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  • Wiley  (6)
  • Hou, Jinlin  (6)
  • 1
    In: Alimentary Pharmacology & Therapeutics, Wiley, Vol. 54, No. 3 ( 2021-08), p. 329-338
    Abstract: Obesity is typically associated with metabolic dysfunction, but its impact on hepatocellular carcinoma (HCC) remains unclear in patients with chronic hepatitis B (CHB). Aim To study the effect of obesity on HCC development in patients with CHB receiving antiviral therapy. Methods We included patients from a Chinese multicentre, prospective, observational, treated CHB cohort in this study. General obesity was evaluated by body‐mass index (BMI). Central obesity was evaluated by waist circumference, waist‐to‐hip ratio and waist‐to‐height ratio. Results A total of 5754 nucleos(t)ide analogue treated patients were enrolled in the analysis. The 5‐year cumulative incidence of HCC was 2.9%. Waist‐to‐height ratio performed better in predicting HCC development than BMI, waist circumference or waist‐to‐hip ratio. Patients with central obesity (defined as waist‐to‐height ratio 〉 0.5) had significantly higher 5‐year incidence of HCC than those without central obesity in the overall population (3.9% vs 2.1%, hazard ratio [HR]: 2.06, P  = 0.0001) and 745 propensity score matched pairs (4.7% vs 2.3%, HR: 2.04, P  = 0.026), respectively. Besides cirrhosis status and aMAP HCC risk score, central obesity was also independently associated with HCC risk (HR: 1.63, P  = 0.013). Waist‐to‐height ratio gain within 1 year was associated with a significantly higher HCC risk with an adjusted HR value of 1.88 (95% confidence interval: 1.12‐3.13, P  = 0.017). Conclusions Central obesity, evaluated by the waist‐to‐height ratio, was associated with a twofold increase in HCC risk among CHB patients receiving antiviral treatment, highlighting the important role of abnormal metabolic function in the progression of liver disease.
    Type of Medium: Online Resource
    ISSN: 0269-2813 , 1365-2036
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2003094-0
    SSG: 15,3
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  • 2
    In: Liver International, Wiley, Vol. 19, No. 5 ( 1999-10), p. 411-417
    Type of Medium: Online Resource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 1999
    detail.hit.zdb_id: 2124684-1
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  • 3
    In: Liver International, Wiley, Vol. 39, No. 8 ( 2019-08), p. 1428-1436
    Abstract: The role of cigarette smoking in the development of chronic hepatitis B (CHB) remains poorly understood. We assessed the potential contributions of cigarette smoking to liver fibrosis and its regression after starting antiviral therapy in CHB patients. Methods In this cohort study, 2144 consecutive male CHB patients under no antiviral therapy were evaluated and 206 patients with significant liver fibrosis (≥F2) initiating antiviral therapy had longitudinal follow‐up. Liver fibrosis was measured by liver stiffness measurement using transient elastography. To adjust for imbalances between smoking history and never smoking groups, propensity score (PS) matching model with 1:1 ratios were performed. Cigarette smoking history and intensity (pack‐years) were collected and documented using a standardized questionnaire. Results Before PS matching, 432/2144 patients had advanced fibrosis in prevalence cohort. Patients with smoking history (n = 1002) had a greater prevalence of advanced fibrosis than those without (n = 1142) (24.4% vs 16.5%, P  = 0.001). Multivariate logistic regression analysis demonstrated that smoking contributed to advanced fibrosis (OR, 1.458; 95% CI, 1.114‐1.908). In longitudinal cohort, multivariate logistic regression analysis demonstrated retarded fibrosis regression in patients with history of smoking ≥10 pack‐years (OR, 0.288; 95% CI, 0.1‐0.825). After PS matching, patients with smoking history had higher prevalence of advanced fibrosis (22.8% vs 18%, P  = 0.024) than those non‐smokers. In post‐PS‐matching logistic regression, the effect of smoking on advanced fibrosis persisted (OR, 1.415; 95% CI, 1.047‐1.912; P  = 0.024). Conclusions Cigarette smoking in male CHB patients aggravated liver fibrosis prior to and delayed fibrosis regression under antiviral therapy.
    Type of Medium: Online Resource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2124684-1
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  • 4
    In: Liver International, Wiley, Vol. 44, No. 3 ( 2024-03), p. 749-759
    Abstract: aMAP score, as a hepatocellular carcinoma risk score, is proven to be associated with the degree of chronic hepatitis B‐related liver fibrosis. We aimed to evaluate the ability of aMAP score for metabolic dysfunction‐associated steatotic liver disease (MASLD; formerly NAFLD)‐related fibrosis diagnosis and establish a machine‐learning (ML) model to improve the diagnostic performance. Methods A total of 946 biopsy‐proved MASLD patients from China and the United States were included in the analysis. The aMAP score, demographic/clinical indices and liver stiffness measurement (LSM) were included in seven ML algorithms to build fibrosis diagnostic models in the training set ( N = 703). The performance of ML models was evaluated in the external validation set ( N = 125). Results The AUROCs of aMAP versus fibrosis‐4 index (FIB‐4) and aspartate aminotransferase‐platelet ratio (APRI) in cirrhosis and advanced fibrosis were (0.850 vs. 0.857 [ P = 0.734], 0.735 [ P = 0.001]) and (0.759 vs. 0.795 [ P = 0.027], 0.709 [ P = 0.049]). When using dual cut‐off values, aMAP had a smaller uncertainty area and higher accuracy (26.9%, 86.6%) than FIB‐4 (37.3%, 85.0%) and APRI (59.0%, 77.3%) in cirrhosis diagnosis. The seven ML models performed satisfactorily in most cases. In the validation set, the ML model comprising LSM and 5 indices (including age, sex, platelets, albumin and total bilirubin used in aMAP calculator), built by logistic regression algorithm (called LSM‐plus model), exhibited excellent performance. In cirrhosis and advanced fibrosis detection, the LSM‐plus model had higher accuracy (96.8%, 91.2%) than LSM alone (86.4%, 67.2%) and Agile score (76.0%, 83.2%), respectively. Additionally, the LSM‐plus model also displayed high specificity (cirrhosis: 98.3%; advanced fibrosis: 92.6%) with satisfactory AUROC (0.932, 0.875, respectively) and sensitivity (88.9%, 82.4%, respectively). Conclusions The aMAP score is capable of diagnosing MASLD‐related fibrosis. The LSM‐plus model could accurately identify MASLD‐related cirrhosis and advanced fibrosis.
    Type of Medium: Online Resource
    ISSN: 1478-3223 , 1478-3231
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2024
    detail.hit.zdb_id: 2124684-1
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  • 5
    In: Journal of Medical Virology, Wiley, Vol. 83, No. 9 ( 2011-09), p. 1544-1550
    Abstract: The existence of statistical associations between hepatitis B‐related acute‐on‐chronic liver failure and both hepatitis B virus (HBV) genotype and mutations in the basal core promoter (BCP) and precore (PC) regions needs to be confirmed. A total of 322 patients with a chronic HBV infection, including 77 with hepatitis B‐related acute‐on‐chronic liver failure, 109 with hepatocellular carcinoma (HCC) and 136 with chronic hepatitis B (CHB) were enrolled. The HBV genotype and the presence of mutations in the BCP/PC regions were determined by direct sequencing, and the frequencies were compared in the three patient groups. Overall, 198/322 (61.5%) were infected with genotype B and 124/322 (38.5%) with genotype C. Genotype B was significantly more frequent in patients with acute‐on‐chronic liver failure than CHB (92.2% vs. 60.3%, P   〈  0.001). As a contrast, genotype C was more common in patients with HCC than CHB (58.7% vs. 39.7%, P  = 0.003). In genotype B patients, the A1762T/G1764A, A1846T, and G1896A mutations were significantly more prevalent in patients with acute‐on‐chronic liver failure than CHB (50.7% vs. 28.0%, P  = 0.004; 59.2% vs. 34.1%, P  = 0.002; 69.0% vs. 41.5%, P  = 0.001, respectively). In multivariate analysis, the risk factors for acute‐on‐chronic liver failure were genotype B, A1762T/G1764A, and G1896A. In conclusion, CHB patients with genotype B, G1896A, and A1762T/G1764A had a higher tendency to develop liver failure than patients with genotype C. Therefore, HBV genotyping and detecting G1896A and A1762T/G1764A mutations might have important clinical implications as predictive risk factors for hepatitis B‐related acute‐on‐chronic liver failure. J. Med. Virol. 83:1544–1550, 2011. © 2011 Wiley‐Liss, Inc.
    Type of Medium: Online Resource
    ISSN: 0146-6615 , 1096-9071
    URL: Issue
    RVK:
    Language: English
    Publisher: Wiley
    Publication Date: 2011
    detail.hit.zdb_id: 752392-0
    detail.hit.zdb_id: 1475090-9
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  • 6
    In: Journal of Gastroenterology and Hepatology, Wiley, Vol. 36, No. 1 ( 2021-01), p. 208-216
    Abstract: Tri‐typing of acute‐on‐chronic liver failure (ACLF), as proposed by the World Gastroenterology Organization (WGO), has not been validated in patients infected with hepatitis B virus (HBV). We aim to compare the three types of ACLF patients in clinic characteristics. Methods Hospitalized ACLF patients with chronic hepatitis B from five hepatology centers were retrospectively selected and grouped according to the WGO classification. For each group, we investigated laboratory tests, precipitating events, organ failure, and clinical outcome. Results Compared with type‐B ( n  = 262, compensated cirrhosis) and type‐C ( n  = 129, decompensated cirrhosis) ACLF, type‐A patients ( n  = 195, non‐cirrhosis) were associated with a younger age, the highest platelet counts, the highest aminotransferase levels, and the most active HBV replications. HBV reactivation were more predominant in type‐A, while bacterial infections in type‐B and type‐C ACLF cases. Liver failure (97.4%) and coagulation failure (86.7%) were most common in type‐A compared with type‐B or type‐C ACLF patients. Kidney failure was predominantly identified in type‐C subjects (41.9%) and was highest (23/38, 60.5%) in grade 1 ACLF patients. Furthermore, type‐C ACLF showed the highest 28‐day (65.2%) and 90‐day (75.3%) mortalities, compared with type‐A (48.7% and 54.4%, respectively) and type‐B (48.4% and 62.8%, respectively) ACLF cases. Compared with type‐A (11.7%) ACLF patients, the increased mortality from 28 to 90 days was higher in type‐B (31.6%) and type‐C (37.5%). Conclusion Tri‐typing of HBV‐related ACLF in accordance with the WGO definition was able to distinguish clinical characteristics, including precipitating events, organ failure, and short‐term prognosis in ACLF patients.
    Type of Medium: Online Resource
    ISSN: 0815-9319 , 1440-1746
    URL: Issue
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2006782-3
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