Liver diseases in pregnancy are more common in pregnancy. Common liver diseases in pregnancy mainly include pregnancy-associated viral hepatitis (type A, type B, type C, type D, type E), pregnancy-specific liver diseases (intrahepatic cholestasis in pregnancy, acute fatty liver during pregnancy) and liver diseases caused by pregnancy complications (hyperemesis, HELLP syndrome, severe vomiting in pregnancy), among which pregnancy-associated viral hepatitis occupies the first place and pregnancy-associated The first is viral hepatitis and the second is intrahepatic cholestasis. Viral hepatitis in pregnancy Viral hepatitis is the most common serious liver disease in pregnant women, and there are hepatitis A, hepatitis B, hepatitis C, hepatitis D and hepatitis E. Among them, hepatitis A and hepatitis E are transmitted maternally through the gastrointestinal tract and usually do not develop into chronic hepatitis; hepatitis C, hepatitis B and hepatitis D are mainly transmitted through blood transmission, sexual transmission and vertical transmission from mother to child. Pregnant women are more susceptible to viral hepatitis during pregnancy and are sicker than when they are not pregnant and can worsen early pregnancy reactions. The later in pregnancy viral hepatitis occurs, the more likely it is to develop into severe hepatitis. Hepatitis B is the most common in pregnancy, and hepatitis E has the highest mortality rate of 63.4% or more. Viral hepatitis can cause miscarriage, premature birth, stillbirth, and intrauterine infection of the fetus. The clinical manifestations of viral hepatitis are: progressive worsening of malaise, loss of appetite, nausea, vomiting, abdominal distension and other gastrointestinal symptoms, darkening of urine, itchy skin, yellow sclera, etc. The liver is enlarged and there is pressure pain. Laboratory tests: serum total bilirubin and transaminases are elevated, and serum hepatitis virus marker tests can clarify the diagnosis. Before the occurrence of severe hepatitis, frequent nausea, vomiting, and progressive deepening of jaundice are the precursors. when severe hepatitis occurs, the hepatic turbinate boundary gradually narrows, and serum total bilirubin ≥ 170 μmol/L, or increases by 17 μmol/L per day. transaminases first rise and then fall, and the characteristic contrast with elevated bilirubin is a peculiar bile enzyme separation phenomenon. Prothrombin time is prolonged, diffuse intravascular coagulation (DIC) may occur in some patients, and patients have the possibility of hemorrhage at any time. There may also be manifestations of hepatic coma and hepatorenal syndrome. Hepatitis A during pregnancy is not considered to be transmitted from mother to child, and anti-HAV-IgG protects the fetus through the placenta. Mother-to-child transmission of hepatitis B exists and is mainly associated with HBeAg-positive and HBV-DNA-positive mothers. In general, infants are more likely to be infected when their mothers are e antigen positive and HBV-DNA positive, and less likely to be infected when their mothers are e antibody positive and HBV-DNA negative. The ultimate goal of hepatitis B vaccination is to eliminate hepatitis B infection. The immunization measures currently used can interrupt most of the mother-to-child transmission of hepatitis B. However, there are still cases of immunization failure. However, there is still a possibility that hepatitis B infection may occur as a result of immunization failure. At present, China mainly uses recombinant yeast hepatitis B vaccine, 10 micrograms per dose, according to the 0, 1, 6 procedure. Active-passive combination immunization is recommended for newborns of Australian antibodies ( HbsAg)-positive mothers. Intrapartum blockade is most important. Immediately after birth, the newborn should be bathed to remove the contaminated mother’s body fluids, given hepatitis B immunoglobulin as soon as possible (no later than 24 hours), and given hepatitis B vaccine at different sites, which can protect the newborn by more than 90%. Hepatitis C can also be transmitted vertically from mother to child, but its transmission rate is much lower than that of hepatitis B (about 4-5%), but there is no good method of interruption, and the occurrence of vertical infection from mother to child is related to the mother’s HCV-RNA blood load. Since anti-HCV can pass through the placenta, detection of positive anti-HCV in newborns cannot be considered as HCV infection. Mother-to-child transmission of type D infection and hepatitis E is rare. The pathogenesis of ICP is not yet clear, but may be related to genetic factors and estrogen, and is familial, recurrent, and prone to occur in sensitive women with high estrogen concentration, accounting for 1/5 of jaundice in pregnancy. The main histological lesion of ICP is intrahepatic cholestasis with intact liver structure and no inflammatory changes or proliferation of interstitial cells. bile acids in pregnant women with ICP are not completely cleared by the liver and collect in the serum, so the total bile acid level may be 10-100 times higher and has diagnostic significance as it appears earlier than clinical symptoms. Serum transaminases are mildly to moderately elevated but rarely exceed 250 IU/L. The clinical features of ICP are pruritus and jaundice, with pruritus often being the first symptom to appear, often starting at 28-32 weeks, with the palms of the hands, feet and abdomen being the common sites of pruritus, with a diurnal pattern of lightness and severity, which mostly persists until delivery, usually within 2 days after delivery, and rarely lasting more than 2 weeks. Jaundice occurs several days to weeks after the onset of pruritus and is usually mild. ICP is less harmful to the mother and mainly endangers the fetus. The normal fetal-maternal transport of bile acids through the placental trophoblast is disrupted, resulting in abnormal accumulation of bile acids, resulting in fetal growth restriction, spontaneous preterm delivery, intrauterine distress, and intrauterine death. Therefore, the incidence of preterm delivery and intrauterine distress in ICP women is significantly higher. According to the literature, the incidence of stillbirth and fetal distress is much higher in those with pruritus combined with jaundice than in those with pruritus alone, and is related to the bile acid level of the pregnant woman, the higher the bile acid level, the higher the incidence of fetal distress. 2, acute fatty liver in pregnancy (AFLP) Acute fatty liver in pregnancy is a serious, rare (about 1/13328-1/15900) disease that occurs in late pregnancy and is fatal to the mother and fetus, with clinical manifestations and liver function laboratory tests resembling heavy hepatitis. It is common in primiparous mothers, usually occurring at 31-42 weeks, especially at 32-36 weeks, and is more likely to occur in twin, male fetuses. The initial stage of the disease is characterized by persistent nausea, vomiting, malaise, and epigastric pain, with vomiting often being the main symptom, followed by jaundice with progressive deepening in a few days to a week, often without pruritus, hypertension, proteinuria, and edema. If the pregnancy is not terminated in time, the condition will deteriorate rapidly and multiple organ failure such as coagulation dysfunction, DIC, hypoglycemia, hepatic coma, and renal failure will occur soon, and the patient will often die within a short period of time. The fetus may die in utero, stillbirth or preterm delivery. The cause is unknown, but may be related to a defect in fatty acid B oxidase in the mitochondria. Physical examination and ancillary tests may reveal jaundice, hypertension, ascites, edema and renal failure, and the liver may be normal or reduced in size. Liver tissue biopsy reveals acute diffuse vesicular hepatic steatosis, which is the gold standard for diagnosis. Laboratory abnormalities include low blood fibrinogen (often less than 0.1g /L), prolonged clotting time, serum transaminase levels of 300-5000 IU/L, elevated blood uric acid, myohepatitis, urea nitrogen, especially the degree of increase in uric acid is disproportionate to renal failure, elevated peripheral blood leukocyte count, and may have mild thrombocytopenia and hemolysis, in addition to persistent severe hypoglycemia is AFLP is characterized by persistent and severe hypoglycemia, often down to 1/3-1/2 of normal values, hyperbilirubinemia with negative urobilinogen, ultrasound with fatty liver features, and CT with a high positive detection rate. The disease improves rapidly after delivery without permanent liver damage and the chance of reoccurrence is very low. In the past, the maternal and infant mortality rate was as high as 95%, but in recent years, due to improved diagnostic techniques, early diagnosis and treatment have become possible, so the maternal and infant mortality rate has decreased significantly. However, in recent years, the incidence has been increasing significantly. Liver disease caused by pregnancy complications 1. Liver function damage caused by severe gestational hypertensive disease Liver function damage can be caused when arterial spasm caused by severe gestational hypertensive disease leads to impaired blood supply to the liver. Mild cases commonly have varying degrees of elevated serum transaminases and alkaline phosphatase, and thrombocytopenia and jaundice appear in the late stages of the disease. Most serum transaminases are mildly elevated, rarely exceeding 200-500 IU/L, and serum bilirubin rarely exceeds 35-70 μmol/L (2-4 mg /dl). In severe cases, cerebral edema, hepatic embolism, liver rupture with shock, acute renal failure, eclampsia, pancreatitis, pulmonary edema and respiratory distress are seen. When pregnancy is interrupted, the condition mostly resolves rapidly and liver function is restored without sequelae of liver disease. If multiple organ damage is combined, the prognosis for mother and child is poor. Liver complications are subperitoneal hematoma and rupture, infarct formation and fulminant liver failure are the remaining causes of death. Complications affecting the fetus are early placental abruption, preterm delivery and intrauterine growth retardation. HELLP syndrome is common in severe preeclampsia and includes hemolysis, elevated liver enzymes and thrombocytopenia. It accounts for 4-12% of patients with preeclampsia, and the incidence is about 0.1%-0.6% in pregnant women in general. 70% of cases occur at 27-36 weeks of gestation, 1/3 in the postpartum period, and it is common in menstruating mothers. It usually develops before 36 weeks of gestation, 65%-90% have epigastric or right upper abdominal pain, 36%-50% nausea and vomiting, 31% headache, 5% jaundice, 80% right upper abdominal tenderness on physical examination, 60% edema and weight gain, a few visible convulsions, gastrointestinal bleeding. The diagnosis can be made based on clinical manifestations such as nausea, vomiting, malaise, as well as hypertension and edema, and laboratory tests such as hemolysis, elevated liver enzymes and thrombocytopenia. In case of sudden and persistent right upper abdomen or epigastric pain with vomiting and shock, liver infarction, subperitoneal hemorrhage and liver rupture should be considered, and B ultrasound, CT or MRI and laparoscopy can clarify the diagnosis. The prognosis depends mainly on the maternal age and the severity of HELLP syndrome at the time of delivery. HELLP syndrome has a recurrence rate of 3%-27% in repeat pregnancies. The survival rate after hepatic pericardial rupture is 25%. 3. Liver damage caused by hyperemesis gravidarum The hyperemesis gravidarum is usually seen in the first child, with an incidence of 1%-1.5%, and develops around 8 weeks after menopause from the general early pregnancy reaction. Due to repeated vomiting and long-term starvation, it can cause disorders of water and electrolyte balance and metabolic acidosis, and in severe cases, liver and kidney function damage, jaundice, mild elevation of serum bilirubin and transaminases, which can rapidly improve and liver function recover after early pregnancy reaction is reduced, hydration, correction of acid-base imbalance and electrolyte disorders, but if urinary ketone bodies appear repeatedly, it can lead to fetal malformation and fetal stoppage. Severe liver damage and pregnancy should be terminated.