Physical liver dysfunction jaundice (gilbert syndrome)

Physical jaundice is a chronic jaundice caused by ingestion, binding or excretion of bilirubin by congenital hepatocytes, mainly characterized by long-term persistent or fluctuating jaundice, mild or asymptomatic and normal liver function. Physical jaundice is also known as constitutional hyperbilirubinemia and hereditary hyperbilirubinemia. It is rare in clinical practice. According to the nature of serum bilirubin, the clinical introduction of diseases can be divided into two categories, namely, Huangqi (highly non-conjugated bilirubinemia UCHB) with unconjugated bilirubin and increased bilirubin. The main jaundice (high binding bilirubinemia CHB). Physical jaundice is often misdiagnosed as chronic hepatitis or chronic biliary tract disease due to long-lasting persistent or fluctuating jaundice, and even unnecessary surgery is mistaken. Clinical identification with other types of jaundice is important, which is related to treatment and prognosis. The key to the diagnosis of this type of jaundice is to have a basic concept for it. Any clinically encountered long-term jaundice with mild clinical symptoms, the course of the disease is different from viral hepatitis, hemolytic jaundice and biliary tract disease, except for bilirubin metabolism. In addition to abnormalities, other liver function tests are normal, especially when there is a family history, such rare jaundice should always be considered. General constitutional jaundice has four characteristics: 1. Most have a family history or a genetic predisposition; 2. The clinical symptoms are mild or asymptomatic, mainly characterized by chronic volcanic jaundice; 3. In addition to elevated serum bilirubin, normal liver function 4. Outside of crigler najjar, most of them do not require treatment and have a good prognosis. Physical jaundice, the name of the disease. Also known as constitutional liver dysfunction jaundice, is a more common hereditary unconjugated bilirubinemia. Gilbert syndrome, also known as constitutional hepatic dysfunction, is a more common hereditary unconjugated bilirubinemia, first reported by Gilbert in 1901. The clinical manifestations of Gilbert syndrome are characterized by long-term intermittent mild jaundice with no obvious symptoms. Gilbert syndrome is an autosomal dominant hereditary disease. The majority of patients are adolescents and males are more common. The incidence rate is about 5%. Symptoms and symptoms 1. There may be no obvious symptoms; 2. Long-term intermittent mild jaundice; 3. Some cases have fatigue, indigestion, liver discomfort; 4. Liver and spleen without swelling. Diagnosis based on 1. Adolescent onset, with increasing age, jaundice gradually declines, often family history; 2. Chronic recurrent jaundice, fatigue, alcohol, infection or menstrual period jaundice. 3. Phenobarbital or guided sleep can reduce or eliminate jaundice. 4. Serum unbound bilirubin increased, urinary bilirubin was negative, and urinary biliary content was normal. No dominant or latent hemolytic jaundice; 5. Liver function test, bromosulfate sodium test, liver biopsy normal. Principles of treatment 1. Gilbert syndrome does not require special treatment; 2. If necessary, phenobarbital can reduce the effect of blood bilirubin. Efficacy evaluation 1. Cure: jaundice subsided, symptoms disappeared; 2. improved: jaundice relieved, symptoms improved; 3. Unhealed: symptoms did not improve. Experts suggest that the cause of Gilbert syndrome is a decrease in bilirubin clearance, which may be a decrease in the ability of hepatocytes to take up bilirubin and a decrease in the activity of intrahepatic bilirubin glucuronide. In the diagnosis of Gilbert syndrome, attention should be paid to the identification of hemolytic jaundice, obstructive jaundice, fatty liver, alcoholism, viral hepatitis, cirrhosis, Dubin-Johnson syndrome. Gilbert's syndrome has a good prognosis and generally requires no special treatment. However, the cause of the increase in jaundice should be avoided. Diet therapy oyster meat corn soup Read more...