Late-stage presentation with decompensated cirrhosis is alarmingly common but successful etiologic therapy allows for favorable clinical outcomes (pdf)

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Late-stage presentation with decompensated cirrhosis is alarmingly common but successful etiologic therapy allows for favorable clinical outcomes

PLOS ONE RESEARCH ARTICLE Late-stage presentation with decompensated cirrhosis is alarmingly common but successful etiologic therapy allows for favorable clinical outcomes a1111111111 a1111111111 a1111111111 a1111111111 a1111111111 Michael Schwarz ID1,2, Caroline Schwarz ID1,2, Lukas Burghart1,2, Nikolaus Pfisterer3, David Bauer ID1,2, Wolfgang Hübl4, Mattias Mandorfer2, Michael Gschwantler1,5, Thomas Reiberger ID2* 1 Department of Internal Medicine IV, Department for Gastroenterology and Hepatology, Klinik Ottakring, Vienna, Austria, 2 Department of Medicine III, Division of Gastroenterology and Hepatology, Medical University of Vienna, Vienna, Austria, 3 Department for Gastroenterology and Hepatology, Department of Internal Medicine IV, Klinik Landstraße, Vienna, Austria, 4 Klinik Ottakring, Institute for Laboratory Medicine, Vienna, Austria, 5 Sigmund Freud University, Vienna, Austria * OPEN ACCESS Citation: Schwarz M, Schwarz C, Burghart L, Pfisterer N, Bauer D, Hübl W, et al. (2023) Latestage presentation with decompensated cirrhosis is alarmingly common but successful etiologic therapy allows for favorable clinical outcomes. PLoS ONE 18(8): e0290352. https://doi.org/ 10.1371/journal.pone.0290352 Editor: Ashraf Elbahrawy, Al-Azhar University, EGYPT Received: February 14, 2023 Accepted: August 4, 2023 Published: August 24, 2023 Copyright: © 2023 Schwarz et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Data Availability Statement: All relevant data are within the paper and its Supporting Information files. Funding: The authors received no specific funding for this work. Competing interests: I have read the journal’s policy and the authors of this manuscript have the following competing interests: M.S. received travel support from MSD, Sandoz, BMS, Abbvie and Gilead; and speaking honoraria from BMS. C.S. Abstract Introduction Liver cirrhosis accounts for considerable morbidity and mortality worldwide and late presentation limits therapeutic options. We aimed to assess characteristics of patients with liver cirrhosis at the time of first presentation and during their clinical course. Methods Patients with cirrhosis as evident by presence of varices at endoscopy, liver stiffness �15kPa at elastography, or ascites requiring paracentesis between Q1/2015-Q2/2020 were retrospectively included. Clinical, laboratory, and imaging data were collected from medical records at presentation and last follow-up. Results 476 patients were included (alcohol-related liver disease, ALD: 211, 44.3%; viral hepatitis: 163, 34.2%). Of these, 106 patients (22.3%) and 160 patients (33.6%) presented already with Child-Pugh C and MELD >15, respectively, and decompensation events were registered in 50% (238 patients) at baseline, and even in 75.4% of ALD patients. During a median follow-up of 11.0 (IQR 4–24) months, 116 patients died. Two-year survival was worse for patients with ALD than for viral hepatitis (71.1% vs. 90.2%, log rank p<0.001). We observed the highest percentage of portal-vein thrombosis (30.0%), hepatocellular carcinoma (15.0%), and death (45.0%) in the MAFLD group (n = 20). Patients cured from hepatitis C showed significant improvements in platelet count (147 to 169 G/L, p<0.001) and liver stiffness (26.2 to 17.7 kPa, p<0.001), while ALD patients improved in Child-Pugh score (8.6 to 7.6, p<0.001) during follow-up. With increasing Child Pugh score PLOS ONE | https://doi.org/10.1371/journal.pone.0290352 August 24, 2023 1 / 17 PLOS ONE received travel support from Gilead, Abbvie, and Gebro; speaking honoraria from Abbvie and Gilead; and payments for consulting from Gilead. L.B. has nothing to disclose. N.P. has nothing to disclose. D.B. received travel support from Gilead and Siemens, served as advisor/speaker for AbbVie and Siemens, as well as grant support from Gilead, Siemens,Philips, and AbbVie. W.H. has nothing to disclose. M.M. served as a speaker and/or consultant and/or advisory board member for AbbVie, Bristol-Myers Squibb, Gilead, Collective Acumen, and W. L. Gore & Associates and received travel support from AbbVie, Bristol-Myers Squibb, and Gilead. M.G. received grant support from Abbvie, Gilead and MSD; speaking honoraria from Abbvie, Gilead, Janssen, Roche, Intercept, and MSD; consulting/advisory board fees from Abbvie, Gilead, Janssen, Roche, Intercept, Norgine, AstraZeneca, Falk, Shionogi and MSD; and travel support from Abbvie and Gilead. T.R. received grant support from AbbVie, Boehringer-Ingelheim, Gilead, MSD, Philips Healthcare, Gore; speaking honoraria from AbbVie, Gilead, Gore, Intercept, Roche, MSD; consulting/advisory board fees from AbbVie, Bayer, Boehringer-Ingelheim, Gilead, Intercept, MSD, Siemens; and travel support from Boehringer-Ingelheim, Gilead and Roche. This does not alter our adherence to PLOS ONE policies on sharing data and materials. Late-stage presentation with decompensated cirrhosis is alarmingly common and MELD, we found increasing serum concentrations of CRP (p<0.001) and an inverse correlation with serum HDL (Spearman’s ρ = -0.573 and -0.529, respectively, p<0.001). Conclusion Half of the patients with cirrhosis had decompensated cirrhosis at presentation. This calls for increased awareness and strategies for earlier diagnosis of chronic liver disease and cirrhosis. Introduction Worldwide, liver cirrhosis accounts for substantial mortality and morbidity with approximately two million deaths each year [1,2]. Most common causes are viral hepatitis (i.e. chronic hepatitis B, C or D [CHB, CHC, CHD]), alcoholic liver disease (ALD), and metabolic dysfunction-associated fatty liver disease (MAFLD) [3,4]. Cirrhosis is caused by prolonged damage to the liver parenchyma, subsequent inflammation, and scarring, as well as changes in vascular resistance and perfusion [5,6]. Fibrotic rearrangement of the liver, intrahepatic vasoconstriction, and extrahepatic (splanchnic) vasodilation result in portal hypertension, which causes the formation of venous collaterals (e.g., gastroesophageal varices) and decompensation events like ascites, variceal bleeding, and hepatic encephalopathy [7–9]. Thus, cirrhosis be divided into a compensated and decompensated state, where the occurrence of decompensation is associated with a marked reduction in prognosis with a median survival of about two years after the first event [10,11]. Although there is no predictable sequence of events, ascites is the most common and regularly the first decompensation event [10,12,13]. Despite the severe morbidity of chronic liver disease, its progression to cirrhosis, and the burden on healthcare systems worldwide, underdiagnosis is prevalent [14,15], even though etiological treatment for viral hepatitis or pathogen abstinence for ALD can potentially reverse the damage done (...truncated)