Patient: born on September 28, 2010, full term, blood type O, weight at birth 7.42 pounds, parents without genetic diseases such as hepatitis B and thalassemia, father blood type O, mother type B. The medical history has been mainly high indirect bilirubin, transaminases have risen and fallen, examined endocrine, eugenics five, cytomegalovirus, EBV, NICCD, hearing screening, fasting 3 hours blood test, urine and stool, fasting 4 hours liver, gallbladder and spleen ultrasound, electrocardiogram and so on have not found the cause. Jaundice appeared three days after birth and was discharged after 3 days of blue light treatment with mild jaundice, feeling aggravated at 36 days and hospitalized, with rebound during the treatment. Among them, when he was hospitalized in a hospital in Guangzhou on November 4, the total bilirubin was 399, which dropped to 287 three days later and rebounded to about 390 on November 11; now he is treated in Guangzhou Children’s Hospital, and the total bilirubin was 399 (direct bilirubin 80, indirect bilirubin 319) on November 11, which kept dropping to total bilirubin 129 (direct bilirubin 21, indirect bilirubin 108) on December 9. Then it started to rebound on December 22 with a total bilirubin of 189 (direct bilirubin 12, indirect bilirubin 177). On December 22, ALT rose to 438 and AST rose to 480. 2. Medication: At the Southern Hospital, we used: Alto Moran, anti-inflammatory and biliary tablets, Glycine, and Eusebio. Vitamin E, hydrocortisone (15mg), cimetidine. Now in Guangzhou Children’s Hospital for infusion: Spartacan, Guradin, Simitet, potassium magnesium menadione, Xiangdan injection, Viagra, Neoterein (for cough). Oral medications: Mennen, Ursodeoxycholic Acid Tablets, Yin Zhi Huang Oral Liquid, Yin Gardenia Huang Granules, Mamia, Anti-inflammatory and Biliary Tablets, Ai Chang. The baby has been mainly with high indirect bilirubin, and there is recurrence during the treatment. Doctor: There is a possibility of Criger-najjar syndrome. Many similar cases have been diagnosed in the outpatient clinic. Patient: We have a few more questions for you: 1. We are surprised that many hospitals here in Guangzhou have never heard of this condition, including the Children’s Hospital. 2. I was looking up about criger-najjar type II on the internet, and it says online that it is autosomal dominant with incomplete epiphenomenon. We have no such symptoms within three generations in both sides of our family, not even those suffering from jaundice, so we would like to ask you, could there be a possibility of genetic mutation? 3. We adults also want to do a genetic diagnosis about this condition, can your hospital do it, we pay the money, we asked several on the Guangzhou side do not do it. We want to have a second child, and you said the probability of a normal fetus is 1/4. (We checked the internet, and it says that dominant inheritance is 1/4 is normal, 1/4 is diseased, and 1/2 is a carrier.) Can your hospital currently do IVF, and can the current technology perform pre-implantation diagnosis to ensure that a normal fetus is conceived? How many hospitals do you recommend? 4. Luminaria has a lot of side effects, is there any other derivative or alternative medicine. When we checked online, it said that aspirin-based drugs should not be used for this condition, is this true? 5.The Internet says that liver cells can be transplanted, is there any liver cell transplant for this disease? We just had a liver function and reticulocyte review on April 8 (photos attached), and both of the child’s transaminases are normal, but the interstitial bile is high and the total bilirubin is 189, so can we get a preventive injection? Is it possible to get the vaccination if the liver function is normal and the total bilirubin is less than 200? It is very painful and problematic for both sides of our family to encounter this condition, so please, thank you very much! You often communicate with foreign experts, if there is any new research progress for the treatment of this disease, please tell us. Doctor: You can take precautions. Some problems are difficult to say clearly through words alone, it is better to discuss in person. Patients: 1, this disease belongs to the autosomal dominant or recessive inheritance, we asked several doctors, the answer is not uniform, some said dominant, but also said recessive? 2. The test results say that both of us are carriers of this disease, what is the percentage of normal babies if we have a second child? What is the percentage of carriers? If we do IVF, can the gene be tested out before implantation into the mother? Or through amniotic fluid testing after pregnancy? Doctor: It is a kind of UGT1A1 gene defect. The lighter cases are more consistent with autosomal dominant inheritance, while the heavier ones are more consistent with recessive inheritance, which is actually a quantitative inheritance relationship, lighter in heterozygous cases and heavier in pure cases. It is also related to the type of mutation. Since satisfactory results can be achieved with good management, it is not necessary to perform genetic testing before maternal implantation or through amniotic fluid testing after pregnancy.