Infant hepatitis syndrome

　　Section 1: Infection

　　The most common cause is viral infection, including hepatitis A virus, hepatitis B virus, hepatitis C virus, cytomegalovirus, rubella virus, Echovirus, adenovirus, varicella virus, and Epstein-Barr virus, etc. In China, infections caused by cytomegalovirus (CMV) are more common, accounting for about 40%-80% of this syndrome.

　　Section 2: Hereditary Metabolic Defects

　　1. Glucose metabolic disorders such as galactosemia, hereditary fructose intolerance, and glycogen storage disease type IV, etc.

　　2. Amino acid metabolic disorders such as phenylketonuria, etc.

　　3. Lipid metabolic disorders such as Niemann-Pick disease, Gaucher disease, and dyoxuria, etc.

　　4. Other metabolic disorders such as abnormal bile acid metabolism, hereditary hemochromatosis, and α1-antitrypsin deficiency, etc.

　　Section 3: Developmental Disorders of Intrahepatic Bile Ducts and Interstitium

　　如肝内胆管缺加入胆管发育不良、胆管囊性扩张、肝纤维化等。

　　四、其他

　　4. Other conditions such as intrahepatic bile duct atresia, bile duct dysplasia, bile duct cystic dilatation, liver fibrosis, etc.

　　In addition to its clinical manifestations, infantile hepatitis syndrome can also cause other diseases. Inflammatory cell infiltration in the liver lobules and portal areas can lead to cirrhosis, which should attract the attention of clinicians and patients.

　　Symptoms can generally be divided into two types:

　　1. Gastrointestinal symptoms of hepatitis type are generally more obvious, with anorexia, nausea, vomiting, abdominal distension, diarrhea, normal or slightly yellow stools. Jaundice is mild to moderate, the liver is slightly to moderately enlarged, and the texture is generally slightly hard or medium hardness. With the improvement of the condition, jaundice gradually subsides, and the liver shrinks. A few children may present with acute severe or subacute severe hepatitis, with progressive jaundice, marked mental and neurological symptoms, bleeding tendency, and multi-system organ failure, with poor prognosis.

　　2. Cholestatic jaundice is deeper and lasts longer, with pale or clay-colored stools. The liver gradually enlarges with moderate to severe hardness. Due to bile stasis, the bile in the duodenum is reduced or absent, often accompanied by steatorrhea, malabsorption of fat-soluble vitamins, growth retardation, and bleeding. If the condition worsens further, it can lead to biliary cirrhosis.

　　Infantile hepatitis syndrome severely affects patients' daily lives, so it should be actively prevented. Due to the complex etiology, prevention is relatively difficult. Blocking maternal-child transmission of hepatitis B virus can prevent the occurrence of infantile hepatitis caused by HBV.

　　1. Liver function tests

　　(1) Serum bilirubin, both conjugated and unconjugated bilirubin levels in the blood are elevated, usually with an increase in conjugated bilirubin.

　　(2) The degree of elevation of serum alanine aminotransferase (ALT) is different and related to the degree of liver cell damage. It gradually returns to normal as the condition recovers.

　　(3) Serum gamma-glutamyl transferase (γ-GT), 5'-nucleotidase (5'-NT), alkaline phosphatase (AKP), and serum bile acids, etc., are significantly elevated when there is bile stasis.

　　(4) Prothrombin time can reflect liver function early, and it is significantly prolonged when liver cells are damaged.

　　2. Pathogen detection

　　(1) Viral infection marker tests, such as blood anti-HAV-IgM test for the detection of hepatitis A virus infection; serum HBsAg and HBV-DNA test for the detection of hepatitis B virus infection; serum anti-CMV-IgM and serum anti-EBV-IgM test for the detection of cytomegalovirus and Epstein-Barr virus infection. In newborns, due to the weaker ability to produce IgM antibodies, false negatives may occur. In addition, urine CMV culture can improve the diagnostic rate.

　　(2) Blood culture and midstream urine culture are performed to detect sepsis and urinary tract infections.

　　(3) Blood antitoxoplasma antibody test to detect toxoplasmosis infection.

　　3. Metabolic Disease Screening

　　Measurement of urinary reducing substances and fasting blood glucose, galactose values to detect galactosemia, fructose intolerance, or glycogen storage disease. Measurement of serum α1-AT values to detect α1-AT deficiency, etc.

　　4. Imaging Examination

　　Liver ultrasound, CT, or MRI, or percutaneous biliary duct selective imaging can reveal intrahepatic biliary atresia.

　　The diet of infants with hepatitis syndrome should be light, easy to digest, with an emphasis on fruits and vegetables, a reasonable diet, and attention to adequate nutrition. In addition, patients should also avoid spicy, greasy, and cold foods.

　　1. General Treatment

　　1. Liver-protecting and jaundice-relieving Yinyu Huang 5-10ml per dose, added to 50ml of glucose solution, intravenously once a day; Dahuang 0.5g/kg, taken by infusion daily; albumin at a dose of 1g/kg intravenously, once every 1-2 days.

　　2. Prevention and treatment of bleeding tendency can be initiated with vitamin K, fresh blood intravenously, or thromboplastin complex (factors II, VII, IX, X) dissolved in 5ml of normal saline for intravenous injection.

　　3. Proper nutritional supply is extremely important for liver repair, as both excessive and insufficient nutritional supply are harmful to the liver.

　　4. Adequate supplementation of fat-soluble vitamins is especially necessary for cholestatic patients, 110mg vitamin K1 intravenously every 2 weeks; 10mg/kg vitamin E (total not exceeding 200mg) intramuscularly every 2 weeks; 100,000 IU vitamin A intramuscularly every 2 months; 300,000-600,000 IU vitamin D3 intramuscularly once a month.

　　2. Treatment of the Etiology

　　1. If CMV infection is present, ganciclovir can be tried at a dose of 5mg/kg intravenously (for more than 1h), twice a day, with an interval of 12h between doses, usually for a course of 2-4 weeks, with attention to side effects such as bone marrow suppression.

　　2. For certain hereditary metabolic defects such as galactosemia, all dairy products should be discontinued and soy milk and sucrose should be used for feeding; for phenylketonuria, a low phenylalanine and low tyrosine diet should be provided.

　　3. Liver Transplantation

　　In cases where there are conditions for genetic metabolic diseases such as liver fibrosis, liver transplantation can be considered.