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Article ; Online: Shunt-Induced Hepatic Encephalopathy in TIPS

Philipp Schindler / Hauke Heinzow / Jonel Trebicka / Moritz Wildgruber

Journal of Clinical Medicine, Vol 9, Iss 3784, p

Current Approaches and Clinical Challenges

2020 Volume 3784

Abstract: Transjugular intrahepatic portosystemic shunt (TIPS) is an established treatment tool in decompensated liver cirrhosis that has been shown to prolong transplant-free survival. Hepatic encephalopathy (HE) is a frequent complication of decompensated ... ...

Abstract	Transjugular intrahepatic portosystemic shunt (TIPS) is an established treatment tool in decompensated liver cirrhosis that has been shown to prolong transplant-free survival. Hepatic encephalopathy (HE) is a frequent complication of decompensated cirrhosis, eventually induced and/or aggravated by TIPS, that remains a clinical challenge especially in these patients. Therefore, patient selection for TIPS requires careful assessment of risk factors for HE. TIPS procedural parameters regarding stent size and invasive portosystemic pressure gradient measurements thereby have an important role. Endovascular shunt modification, in combination with a conservative medical approach, often results in a significant reduction of symptoms. This review summarizes HE molecular mechanisms and pathophysiology as well as diagnostic and therapeutic approaches targeting shunt-induced HE.
Keywords	hepatic encephalopathy ; transjugular portosystemic intrahepatic shunt ; liver cirrhosis ; Medicine ; R
Subject code	610
Language	English
Publishing date	2020-11-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Hepatobiliary manifestations in patients with ulcerative colitis

Katharina Stratmann / Songül Aydolmus / Wenyi Gu / Dominik Heling / Ulrich Spengler / Birgit Terjung / Christian P. Strassburg / Richard Vollenberg / Irina Blumenstein / Jonel Trebicka

Frontiers in Medicine, Vol

a retrospective analysis

2024 Volume 10

Abstract: BackgroundInflammatory bowel diseases (IBDs) are often associated with altered liver function tests (LFTs). There is little data on the relationship between abnormal LFT and IBD. Our study aimed to evaluate the prevalence and etiology of elevated LFT in ... ...

Abstract	BackgroundInflammatory bowel diseases (IBDs) are often associated with altered liver function tests (LFTs). There is little data on the relationship between abnormal LFT and IBD. Our study aimed to evaluate the prevalence and etiology of elevated LFT in patients with ulcerative colitis (UC) and to determine whether there is an association with clinical and demographic parameters.MethodsThe clinical records of the Gastroenterology Outpatients Clinic at a single center were reviewed and screened for patients with UC from 2005 to 2014. In total, 263 patients were included. Patients with Crohn’s disease (CD), colitis indeterminate, and colitis of other origins were excluded. Abnormal LFT and liver injuries were analyzed.ResultsA cohort of 182 patients was analyzed (114 males, 68 females; mean age = 50.2 ± 16.1 years). 58 patients had already been diagnosed with a hepatobiliary disorder. Patients with a known hepatobiliary disorder suffered from UC for a significantly longer duration. Elevated LFT in patients without known hepatobiliary disorders was 69.4%. Liver injury was found in 21.8%. A transient increase in abnormal LFT was shown in 59 patients (68.6%), a persistent increase was found in 27 patients (31.4%). Treatment with thiopurines was a risk factor for persistent elevated LFT (p = 0.029), steroids had a protective impact (p = 0.037).ConclusionThis study clearly highlights the importance of screening for hepatobiliary disorders and abnormal LFT in patients with UC, as the prevalence of hepatobiliary disorders and abnormal LFT is detected very often among this patient group.
Keywords	inflammatory bowel disease ; ulcerative colitis ; hepatobiliary disorder ; liver function test (LFT) ; risk factor ; Medicine (General) ; R5-920
Subject code	610
Language	English
Publishing date	2024-01-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Cyclic GMP in Liver Cirrhosis—Role in Pathophysiology of Portal Hypertension and Therapeutic Implications

Wolfgang Kreisel / Adhara Lazaro / Jonel Trebicka / Markus Grosse Perdekamp / Annette Schmitt-Graeff / Peter Deibert

International Journal of Molecular Sciences, Vol 22, Iss 10372, p

2021 Volume 10372

Abstract: The NO-cGMP signal transduction pathway plays a crucial role in tone regulation in hepatic sinusoids and peripheral blood vessels. In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and ... ...

Abstract	The NO-cGMP signal transduction pathway plays a crucial role in tone regulation in hepatic sinusoids and peripheral blood vessels. In a cirrhotic liver, the key enzymes endothelial NO synthase (eNOS), soluble guanylate cyclase (sGC), and phosphodiesterase-5 (PDE-5) are overexpressed, leading to decreased cyclic guanosine-monophosphate (cGMP). This results in constriction of hepatic sinusoids, contributing about 30% of portal pressure. In contrast, in peripheral arteries, dilation prevails with excess cGMP due to low PDE-5. Both effects eventually lead to circulatory dysfunction in progressed liver cirrhosis. The conventional view of portal hypertension (PH) pathophysiology has been described using the “NO-paradox”, referring to reduced NO availability inside the liver and elevated NO production in the peripheral systemic circulation. However, recent data suggest that an altered availability of cGMP could better elucidate the contrasting findings of intrahepatic vasoconstriction and peripheral systemic vasodilation than mere focus on NO availability. Preclinical and clinical data have demonstrated that targeting the NO-cGMP pathway in liver cirrhosis using PDE-5 inhibitors or sGC stimulators/activators decreases intrahepatic resistance through dilation of sinusoids, lowering portal pressure, and increasing portal venous blood flow. These results suggest further clinical applications in liver cirrhosis. Targeting the NO-cGMP system plays a role in possible reversal of liver fibrosis or cirrhosis. PDE-5 inhibitors may have therapeutic potential for hepatic encephalopathy. Serum/plasma levels of cGMP can be used as a non-invasive marker of clinically significant portal hypertension. This manuscript reviews new data about the role of the NO-cGMP signal transduction system in pathophysiology of cirrhotic portal hypertension and provides perspective for further studies.
Keywords	liver cirrhosis ; liver fibrosis ; portal hypertension ; NO-cGMP pathway ; sGC ; PDE-5 ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Subject code	571 ; 610
Language	English
Publishing date	2021-09-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Managing portal hypertension in patients with liver cirrhosis [version 1; referees

Tilman Sauerbruch / Robert Schierwagen / Jonel Trebicka

F1000Research, Vol

2 approved]

2018 Volume 7

Abstract: Portal hypertension is one cause and a part of a dynamic process triggered by chronic liver disease, mostly induced by alcohol or incorrect nutrition and less often by viral infections and autoimmune or genetic disease. Adequate staging - continuously ... ...

Abstract	Portal hypertension is one cause and a part of a dynamic process triggered by chronic liver disease, mostly induced by alcohol or incorrect nutrition and less often by viral infections and autoimmune or genetic disease. Adequate staging - continuously modified by current knowledge - should guide the prevention and treatment of portal hypertension with defined endpoints. The main goals are interruption of etiology and prevention of complications followed, if necessary, by treatment of these. For the past few decades, shunts, mostly as intrahepatic stent bypass between portal and hepatic vein branches, have played an important role in the prevention of recurrent bleeding and ascites formation, although their impact on survival remains ambiguous. Systemic drugs, such as non-selective beta-blockers, statins, or antibiotics, reduce portal hypertension by decreasing intrahepatic resistance or portal tributary blood flow or by blunting inflammatory stimuli inside and outside the liver. Here, the interactions among the gut, liver, and brain are increasingly examined for new therapeutic options. There is no general panacea. The interruption of initiating factors is key. If not possible or if not possible in a timely manner, combined approaches should receive more attention before considering liver transplantation.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2018-05-01T00:00:00Z
Publisher	F1000 Research Ltd
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Diagnostic and prognostic significance of cell death markers in patients with cirrhosis and acute decompensation.

Philipp Stoffers / Sabrina Guckenbiehl / Martin Walter Welker / Stefan Zeuzem / Christian Markus Lange / Jonel Trebicka / Eva Herrmann / Christoph Welsch

PLoS ONE, Vol 17, Iss 2, p e

2022 Volume 0263989

Abstract: Background The transition from compensated to decompensated liver cirrhosis is a hallmark of disease progression, however, reliable predictors to assess the risk of decompensation in individual patients from routine diagnostics are lacking. Here, we ... ...

Abstract	Background The transition from compensated to decompensated liver cirrhosis is a hallmark of disease progression, however, reliable predictors to assess the risk of decompensation in individual patients from routine diagnostics are lacking. Here, we characterize serum levels of cell death-associated markers and routine biochemistry from patients with chronic liver disease with and without decompensation. Methods A post-hoc analysis was based on prospectively collected clinical data from 160 patients with chronic liver disease, stably compensated or decompensated at baseline or during follow-up, over a median period of 721 days. Serum levels of damage-associated molecular patterns (DAMPs) and routine biochemistry are quantified at baseline (for all patients) and during follow-up (for patients with acute decompensation). The panel of DAMPs assessed in this study comprises high-mobility group-box protein 1 (HMGB1), cytochrome C (cyt C), soluble Fas-ligand (sFasL), interleukin 6 (IL-6), soluble cytokeratin-18 (CK18-M65) and its caspase-cleaved fragment CK18-M30. Results In this cohort study, 80 patients (50%) were diagnosed with alcoholic liver cirrhosis, 60 patients (37.5%) with hepatitis C virus- and 20 patients (13.5%) with hepatitis B virus-related liver cirrhosis. At baseline, 17 patients (10.6%) showed decompensated liver disease and another 28 patients (17.5%) developed acute decompensation during follow-up (within 24 months). One hundred fifteen patients showed stable liver disease (71.9%). We found DAMPs significantly elevated in patients with decompensated liver disease versus compensated liver disease. Patients with acute decompensation during follow-up showed higher baseline levels of IL-6, sFasL, CK18-M65 and-M30 (P<0.01) compared to patients with stably compensated liver disease. In multivariate analyses, we found an independent association of baseline serum levels of sFasL (P = 0.02; OR = 2.67) and gamma-glutamyl transferase (GGT) (P<0.001; OR = 2.1) with acute decompensation. Accuracy of the ...
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Diagnostic and prognostic significance of cell death markers in patients with cirrhosis and acute decompensation

Philipp Stoffers / Sabrina Guckenbiehl / Martin Walter Welker / Stefan Zeuzem / Christian Markus Lange / Jonel Trebicka / Eva Herrmann / Christoph Welsch

PLoS ONE, Vol 17, Iss

2022 Volume 2

Abstract	Background The transition from compensated to decompensated liver cirrhosis is a hallmark of disease progression, however, reliable predictors to assess the risk of decompensation in individual patients from routine diagnostics are lacking. Here, we characterize serum levels of cell death-associated markers and routine biochemistry from patients with chronic liver disease with and without decompensation. Methods A post-hoc analysis was based on prospectively collected clinical data from 160 patients with chronic liver disease, stably compensated or decompensated at baseline or during follow-up, over a median period of 721 days. Serum levels of damage-associated molecular patterns (DAMPs) and routine biochemistry are quantified at baseline (for all patients) and during follow-up (for patients with acute decompensation). The panel of DAMPs assessed in this study comprises high-mobility group-box protein 1 (HMGB1), cytochrome C (cyt C), soluble Fas-ligand (sFasL), interleukin 6 (IL-6), soluble cytokeratin-18 (CK18-M65) and its caspase‐cleaved fragment CK18-M30. Results In this cohort study, 80 patients (50%) were diagnosed with alcoholic liver cirrhosis, 60 patients (37.5%) with hepatitis C virus- and 20 patients (13.5%) with hepatitis B virus-related liver cirrhosis. At baseline, 17 patients (10.6%) showed decompensated liver disease and another 28 patients (17.5%) developed acute decompensation during follow-up (within 24 months). One hundred fifteen patients showed stable liver disease (71.9%). We found DAMPs significantly elevated in patients with decompensated liver disease versus compensated liver disease. Patients with acute decompensation during follow-up showed higher baseline levels of IL-6, sFasL, CK18-M65 and–M30 (P<0.01) compared to patients with stably compensated liver disease. In multivariate analyses, we found an independent association of baseline serum levels of sFasL (P = 0.02; OR = 2.67) and gamma-glutamyl transferase (GGT) (P<0.001; OR = 2.1) with acute decompensation. Accuracy of the ...
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2022-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The non-selective Rho-kinase inhibitors Y-27632 and Y-33075 decrease contraction but increase migration in murine and human hepatic stellate cells.

Nadine Bachtler / Sandra Torres / Cristina Ortiz / Robert Schierwagen / Olaf Tyc / Christoph Hieber / Marie-Luise Berres / Caroline Meier / Nico Kraus / Stefan Zeuzem / Bart Nijmeijer / Sebas Pronk / Jonel Trebicka / Sabine Klein

PLoS ONE, Vol 18, Iss 1, p e

2023 Volume 0270288

Abstract: Background The Rho-kinase ROCK II plays a major role in the activation of hepatic stellate cells (HSC), which are the key profibrotic and contractile cells contributing to the development of chronic liver disease. Inhibition of ROCK II ultimately blocks ... ...

Abstract	Background The Rho-kinase ROCK II plays a major role in the activation of hepatic stellate cells (HSC), which are the key profibrotic and contractile cells contributing to the development of chronic liver disease. Inhibition of ROCK II ultimately blocks the phosphorylation of the myosin light chain (MLC) and thus inhibits stress fibre assembly and cell contraction. We investigated the effects of the ROCK inhibitors Y-33075 as well as Y-27632 in murine and human hepatic stellate cells. Methods Primary isolated HSC from FVB/NJ mice and the immortalized human HSC line TWNT-4 were culture-activated and incubated with Y-27632 and Y-33075 (10nM to 10μM) for 24h. Protein expression levels were analyzed by Western Blots and transcriptional levels of pro-fibrotic markers and proliferative markers were evaluated using real-time qPCR. Migration was investigated by wound-healing assay. Proliferation was assessed by BrdU assay. Contraction of HSC was measured using 3D collagen matrices after incubation with Y-27632 or Y-33075 in different doses. Results Both Rho-kinase inhibitors, Y-27632 and Y-33075, reduced contraction, fibrogenesis and proliferation in activated primary mouse HSC (FVB/NJ) and human HSC line (TWNT-4) significantly. Y-33075 demonstrated a 10-times increased potency compared to Y-27632. Surprisingly, both inhibitors mediated a substantial and unexpected increase in migration of HSC in FVB/NJ. Conclusion ROCK inhibition by the tested compounds decreased contraction but increased migration. Y-33075 proved more potent than Y27632 in the inhibition of contraction of HSCs and should be further evaluated in chronic liver disease.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Short Versus Long Antibiotic Therapy and Risk of Recurrence of Acute Cholangitis Due to Malignant Biliary Strictures

Philip G. Ferstl / Katharina Bremer / Natalie Filmann / Volkhard A. J. Kempf / Michael Hogardt / Olivier Ballo / Fabian Finkelmeier / Jonel Trebicka / Stefan Zeuzem / Jörg Bojunga / Mireen Friedrich-Rust / Dirk Walter

Journal of Clinical Medicine, Vol 12, Iss 21, p

2023 Volume 6716

Abstract: Malignancies can cause severe stenosis of the biliary tract and therefore predispose a patient to bacterial cholangitis. Upon endoscopic drainage, antibiotic therapy (AT) is performed according to individual clinical judgement, as the optimal duration of ...

Abstract	Malignancies can cause severe stenosis of the biliary tract and therefore predispose a patient to bacterial cholangitis. Upon endoscopic drainage, antibiotic therapy (AT) is performed according to individual clinical judgement, as the optimal duration of AT is unclear to date, especially in the case of multidrug-resistant organisms (MDROs). In a case-based retrospective study, patients with malignant biliary strictures and acute cholangitis were included upon endoscopic retrograde cholangiography (ERC). The outcome of cases treated with short AT (≤6 days) was compared to that of long AT (≥7 days). Recurrent cholangitis (RC) before scheduled stent exchange was the primary end point. In total, 124 patients were included, with 183 cases of proven cholangitis in total. The overall median duration of AT was 7 days (range 1–20), with 74 cases (40%) receiving short AT and 109 (60%) receiving long AT. Short AT was not an independent risk factor for RC (HR = 0.66, p > 0.2), while colonization with MDROs was associated with a higher risk of RC (HR = 2.21, p = 0.005). Placement of a metal stent was associated with minor risk of RC (HR = 0.4, p = 0.038). In conclusion, short AT is possible in selected patients with non-severe cholangitis and malignant biliary strictures. Scheduled screening for MDROs is recommended and placement of a metal stent should be performed if possible.
Keywords	cancer-associated cholangitis ; multidrug resistance ; metal stent ; antibiotic duration ; recurring cholangitis ; Medicine ; R
Subject code	610 ; 616
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: The non-selective Rho-kinase inhibitors Y-27632 and Y-33075 decrease contraction but increase migration in murine and human hepatic stellate cells

PLoS ONE, Vol 18, Iss

2023 Volume 1

Abstract	Background The Rho-kinase ROCK II plays a major role in the activation of hepatic stellate cells (HSC), which are the key profibrotic and contractile cells contributing to the development of chronic liver disease. Inhibition of ROCK II ultimately blocks the phosphorylation of the myosin light chain (MLC) and thus inhibits stress fibre assembly and cell contraction. We investigated the effects of the ROCK inhibitors Y-33075 as well as Y-27632 in murine and human hepatic stellate cells. Methods Primary isolated HSC from FVB/NJ mice and the immortalized human HSC line TWNT-4 were culture-activated and incubated with Y-27632 and Y-33075 (10nM to 10μM) for 24h. Protein expression levels were analyzed by Western Blots and transcriptional levels of pro-fibrotic markers and proliferative markers were evaluated using real-time qPCR. Migration was investigated by wound-healing assay. Proliferation was assessed by BrdU assay. Contraction of HSC was measured using 3D collagen matrices after incubation with Y-27632 or Y-33075 in different doses. Results Both Rho-kinase inhibitors, Y-27632 and Y-33075, reduced contraction, fibrogenesis and proliferation in activated primary mouse HSC (FVB/NJ) and human HSC line (TWNT-4) significantly. Y-33075 demonstrated a 10-times increased potency compared to Y-27632. Surprisingly, both inhibitors mediated a substantial and unexpected increase in migration of HSC in FVB/NJ. Conclusion ROCK inhibition by the tested compounds decreased contraction but increased migration. Y-33075 proved more potent than Y27632 in the inhibition of contraction of HSCs and should be further evaluated in chronic liver disease.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2023-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Differential Lipidomics, Metabolomics and Immunological Analysis of Alcoholic and Non-Alcoholic Steatohepatitis in Mice

Erika Dorochow / Nico Kraus / Nicolas Chenaux-Repond / Sandra Pierre / Anja Kolbinger / Gerd Geisslinger / Cristina Ortiz / Christoph Welsch / Jonel Trebicka / Robert Gurke / Lisa Hahnefeld / Sabine Klein / Klaus Scholich

International Journal of Molecular Sciences, Vol 24, Iss 10351, p

2023 Volume 10351

Abstract: Non-alcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH) are the leading causes of liver disease worldwide. To identify disease-specific pathomechanisms, we analyzed the lipidome, metabolome and immune cell recruitment in livers in both ... ...

Abstract	Non-alcoholic steatohepatitis (NASH) and alcoholic steatohepatitis (ASH) are the leading causes of liver disease worldwide. To identify disease-specific pathomechanisms, we analyzed the lipidome, metabolome and immune cell recruitment in livers in both diseases. Mice harboring ASH or NASH had comparable disease severities regarding mortality rate, neurological behavior, expression of fibrosis marker and albumin levels. Lipid droplet size was higher in NASH than ASH and qualitative differences in the lipidome were mainly based on incorporation of diet-specific fatty acids into triglycerides, phosphatidylcholines and lysophosphatidylcholines. Metabolomic analysis showed downregulated nucleoside levels in both models. Here, the corresponding uremic metabolites were only upregulated in NASH suggesting stronger cellular senescence, which was supported by lower antioxidant levels in NASH as compared to ASH. While altered urea cycle metabolites suggest increased nitric oxide synthesis in both models, in ASH, this depended on increased L-homoarginine levels indicating a cardiovascular response mechanism. Interestingly, only in NASH were the levels of tryptophan and its anti-inflammatory metabolite kynurenine upregulated. Fittingly, high-content immunohistochemistry showed a decreased macrophage recruitment and an increased polarization towards M2-like macrophages in NASH. In conclusion, with comparable disease severity in both models, higher lipid storage, oxidative stress and tryptophan/kynurenine levels were seen in NASH, leading to distinct immune responses.
Keywords	non-alcoholic fatty liver disease ; alcoholic fatty liver disease ; lipid droplets ; metabolomics ; lipidomics ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
Language	English
Publishing date	2023-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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