scholarly journals The Lymphatic Headmaster of the Mast Cell-Related Splanchnic Inflammation in Portal Hypertension

Cells ◽  
2019 ◽  
Vol 8 (7) ◽  
pp. 658
Author(s):  
Maria-Angeles Aller ◽  
Javier Blanco-Rivero ◽  
Natalia Arias ◽  
Luis Santamaria ◽  
Jaime Arias
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Mast Cells ◽  
Inflammatory Response ◽  
Blood Circulation ◽  
Venous Pressure ◽  
Hepatic Metabolism ◽  
Molecular Pattern ◽  
Intestinal Origin ◽  
Collateral Vessels

Portal hypertension is a common complication of liver disease, either acute or chronic. Consequently, in chronic liver disease, such as the hypertensive mesenteric venous pathology, the coexisting inflammatory response is classically characterized by the splanchnic blood circulation. However, a vascular lymphatic pathology is produced simultaneously with the splanchnic arterio-venous impairments. The pathological increase of the mesenteric venous pressure, by mechanotransduction of the venous endothelium hyperpressure, causes an inflammatory response involving the subendothelial mast cells and the lymphatic endothelium of the intestinal villi lacteal. In portal hypertension, the intestinal lymphatic inflammatory response through the development of mesenteric-systemic lymphatic collateral vessels favors the systemic diffusion of substances with a molecular pattern associated with damage and pathogens of intestinal origin. When the chronic hepatic insufficiency worsens the portal hypertensive inflammatory response, the splanchnic lymphatic system transports the hyperplasied intestinal mast cells to the mesenteric lymphatic complex. Then, an acquired immune response regulating a new hepato-intestinal metabolic scenario is activated. Therefore, reduction of the hepatic metabolism would reduce its key centralized functions, such as the metabolic, detoxifying and antioxidant functions which would try to be substituted by their peroxisome activity, among other functions of the mast cells.

Portal Angiogenesis in Chronic Liver Disease Patients Correlates with Portal Pressure and Collateral Formation

2019 ◽  
Vol 37 (6) ◽  
pp. 498-508 ◽  
Author(s):  
Carolina A. Serrano ◽  
Simon C. Ling ◽  
Sofia Verdaguer ◽  
Miguel León ◽  
Nicolás Jarufe ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Peripheral Circulation ◽  
Chronic Liver ◽  
Noninvasive Markers ◽  
Collateral Formation

Background/Aims: One hallmark of chronic liver disease in patients with portal hypertension is the formation of portal-systemic collaterals in which angiogenesis has a fundamental role. We studied patients with chronic liver disease undergoing liver transplantation to correlate levels of circulating angiogenic factors in portal and peripheral circulation with portal pressure and portal-systemic collaterals. Methods: Sixteen patients who underwent liver transplantation were enrolled. During transplant surgery, we determined portal venous pressure and portal-systemic collateral formation. We determined angiogenics mediator levels in systemic and portal plasma. Peripheral plasma from healthy donors was measured as controls. Results: Vascular endothelial growth factor (VEGF)-R1 and 2, Ang-1 and 2, Tie2, FGF- 1 and 2, CD163, PDGFR-β, PDGFsRα, PDGF-AB and BB, CD163, TGF-β VASH-1 levels were significantly different in the controls in comparison to cases. Significantly decreased portal venous levels of Ang-1, FGF-1, PDGF-AB/BB, and CC were observed in patients with higher portal pressure. Peripheral VEGF, Ang-1, pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation. While peripheral VEGF-R1 was higher in patients with severe collateral formation. For portal circulation, VEGF, Ang-1, ­pPDGF-AB, BB, and CC were significantly decreased in patients with more severe collateral formation Conclusions: Angiogenesis factors correlated with portal pressure and collateral formation and different patterns of circulating angiogenesis mediators were found in peripheral and portal blood of patients with chronic liver disease. These results support the importance of angiogenic pathways in cirrhosis and portal hypertension and highlight areas for further study to identify clinically useful noninvasive markers of portal pressure and collateral formation.

scholarly journals A72 VARICEAL BLEED & PORTAL HYPERTENSIVE GASTROPATHY IN A NON-CIRRHOTIC PATIENT WITH ISOLATED SPLENOMEGALY

2020 ◽  
Vol 3 (Supplement_1) ◽  
pp. 85-86
Author(s):  
S Hasan ◽  
M Dmitriew ◽  
J Leonard
Keyword(s):  
Intensive Care ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Cirrhotic Patient ◽  
Rare Case ◽  
Treatment Plan ◽  
Venous Pressure ◽  
Retinal Dystrophy ◽  
Ct Guided ◽  
Variceal Bleed

Abstract Background Portal hypertension caused by cirrhosis is the most common etiology of esophageal varices. However, abnormalities of the spleno-portal axis in the absence of liver disease may also cause portal hypertension resulting in varices. We report a rare case of esophageal variceal bleed in a non-cirrhotic patient with isolated splenomegaly secondary to chronic G-CSF therapy. Aims This report outlines the case of a patient with Cohen Syndrome (CS) who presented with an upper gastrointestinal (GI) bleed in the setting of previously documented splenomegaly and portal hypertension. We expand on the clinical investigations, diagnosis, treatment plan and hospital course of this patient. Methods Case report, review of literature. Results A 26-year old male with previously diagnosed CS presented with large volume hematemesis and pancytopenia. CS is a rare autosomal recessive disorder. In our patient this manifested with congenital neutropenia, microcephaly, retinal dystrophy and global developmental delay. He required long term G-CSF therapy to manage chronic neutropenia and subsequently developed splenomegaly, a known side effect. The most recent MRI identified stable splenomegaly with a craniocaudal length of 23 cm, normal liver size and no radiographic evidence of cirrhosis. The imaging was also significant for gastroesophageal and splenorenal varices but no ascites or recanalization of the umbilical vein. A recent liver biopsy had shown mild pericellular fibrosis with no active liver disease or cirrhosis. In the past, the patient had declined EGD, therapeutic splenectomy or assessment of hepatic venous pressure gradient through invasive venography. His liver enzymes, bilirubin and albumin had always been within normal limits. The patient had no history of GI bleeding. Previous investigations for hematologic malignancies or myelodysplastic syndrome had been negative. Upon admission, an urgent EGD revealed active variceal bleeding in the esophagus and portal gastropathy. Given the extent of his congenital orofacial abnormalities a variceal band ligator could not be passed for appropriate intervention. The patient was transferred to the Intensive Care Unit and managed with intravenous proton pump inhibitor, octreotide, as well as transfusions of packed red blood cells, platelets and fresh frozen plasma. Within the next 48 hours, the patient underwent successful transjugular intrahepatic portosystemic shunt and CT-guided coil placements for the bleeding varices. Conclusions This is a rare case of variceal bleed in a non-cirrhotic patient with portal hypertension from iatrogenic splenomegaly. While there are previous reports of spontaneous splenic rupture secondary to G-CSF therapy we are the first to report variceal bleed as a complication. This is a life-threatening consequence that requires urgent intervention and intensive care. Funding Agencies None

Urotensin II modulates hepatic fibrosis and portal hemodynamic alterations in rats

2009 ◽  
Vol 297 (4) ◽  
pp. G762-G767 ◽  
Author(s):  
William Kemp ◽  
Andrew Kompa ◽  
Arintaya Phrommintikul ◽  
Chandana Herath ◽  
Jia Zhiyuan ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Growth Factor ◽  
Hepatic Fibrosis ◽  
Transforming Growth Factor ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Hepatic Tissue ◽  
High Dose ◽  
Urotensin Ii

The influence of circulating urotensin II (UII) on liver disease and portal hypertension is unknown. We aimed to evaluate whether UII executes a pathogenetic role in the development of hepatic fibrosis and portal hypertension. UII was administered by continuous infusion over 4 wk in 20 healthy rats divided into three treatment groups, controls (saline, n = 7), low dose (UII, 1 nmol·kg−1·h−1, n = 8), and high dose (UII, 3 nmol·kg−1·h−1, n = 5). Hemodynamic parameters and morphometric quantification of fibrosis were assessed, and profibrotic cytokines and fibrosis markers were assayed in hepatic tissue. UII induced a significant dose-dependent increase in portal venous pressure (5.8 ± 0.4, 6.4 ± 0.3, and 7.6 ± 0.7, respectively, P = 0.03). High-dose UII infusion was associated with an increase in hepatic transcript for transforming growth factor-β ( P < 0.05) and platelet-derived growth factor-β ( P = 0.06). Liver tissue hydroxyproline was elevated in the high-dose group ( P < 0.05). No systemic hemodynamic alterations were noted. We concluded that UII infusion elevates portal pressure and induces hepatic fibrosis in normal rats. This response may be mediated via induction of fibrogenic cytokines. These findings have pathophysiological implications in human liver disease where increased plasma UII levels have been observed.

scholarly journals Nonalcoholic fatty liver disease and portal hypertension

2020 ◽  
Vol 1 (3) ◽  
pp. 149-169 ◽  
Author(s):  
Marvin Ryou ◽  
Nicholas Stylopoulos ◽  
Gyorgy Baffy
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Pressure Gradient ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Venous Pressure ◽  
Portal Venous Pressure ◽  
Invasive Technique ◽  
Nonalcoholic Fatty Liver

Nonalcoholic fatty liver disease (NAFLD) is a substantial and growing problem worldwide and has become the second most common indication for liver transplantation as it may progress to cirrhosis and develop complications from portal hypertension primarily caused by advanced fibrosis and erratic tissue remodeling. However, elevated portal venous pressure has also been detected in experimental models of fatty liver and in human NAFLD when fibrosis is far less advanced and cirrhosis is absent. Early increases in intrahepatic vascular resistance may contribute to the progression of liver disease. Specific pathophenotypes linked to the development of portal hypertension in NAFLD include hepatocellular lipid accumulation and ballooning injury, capillarization of liver sinusoidal endothelial cells, enhanced contractility of hepatic stellate cells, activation of Kupffer cells and pro-inflammatory pathways, adhesion and entrapment of recruited leukocytes, microthrombosis, angiogenesis and perisinusoidal fibrosis. These pathological events are amplified in NAFLD by concomitant visceral obesity, insulin resistance, type 2 diabetes and dysbiosis, promoting aberrant interactions with adipose tissue, skeletal muscle and gut microbiota. Measurement of the hepatic venous pressure gradient by retrograde insertion of a balloon-tipped central vein catheter is the current reference method for predicting outcomes of cirrhosis associated with clinically significant portal hypertension and guiding interventions. This invasive technique is rarely considered in the absence of cirrhosis where currently available clinical, imaging and laboratory correlates of portal hypertension may not reflect early changes in liver hemodynamics. Availability of less invasive but sufficiently sensitive methods for the assessment of portal venous pressure in NAFLD remains therefore an unmet need. Recent efforts to develop new biomarkers and endoscopy-based approaches such as endoscopic ultrasound-guided measurement of portal pressure gradient may help achieve this goal. In addition, cellular and molecular targets are being identified to guide emerging therapies in the prevention and management of portal hypertension.

scholarly journals Machine Learning Analysis of Volatolomic Profiles in Breath Can Identify Non-invasive Biomarkers of Liver Disease

2021 ◽  
Author(s):  
Jonathan Thomas ◽  
Joanna Roopkumar ◽  
Tushar Patel
Keyword(s):  
Machine Learning ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Hepatic Metabolism ◽  
Molecular Feature ◽  
Non Invasive ◽  
Molecular Features ◽  
Signature Pattern ◽  
Ion Mobility Spectroscopy ◽  
Learning Analysis

Abstract Disease-related effects on hepatic metabolism can alter the composition of chemicals in the circulation and subsequently in breath. The presence of disease related alterations in exhaled volatile organic compounds (VOC) could provide a basis for non-invasive biomarkers of hepatic disease. This study examined the feasibility of combining global VOC (volatolomic) profiles from breath analysis and machine learning to develop signature pattern-based biomarkers for cirrhosis. Breath samples were analyzed using thermal desorption-gas chromatography-field asymmetric ion mobility spectroscopy to generate volatolomic profiles. Samples were collected from 35 persons with cirrhosis, 4 with non-cirrhotic portal hypertension, and 11 healthy participants. Molecular features of interest were identified to determine their ability to classify cirrhosis or portal hypertension. A molecular feature score was derived that increased with the stage of cirrhosis and had an AUC of 0.78 for detection. Chromatographic breath profiles were utilized to generate machine learning-based classifiers. Algorithmic models could discriminate presence or stage of cirrhosis with a sensitivity of 88-92% and specificity of 75%. These results demonstrate the feasibility of volatolomic profiling to classify clinical phenotypes without identifying specific compounds. These studies will pave the way in developing non-invasive biomarkers of liver disease based on volatolomic signatures found in breath.

scholarly journals Machine learning analysis of volatolomic profiles in breath can identify non-invasive biomarkers of liver disease: A pilot study

PLoS ONE ◽  
2021 ◽  
Vol 16 (11) ◽  
pp. e0260098
Author(s):  
Jonathan N. Thomas ◽  
Joanna Roopkumar ◽  
Tushar Patel
Keyword(s):  
Machine Learning ◽  
Portal Hypertension ◽  
Liver Disease ◽  
Hepatic Metabolism ◽  
Supervised Machine Learning ◽  
Molecular Feature ◽  
Non Invasive ◽  
Molecular Features ◽  
Signature Pattern ◽  
Ion Mobility Spectroscopy

Disease-related effects on hepatic metabolism can alter the composition of chemicals in the circulation and subsequently in breath. The presence of disease related alterations in exhaled volatile organic compounds could therefore provide a basis for non-invasive biomarkers of hepatic disease. This study examined the feasibility of using global volatolomic profiles from breath analysis in combination with supervised machine learning to develop signature pattern-based biomarkers for cirrhosis. Breath samples were analyzed using thermal desorption-gas chromatography-field asymmetric ion mobility spectroscopy to generate breathomic profiles. A standardized collection protocol and analysis pipeline was used to collect samples from 35 persons with cirrhosis, 4 with non-cirrhotic portal hypertension, and 11 healthy participants. Molecular features of interest were identified to determine their ability to classify cirrhosis or portal hypertension. A molecular feature score was derived that increased with the stage of cirrhosis and had an AUC of 0.78 for detection. Chromatographic breath profiles were utilized to generate machine learning-based classifiers. Algorithmic models could discriminate presence or stage of cirrhosis with a sensitivity of 88–92% and specificity of 75%. These results demonstrate the feasibility of volatolomic profiling to classify clinical phenotypes using global breath output. These studies will pave the way for the development of non-invasive biomarkers of liver disease based on volatolomic signatures found in breath.

Transjugular Intrahepatic Portosystemic Shunt in Patients with Portal Hypertension: Patency Depends on Coverage and Interventionalist’s Experience

2018 ◽  
Vol 36 (3) ◽  
pp. 218-227 ◽  
Author(s):  
Matthias Buechter ◽  
Paul Manka ◽  
Guido Gerken ◽  
Ali Canbay ◽  
Sandra Blomeyer ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Transjugular Intrahepatic Portosystemic Shunt ◽  
Venous Pressure ◽  
Portosystemic Shunt ◽  
Refractory Ascites ◽  
Control Group ◽  
Covered Stents ◽  
Group I ◽  
Intrahepatic Portosystemic Shunt

Background and Aims: Transjugular intrahepatic portosystemic shunt (TIPS) is the treatment of choice in decompensated portal hypertension. TIPS revision due to thrombosis or stenosis increases morbidity and mortality. Our aim was to investigate patient- and procedure-associated risk factors for TIPS-revision. Patients and Methods: We retrospectively evaluated 189 patients who underwent the TIPS procedure. Only patients who required TIPS revision within 1 year (Group I, 34 patients) and patients who did not require re-intervention within the first year (Group II [control group], 54 patients) were included. Results: Out of 88 patients, the majority were male (69.3%) and mean age was 56 ± 11 years. Indications for TIPS were refractory ascites (68%), bleeding (24%), and Budd-Chiari syndrome (8%). The most frequent liver disease was alcohol-induced cirrhosis (60%). Forty-three patients (49%) received bare and 45 patients (51%) covered stents, thus resulting in reduction of hepatic venous pressure gradient (HVPG) from 19.0 to 9.0 mm Hg. When comparing patient- and procedure-related factors, the type of stent (p < 0.01) and interventionalist’s experience (number of performed TIPS implantations per year; p < 0.05) were the only factors affecting the risk of re-intervention due to stent dysfunction, while age, gender, indication, Child-Pugh, and model of end-stage liver disease score, platelet count, pre- and post-HVPG, additional variceal embolization, stent diameter, and number of stents did not significantly differ. Conclusion: Patients undergoing TIPS procedure should be surveilled closely for shunt dysfunction while covered stents and high-level experience are associated with increased ­patency.

scholarly journals Vitamin A levels reflect disease severity and portal hypertension in patients with cirrhosis

2020 ◽  
Author(s):  
Benedikt Simbrunner ◽  
Georg Semmler ◽  
Alexander Stadlmann ◽  
Bernhard Scheiner ◽  
Philipp Schwabl ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Bile Acid ◽  
Hepatic Dysfunction ◽  
Venous Pressure ◽  
Serum Levels ◽  
Serum Bile Acid ◽  
Reflect Disease Severity ◽  
Registration Number ◽  
Ctp Score

Abstract Background and Aims The liver plays a key role in the storage, metabolism and homeostasis of fat-soluble vitamins. We investigated the relation of Vitamin(Vit)A/D/E serum levels with severity of liver disease and portal hypertension (PHT). Methods VitA/D/E serum levels were assessed in 234 patients with advanced chronic liver disease (ACLD, i.e. hepatic venous pressure gradient [HVPG] ≥ 6 mmHg). Patients with hepatocellular carcinoma, pre-/post-hepatic PHT, TIPS or liver transplantation were excluded. Results Most patients were male (n = 153; 65%) with a median age of 57.6 (49.7–64.5) years. Thirty-two (14%) patients had HVPG 6–9 mmHg, 66 (28%) 10-15 mmHg, and 136 (58%) ≥ 16 mmHg, respectively. VitD deficiency (25-OH-vitamin-D <50 nmol/L) was found in 133 (57%) with higher prevalence in Child-Turcotte-Pugh (CTP)-C: 85% vs. B: 66% vs. A: 47% (p < 0.001). VitD levels displayed significant but weak correlations with hepatic dysfunction and PHT. VitE levels were normal in 227 (97%) patients and displayed no relevant association with hepatic dysfunction or PHT. Only 63 (27%) patients had normal (>1.05 µmol/L) VitA levels, while 58 (25%) had mild (0.70–1.04 µmol/L), 71 (30%) moderate (0.35–0.69 µmol/L), and 42(18%) severe(<0.35 µmol/L) VitA deficiency. VitA correlated with HVPG (Rho = −0.409), CTP score (Rho = −0.646), and serum bile acid levels (Rho = −0.531; all p < 0.001). The prevalence of decompensated ACLD (dACLD) continuously increased with severity of VitA deficiency (no: 40% vs. mild: 51% vs. moderate: 67% vs. severe: 91% had dACLD; p < 0.001). CTP score (per point; OR 2.46; 95%CI 1.80–3.37; p <0.001), age (per year; OR 0.95; 95%CI 0.92–0.98; p = 0.001) and elevated bile acid levels(>10 µmol/L; OR 3.62; 95%CI 1.61–8.14; p = 0.002) were independently associated with VitA deficiency. Conclusion VitA and VitD but not VitE deficiencies are highly prevalent in ACLD. VitA deficiency strongly correlates with hepatic dysfunction, PHT and bile acid levels and is associated with decompensated ACLD. Trial registration number NCT03267615.

scholarly journals Diagnosis of portal hypertension by transabdominal ultrasound

2015 ◽  
Vol 47 (1-2) ◽  
pp. 21-24
Author(s):  
Md Saad Ahamed ◽  
Shikha Kabir ◽  
AS Mohiuddin ◽  
Poritosh Kumar Chowdhury
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Superior Mesenteric Vein ◽  
Statistical Significance ◽  
Venous Pressure ◽  
Splenic Vein ◽  
Deep Inspiration ◽  
Mesenteric Veins ◽  
Mesenteric Vein ◽  
Imaging Department

Portal hypertension is pathologic increase in portal venous pressure, with diversion of portal blood to the systemic circulation. The study was directed to measure as well as to compare the diameters of splenic, superior mesenteric and portal veins with their variation with respiration in normal subjects and in patients with portal hypertension. An analytic type of cross-sectional study was conducted at Radiology and Imaging Department of BIRDEM, Shahbag, Dhaka for one year (2011-12) among purposively selected 59 study subjects with chronic liver disease and portal hypertension, and 45 individuals without liver disease. Transabdominal ultrasonograpy of hepatobiliary system was carried out using computed sonography system with multiple probes having multiple frequency depending on physical built of the subjects. The diameters of selected veins were measured in the course of expiration and deep inspiration. In all control subjects, diameter variations of splenic vein and superior mesenteric vein were noted in the phases of respiration, the diameters increased during deep inspiration and decreased during deep expiration mean diameter and standard deviation of splenic vein and superior mesenteric vein were 6.95 ± 1.75 mm and 8.77 ± 2.06 mm respectively and during expiration they were 4.45 ± 1.24 mm and 5.66 ± 1.41 mm respectively. The difference in deep inspiratory and expiratory diameters had high statistical significance (p<0.0001). Patients with portal hypertension diameter variation with breathing at the level of splenic and superior mesenteric veins was observed only in 5 (9.47%) cases. Diminished response of splenic and superior mesenteric veins with respiration in transabdominal ultrasonography is an indicator of portal hypertension. DOI: http://dx.doi.org/10.3329/bmjk.v47i1-2.22558 Bang Med J (Khulna) 2014; 47 : 21-24

scholarly journals Thromboelastometry in patients with advanced chronic liver disease stratified by severity of portal hypertension

2020 ◽  
Author(s):  
Pierre Raeven ◽  
Joanna Baron-Stefaniak ◽  
Benedikt Simbrunner ◽  
Alexander Stadlmann ◽  
Philipp Schwabl ◽  
...  
Keyword(s):  
Portal Hypertension ◽  
Liver Disease ◽  
Chronic Liver Disease ◽  
Venous Pressure ◽  
Portal Pressure ◽  
Cross Sectional Study ◽  
Chronic Liver ◽  
Cross Sectional ◽  
Reactive Protein ◽  
The Impact

Abstract Background Rotational thromboelastometry (ROTEM) has been studied in patients with advanced chronic liver disease (ACLD) without considering the impact of portal hypertension. We evaluated the influence of the hepatic venous pressure gradient (HVPG) on ROTEM results in patients with ACLD. Methods Cross-sectional study; ACLD patients undergoing HVPG measurement within the prospective Vienna Cirrhosis Study (NCT03267615) underwent concomitant ROTEM testing. Results Among 159 patients (68% male; Child–Pugh-A: 53%, Child–Pugh-B: 34%, Child–Pugh-C: 13%), 21 patients (13%) had a HVPG between 6 and 10 mmHg, 84 patients (53%) between 10 and 19 mmHg, and 54 patients (34%) ≥ 20 mmHg. Child–Pugh-C patients (vs. Child–Pugh-A and vs. Child–Pugh-B patients, respectively) showed longer clot formation time (CFT: median 187 s vs. 122 s vs. 122 s, p = 0.007) and lower maximum clot firmness (MCF: median: 45 mm vs. 56 mm vs. 56 mm, p = 0.002) in extrinsic thromboelastometry (EXTEM), while platelet counts were similar across Child–Pugh stages. In the overall cohort, ROTEM parameters did not differ by severity of portal hypertension. However, among compensated Child–Pugh-A patients, MCF decreased with increasing portal pressure, i.e. in higher HVPG strata (HVPG 9–10 mmHg: median MCF: 59 mm vs. HVPG 10–19 mmHg: 56 mm vs HVPG ≥ 20 mmHg: 54 mm, p = 0.023). Furthermore, patients with short CFT and high MCF in EXTEM had higher levels of lipopolysaccharide-binding protein, C-reactive protein, and procalcitonin, as well as higher leukocyte counts (all p < 0.05). Conclusions Portal hypertension seems to impact ROTEM results only in compensated Child–Pugh-A patients. Bacterial translocation and systemic inflammation may trigger a procoagulant state in patients with ACLD.

Sign in / Sign up

Export Citation Format

Share Document