Risk factors for hepatitis B virus recurrence after living donor liver transplantation: A 22-year experience at a single center

Bae, Sung Kwan; Akamatsu, Nobuhisa; Ichida, Akihiko; Maki, Hisaji; Kawahara, Takuya; Hoshikawa, Mayumi; Nagata, Ryuji; Mihara, Yuichiro; Kawaguchi, Yoshikuni; Ishizawa, Takeaki; Arita, Junichi; Kaneko, Junichi; Tamura, Sumihito; Hasegawa, Kiyoshi

doi:10.5582/bst.2020.03336

Cited by 2 publications

(1 citation statement)

References 24 publications

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“…All 4 HCC recurrent patients had received pre-transplant bridging therapy and at least 1 patient was downstaged to within Milan criteria. Other factors associated with a higher risk of HBV recurrence include pre-transplant HCC, especially outside the Milan criteria [ 29 – 31 ], the viral load at time of transplantation [ 32 ], co-infection with human immunodeficiency virus [ 33 ], pre-transplant HBeAg positivity [ 5 ], and immunosuppressive therapy [ 1 ]. All 7 HBV-recurrent patients in our NIS presented with at least 1 of the above-mentioned risk factors.…”

Section: Discussionmentioning

confidence: 99%

Long-Term Effectiveness, Safety, and Patient-Reported Outcomes of Self-Administered Subcutaneous Hepatitis B Immunoglobulin in Liver Post-Transplant Hepatitis B Prophylaxis: A Prospective Non-Interventional Study

et al. 2022

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Background Self-administered subcutaneous hepatitis B immunoglobulin (s.c. HBIg) in combination with nucleos(t)ide analogs (NUCs) has proved to be effective and safe in preventing hepatitis B virus (HBV) reinfection after liver transplantation. Material/Methods This non-interventional, prospective, single-arm, multicenter, international study collected data on long-term effectiveness, safety, patient satisfaction (Treatment Satisfaction Questionnaire for Medication, TSQM-11), and quality of life (EQ-5D questionnaire) in routine practice over a 2-year treatment period. Data analysis was based on 195 adults (82.1% male) transplanted for HBV-related liver diseases and treated with s.c. HBIg with/without NUC(s). Results HBV recurrence (seropositivity of HBV surface antigen and/or HBV DNA) was observed in 7/195 (3.6%) patients (annual rate: 2.01%). Hepatocellular carcinoma (HCC) recurred in 4/83 (4.8%) patients transplanted for HBV-HCC (annual rate: 2.88%). Twenty-nine adverse drug reactions occurred in 16/195 (8.2%) patients. Convenience and overall satisfaction scores of the TSQM-11 were significantly ( P <0.05) improved under treatment at the 3-month, 2-year, and last follow-up visits. Quality of life remained constant over the entire observation period (EQ-5D index [ P ≥0.075]). S.c. HBIg was mainly self-administered (6458/9021 administrations, 71.6%) at home (8514/9021 administrations, 94.4%). Conclusions The results indicate long-term effectiveness and safety of s.c. HBIg in combination with NUC therapy in preventing post-transplant HBV reinfection under real-life conditions. The convenience of the therapy contributed to the high overall treatment satisfaction and acceptance by the patients.

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Section: Discussionmentioning

confidence: 99%

Long-Term Effectiveness, Safety, and Patient-Reported Outcomes of Self-Administered Subcutaneous Hepatitis B Immunoglobulin in Liver Post-Transplant Hepatitis B Prophylaxis: A Prospective Non-Interventional Study

et al. 2022

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Knockdown of NDUFC1 inhibits cell proliferation, migration, and invasion of hepatocellular carcinoma

et al. 2022

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BackgroundNADH: ubiquinone oxidoreductase subunit C1(NDUFC1) encodes a subunit of the Complex I, which may support the structural stability of Complex I and assist in its biogenesis. The expression and functional roles of NDUFC1 in hepatocellular carcinoma (HCC) remain unknown.ResultWe knocked down the expression of NDUFC1 in HCC cell lines to explore the effects of NDUFC1 downregulation on HCC in vitro. MTT assay determined that downregulation of NDUFC1 significantly inhibited cell proliferation. Flow cytometry with (propidium iodide) PI staining indicated silencing of NDUFC1 arrested cell cycle of BEL-7404 cells at G2 phase and SK-HEP-1 cells at S/G2 phase. Annexin V-PI double staining and flow cytometric analysis showed that the downregulation of NDUFC1 significantly increased the population of apoptotic cells. Wound-healing assay and transwell assay indicated that the downregulation of NDUFC1 suppressed the migration and invasion of HCC cells. According to the detection of complex1 activity, we found that the activity of NDUFC1 silenced group decreased, whereas the content of ROS increased. Furthermore, combined with bioinformatics analysis of senescence-related genes, we found that the silence of NDUFC1 in HCC could induce senescence and inhibit autophagy. In addition, NDUFC1 could correlate positively with cancer-related pathways, among which the p53 pathways and the PI3K/Akt/mTOR pathways. Finally, NDUFC1 is high expression in HCC specimens. High NDUFC1 expression was associated with poor prognosis and was an independent risk factor for reduced overall survival (OS).ConclusionsOur study indicated, for the first time, that NDUFC1 is an independent risk factor for the poor prognosis of HCC patients. NDUFC1 may promote tumor progression by inhibiting mitochondrial Complex I and up-regulating ROS through multiple cancer-related and senescence-related pathways of HCC, including p53 pathways and PI3K/Akt/mTOR pathways. We suppose that NDUFC1 might be a potential target for the mitochondrial metabolism therapy of HCC.

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Risk factors for hepatitis B virus recurrence after living donor liver transplantation: A 22-year experience at a single center

Cited by 2 publications

References 24 publications

Long-Term Effectiveness, Safety, and Patient-Reported Outcomes of Self-Administered Subcutaneous Hepatitis B Immunoglobulin in Liver Post-Transplant Hepatitis B Prophylaxis: A Prospective Non-Interventional Study

Long-Term Effectiveness, Safety, and Patient-Reported Outcomes of Self-Administered Subcutaneous Hepatitis B Immunoglobulin in Liver Post-Transplant Hepatitis B Prophylaxis: A Prospective Non-Interventional Study

Knockdown of NDUFC1 inhibits cell proliferation, migration, and invasion of hepatocellular carcinoma

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