TY - JOUR
T1 - Dysmetabolism, Diabetes and Clinical Outcomes in Patients Cured of Chronic Hepatitis C
T2 - A Real-Life Cohort Study
AU - for the NAVIGATORE-Lombardia Network
AU - Valenti, Luca
AU - Pelusi, Serena
AU - Aghemo, Alessio
AU - Gritti, Sara
AU - Pasulo, Luisa
AU - Bianco, Cristiana
AU - Iegri, Claudia
AU - Cologni, Giuliana
AU - Degasperi, Elisabetta
AU - D’Ambrosio, Roberta
AU - del Poggio, Paolo
AU - Soria, Alessandro
AU - Puoti, Massimo
AU - Carderi, Isabella
AU - Pigozzi, Marie Graciella
AU - Carriero, Canio
AU - Spinetti, Angiola
AU - Zuccaro, Valentina
AU - Memoli, Massimo
AU - Giorgini, Alessia
AU - Viganò, Mauro
AU - Rumi, Maria Grazia
AU - Re, Tiziana
AU - Spinelli, Ombretta
AU - Colombo, Maria Chiara
AU - Quirino, Tiziana
AU - Menzaghi, Barbara
AU - Lorini, Gianpaolo
AU - Pan, Angelo
AU - D’Arminio Monforte, Antonella
AU - Buscarini, Elisabetta
AU - Autolitano, Aldo
AU - Bonfanti, Paolo
AU - Terreni, Natalia
AU - Aimo, Gianpiero
AU - Mendeni, Monia
AU - Prati, Daniele
AU - Lampertico, Pietro
AU - Colombo, Massimo
AU - Fagiuoli, Stefano
N1 - Funding Information:
Potential conflict of interest: Dr. Valenti received grants from Gilead. Dr. Pasulo advises AbbVie. Dr. D’Ambrosio consults and received grants from Gilead and AbbVie. Dr. Puoti advises, is on the speakers’ bureau, and received grants from Gilead, AbbVie, and Merck. Dr. Rumi consults and received grants from Gilead. She received grants from AbbVie. Dr. Lampertico advises and is on the speakers’ bureau for Bristol‐Myers Squibb, Roche, Gilead, GlaxoSmithKline, MSD, AbbVie, Arrowhead, Alnylam, Eiger, Myr, and Janssen. Dr. Fagiuoli is on the speakers’ bureau for Gilead, MSD, AbbVie, Novartis, Intercept, and Bayer.
Funding Information:
Supported by Gilead Sciences (Gilead Fellowship 2018 Italy, Gilead_IN‐IT‐989‐5790), Ministero della Salute (CV PREVITAL, RF‐2016‐02364358), Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico (PR‐0391 and RC100017A), and European Commission (101016726 and 777377).
Publisher Copyright:
© 2021 The Authors. Hepatology Communications published by Wiley Periodicals LLC on behalf of American Association for the Study of Liver Diseases.
PY - 2022
Y1 - 2022
N2 - The aim of this study was to examine the impact of features of dysmetabolism on liver disease severity, evolution, and clinical outcomes in a real-life cohort of patients treated with direct acting antivirals for chronic hepatitis C virus (HCV) infection. To this end, we considered 7,007 patients treated between 2014 and 2018, 65.3% with advanced fibrosis, of whom 97.7% achieved viral eradication (NAVIGATORE-Lombardia registry). In a subset (n = 748), liver stiffness measurement (LSM) was available at baseline and follow-up. Higher body mass index (BMI; odds ratio [OR] 1.06 per kg/m2, 1.03-1.09) and diabetes (OR 2.01 [1.65-2.46]) were independently associated with advanced fibrosis at baseline, whereas statin use was protective (OR 0.46 [0.35-0.60]; P < 0.0001 for all). The impact of BMI was greater in those without diabetes (P = 0.003). Diabetes was independently associated with less pronounced LSM improvement after viral eradication (P = 0.001) and in patients with advanced fibrosis was an independent predictor of the most frequent clinical events, namely de novo hepatocellular carcinoma (HCC; hazard ratio [HR] 2.09 [1.20-3.63]; P = 0.009) and cardiovascular events (HR 2.73 [1.16-6.43]; P = 0.021). Metformin showed a protective association against HCC (HR 0.32 [0.11-0.96]; P = 0.043), which was confirmed after adjustment for propensity score (P = 0.038). Diabetes diagnosis further refined HCC prediction in patients with compensated advanced chronic liver disease at high baseline risk (P = 0.024). Conclusion: Metabolic comorbidities were associated with advanced liver fibrosis at baseline, whereas statins were protective. In patients with advanced fibrosis, diabetes increased the risk of de novo HCC and of cardiovascular events. Optimization of metabolic comorbidities treatment by a multi-disciplinary management approach may improve cardiovascular and possibly liver-related outcomes.
AB - The aim of this study was to examine the impact of features of dysmetabolism on liver disease severity, evolution, and clinical outcomes in a real-life cohort of patients treated with direct acting antivirals for chronic hepatitis C virus (HCV) infection. To this end, we considered 7,007 patients treated between 2014 and 2018, 65.3% with advanced fibrosis, of whom 97.7% achieved viral eradication (NAVIGATORE-Lombardia registry). In a subset (n = 748), liver stiffness measurement (LSM) was available at baseline and follow-up. Higher body mass index (BMI; odds ratio [OR] 1.06 per kg/m2, 1.03-1.09) and diabetes (OR 2.01 [1.65-2.46]) were independently associated with advanced fibrosis at baseline, whereas statin use was protective (OR 0.46 [0.35-0.60]; P < 0.0001 for all). The impact of BMI was greater in those without diabetes (P = 0.003). Diabetes was independently associated with less pronounced LSM improvement after viral eradication (P = 0.001) and in patients with advanced fibrosis was an independent predictor of the most frequent clinical events, namely de novo hepatocellular carcinoma (HCC; hazard ratio [HR] 2.09 [1.20-3.63]; P = 0.009) and cardiovascular events (HR 2.73 [1.16-6.43]; P = 0.021). Metformin showed a protective association against HCC (HR 0.32 [0.11-0.96]; P = 0.043), which was confirmed after adjustment for propensity score (P = 0.038). Diabetes diagnosis further refined HCC prediction in patients with compensated advanced chronic liver disease at high baseline risk (P = 0.024). Conclusion: Metabolic comorbidities were associated with advanced liver fibrosis at baseline, whereas statins were protective. In patients with advanced fibrosis, diabetes increased the risk of de novo HCC and of cardiovascular events. Optimization of metabolic comorbidities treatment by a multi-disciplinary management approach may improve cardiovascular and possibly liver-related outcomes.
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U2 - 10.1002/hep4.1851
DO - 10.1002/hep4.1851
M3 - Article
AN - SCOPUS:85119688501
VL - 6
SP - 867
EP - 877
JO - Hepatology Communications
JF - Hepatology Communications
SN - 2471-254X
IS - 4
ER -