The impact of hepatic steatosis on portal hypertension
Studies in animal models have suggested that hepatic steatosis impacts on portal pressure, potentially by inducing liver sinusoidal endothelial dysfunction and thereby increasing intrahepatic resistance. Thus, we aimed to evaluate the impact of hepatic steatosis on hepatic venous pressure gradient (...
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creator | Semmler, Georg Scheiner, Bernhard Schwabl, Philipp Bucsics, Theresa Paternostro, Rafael Chromy, David Stättermayer, Albert Friedrich Trauner, Michael Mandorfer, Mattias Ferlitsch, Arnulf Reiberger, Thomas |
description | Studies in animal models have suggested that hepatic steatosis impacts on portal pressure, potentially by inducing liver sinusoidal endothelial dysfunction and thereby increasing intrahepatic resistance. Thus, we aimed to evaluate the impact of hepatic steatosis on hepatic venous pressure gradient (HVPG) in patients with chronic liver disease.
261 patients undergoing simultaneous HVPG measurements and controlled attenuation parameter (CAP)-based steatosis assessment were included in this retrospective study.
The majority of patients had cirrhosis (n = 205; 78.5%) and n = 191 (73.2%) had clinically significant portal hypertension (CSPH; HVPG≥10mmHg). Hepatic steatosis (S1/2/3; CAP ≥248dB/m) was present in n = 102 (39.1%). Overall, HVPG was comparable between patients with vs. without hepatic steatosis (15.5±7.5 vs. 14.8±7.7mmHg; p = 0.465). Neither in patients with HVPG ( |
doi_str_mv | 10.1371/journal.pone.0224506 |
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261 patients undergoing simultaneous HVPG measurements and controlled attenuation parameter (CAP)-based steatosis assessment were included in this retrospective study.
The majority of patients had cirrhosis (n = 205; 78.5%) and n = 191 (73.2%) had clinically significant portal hypertension (CSPH; HVPG≥10mmHg). Hepatic steatosis (S1/2/3; CAP ≥248dB/m) was present in n = 102 (39.1%). Overall, HVPG was comparable between patients with vs. without hepatic steatosis (15.5±7.5 vs. 14.8±7.7mmHg; p = 0.465). Neither in patients with HVPG (<6mmHg; p = 0.371) nor in patients with mild portal hypertension (HVPG 6-9mmHg; p = 0.716) or CSPH (HVPG≥10mmHg; p = 0.311) any correlation between CAP and HVPG was found. Interestingly, in patients with liver fibrosis F2/3, there was a negative correlation between CAP and HVPG (Pearson's ρ:-0.522; p≤0.001). In multivariate analysis, higher CAP was an independent 'protective' factor for the presence of CSPH (odds ratio [OR] per 10dB/m: 0.92, 95% confidence interval [CI]:0.85-1.00; p = 0.045), while liver stiffness was associated with the presence of CSPH (OR per kPa: 1.26, 95%CI: 1.17-1.36; p≤0.001). In 78 patients, in whom liver biopsy was performed, HVPG was neither correlated with percentage of histological steatosis (p = 0.714) nor with histological steatosis grade (p = 0.957).
Hepatic steatosis, as assessed by CAP and liver histology, did not impact on HVPG in our cohort comprising a high proportion of patients with advanced chronic liver disease. However, high CAP values (i.e. pronounced hepatic steatosis) might lead to overestimation of liver fibrosis by 'artificially' increasing transient elastography-based liver stiffness measurements.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0224506</identifier><identifier>PMID: 31693695</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adult ; Aged ; Animal experimentation ; Animal models ; Attenuation ; Bile ; Biology and Life Sciences ; Biopsy ; Cirrhosis ; Confidence intervals ; Correlation ; Disease control ; Elasticity Imaging Techniques ; Endothelium ; Fatty liver ; Female ; Fibrosis ; Gastroenterology ; Hepatitis ; Hepatology ; Histology ; Humans ; Hypertension ; Hypertension, Portal - diagnosis ; Hypertension, Portal - epidemiology ; Hypertension, Portal - etiology ; Internal medicine ; Laboratories ; Liver ; Liver - blood supply ; Liver - diagnostic imaging ; Liver - pathology ; Liver cancer ; Liver cirrhosis ; Liver Cirrhosis - diagnosis ; Liver Cirrhosis - epidemiology ; Liver Cirrhosis - etiology ; Liver diseases ; Male ; Medicine ; Medicine and Health Sciences ; Metabolic syndrome ; Middle Aged ; Multivariate analysis ; Non-alcoholic Fatty Liver Disease - complications ; Non-alcoholic Fatty Liver Disease - pathology ; Physiology ; Portal hypertension ; Portal Pressure ; Retrospective Studies ; Steatosis ; Stiffness ; Venous pressure</subject><ispartof>PloS one, 2019-11, Vol.14 (11), p.e0224506-e0224506</ispartof><rights>COPYRIGHT 2019 Public Library of Science</rights><rights>2019 Semmler et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 Semmler et al 2019 Semmler et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-3a13790da009ac4cc2861ce7937f3e887267716db39039a3373fd066b0f1d303</citedby><cites>FETCH-LOGICAL-c692t-3a13790da009ac4cc2861ce7937f3e887267716db39039a3373fd066b0f1d303</cites><orcidid>0000-0002-0411-166X ; 0000-0002-4590-3583</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834246/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6834246/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,2103,2929,23871,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31693695$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Strnad, Pavel</contributor><creatorcontrib>Semmler, Georg</creatorcontrib><creatorcontrib>Scheiner, Bernhard</creatorcontrib><creatorcontrib>Schwabl, Philipp</creatorcontrib><creatorcontrib>Bucsics, Theresa</creatorcontrib><creatorcontrib>Paternostro, Rafael</creatorcontrib><creatorcontrib>Chromy, David</creatorcontrib><creatorcontrib>Stättermayer, Albert Friedrich</creatorcontrib><creatorcontrib>Trauner, Michael</creatorcontrib><creatorcontrib>Mandorfer, Mattias</creatorcontrib><creatorcontrib>Ferlitsch, Arnulf</creatorcontrib><creatorcontrib>Reiberger, Thomas</creatorcontrib><title>The impact of hepatic steatosis on portal hypertension</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Studies in animal models have suggested that hepatic steatosis impacts on portal pressure, potentially by inducing liver sinusoidal endothelial dysfunction and thereby increasing intrahepatic resistance. Thus, we aimed to evaluate the impact of hepatic steatosis on hepatic venous pressure gradient (HVPG) in patients with chronic liver disease.
261 patients undergoing simultaneous HVPG measurements and controlled attenuation parameter (CAP)-based steatosis assessment were included in this retrospective study.
The majority of patients had cirrhosis (n = 205; 78.5%) and n = 191 (73.2%) had clinically significant portal hypertension (CSPH; HVPG≥10mmHg). Hepatic steatosis (S1/2/3; CAP ≥248dB/m) was present in n = 102 (39.1%). Overall, HVPG was comparable between patients with vs. without hepatic steatosis (15.5±7.5 vs. 14.8±7.7mmHg; p = 0.465). Neither in patients with HVPG (<6mmHg; p = 0.371) nor in patients with mild portal hypertension (HVPG 6-9mmHg; p = 0.716) or CSPH (HVPG≥10mmHg; p = 0.311) any correlation between CAP and HVPG was found. Interestingly, in patients with liver fibrosis F2/3, there was a negative correlation between CAP and HVPG (Pearson's ρ:-0.522; p≤0.001). In multivariate analysis, higher CAP was an independent 'protective' factor for the presence of CSPH (odds ratio [OR] per 10dB/m: 0.92, 95% confidence interval [CI]:0.85-1.00; p = 0.045), while liver stiffness was associated with the presence of CSPH (OR per kPa: 1.26, 95%CI: 1.17-1.36; p≤0.001). In 78 patients, in whom liver biopsy was performed, HVPG was neither correlated with percentage of histological steatosis (p = 0.714) nor with histological steatosis grade (p = 0.957).
Hepatic steatosis, as assessed by CAP and liver histology, did not impact on HVPG in our cohort comprising a high proportion of patients with advanced chronic liver disease. However, high CAP values (i.e. pronounced hepatic steatosis) might lead to overestimation of liver fibrosis by 'artificially' increasing transient elastography-based liver stiffness measurements.</description><subject>Adult</subject><subject>Aged</subject><subject>Animal experimentation</subject><subject>Animal models</subject><subject>Attenuation</subject><subject>Bile</subject><subject>Biology and Life Sciences</subject><subject>Biopsy</subject><subject>Cirrhosis</subject><subject>Confidence intervals</subject><subject>Correlation</subject><subject>Disease control</subject><subject>Elasticity Imaging Techniques</subject><subject>Endothelium</subject><subject>Fatty liver</subject><subject>Female</subject><subject>Fibrosis</subject><subject>Gastroenterology</subject><subject>Hepatitis</subject><subject>Hepatology</subject><subject>Histology</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension, Portal - diagnosis</subject><subject>Hypertension, Portal - epidemiology</subject><subject>Hypertension, Portal - etiology</subject><subject>Internal medicine</subject><subject>Laboratories</subject><subject>Liver</subject><subject>Liver - blood supply</subject><subject>Liver - diagnostic imaging</subject><subject>Liver - pathology</subject><subject>Liver cancer</subject><subject>Liver cirrhosis</subject><subject>Liver Cirrhosis - diagnosis</subject><subject>Liver Cirrhosis - epidemiology</subject><subject>Liver Cirrhosis - etiology</subject><subject>Liver diseases</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Metabolic syndrome</subject><subject>Middle Aged</subject><subject>Multivariate analysis</subject><subject>Non-alcoholic Fatty Liver Disease - complications</subject><subject>Non-alcoholic Fatty Liver Disease - pathology</subject><subject>Physiology</subject><subject>Portal hypertension</subject><subject>Portal Pressure</subject><subject>Retrospective Studies</subject><subject>Steatosis</subject><subject>Stiffness</subject><subject>Venous pressure</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl2L1DAUhoso7rr6D0QLgujFjElOmjQ3wrL4MbCwoIO3IU2TaYe2qUkq7r8343SXqeyF5CLh5DnvOSd5s-wlRmsMHH_Yu8kPqluPbjBrRAgtEHuUnWMBZMUIgscn57PsWQh7hAooGXuanQFmApgozjO2bUze9qPSMXc2b8yoYqvzEI2KLrQhd0M-Oh9Vlze3o_HRDKF1w_PsiVVdMC_m_SLbfv60vfq6ur75srm6vF5pJkhcgUqtClQrhITSVGtSMqwNF8AtmLLkhHGOWV2BQCAUAAdbI8YqZHENCC6y10fZsXNBzhMHSQCTggIti0RsjkTt1F6Ovu2Vv5VOtfJvwPmdVD5N1BnJqSltKmyVRdRCJXBV1LzChqi6oAiS1se52lT1ptZmiF51C9HlzdA2cud-SVYCJZQlgXezgHc_JxOi7NugTdepwbjp2HeJSs5IQt_8gz483UztVBqgHaxLdfVBVF4yRAXnBeWJWj9ApVWbvtXJHrZN8UXC-0VCYqL5HXdqCkFuvn_7f_bmx5J9e8I2RnWxCa6bYnJMWIL0CGrvQvDG3j8yRvLg7rvXkAd3y9ndKe3V6QfdJ93ZGf4Agqby4Q</recordid><startdate>20191106</startdate><enddate>20191106</enddate><creator>Semmler, 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impact of hepatic steatosis on portal hypertension</title><author>Semmler, Georg ; Scheiner, Bernhard ; Schwabl, Philipp ; Bucsics, Theresa ; Paternostro, Rafael ; Chromy, David ; Stättermayer, Albert Friedrich ; Trauner, Michael ; Mandorfer, Mattias ; Ferlitsch, Arnulf ; Reiberger, Thomas</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-3a13790da009ac4cc2861ce7937f3e887267716db39039a3373fd066b0f1d303</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Animal experimentation</topic><topic>Animal models</topic><topic>Attenuation</topic><topic>Bile</topic><topic>Biology and Life Sciences</topic><topic>Biopsy</topic><topic>Cirrhosis</topic><topic>Confidence intervals</topic><topic>Correlation</topic><topic>Disease control</topic><topic>Elasticity Imaging Techniques</topic><topic>Endothelium</topic><topic>Fatty liver</topic><topic>Female</topic><topic>Fibrosis</topic><topic>Gastroenterology</topic><topic>Hepatitis</topic><topic>Hepatology</topic><topic>Histology</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension, Portal - diagnosis</topic><topic>Hypertension, Portal - epidemiology</topic><topic>Hypertension, Portal - etiology</topic><topic>Internal medicine</topic><topic>Laboratories</topic><topic>Liver</topic><topic>Liver - blood supply</topic><topic>Liver - diagnostic imaging</topic><topic>Liver - pathology</topic><topic>Liver cancer</topic><topic>Liver cirrhosis</topic><topic>Liver Cirrhosis - diagnosis</topic><topic>Liver Cirrhosis - epidemiology</topic><topic>Liver Cirrhosis - etiology</topic><topic>Liver diseases</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine and Health Sciences</topic><topic>Metabolic syndrome</topic><topic>Middle Aged</topic><topic>Multivariate analysis</topic><topic>Non-alcoholic Fatty Liver Disease - complications</topic><topic>Non-alcoholic Fatty Liver Disease - pathology</topic><topic>Physiology</topic><topic>Portal hypertension</topic><topic>Portal Pressure</topic><topic>Retrospective Studies</topic><topic>Steatosis</topic><topic>Stiffness</topic><topic>Venous pressure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Semmler, Georg</creatorcontrib><creatorcontrib>Scheiner, Bernhard</creatorcontrib><creatorcontrib>Schwabl, Philipp</creatorcontrib><creatorcontrib>Bucsics, Theresa</creatorcontrib><creatorcontrib>Paternostro, Rafael</creatorcontrib><creatorcontrib>Chromy, David</creatorcontrib><creatorcontrib>Stättermayer, Albert Friedrich</creatorcontrib><creatorcontrib>Trauner, Michael</creatorcontrib><creatorcontrib>Mandorfer, Mattias</creatorcontrib><creatorcontrib>Ferlitsch, Arnulf</creatorcontrib><creatorcontrib>Reiberger, Thomas</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE 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USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Semmler, Georg</au><au>Scheiner, Bernhard</au><au>Schwabl, Philipp</au><au>Bucsics, Theresa</au><au>Paternostro, Rafael</au><au>Chromy, David</au><au>Stättermayer, Albert Friedrich</au><au>Trauner, Michael</au><au>Mandorfer, Mattias</au><au>Ferlitsch, Arnulf</au><au>Reiberger, Thomas</au><au>Strnad, Pavel</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The impact of hepatic steatosis on portal hypertension</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2019-11-06</date><risdate>2019</risdate><volume>14</volume><issue>11</issue><spage>e0224506</spage><epage>e0224506</epage><pages>e0224506-e0224506</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Studies in animal models have suggested that hepatic steatosis impacts on portal pressure, potentially by inducing liver sinusoidal endothelial dysfunction and thereby increasing intrahepatic resistance. Thus, we aimed to evaluate the impact of hepatic steatosis on hepatic venous pressure gradient (HVPG) in patients with chronic liver disease.
261 patients undergoing simultaneous HVPG measurements and controlled attenuation parameter (CAP)-based steatosis assessment were included in this retrospective study.
The majority of patients had cirrhosis (n = 205; 78.5%) and n = 191 (73.2%) had clinically significant portal hypertension (CSPH; HVPG≥10mmHg). Hepatic steatosis (S1/2/3; CAP ≥248dB/m) was present in n = 102 (39.1%). Overall, HVPG was comparable between patients with vs. without hepatic steatosis (15.5±7.5 vs. 14.8±7.7mmHg; p = 0.465). Neither in patients with HVPG (<6mmHg; p = 0.371) nor in patients with mild portal hypertension (HVPG 6-9mmHg; p = 0.716) or CSPH (HVPG≥10mmHg; p = 0.311) any correlation between CAP and HVPG was found. Interestingly, in patients with liver fibrosis F2/3, there was a negative correlation between CAP and HVPG (Pearson's ρ:-0.522; p≤0.001). In multivariate analysis, higher CAP was an independent 'protective' factor for the presence of CSPH (odds ratio [OR] per 10dB/m: 0.92, 95% confidence interval [CI]:0.85-1.00; p = 0.045), while liver stiffness was associated with the presence of CSPH (OR per kPa: 1.26, 95%CI: 1.17-1.36; p≤0.001). In 78 patients, in whom liver biopsy was performed, HVPG was neither correlated with percentage of histological steatosis (p = 0.714) nor with histological steatosis grade (p = 0.957).
Hepatic steatosis, as assessed by CAP and liver histology, did not impact on HVPG in our cohort comprising a high proportion of patients with advanced chronic liver disease. However, high CAP values (i.e. pronounced hepatic steatosis) might lead to overestimation of liver fibrosis by 'artificially' increasing transient elastography-based liver stiffness measurements.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>31693695</pmid><doi>10.1371/journal.pone.0224506</doi><tpages>e0224506</tpages><orcidid>https://orcid.org/0000-0002-0411-166X</orcidid><orcidid>https://orcid.org/0000-0002-4590-3583</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1932-6203 |
ispartof | PloS one, 2019-11, Vol.14 (11), p.e0224506-e0224506 |
issn | 1932-6203 1932-6203 |
language | eng |
recordid | cdi_plos_journals_2312543485 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Adult Aged Animal experimentation Animal models Attenuation Bile Biology and Life Sciences Biopsy Cirrhosis Confidence intervals Correlation Disease control Elasticity Imaging Techniques Endothelium Fatty liver Female Fibrosis Gastroenterology Hepatitis Hepatology Histology Humans Hypertension Hypertension, Portal - diagnosis Hypertension, Portal - epidemiology Hypertension, Portal - etiology Internal medicine Laboratories Liver Liver - blood supply Liver - diagnostic imaging Liver - pathology Liver cancer Liver cirrhosis Liver Cirrhosis - diagnosis Liver Cirrhosis - epidemiology Liver Cirrhosis - etiology Liver diseases Male Medicine Medicine and Health Sciences Metabolic syndrome Middle Aged Multivariate analysis Non-alcoholic Fatty Liver Disease - complications Non-alcoholic Fatty Liver Disease - pathology Physiology Portal hypertension Portal Pressure Retrospective Studies Steatosis Stiffness Venous pressure |
title | The impact of hepatic steatosis on portal hypertension |
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