamins and minerals. Vitamins play an important role in detoxification, regeneration, and immune enhancement of liver cells. Vitamins are often used as adjuvant treatment for chronic hepatitis. The main way to supplement vitamins is through food, and it is still beneficial to supplement vitamin preparations in cases of insufficient intake. Chronic hepatitis patients are prone to calcium deficiency and osteoporosis. It is necessary to persistently drink milk or take calcium supplements appropriately.

　　6. Abstain from alcohol and avoid the intake of substances that damage the liver. Ethanol can cause damage to liver cells, and the detoxification ability of the liver of chronic hepatitis patients decreases. Even a small amount of alcohol can worsen liver cell damage, leading to the aggravation of liver disease. Therefore, patients with hepatitis should abstain from alcohol.

　　What is the treatment method for post-transfusion hepatitis? The introduction is as follows:

　　1. Treatment for type A and E viral hepatitis does not require antiviral treatment, mainly supported by treatment, supplemented with appropriate liver-protective drugs such as glycyrrhizin preparations, silymarin, reduced glutathione, and phosphatidylcholine, etc., to avoid alcohol and fatigue, and to avoid using liver-damaging drugs. Emphasize early bed rest until symptoms are significantly reduced, and gradually increase activity, following the principle of not feeling tired. Hospitalization and isolation treatment is required for 3 weeks after onset, with clinical symptoms disappearing, and serum total bilirubin below 17.1 umol/L.Alanine aminotransferase (. ALT) is below twice the normal value, can be discharged from the hospital, but should still rest for 1-3 months after discharge, and should have regular physical examinations every half year to one year after returning to work.

　　2. Chronic hepatitis C, whether acute or chronic, as long asHepatitis C virus (. RNA of HCV can be detected, antiviral treatment is needed. The standard antiviral treatment regimen is pegylated interferon and ribavirin. If pegylated interferon is not affordable due to economic conditions, ordinary interferon can be used instead, and the duration of treatment is determined according to the patient's response at 4 weeks, 12 weeks, and 24 weeks of treatment (i.e., response-guided therapy - RGT). For patients with genotype 1 who have poor response, direct-acting antiviral drugs such as boceprevir (Boceprevir, BOC) or telaprevir (Telaprevir, TVR) can be considered for treatment.