Objective:To explore the diagnostic key points, treatment strategies, and prognosis of graft-versus-host disease (GVHD) after liver transplantation.Methods:The clinical data of 5 recipients diagnosed with GVHD after liver transplantation at the Liver Transplantation Center of the First Affiliated Hospital of Army Medical University from May 1999 to October 2024 were retrospectively analyzed. The causes, onset, diagnosis, treatment, and prognosis of GVHD after liver transplantation were summarized and analyzed. Literature was searched in CNKI, Wanfang, VIP, Chinese Medical Journal Full-text Database, PubMed, Web of Science, and Google Scholar using the Chinese keywords "移植物抗宿主病+肝移植", and the English keywords "graft versus host disease + liver transplantation". The search time ranged from January 1988 to January 2025. Inclusion criteria for the literature: (1) meeting the clinical or pathological diagnostic criteria of GVHD after liver transplantation; (2) recipient age >18 years; (3) case number ≥2. Exclusion criteria: incomplete clinical data such as incidence, mortality, and clinical manifestations of GVHD after liver transplantation. The retrieved literature was reviewed.Results:All 5 recipients were male. Among them, 4 cases underwent liver transplantation at this center. The incidence of GVHD after liver transplantation in this center was 0.46% (4/872). All 5 cases developed symptoms such as fever, rash, diarrhea, oral ulcers, and pancytopenia on the 19th (5-21) day after liver transplantation. One case had gastrointestinal bleeding. Two cases were diagnosed by skin pathological biopsy, and three cases were diagnosed based on clinical manifestations such as fever, rash, diarrhea, and bone marrow suppression. One case discontinued immunosuppressants, and four cases reduced the dosage of immunosuppressants. Four cases were treated with high-dose glucocorticoids, four with intravenous immunoglobulin (IVIG), three with ruxolitinib, and three with hematopoietic factors. All five cases received protective isolation, anti-infection, and symptomatic supportive treatment. Among the three recipients treated with ruxolitinib, body temperature returned to normal, rash gradually faded, oral ulcers gradually healed, blood cells returned to normal, and they were eventually discharged after recovery. The remaining two cases showed no symptom improvement and died of severe lung infection and multiple organ failure. Literature review A total of 34 articles were included. The incidence of GVHD after liver transplantation was 1.03% (279/27 018), and the onset time ranged from 7 to 1,865 days post-transplantation; 272 cases (97.49%) occurred within 1-8 weeks. The main clinical manifestations included fever (195 cases, 69.89%), rash (267 cases, 95.70%), diarrhea (173 cases, 62.01%), and bone marrow suppression (214 cases, 76.70%). Treatment mainly involved adjustment of immunosuppressants (201 cases, 72.04%), high-dose corticosteroids (215 cases, 77.06%), and IVIG pulse therapy (146 cases, 52.33%). In the end, 83 cases (29.75%) recovered and were discharged, while the mortality rate was 70.25% (196/279), with causes of death including infection, gastrointestinal bleeding, and multiple organ failure.Conclusions:GVHD after liver transplantation has a low incidence, high mortality, and poor prognosis. Diagnosis mainly relies on typical clinical manifestations and pathological results of tissue biopsy. Early administration of high-dose corticosteroids combined with IVIG pulse therapy, timely reduction or discontinuation of immunosuppressants, use of ruxolitinib, active infection management, and enhanced symptomatic and supportive care are effective strategies for treating GVHD after liver transplantation.

Objective:To explore the diagnostic key points, treatment strategies, and prognosis of graft-versus-host disease (GVHD) after liver transplantation.Methods:The clinical data of 5 recipients diagnosed with GVHD after liver transplantation at the Liver Transplantation Center of the First Affiliated Hospital of Army Medical University from May 1999 to October 2024 were retrospectively analyzed. The causes, onset, diagnosis, treatment, and prognosis of GVHD after liver transplantation were summarized and analyzed. Literature was searched in CNKI, Wanfang, VIP, Chinese Medical Journal Full-text Database, PubMed, Web of Science, and Google Scholar using the Chinese keywords "移植物抗宿主病+肝移植", and the English keywords "graft versus host disease + liver transplantation". The search time ranged from January 1988 to January 2025. Inclusion criteria for the literature: (1) meeting the clinical or pathological diagnostic criteria of GVHD after liver transplantation; (2) recipient age >18 years; (3) case number ≥2. Exclusion criteria: incomplete clinical data such as incidence, mortality, and clinical manifestations of GVHD after liver transplantation. The retrieved literature was reviewed.Results:All 5 recipients were male. Among them, 4 cases underwent liver transplantation at this center. The incidence of GVHD after liver transplantation in this center was 0.46% (4/872). All 5 cases developed symptoms such as fever, rash, diarrhea, oral ulcers, and pancytopenia on the 19th (5-21) day after liver transplantation. One case had gastrointestinal bleeding. Two cases were diagnosed by skin pathological biopsy, and three cases were diagnosed based on clinical manifestations such as fever, rash, diarrhea, and bone marrow suppression. One case discontinued immunosuppressants, and four cases reduced the dosage of immunosuppressants. Four cases were treated with high-dose glucocorticoids, four with intravenous immunoglobulin (IVIG), three with ruxolitinib, and three with hematopoietic factors. All five cases received protective isolation, anti-infection, and symptomatic supportive treatment. Among the three recipients treated with ruxolitinib, body temperature returned to normal, rash gradually faded, oral ulcers gradually healed, blood cells returned to normal, and they were eventually discharged after recovery. The remaining two cases showed no symptom improvement and died of severe lung infection and multiple organ failure. Literature review A total of 34 articles were included. The incidence of GVHD after liver transplantation was 1.03% (279/27 018), and the onset time ranged from 7 to 1,865 days post-transplantation; 272 cases (97.49%) occurred within 1-8 weeks. The main clinical manifestations included fever (195 cases, 69.89%), rash (267 cases, 95.70%), diarrhea (173 cases, 62.01%), and bone marrow suppression (214 cases, 76.70%). Treatment mainly involved adjustment of immunosuppressants (201 cases, 72.04%), high-dose corticosteroids (215 cases, 77.06%), and IVIG pulse therapy (146 cases, 52.33%). In the end, 83 cases (29.75%) recovered and were discharged, while the mortality rate was 70.25% (196/279), with causes of death including infection, gastrointestinal bleeding, and multiple organ failure.Conclusions:GVHD after liver transplantation has a low incidence, high mortality, and poor prognosis. Diagnosis mainly relies on typical clinical manifestations and pathological results of tissue biopsy. Early administration of high-dose corticosteroids combined with IVIG pulse therapy, timely reduction or discontinuation of immunosuppressants, use of ruxolitinib, active infection management, and enhanced symptomatic and supportive care are effective strategies for treating GVHD after liver transplantation.

Objective To analyze the clinical efficacy and safety of transcatheter arterial chemoembolization(TACE)combined with lenvatinib and PD-1 antibody in the treatment of intermediate-advanced hepatocellular carcinoma(HCC).Methods A retrospective cohort trial was conducted on 105 patients with intermediate-advanced HCC(BCLC B or C stage)treated with TACE combined with lenvatinib and PD-1 antibody in our institute from January 2021 to June 2023.The blood biochemical indicators and imaging characteristics of the patients were collected before and after TACE.Objective response rate(ORR),disease control rate(DCR),conversion resection rate,overall survival(OS)and progression-free survival(PFS)were analyzed to evaluate the clinical efficacy of the triple therapy,and the frequency and severity of all adverse reactions during treatment were recorded to evaluate the safety of the therapy.Results Among the 105 patients with intermediate-advanced HCC who received triple therapy,33 died and 72 survived.The ORR was 62.8％and the DCR was 72.3％.The conversion resection rate was 11.4％.The median OS(mOS)was not reached.The median PFS(mPFS)was(10.3±0.8)months.The incidence of adverse reactions of all grades was 97.1％,and the incidence of those of grade 3～4 was 33.3％.No treatment-related death occurred.Conclusion The triple therapy of TACE combined with lenvatinib and PD-1 antibody is a safe and effective comprehensive treatment regimen,which provides a new treatment strategy for improving the prognosis of intermediate-advanced HCC.

Objective To study the role of bone marrow mesenchymalstem cells in recovery process of hepatocyteinjury and to explore the possible mechanism. Methods BMSCs and primary generation of hepatocytes were cultured and identified. A model of hepatocyte injure was established. Liver cell proliferation at different conditionswas detected by MTT method. Hepatocytes were added with BMSCs,baxinhibitor and mixture of BMSCs and baxinhibitor for co?cultured.Expressions of TGF?β1,bcl?2,and baxwere detected by Westernblot and real?time PCR. Results BMSCs and primary generation of hepatocyte were successfully cultured and identified, and a model of hepatocyte injury was successfully established. MTT tests revealed that the OD value of the mixture wassignificant higher in BMSCs and HGF co?culture group than in BMSCs co?culture group or HGF co?culture group;there was no significant difference between BMSCs co?culture group and HGF co?culture group,while both groups were significant higher than control group. The MTT tests also revealed that the OD value of the mixture of BMSCs and Baxinhibitor co?culture group had no significant difference as compared with BMSCs co?culture group or Baxinhibitor co?culture group. There was no significant difference between BMSCs co?culture group and Baxinhibitor co?culture group,while the OD value was significant higher in both groups than in the control group. Westernb lot and real?time PCR results revealed that the value of TGF?β1 and bax in the mixture of BMSCs and Baxinhibitor co?culture group had no significant difference as compared with BMSCs co?culture group or Baxinhibitor co?culture group. There was no significant difference between BMSCs co?culture group and Baxinhibitor co?culture group,while both groups had a significant higher value than the control group. The value of Bcl?2 in the mixture of BMSCs and Baxinhibitor co?culture group had no significant difference as compared with BMSCs co?culture group or Baxinhibitor co?culture group. There was no significant difference between BMSCs co?culture group and Baxinhibitor co?culture group,while both groups had a significant lower value than the control group. Conclusions BMSCs can promote hepatocyte proliferation during the recovery process of hepatocyte injury,BMSCs and HGF promote liver cell proliferation have synergy effect,the effect of BMSCs probably through regulate TGF?β1/bcl?2(bax)correlation pathway.

Objective To lay the foundation for analyzing the mechanism of liver cell injury caused by mtDNA deletion and mutation in patients with obstructive jaundice. Methods 30 patients were randomly selected as obstructive jaundice group (case group) and 10 patients as control group according to the strict condition. Author makes use of the methods of PCR amplification of the entire human mitochondrial genome in 17 mismatch-specific overlapping fragments and gene sequencing results to Preliminary estimate the localizathion of hepatocyte mtDNA damage in patients with obstructive jaundice. Result Deletions and length of partial liver cells were 8429-9591 of about 1. 1 kb, 16024-60 of about 0. 6 kb, 1889-3031 of about 1. 1 kb and 4977bps common deletion and the high mutation rate of some bases in D-loop region. Conclusion There are multiple mtDNA deletions and multiple point mutations in patients with obstructive jaundice