Patient 1, female, 36 years old. Hepatitis B virus surface antigen was found positive in 2009. For further diagnosis and treatment, she was admitted to Beijing Ditan Hospital Affiliated to Capital Medical University on August 4, 2010. The results showed that HBsAg, HBeAg and HBV DNA were 5742.92 IU/ml, 3.34 S/CO and 5.30x103 IU/ml, respectively. Alanine aminotransferase (ALT) 42.0U/L, Aspartate aminotransferase (AST) 47.2U/L, total bilirubin(TBIL)11.8umol/L, direct bilirubin (DBil) 1.8umol/L, gamma-glutaminase (GGT) 30.5U/L, Cholinesterase (CHE) 11126U/L. Creatinine (CR) 51.3umol/L, thyroid hormone 8.22ug/DL. Ultrasound showed that the echo of liver parenchyma was thicker and the thickness of spleen was 38 mm. She was diagnosed as "chronic hepatitis B".
The patient denied the history of trauma, operation and blood transfusion. She had no history of smoking and drinking, no family history of chronic hepatitis B, and denied the history of cancer and heredity. The patient was treated with subcutaneous injection of PEG-IFN α-2a 180 µg, Qw antiviral therapy in August 2010. After that, the patient was reexamined every 24 weeks. After 72 weeks of treatment, the surface antigen decreased to 18.71 IU/ml and the e antigen decreased to 3. 34 S/CO, HBV DNA level < 20 IU/ml, WBC and PLT decreased slightly during treatment. Continued with 12 weeks of PEG-IFNα-2a treatment, there was no significant decrease in surface antigens, and there was a trend toward an increase. So PEG-IFNα-2a treatment was discontinued for about 12 weeks, and oral entecavir was used to maintain antiviral treatment. After 12 weeks, PEG-IFNα-2a was added and joint with entecavir .After 24 weeks of joint therapy, the surface antigen was reduced to 0. 02 IU/ml, e antigen was 0. 62 S/CO, and HBV DNA was undetectable. After reaching the clinical cure level, we continued a 24-week consolidation treatment, then the drug was stopped. Regular follow-up was made after that. By June 2021, the surface antigen remained negative, HBV DNA could not be detected, and no hepatitis recurrence was found.
Patient 2, male, 14 years old, had a mother-child relationship with patient 1. In 2012, he was found positive in surface antigen at the same time with his mother. The results were as follows: surface antigen 4742.22 IU/ml, e antigen 149.25 S/CO, e antibody 23.76 S/CO, HBV DNA 5.25x105, ALT 110.2 U/L, AST 114.5 U/L, TBil 6.3 umol/L and DBil 2.6 umol/L, GGT 45.7 U/L, CHE 10612 U/L, CR 55.7 umol/L and thyroid hormone 7.70 UG/DL.
The patient regularly vaccinated with hepatitis B vaccine after birth, so was considered to be vertical transmission from mother to child. After birth, he denied the history of hepatitis and other infectious diseases, trauma and blood transfusion. At the age of 5 years, the patient was treated with subcutaneous injection of PEG-IFN α-2a 135 µg, Qw antiviral therapy. After 36 weeks of treatment, HBV DNA decreased from 5.25x105 to 5. 30x102, but had not yet reached negative, so oral entecavir was added. After 48 weeks of treatment, HBV DNA turned negative; after 72 weeks of continuous treatment, e antigen turned negative and reached 0.33 S/CO; after 439 weeks, the surface antigen was negative (0.03 IU/ml). Consolidation continued after about 24 weeks then stopped. By June 2021, the surface antigen remained negative, HBV DNA could not be detected, and no hepatitis recurrence was found.