ABSTRACT
BACKGROUND AND AIM: It has been reported that serum quantification of anti-HBc (qAnti-HBc) could predict antiviral response in chronic hepatitis B (CHB) patients, while its role in hepatitis B virus-related acute-on-chronic liver failure (HBV-ACLF) remains unclear. Its implication in HBV-ACLF was evaluated in this study. METHODS: Baseline serum qAnti-HBc levels were retrospectively detected in HBV-ACLF and CHB patients using recently developed double-sandwich immunoassay. The association of qAnti-HBc level with clinical outcomes was evaluated by multiple logistic regression. Nomogram was adopted to formulate an algorithm incorporating qAnti-HBc for the prediction of survival in HBV-ACLF. The post-hospitalization of HBV-ACLF patients were followed-up for 1 year. RESULTS: Eighty-eight HBV-ACLF as training set, 80 HBV-ACLF as validation set and 216 CHB cases were included. Serum qAnti-HBc level was significantly higher in HBV-ACLF (4.95 ± 0.54 log10 IU/mL) than CHB patients (4.47 ± 0.84 log10 IU/mL) (P < 0.01). Among HBV-ACLF cases, both in training and validation set, patients with poor outcomes had lower qAnti-HBc level. Area under receiver operating characteristic curve of the novel qAnti-HBc inclusive model was 0.82, superior to 0.73 from model for end-stage liver disease scores (P = 0.018), which was confirmed in validation set. During follow-up, the qAnti-HBc level declined at month 3 and month 6, then plateaued at 3.84 log10 IU/mL. CONCLUSIONS: Serum qAnti-HBc level was associated with disease severity and might be served as a novel biomarker in the prediction of HBV-ACLF clinical outcomes. The underlying immunological mechanism warrants further investigation.
Subject(s)
Acute-On-Chronic Liver Failure/diagnosis , Acute-On-Chronic Liver Failure/etiology , Hepatitis B Antibodies/blood , Hepatitis B Core Antigens/immunology , Hepatitis B virus/immunology , Hepatitis B, Chronic/complications , Hepatitis B, Chronic/diagnosis , Adult , Biomarkers/blood , Female , Follow-Up Studies , Humans , Logistic Models , Male , Middle Aged , Predictive Value of Tests , Prognosis , Severity of Illness IndexABSTRACT
BACKGROUND: Hypertrophic scars (HS) are common pathologic processes emerged during wound-healing process. The receptor-interacting protein kinase (RIP) might participate in keloid formation. AIMS: This study aimed to investigate Necrostatin-1 (Nec-1), a RIP1/RIP3 inhibitor, in the formation of hypertrophic scar. METHODS: Human hypertrophic scar fibroblasts (HSF) were extracted from patients with hypertrophic scar. Transforming growth factor-ß1 (TGF-ß1) was performed to induce wound-healing process including cell proliferation (CCK-8, Flow cytometry, and Western blot), migration (Transwell assay, Western blot), collagen production (Western blot), and extracellular matrix dysfunction (Western blotting and immunofluorescence). RESULTS: Our results reported that Nec-1 inhibited TGF-ß1-induced cell proliferation and promoted G0/G1 phase arrest in HSF. In addition, Nec-1 attenuated TGF-ß1-induced cell migration and inhibited the expression of MMP2 and MMP9 in TGF-ß1-induced HSF. Besides, Nec-1 also reduced TGF-ß1-induced collagen production and α-smooth muscle actin expression in HSF. CONCLUSIONS: The present data in this study showed the potential role of Nec-1 as a novel treatment for HS.
