Post-transfusion hepatitis

Introduction to hepatitis after transfusion Anyone who has hepatitis due to blood transfusion and blood products, or has no clinical signs and symptoms of hepatitis, but has a positive serological marker, is called post-transfusion hepatitis (PTH). Hepatitis A and E are mainly transmitted through the digestive tract and do not turn into chronic hepatitis or carriers of chronic viruses, so they generally do not cause post-transfusion hepatitis, but individual recipients of blood, after receiving blood from those who are in the latent period, may also cause Hepatitis A or E after transfusion. Type B, C, D and G hepatitis can cause chronic hepatitis or chronic hepatitis virus carriers mainly through blood transmission. Among them, hepatitis D virus is a defective RNA virus, which is often present in HBV-infected patients. HDV in the body can only occur with the help of HBV. HDV can re-infect with HBV at the same time as the infection of the axillary BV infection, thereby aggravating hepatitis B or causing hepatitis B to develop fulminant hepatitis. The blood donors generally do not consider hepatitis A, hepatitis B, and hepatitis D, but focus on hepatitis B, C, and G hepatitis that are easily transmitted through the blood. Recently, some scholars have discovered that some new hepatitis viruses, such as the transfusion-transmitted virus TTV and SEN virus, may cause hepatitis. At present, China has generally used enzyme immunoassay to screen out hbv carriers in blood donors. Hepatitis B has been rare after blood transfusion caused by missed detection of hbsag(+). The missed test may be blood with a low level of virus, and the blood transfusion can still infect a large number of viruses. At present, more than 90% of post-transfusion hepatitis in China is hepatitis C. Hepatitis C was a serious problem of clinical blood transfusion after transfusion a few years ago. In recent years, the progress of blood transfusion management has been greatly alleviated, and the hcv pollution rate of blood products is also Greatly reduced. basic knowledge Sickness ratio: 0.1% Susceptible people: no special people Mode of infection: blood transmission Complications: liver cancer

Causes of hepatitis after transfusion

First, hepatitis B after transfusion

HBsAg is the most common and important indicator of hepatitis B virus. Detection of HBsAg is one of the routine items for screening blood donors in China. At present, the EIA method is used to screen blood donor HBsAg, which greatly reduces the occurrence of hepatitis B after transfusion, but it is still impossible to completely prevent it. the reason:

1. Acute hepatitis is in an incubation period: HBsAg does not appear or has a low concentration;

2. HBsAg carriers of chronic hepatitis may be lower than the detection level;

3. Gene mutations in HBV;

4. Detection of technical errors;

5. Non-transfusion pathways;

6, contagious, 0.00004ml of blood containing HBV is enough to cause infection.

Entering hbv(+) blood is infected, depending 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 hbsag(+) recipients was 50.0%, only one case of post-transfusion hepatitis and fulminant hepatitis; receiving anti-hbc(+) blood supply of 21.4% and receiving hbsas (-)/anti-hbc(-) 5.9% of blood donors were infected, all were transient asymptomatic infections, no dominant hepatitis. It is possible that the blood content of hbsag(-) blood is low, and in fact such transmission is rarely detected clinically.

Hepatitis B is mostly acute after a dominant blood transfusion. Due to the large amount of virus infected by blood transfusion, many transfusions of hepatitis are fulminant; about 1/4 of fulminant hepatitis B is due to blood transfusion, of which 45%-60% is caused by hbv.

Second, hepatitis C after transfusion

At the International Conference on Non-A, Non-B Hepatitis, held in Tokyo, Japan in September 1989, NANBH was officially divided into HC and HE. According to reports, 90% of PTH is HC, of which 50%-60% PTH-C can develop into chronic hepatitis, and 20% of chronic hepatitis develops cirrhosis and primary liver cancer. The incidence of PTH-C in early US research data was 21%, and now it is down to 1%-4%. The positive rate of anti-HCV in normal population in China was 1.35%, and that in individual blood donors was 13.6%.

With the promulgation of the blood donation law and the implementation of the voluntary blood donation system in China, blood quality has been guaranteed from the blood source, and blood safety has been greatly improved. The positive rate of blood donors in various places is also inconsistent.

The clinical manifestations of acute HCV infection have an incubation period of 2-26 weeks, with an average of 7-4 weeks. About 40% of patients fail to find a clear route of transmission and their latency is difficult to determine. 40%-75% are asymptomatic, only elevated ALT is found, and serological detection of HCV RNA is accidentally discovered. If there are symptoms, it is generally lighter. Studies of the natural course of hepatitis C have shown that approximately 50% (30%-60%) of those with acute HCV infection will evolve into a sustained state of the virus. It can be an important source of infection due to its presence of viremia.

Chronic hepatitis C, including chronic persistent hepatitis and chronic active hepatitis, can be evolved from acute hepatitis and can also be concealed. Compared with hepatitis B, hepatitis C has a stronger chronic tendency, and about 20% of patients with chronic hepatitis C will develop cirrhosis within 20-30 years. These patients can develop liver cancer in the next 10 years. . The incidence and mortality of severe hepatitis were lower than those of hepatitis B.

Third, after transfusion of Geng liver

Hepatitis G virus is a suspected hepatitis virus isolated from hepatitis patients using modern molecular virology technology, called GBV-C type and HGV, respectively. Sequence analysis shows that the nucleotide and amino acid level homology is 85%. And 95%, therefore, GBV-C and HGV are different isolates of the same virus and have similar structural genes to HCV.

Transmission routes have been shown to be transmitted through blood transfusions, including those who receive hemodialysis and medical personnel who are exposed to blood; in addition, intravenous drug use is another important route. In patients with intravenous drug use, the detection rate of serum hepatitis G virus RNA was 11.6%; pregnant women infected with hepatitis G virus, the mother-to-child transmission rate was up to 33%; thus, the focus of prevention of hepatitis G is Put a good blood transfusion; early detection, early prevention.

Hepatitis prevention after transfusion

The occurrence of hepatitis after transfusion is related to the source of blood, the inactivation treatment of blood products, and the preparation method.

It is generally believed that if screening is not carried out, the blood of professional blood donors often causes a greater risk of post-transfusion hepatitis than the blood of a truly volunteer blood donor; blood products that are not inactivated are larger than those that have been inactivated; mixed plasma It is larger than a single plasma; this is because the cultural level of professional blood donors is often low, especially after repeated blood donation, the chance of being infected is greater: especially among blood donors who have plasma and blood transfusions, The positive rate of HCV can reach more than 50%. Therefore, blood that is not screened for blood donors is prone to post-transfusion hepatitis. The inactivation of blood products is not strict or disinfected without inactivation. There is a high possibility of hepatitis virus. After losing this blood, the possibility of hepatitis after transfusion is also high. Mixing plasma with a positive hepatitis C virus can contaminate the entire plasma, although the risk of mixing plasma is greater than that of a single plasma.

Hepatitis after transfusion is related to the above factors. It is also related to the body resistance of the recipient, the number of blood transfusions, and the amount of blood transfusion. The lower the resistance of the recipient's body, the more blood transfusions and blood transfusions, the higher the incidence of hepatitis after transfusion: therefore, the inactivation of blood products and the screening of blood donors, improve the preparation of blood products. The law advocates component blood transfusion, strictly controls blood transfusion indications, and does not indiscriminate blood transfusion products, which is very important to prevent post-transfusion hepatitis.

Hepatitis complications after transfusion Complications

Approximately 50% (30%-60%) of people with acute HCV infection will evolve into a sustained carrier state of the virus. It can be an important source of infection due to its presence of viremia. Chronic hepatitis C, including chronic persistent hepatitis and chronic active hepatitis, can be evolved from acute hepatitis and can also be concealed. Compared with hepatitis B, hepatitis C has a stronger chronic tendency, and about 20% of patients with chronic hepatitis C will develop cirrhosis within 20-30 years. These patients can develop liver cancer in the next 10 years. .

Hepatitis G can be combined with other hepatitis viruses, and most of them are infected with HBV and HCV. According to statistics, 10%-20% of adult chronic hepatitis B and C patients are infected with GBV-C/HGV at the same time. In China, investigations have shown that the infection rates of GBV-C/HGV in clinical hepatitis B, hepatitis C and non-methyl 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 people have no symptoms, and ALT levels are usually normal.

Hepatitis symptoms after transfusion Common symptoms Liver gas spleen fatigue nausea vomiting liver pain jaundice

Symptoms of hepatitis patients

The whole body is weak, do not want to eat, fever, nausea, vomiting, fear of eating greasy food, upper abdominal blockage or fullness discomfort, obvious yellow urine.

After suffering from hepatitis, the function of the bilirubin is reduced due to the function of the liver cells, so that the bile can not be discharged to the small intestine according to the normal pathway, and the bilirubin in the blood is increased. Therefore, hepatitis patients often have symptoms such as jaundice and yellow urine. Due to the inflammation and swelling of the liver, the liver capsule on the surface of the liver is too tight, and the patient may have pain in the liver area.

Chronic hepatitis and cirrhosis patients also often have signs of sexual dysfunction. For example, male patients may decline or disappear, pubic hair, pubic hair may decrease and fall off, testicular atrophy becomes smaller, impotence, infertility, breast enlargement, and liver palm, spider mites, etc.; female patients may cause irregular menstruation, such as menstruation Not allowed, less or too much menstruation, amenorrhea, dysmenorrhea, etc. This phenomenon is caused by the liver's regulation of sexual hormones, resulting in the imbalance of sex hormones.

Patients with severe hepatitis and cirrhosis, elevated portal pressure in patients with cirrhosis, etc., can cause edema or ascites in patients.

Common signs of hepatitis patients:

1, liver enlargement: the vast majority will have varying degrees of liver enlargement, usually 1 to 3 cm under the rib arch. However, due to the massive necrosis of liver cells in patients with severe hepatitis, the liver is not only not swollen, but tends to shrink to varying degrees.

2, liver tenderness and snoring pain: liver swelling accompanied by tenderness and snoring pain, is the most important and most common signs of hepatitis.

3, jaundice: jaundice light, often only white eyes (sclera) yellow; jaundice is heavier, the whole body skin can have obvious yellow stain.

4, splenomegaly: patients with acute hepatitis, generally have varying degrees of spleen enlargement.

5, gray complexion: chronic hepatitis and cirrhosis patients often look dull, dull, or black complexion.

Examination of hepatitis after transfusion

(1) Blood image

The total number of white blood cells is normal or slightly lower, lymphocytes are relatively increased, and occasional abnormal lymphocytes appear. The number of white blood cells and neutrophils in patients with severe hepatitis can be increased. Thrombocytopenia in some patients with chronic hepatitis.

(two) liver function test

There are many types of liver function tests, which should be selected according to specific conditions.

1. Astragalus index, bilirubin quantitative test: the above indicators of jaundice hepatitis can be increased. Urinary examination increased bilirubin, urobilinogen and urinary bilirubin.

2. Serum enzyme assay: commonly used alanine aminotransferase (ALT) and aspartate aminotransferase (AST), serum aminotransferase in the hepatitis incubation period, early onset and latent infection can be elevated, it is helpful for early diagnosis. It has been confirmed that there are two types of AST, one is ASTs, which is present in the liver cytoplasm, and the other is ASTm, which is present in the shallow cells of hepatocytes. When liver cells are extensively necrotic, ASTm in the serum is increased, so ASTm is mainly increased in severe hepatitis.

Since the half-life of ASTm is shorter than ASTs, recovery is also earlier. When ASTm continues to increase in acute hepatitis, it may become chronic hepatitis. Chronic hepatitis should continue to be considered as chronic active hepatitis. Glutathione-S-transferase (GST) is the earliest elevated in severe hepatitis and is helpful in early diagnosis. Fructose 1,6-bisphosphatase is one of glycogen synthase, and the serum content of various types of chronic hepatitis is significantly increased. Serum guaninease (GDA) is consistent with ALT activity and is organ specific.

3. Determination of cholesterol, cholesterol ester, and cholesterol cholesterase: When liver cells are damaged, total cholesterol in the blood is reduced, and cholesterol is increased when obstructive jaundice. Cholesterol, cholesterol esters, and cholesterol cholesterase in patients with severe hepatitis can be significantly decreased, suggesting a poor prognosis.

4. Determination of serum protein and amino acid: protein electrophoresis in chronic active hepatitis indicates that -globulin is often >26%, and -globulin can be >30% in cirrhosis. However, the percentage of -globulin in cirrhosis, autoimmune diseases, myeloma, sarcoidosis, etc. of schistosomiasis can be increased.

Serum prealbumin is synthesized by the liver, also known as thyroid-binding protein and vitamin A transporter. Its molecular weight is 60,000, half-life is 1.9 days, pH is 8.6, and its electrophoretic movement speed is faster than serum albumin, so it is called prealbumin. When the liver parenchymal cells are damaged, the concentration decreases, and the extent of the decline is consistent with the degree of hepatocyte damage. In severe hepatitis, the value is very low, even close to zero. The serum prealbumin value of patients with acute hepatitis and chronic active hepatitis decreased by 92% and 83.8%, respectively, and returned to normal as the condition recovered. However, the value of liver cancer, cirrhosis, obstructive jaundice and other diseases can also be reduced, and should be noted.

The ratio of plasma branched chain amino acid (BCAA) to aromatic amino acid (AAA) is detected. If the ratio decreases or is inverted, it reflects liver parenchymal dysfunction. It has reference significance for judging the prognosis of severe hepatitis and evaluating the efficacy of branched chain amino acids.

5. Serum procollagen III: (PIIIP) determination of elevated serum PIIIP, suggesting that fibrosis in the liver will form a possible literature reported sensitivity of 31.4%, specificity of 75.0%. The normal value of PIIIP was <175 g/L.

(three) serum immunological examination

Hepatitis A: Determination of anti-HAV-IgM has early diagnostic value; determine whether there is hepatitis B infection: HBV markers (HBsAg, HBEAg, HBCAg and anti-HBs, anti-HBe, anti-HBc); determine hepatitis B patients HBV replication in vivo: HBV-DNA, DNA-P and PHSA receptor assay; diagnosis of acute hepatitis B: high titer anti-HBc-IgM positive. Localization of pre-S antigen in blood cells of patients with acute and chronic hepatitis B: it can be studied by histochemistry and solid phase radioimmunoassay; anti-pre-S1 positive can be used as an early diagnostic indicator for acute hepatitis B, anti-pre-S2 An indicator for the recovery of hepatitis.

Hepatitis C is often diagnosed by queuing with type A, B, E and other viruses (CMV, EBV), and serum anti-HCV-IgM or / and HCV-RNA positive can be diagnosed.

Serological diagnosis of hepatitis D depends on serum anti-HDV-IgM-positive or HDAg or HDV cDNA hybridization positive; HDAg-positive or HDV cDNA hybridization positive in hepatocytes can be confirmed.

The diagnosis of hepatitis E depends on serum anti-HEV-IgM positive or immunoelectron microscopy to see 30 to 32 nm virus particles in the feces.

Polymerase chain reaction (PCR) is a new method for detecting viral hepatitis with high specificity and sensitivity. PCR is a polymerase chain reaction of specific DNA in a test tube under the action of a primer. It can synthesize millions of the same DNA in a few hours, greatly increasing the sensitivity and specificity of the assay. In the case of viral hepatitis, because the amount of virus in the serum is too small, the current detection method is not sensitive enough, which may cause missed diagnosis. PCR can also detect a positive reaction when the virus content of the virus is 104/ml, which greatly improves the sensitivity of the detection. PCR was originally applied to the diagnosis of hepatitis B. Currently, hepatitis C can also be diagnosed by this method.

Immune complex (IC), complement (C3, C4), IgG, IgA, IgM, IgE, and autoantibodies (anti-LSP, anti-LMA, etc.) have a reference for the diagnosis of chronic active hepatitis.

(4) Liver puncture pathological examination

It is of great value for the diagnosis of various types of hepatitis. Through liver electron microscopy, immunohistochemistry and Knodell HAI scoring system, the correct data are obtained for the pathogen, etiology, inflammatory activity and degree of fibrosis of chronic hepatitis. Conducive to clinical diagnosis and differential diagnosis.

Diagnostic diagnosis of hepatitis after transfusion

The diagnosis of viral hepatitis is based on the clinical manifestations of hepatitis combined with epidemiological history and detection of virus-specific markers.

The marker for the diagnosis of hepatitis A is anti-HAVIgM-positive and is usually measured in serum about 1 week after onset. The marker for diagnosis of hepatitis B is at least 2-3 positive for hepatitis B (HBsAg, anti-HBs, HBeAg, anti-HBe, anti-HBc) (Da Sanyang: HBsAg, HBeAg, anti-HBc or Xiaosanyang) : HBsAg, anti-HBe, anti-HBc), the load of hepatitis B HBV DNA can reflect the activity of viral replication, the degree of liver function abnormality reflects the degree of activity of liver inflammation; the marker of hepatitis C diagnosis is anti-HCV positive; The marker for diagnosis of hepatitis E is anti-HEVIgM anti-HEV positive; the marker for diagnosis of hepatitis D is anti-HDV positive or HDV antigen positive.

Viral hepatitis needs to be differentiated from hemolytic jaundice, extrahepatic obstructive jaundice, non-hepatovirus (such as cytomegalovirus, Epstein-Barr virus) hepatitis, drug-induced liver damage, alcoholic liver disease, autoimmune hepatitis and other diseases. .

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