内皮素性大鼠门静脉高压模型的建立

目的： 建立内皮素-1(ET-1)引起门静脉压力升高的动物模型。方法: 正常雄性SD大鼠48只，随机分为生理盐水组、ET-1低剂量组(0.3 μg/kg)，ET-1中剂量组(1.0 μg/kg)和ET-1高剂量组(3.0 μg/kg)。生理盐水组大鼠经股静脉注入生理盐水，其余各组大鼠按相应剂量经股静脉注入ET-1溶液，观察门静脉压力和颈动脉压力的变化情况,并筛选出能使门静脉压力升高最适宜的剂量；另取15只大鼠随机分为对照组、ETAR阻断剂(BQ-123)组和ETBR阻断剂(BQ-788)组，实验开始前30 min经各组大鼠股静脉分别注入生理盐水、ETR阻断剂BQ-123(给药剂量为12.5 μg/kg)和BQ-788(给药剂量为15 μg/kg)，然后以选定的适宜剂量匀速注入ET-1溶液，观察各组大鼠门静脉压力变化。结果: 不同剂量的ET-1均能使门静脉压力升高，尤以高剂量组最为明显；而提前注入ETR阻断剂之后，再注入ET-1溶液门静脉压力虽然升高，但升高的幅度较小。结论: 成功创建了内皮素性大鼠门静脉高压模型，此模型可用于研究ET-1在PHT发病机制中的作用和药物对PHT时血中ET-1的影响。     

Mast cell leukemia with rapidly progressing portal hypertension

Reported herein is an autopsy case of mast cell leukemia, a rare form of systemic mastocytosis, complicated with portal hypertension. A 52-year-old woman presented with urticaria-like skin symptoms, anemia, and thrombocytopenia. Atypical mast cells (CD2+, CD25+, CD117+) with toluidine blue metachromasia were found in the peripheral blood and on bone marrow aspiration smears. Chemotherapy with cytosine arabinoside and idarubicin was ineffective and the patient died of multi-organ failure with rapidly progressing hepatosplenomegaly and large-volume ascites 3 months after admission. At autopsy the bone marrow, spleen, liver, and lymph nodes were extensively infiltrated by atypical tumor cells with occasional bi- or multi-lobated nuclei. They were positive for mast cell tryptase and possessed an activating mutation of the c-kit gene (D816V). Ascites (2200 mL) and non-ruptured esophageal varices with submucosal hemorrhage indicated the presence of severe portal hypertension. Although there was no evidence of liver cirrhosis, the hepatic sinusoids were clogged with tumor cells, with a tendency to be more severe in the perivenular areas, and the lumens of central veins were obliterated by tumor cell infiltration. The present case demonstrates that non-cirrhotic portal hypertension due to blocking of sinusoidal and venous flow could be a serious complication in mast cell leukemia.     

The mast cell integrates the splanchnic and systemic inflammatory response in portal hypertension

Portal hypertension is a clinical syndrome that is difficult to study in an isolated manner since it is always associated with a greater or lesser degree of liver functional impairment. The aim of this review is to integrate the complications related to chronic liver disease by using both, the array of mast cell functions and mediators, since they possibly are involved in the pathophysiological mechanisms of these complications. The portal vein ligated rat is the experimental model most widely used to study this syndrome and it has been considered that a systemic inflammatory response is produced. This response is mediated among other inflammatory cells by mast cells and it evolves in three linked pathological functional systems. The nervous functional system presents ischemia-reperfusion and edema (oxidative stress) and would be responsible for hyperdynamic circulation; the immune functional system causes tissue infiltration by inflammatory cells, particularly mast cells and bacteria (enzymatic stress) and the endocrine functional system presents endothelial proliferation (antioxidative and antienzymatic stress) and angiogenesis. Mast cells could develop a key role in the expression of these three phenotypes because their mediators have the ability to produce all the aforementioned alterations, both at the splanchnic level (portal hypertensive enteropathy, mesenteric adenitis, liver steatosis) and the systemic level (portal hypertensive encephalopathy).     

Hemodynamic alterations in cirrhosis and portal hypertension

Portal hypertension (PHT) is associated with hemodynamic changes in intrahepatic, systemic, and portosystemic collateral circulation. Increased intrahepatic resistance and hyperdynamic circulatory alterations with expansion of collateral circulation play a central role in the pathogenesis of PHT. PHT is also characterized by changes in vascular structure, termed vascular remodeling, which is an adaptive response of the vessel wall that occurs in response to chronic changes in the environment such as shear stress. Angiogenesis, the formation of new blood vessels, also occurs with PHT related in particular to the expansion of portosystemic collateral circulation. The complementary processes of vasoreactivity, vascular remodeling, and angiogenesis represent important targets for the treatment of portal hypertension. Systemic and splanchnic vasodilatation can induce hyperdynamic circulation which is related with multi-organ failure such as hepatorenal syndrome and cirrhotic cadiomyopathy.     

Prehepatic portal hypertension worsens the enterohepatic redox balance in thioacetamide-cirrhotic rats

Background: Oxidative stress has been reported as a key pathogenic factor in many human liver diseases and in experimental models of cirrhosis related to hepatotoxin administration. The aim of this study was to verify the hypothesis that prehepatic portal hypertension aggravates the enterohepatic redox imbalance in thioacetamide-cirrhotic rats. Materials and methods: Wistar male rats were used: Control (n = 9); rats with prehepatic portal hypertension by triple partial portal vein ligation (TPVL; n = 9); thioacetamide-cirrhotic rats (TAA; n = 9) and TPVL-rats associated to TAA administration (TPVL + TAA; n = 9). Three months after the operation, portal pressure (PP), mesenteric venous vasculopathy (MVV) and portosystemic collateral circulation were studied. Liver and ileal levels of malondialdehyde (MDA), as a lipid peroxidation marker, and catalase (CAT), glutathione peroxidase (GSH-Px), glutathione transferase (GSH-t) and cytosolic and mitochondrial superoxide dismutases (cSOD and mSOD), as antioxidative enzymatic mechanisms, were measured. Results: Liver and ileal MDA increased in all the experimental groups, although the higher increase occurred in the ileum of rats with portal hypertension. CAT levels decreased in the liver and the ileum in the three experimental groups. The decrease in liver and ileal GSH-Px and GSH-t was greater in rats with portal hypertension, alone or associated with TAA. mSOD activation was demonstrated in the liver when portal hypertension was added to TAA. On the contrary, this compensatory response was not activated in the ileum, where mSOD was significantly decreased. Conclusion: Prehepatic portal hypertension by triple partial portal vein ligation impaired the enterohepatic antioxidative activity and aggravated the intestinal oxidative stress in thioacetamide-cirrhotic rats.     

辛伐他汀通过抑制p38 MAPK活化降低肝硬化门静脉高压大鼠门静脉压力

 目的:探讨p38 MAPK信号通路在辛伐他汀降低肝硬化门静脉高压症大鼠门静脉压力（PP）中的作用。方法:采用四氯化碳复合因素法构建大鼠肝硬化门静脉高压症模型,成模后将存活大鼠随机分为模型组（n=10）、辛伐他汀治疗组（n=11）和p38 MAPK信号通路抑制剂SB203580处理组（n=10）,后2组分别给予辛伐他汀及SB203580干预处理;另设正常对照组（n=8）。处理结束后检测大鼠PP、肝脏总p38 MAPK蛋白、磷酸化p38 MAPK蛋白、总eNOS蛋白、磷酸化eNOS蛋白表达水平以及肝脏一氧化氮（NO）含量的变化。结果:（1）模型组大鼠PP明显高于正常对照组;辛伐他汀治疗组及SB203580处理组PP均明显低于模型组（P＜0.01）,辛伐他汀治疗组PP明显低于SB203580处理组（P＜0.01）。（2）与正常大鼠相比,模型组大鼠肝脏总p38 MAPK蛋白及总eNOS蛋白表达水平无明显变化（P＞0.05）,而磷酸化p38 MAPK蛋白及磷酸化eNOS蛋白表达水平分别增高与降低（P＜0.01）;辛伐他汀治疗组大鼠肝脏磷酸化p38 MAPK蛋白及磷酸化eNOS蛋白表达水平分别降低与增高（P＜0.01）;SB203580处理组大鼠肝脏磷酸化p38 MAPK蛋白及磷酸化eNOS蛋白表达水平分别降低与增高（P＜0.01）,但磷酸化eNOS蛋白表达水平增高的程度低于辛伐他汀治疗组（P＜0.01）。(3)辛伐他汀治疗组肝脏NO含量［（15.73±1.59） μmol/(g protein)］及SB203580处理组肝脏NO含量［（13.98±1.27) μmol/(g protein)］明显高于模型组［（9.81±1.12） μmol/（g protein）］（P＜0.01）,辛伐他汀治疗组NO含量明显高于SB203580处理组（P＜0.01）。结论: 辛伐他汀降低肝硬化门静脉高压症大鼠门静脉压力可能与其抑制p38 MAPK信号通路的活化有关。     

The role of the mast cell in acute inflammatory responses of copper-deficient rats

Macromolecular leakage associated with mast cell degranulation was studied in the cremaster muscle microcirculation of copper-deficient rats. Male Sprague-Dawley rats were fed a purified diet either adequate for copper (6 g copper/gram diet) or deficient (no added copper) 4 weeks prior to experimentation. The rats were anesthetized and the cremasters (with nerve and blood supply intact) were spread in a tissue bath filled with Kreb's solution.In vivo television microscopy was used to observe the microcirculation. Intravascular fluorescein isothiocyanate conjugated to bovine serum albumin was injected and interstitial fluorescent emission intensity was used as an index of macromolecular leakage. Topical administration of the mast cell degranulator compound 48/80 (1.0 and 10.0 g/ml) induced a significantly greater macromolecular leakage in the copper-deficient animals. The compound 48/80 leakage was blocked in both groups of rats by pretreatment with diphenhydramine which is a histamine H₁ receptor blocker. Topical administration of the inflammatory mediators histamine, serotonin, and bradykinin all induced macromolecular leakage which was not significantly different between groups. These results suggest that copper deficiency increases macromolecular leakage associated with mast cell degranulation by a primary effect on the mast cell rather than on the endothelium.This material is based upon work supported by the Cooperative State Research Service, U.S. Department of Agriculture, under Agreement No. 92-37200-7676. Mention of a trademark of proprietary product does not constitute a guarantee or warranty of the product by the U.S. Department of Agriculture, and does not imply its approval to the exclusion of other products that may also be suitable.     

肝硬化患者血管紧张素Ⅱ-RIA水平与门脉血流动力学的关系

目的 :探讨肝硬化门脉高 (PTH)的血流动力学变化及其与血中AT Ⅱ的关系。方法 :4 8例肝硬化PTH患者 (代偿期 18例、失代偿期 30例 )及 32例正常人作为研究对象 ,应用双功能多普勒测定门、脾静脉血流量 (PVBF&SVBF) ,同步测定血中AT Ⅱ的水平 ,并分析PVBF&SVBF与AT Ⅱ的相关性。结果 :门脉系统高血流动力学改变存在于肝硬化PTH发病的始终 ,代偿期显著下降的AT Ⅱ与门脉高血流动力学变化无相关性 ,失代偿期显著升高的AT Ⅱ与门脉高血流动力变化呈正相关。结论 :此研究对临床诊治有指导意义。     

Gln和rhGH对门脉高压症术后肠粘膜屏障及增殖细胞核抗原表达的影响

目的：研究单独或联合应用谷氨酰胺（Gln）和重组人生长激素（rhGH）对门脉高压症术后肠粘膜屏障功能的保护作用及机制。方法:29例门静脉高压症术后患者随机分为4组：①Gln组（n=6），②rhGH组（n=8），③Gln+rhGH组（n=7）和④对照组（n=8）。术后3 d开始进行等氮、等热量的全胃肠外营养支持（TPN），持续7 d。对手术前、后的尿乳果糖排泄率/甘露醇排泄率（L/M）、十二指肠粘膜绒毛高度、陷窝深度及肠粘膜增殖细胞核抗原（PCNA）表达指数进行对比。结果:Gln+rhGH组术后L/M值升高小于对照组（P<0.05），肠粘膜绒毛高度和陷窝深度大于对照组（P<0.05）及术前（P<0.05），肠粘膜上皮PCNA表达指数大于术前及其它3组（P<0.05）；对照组术后绒毛高度小于术前（P<0.05），陷窝深度变化无显著（P＞0.05）。结论：联合应用Gln和rhGH能降低门脉高压症术后肠壁通透性并维护肠粘膜形态学完整性，单用Gln或rhGH无此作用。这种作用可能与增加肠黏膜PCNA表达而促进肠黏膜上皮细胞增殖有关。     

门静脉高压症猪肝动脉的结构重建

目的 建立猪门静脉高压症模型,探讨门静脉高压症时肝动脉的结构重建.方法猪以四氯化碳、苯巴比妥、乙醇配合高脂、低蛋白、低胆碱饮食进行混合饲养.通过脾静脉插管测压,取肝动脉常规石蜡包埋、切片,用HE 法、Weigert 法、Aniline blue法,Organge G法分别染组织结构、弹性纤维、胶原纤维和平滑肌,用计算机...     

Mast cell functions in the innate skin immune system

Mast cells are not only potent effector cells in allergy, but are also important players in protective immune responses against pathogens. Most of our knowledge about mast cells in innate immunity is derived from models of sepsis, whereas their role in innate immune responses of the skin has largely been neglected in the past. Their particular pattern of distribution in the skin and their ability to sense and react to pathogens and other danger signals indicate that mast cells can be important sentinels and effector cells in skin immune responses. The recent findings reviewed here have confirmed this hypothesis and have established a prominent role for skin mast cells in innate immunity.     

Effects of ocreotide on intestinal mucosa in rats with portal hypertensive enteropathy

To clarify the effects of long-term ocreotide (a long-acting somatostatin analogue) treatment on mucosal changes in a rat model of portal hypertensive enteropathy, groups of male Swiss albino rats (n=15 each) were randomly assigned to one of three treatment arms. These were: sham laparotomy+twice daily subcutaneous saline 0.5 mL (Group 1); portal hypertension induction+twice daily subcutaneous saline 0.5 mL (Group 2); and portal hypertension induction+subcutaneous ocreotide 100 microg/kg/12h (Group 3). After 12 weeks of treatment, jejunal and ileal tissue specimens were obtained and evaluated histopathologically (villus/crypt ratio, mean diameter of dilated vessels, mucosal edema, and fibromuscular proliferation in the lamina propria) and immunohistochemically (vascular endothelial growth factor (VEGF), von Willebrand factor (F8), and cluster of differentiation 34 (CD34) labelling). In jejunal specimens, the villus/crypt ratio was markedly lower in Group 2 (2.38+/-0.46 microm) than in Group 1 (5.07+/-2.25 microm) or Group 3 (4.97+/-2.19 microm); mean diameter of dilated vessels was markedly higher in Group 2 (43.30+/-5.71 microm) than in Group 1 (33.53+/-4.00 microm) or Group 3 (36.76+/-3.96 microm); mucosal edema and fibromuscular proliferation were universally absent in Group 1 when compared with the other groups. There were statistically significant differences (p<0.05) between Groups 1 and 2 for villus/crypt ratio, mean diameter of dilated vessels, VEGF immunolabelling intensity, and CD34 immunolabelling intensity; between Groups 1 and 3 for mean diameter of dilated vessels, VEGF immunolabelling intensity, and CD34 immunolabelling intensity; and between Groups 2 and 3 for villus/crypt ratio, mean diameter of dilated vessels, and VEGF immunolabelling intensity. In ileal tissue specimens, the villus/crypt ratio was markedly lower in Group 2 (5.51+/-0.67 microm) than in either Group 1 (7.19+/-2.18 microm) or Group 3 (7.62+/-2.58 microm); mean diameter of dilated vessels was markedly higher in Group 2 (46.36+/-4.77 microm) than in either Group 1 (36.43+/-4.57 microm) or Group 3 (41.31+/-4.70 microm); while mucosal edema was absent in Group 1, it was present in Group 2 and Group 3; and fibromuscular proliferation was universally absent. There were statistically significant differences (p<0.05) between Groups 1 and 2 for villus/crypt ratio and mean diameter of dilated vessels; between Groups 1 and 3 for mean diameter of dilated vessels; and between Groups 2 and 3 for villus/crypt ratio, mean diameter of dilated vessels, and VEGF immunolabelling intensity. Together, these findings indicate that ocreotide treatment ameliorates histomorphological changes in a rat model of portal hypertensive enteropathy.     

Radiological score for hemorrhage in the patients with portal hypertension

Goal: To analyze the risk factors from radiological indices for hemorrhage in the patients with portal hypertension and weight risk factors. Method: We retrospectively analyzed all cases of portal hypertension with hepatitis B from June 2008 to June 2014 in Nanjing Drum Tower hospital. Patients with hepatocellular carcinoma, portal vein thrombosis, or portal hypertension with other causes, such as autoimmune hepatitis, pancreatitis, or hematological diseases were excluded. Results: Ninety-eight patients were recruited and divided into hemorrhage and non-hemorrhage groups. There were no statistical differences in clinical indexes such as age, prothrombin time, serum albumin, serum creatinine, serum sodium, hemameba, and blood platelet count. However, the differences were statistically significant in total bilirubin, hemoglobin, and liver function with the p values of 0.023, 0.000, and 0.039 respectively. For radiological indices, hemorrhage was correlated with diameter of inferior mesenteric vein (P=0.0528), posterior gastric vein (P=0.0283), and esophageal varices scores (P=0.0221). Logistic procedure was used to construct the model with stepwise selection and finally inferior mesenteric vein, posterior gastric vein, esophageal varices, and short gastric vein were enrolled into the model. These veins were scored according to the diameters and the rates of hemorrhage were increased with the score. We then validated the model with 26 patents from July 2014 to December 2014. The AUC value was 0.8849 in ROC curves for this radiological model. Conclusions: A risk model was constructed including inferior mesenteric vein, esophageal varices, posterior gastric vein, and short gastric vein. This radiological scoring model may be a valuable indicator for hemorrhage of portal hypertension.     

Mast cell activation markers for in vitro study

ABSTRACT

Mast cells (MCs) are well known for their role in allergic conditions. This cell can be activated by various types of secretagogues, ranging from a small chemical to a huge protein. Mast cell activation by secretagogues triggers the increase in intracellular calcium (iCa²⁺) concentration, granule trafficking, and exocytosis. Activated mast cells release their intra-granular pre-stored mediator or the newly synthesized mediator in the exocytosis process, in the form of degranulation or secretion. There are at least three types of exocytosis in mast cells, which are suggested to contribute to the release of different mediators, i.e.,, piecemeal, kiss-and-run, and compound exocytosis. The status of mast cells, i.e., activated or resting, is often determined by measuring the concentration of the released mediator such as histamine or β-hexosaminidase. This review summarizes several mast cell components that have been and are generally used as mast cell activation indicator, from the classical histamine and β-hexosaminidase measurement, to eicosanoid and granule trafficking observation. Basic principle of the component determination is also explained with their specified research application and purpose. The information will help to predict the experiment results with a certain study design.     

门静脉高压征模型大鼠构建及门静脉侧支血管和内脏血管的形成

背景：Apelin/APJ系统在心血管调节中具有降低血压、加强心脏收缩及Apelin刺激血管生成等作用已为人们所证实。 目的：确认apelin和APJ在内脏组织中的表达,及检验apelin在门脉高压征大鼠的内脏新生血管发育、内脏充血及门静脉侧支化中的关联作用。 方法：36只大白鼠随机分为模型组18只和假手术组18只,模型组采用局部门静脉结扎构建门脉高压征大鼠模型,腹腔注射生理盐水或特定Apelin受体拮抗剂F13A。假手术组除不行结扎外,其余同模型组。 结果与结论：Apelin及其受体APJ在门静脉高压征的大鼠内脏血管系统过度表达。F13A在门静脉高压征的大鼠中能有效减少内脏血管再生和减少血管内皮生长因子、血小板衍生生长因子和血管生成素2的表达,也能减少门静脉侧支血管的形成。     

Splenectomy ameliorates portal pressure and anemia in animal models of cirrhotic and non-cirrhotic portal hypertension

PurposePortal hypertension (PH)-associated splenomegaly is caused by portal venous congestion and splanchnic hyperemia. This can trigger hypersplenism, which favors the development of cytopenia. We investigated the time-dependent impact of splenectomy on portal pressure and blood cell counts in animal models of non-cirrhotic and cirrhotic PH.Materials and methodsNinety-six rats underwent either partial portal vein ligation (PPVL), bile duct ligation (BDL), or sham operation (SO), with subgroups undergoing additional splenectomy. Portal pressure, mean arterial pressure, heart rate, blood cell counts and hemoglobin concentrations were evaluated throughout 5 weeks following surgery.ResultsFollowing PPVL or BDL surgery, the animals presented a progressive rise in portal pressure, paralleled by decreased mean arterial pressure and accelerated heart rate. Splenectomy curbed the development of PH in both models (PPVL: 16.25 vs. 17.93 ?mmHg, p ?= ?0.083; BDL: 13.55 vs. 15.23 ?mmHg, p ?= ?0.028), increased mean arterial pressure (PPVL: +7%; BDL: +9%), and reduced heart rate (PPVL: ?10%; BDL: ?13%). Accordingly, splenectomized rats had lower von Willebrand factor plasma levels (PPVL: ?22%; BDL: ?25%). Splenectomy resulted in higher hemoglobin levels in PPVL (14.15 vs. 13.08 ?g/dL, p ?< ?0.001) and BDL (13.20 vs. 12.39 ?g/dL, p ?= ?0.097) animals, and significantly increased mean corpuscular hemoglobin concentrations (PPVL: +9%; BDL: +15%). Thrombocytopenia only developed in the PPVL model and was alleviated in the splenectomized subgroup. Conversely, BDL rats presented with thrombocytosis, which was not affected by splenectomy.ConclusionsSplenectomy improves both cirrhotic and non-cirrhotic PH, and ameliorates the hyperdynamic circulation. Hypersplenism related anemia and thrombocytopenia were only significantly improved in the non-cirrhotic PH model.     

Mast cell populations in the chick embryo lung and their response to compound 48/80 and dexamethasone

Summary Two mast cell populations, connective tissue mast cells (CTMCs) and mucosal mast cells, (MMCs) containing different proteoglycans in their granules, can be distinguished in several animal species by means of histochemical methods. In this study we documented the presence of these two types of mast cell in the chick embryo lung, from the 15th incubation day for the MMCs, and from the 18th incubation day for the CTMCs. Lungs of embryos treated with compound 48/ 80, which produces degranulation of the CTMCs, showed a decrease in the number of this type of mast cell and an unchanged number of MMCs. In the lungs of embryos treated with dexamethasone, which degranulates MMCs, a reduction in the number of these cells and an unchanged number of the CTMs were found.     

Mast cell plasticity and sphingosine-1-phosphate in immunity,inflammation and cancer

Mast cells (MC) are found in all vascularized tissues at homeostasis and, until recently, were viewed only as effector cells of allergic reactions via degranulation, the canonical process through which MC release mediators, including histamine and pre-formed proteases and cytokines such as TNF. Cross-linking of IgE bound to surface high affinity receptors for IgE (Fc?RI) by a specific antigen (Ag) triggers signaling events leading to degranulation. We and others have reported the concomitant production and export of an influential multifaceted sphingolipid mediator, sphingosine-1-phosphate (S1P) transported outside of MC by ATP-binding cassettes (ABC) transporters, i.e., independently of degranulation. Indeed, the MC horizon expanded by the discovery of their unique ability to selectively release mediators depending upon the stimulus and receptors involved. Aside from degranulation and transporter usage, MC are also endowed with piecemeal degranulation, a slower process during which mediator release occurs with minor morphological changes. The broad spectrum of pro- and anti-inflammatory bioactive substances MC produce and release, their amounts and delivery pace render these cells bona fide fine-tuners of the immune response. In this viewpoint article, MC developmental, phenotypic and functional plasticity, its modulation by microRNAs and its relevance to immunity, inflammation and cancer will be discussed.     

The usefulness of non-invasive liver stiffness measurements in predicting clinically significant portal hypertension in cirrhotic patients: Korean data

Background/Aims

Liver stiffness measurement (LSM) has been proposed as a non-invasive method for estimating the severity of fibrosis and the complications of cirrhosis. Measurement of the hepatic venous pressure gradient (HVPG) is the gold standard for assessing the presence of portal hypertension, but its invasiveness limits its clinical application. In this study we evaluated the relationship between LSM and HVPG, and the predictive value of LSM for clinically significant portal hypertension (CSPH) and severe portal hypertension in cirrhosis.

Methods

LSM was performed with transient elastography in 59 consecutive cirrhotic patients who underwent hemodynamic HVPG investigations. CSPH and severe portal hypertension were defined as HVPG ≥10 and ≥12 mmHg, respectively. Linear regression analysis was performed to evaluate the relationship between LSM and HVPG. Diagnostic values were analyzed based on receiver operating characteristic (ROC) curves.

Results

A strong positive correlation between LSM and HVPG was observed in the overall population (r²=0.496, P<0.0001). The area under the ROC curve (AUROC) for the prediction of CSPH (HVPG ≥10 mmHg) was 0.851, and the sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) for an LSM cutoff value of 21.95 kPa were 82.5%, 73.7%, 86.8%, and 66.7%, respectively. The AUROC at prediction of severe portal hypertension (HVPG ≥12 mmHg) was 0.877, and the sensitivity, specificity, PPV, and NPV at LSM cutoff value of 24.25 kPa were 82.9%, 70.8%, 80.6%, and 73.9%, respectively.

Conclusions

LSM exhibited a significant correlation with HVPG in patients with cirrhosis. LSM could be a non-invasive method for predicting CSPH and severe portal hypertension in Korean patients with liver cirrhosis.