TIPS insertion and systemic inflammation: Is it ever too late to lower portal pressure? Correspondence to editorial on “Insertion of a transjugular intrahepatic portosystemic shunt leads to sustained reversal of systemic inflammation in patients with deco Anja Tiede, Benjamin Maasoumy Clinical and Molecular Hepatology.2025; 31(2): e176. CrossRef
Decreasing systemic inflammation after TIPS: Still hope for the liver: Reply to correspondence on “Insertion of a transjugular intrahepatic portosystemic shunt leads to sustained reversal of systemic inflammation in patients with decompensated liver cirrh Georg Semmler, Lorenz Balcar, Mattias Mandorfer Clinical and Molecular Hepatology.2025; 31(2): e224. CrossRef
Refining Prognosis in Cirrhosis Patients With Ascites: Impact of Acute vs. Non‐Acute Decompensation Lucie Simonis, Lorenz Balcar, Anna Schedlbauer, Marta Tonon, Nikolaj Torp, Valeria Santori, Katharina Stopfer, Jan Embacher, Christian Sebesta, Leonie Hafner, Benedikt Silvester Hofer, Nina Dominik, Georg Kramer, Paul Thöne, Michael Trauner, Aleksander Kr Alimentary Pharmacology & Therapeutics.2025; 62(11-12): 1202. CrossRef
Systemic inflammatory indexes as predictors of 18-month mortality among cirrhotic patients receiving transjugular intrahepatic portosystemic shunt Jie Cheng, Xiaobing Wang, Lihua Zhou, Xiaojia Chen, Nuer Tang, Feng Zhou, Feng Ding, Yuan Yang, Jun Lin, Liping Chen Annals of Medicine.2025;[Epub] CrossRef
Background/Aims Spontaneous bacterial peritonitis (SBP) is a major problem associated with liver cirrhosis which has high mortality. Increased production of inflammatory mediators, such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) may be associated with development of renal impairment, one of the most important prognostic parameters in SBP. The aim of this study is to investigate the changes of these cytokines in ascitic fluid and plasma in patients with SBP and the relationship between these cytokines and development of renal impairment. Methods: Forty patients with liver cirrhosis and ascites were studied 21 with SBP and 19 with sterile ascites. TNF-α and IL-6 levels in ascitic fluid and plasma were determined by ELISA at the time of diagnosis in both groups and 48 hours after antibiotics treatment in SBP patients. Results: TNF- and IL-6 levels in ascitic fluid and plasma were significantly higher in patients with SBP than those without SBP (ascitic fluid TNF-α: 2.5±0.5 vs. 1.6±0.2; plasma TNF-α: 2.3±0.5 vs. 1.5±0.2; ascitic fluid IL-6: 3.8±0.5 vs. 3.0±0.4; plasma IL-6: 3.4±0.5 vs. 2.3±0.3, log pg/mL) (p<0.001). In patients with SBP, levels of TNF-α and IL-6 in ascitic fluid and plasma decreased 48 hours after antibiotics treatment. Eleven patients with SBP (11/21, 52%) developed renal impairment. Patients with renal impairment had significantly higher ascitic fluid and plasma TNF-α levels than those without renal impairment (median 2.5 vs. 2.1 for ascitic fluid, p=0.006; median 2.4 vs. 2.0, log pg/mL for plasma, p=0.04). Although four out of eleven (36%) patients who developed renal impairment died during hospitalization, all the patients without renal impairment survived (p=0.09). Conclusion: Our results suggest that the levels of TNF-α and IL-6 in ascitic fluid and plasma are increased in SBP and elevated levels of TNF-α in ascitic fluid and plasma may be associated with development of renal impairment, thus indicating poor prognosis in patients with SBP. (Korean J Hepatol 1999;5:314-321)