腹部B超在肝硬化门脉高血压诊断中的应用

目的:探讨腹部B超对肝硬化门脉高血压患者诊断的临床价值。方法:选取肝硬化门脉高血压患者80例作为观察组,同时随机选取健康人50例作为对照组,分别给予腹部B超检查。结果:观察组门静脉内径、脾静脉内径、Qsv/Qpv值均高于对照组,差异具有统计学意义(P<0.05)。结论:腹部B超可准确反映肝硬化门脉高血压患者的门静脉和脾静脉情况,具有重要的临床诊断价值。

分析影响肝硬化门脉高压患者胃肠道出血的相关危险因素

目的研究分析影响肝硬化门脉高压患者胃肠道出血的相关危险因素。方法选取2018年1月至2019年1月我院收治的120例肝硬化门脉高压患者,将所有患者按照出血与未出血的标准分为对照组(60例,胃肠道出血)和研究组(60例,肠胃道未出血),比较两组患者的肺功能Child-Pugh分级、门静脉内径、脾静脉内径、食管静脉曲张、胃底静脉曲张、冠状静脉怒张、红色征。结果对照组的门静脉内径、脾静脉内径明显大于研究组,差异具有统计学意义(P<0.05),研究组的肺功能Child-Pugh分级、食管静脉曲张、胃底静脉曲张、冠状静脉怒张、红色征明显优于对照组,差异具有统计学意义(P<0.05)。结论门静脉内径、脾静脉内径、肺功能Child-Pugh分级、食管静脉曲张、胃底静脉曲张、冠状静脉怒张、红色征都是影响肝硬化门脉高压患者胃肠道出血的因素。

介入断流术治疗肝硬化门脉高压合并上消化道出血效果探讨

目的：研究介入断流术治疗肝硬化门脉高压合并上消化道出血的效果。方法：选取我院2012年1月-2014年10月间诊治的肝硬化门脉高血压合并上消化道出血患者110例，将其随机分为观察组和对照组各55例，对观察组患者采用联合断流术治疗，对对照组患者进行中西医结合治疗，对比观察2组患者的临床治疗效果及不良反应。结果：观察组患者的总有效率为92．73％，对照组患者的总有效率为78．18％，观察组明显高于对照组，差异具有统计学意义（P〈0．05）；在不良反应发生率方面，观察组患者为5．45％，对照纽患者为12．73％，观察纽明显低于对照组，差异具有统计学意义（P〈0．05）。结论：采用联合断流术治疗肝硬化门脉高血压合并上消化道出血不仅可以提高临床治疗效果，而且还能降低并发症的发生率，值得临床推广使用。

Adrenomedullin in cirrhotic and non-cirrhotic portal hypertension

AIM:Adrenomedullin (ADM) is a potent vasodilator peptide. ADM and nitric oxide (NO) are produced in vascular endothelial cells.Increased ADM level has been linked to hyperdynamic circulation and arterial vasodilatation in cirrhotic portal hypertension (CPH).The role of ADM in non-cirrhotic portal hypertension (NCPH) is unknown,plasma ADM levels were studied in patients with NCPH,compensated and decompensated cirrhosis in order to determine its contribution to portal hypertension (PH) in these groups. METHODS:There were 4 groups of subjects.Group 1 consisted of 27 patients (F/M:12/15) with NCPH due to portal and/or splenic vein thrombosis (mean age:41±12 years),group 2 consisted of 14 patients (F/M:6/8) with compensated (Child-Pugh A) cirrhosis (mean age:46±4), group 3 consisted of 16 patients (F/M:6/10) with decompensated (Child-Pugh C) cirrhosis (mean age:47±12). Fourteen healthy subjects (F/M:6/8) (mean age:44±8) were used as controls in Group 4.ADM level was measured by ELISA.NO was determined as nitrite/nitrate level by chemoluminescence. RESULTS:ADM level in Group 1 (236±61.4 pg/mL) was significantly higher than that in group 2 (108.4±28.3 pg/mL) and group 4 (84.1±31.5 pg/mL) (both P<0.0001) but was lower than that in Group3 (324±93.7 pg/mL) (P=0.002).NO level in group 1 (27±1.4 μmol/L) was significantly higher than that in group 2 (19.8±2.8 μmol/L) and group 4 (16.9±1.6 μmol/L) but was lower than that in Group 3 (39±3.6 μmol/L) (for all three P<0.0001).A strong correlation was observed between ADM and NO levels (r=0.827,P<0.0001). CONCLUSION:Adrenomedullin and NO levels were high in both non-cirrhotic and cirrhotic portal hypertension and were closely correlated,Adrenomedullin and NO levels increased proportionally with the severity of cirrhosis,and were significantly higher than those in patients with NCPH. Portal hypertension plays an important role in the increase of ADM and NO.Parenchymal damage in cirrhosis may contribute to the increase in these parameters.

Serum omentin and vaspin levels in cirrhotic patients with and without portal vein thrombosis

AIMTo investigate serum omentin and vaspin levels in cirrhotic patients; and to assess the relationship of these levels with hemostatic parameters, metabolic abnormalities, cirrhosis severity and etiology.METHODSFifty-one cirrhotic patients (17 with portal vein thrombosis) were analyzed. Serum omentin and vaspin levels were measured with commercially available direct enzyme-linked immunosorbent assays (ELISAs). To assess platelet activity, the following tests were performed using a MULTIPLATE®PLATELET FUNCTION ANALYZER: (1) an ADP-induced platelet activation test; (2) a cyclooxygenase dependent aggregation test (ASPI test); (3) a von Willebrand factor and glycoprotein Ib-dependent aggregation (using ristocetin) test (RISTO test); and (4) a test for thrombin receptor-activating peptide-6 induced activation of the thrombin receptor, which is sensitive to IIb/IIIa receptor antagonists.RESULTSOmentin, but not vaspin, serum concentrations were significantly decreased in patients with portal vein thrombosis (PVT) (P = 0.01). Prothrombin levels were significantly increased in patients with PVT (P = 0.01). The thrombin receptor activating peptide (TRAP) test results were significantly lower in the PVT group (P = 0.03). No significant differences in adipokines serum levels were found regarding the etiology or severity of liver cirrhosis assessed according to the Child-Pugh or Model of End-Stage Liver Disease (MELD) scores. There was a significant increase in the TRAP (P = 0.03), ASPI (P = 0.001) and RISTO high-test (P = 0.02) results in patients with lower MELD scores. Serum omentin and vaspin levels were significantly down-regulated in patients without insulin resistance (P = 0.03, P = 0.02, respectively). A positive relationship between omentin and vaspin levels were found both when all of the patients were analyzed (r = 0.41, P = 0.01) and among those with PVT (r = 0.94, P < 0.001).CONCLUSIONSerum omentin levels are increased in patients without PVT. Cirrhosis origin and grade do not affect omentin and vaspin levels. The analyzed adipokines do not influence platelet activity.

Presence of columnar-lined esophagus is negatively associated with the presence of esophageal varices in Japanese alcoholic men

AIM To determine whether the presence of columnar-lined esophagus(CLE) is associated with the presence of esophageal varices(EVs) in male Japanese alcoholics. METHODS The subjects were 1614 Japanese alcohol-dependent men(≥ 40 years of age) who had undergone upper gastrointestinal endoscopic screening. Digitalized records of high-quality endoscopic images that included the squamocolumnar junction and esophagogastric junction were retrospectively jointly reviewed by four expert endoscopists for the purpose of diagnosing CLE. The authors investigated whether and to what extent there were associations between the presence of CLE and the presence of EVs, especially in the group with liver cirrhosis(LC).RESULTS CLE ≥ 5 mm in length was found in 355 subjects(≥ 30 mm in 6 of them), LC without EVs in 152 subjects, LC with EVs in 174 subjects, and EVs without LC in 6 subjects. Advanced EVs, i.e., nodular, large or coiled forms, red color sign, or post-treatment, were found in 88 subjects. The incidence of CLE ≥ 5 mm decreased in the following order(P < 0.0001): 23.3% in the group without EVs, 17.4% in the group with small and straight EVs, and 5.7% in the group with advanced EVs. The multivariate ORs(95%CI) for EVs and advanced EVs in the group with LC were lower when CLE ≥ 5 mm was present [0.46(0.23-0.93) and 0.24(0.08-0.74), respectively, vs 0-4 mm CLE]. CONCLUSION The presence of CLE in male Japanese alcoholics was negatively associated with the presence of EVs.

Attenuation of portal hypertension by natural taurine in rats with liver cirrhosis

AIM： To investigate the inhibitory effect of natural taurine （NTau） on portal hypertension （PHT） in rats with experimentally-induced liver cirrhosis （LC）. METHODS： Experimentally-induced LC Wistar rats （20 rats/group） were treated with either oral saline or oral NTau for 6 consecutive weeks. Evaluation parameters included portal venous pressure （PVP）, portal venous resistance （PVR）, portal venous flow （PVF）, splanchnic vascular resistance （SVR） and mean arterial pressure （NAP）. Vasoactive substance levels including nitric oxide （NO）, nitric oxide synthase （NOS） and cyclic guanosine monophosphate （cGMP） were also measured. Histological investigation of type Ⅰ and Ⅲ collagen （COL Ⅰ and Ⅲ） and transforming growth factor-β1 （TGF-β1） was also performed. RESULTS： Treatment with NTau （1） significantly decreased PVP, PVR and PVF, and increased MAP and SVP; （2） markedly increased the vascular compliance and reduced the zero-stress of the portal vein; （3） markedly decreased the amount of NO and cGMP and activity of NOS; and （4） improved the pathological status of the liver tissue and reduced the expression of COL Ⅰ, COL Ⅲ and TGF-β1. CONCLUSION： NTau inhibited the LC-induced PHT by improving hyperdynamic circulation, morphology of liver and biomechanical properties of the portal vein in experimentally-induced LC rats.

Ascites, refractory ascites and hyponatremia in cirrhosis

Ascites is the most common complication related to cirrhosis and is associated with increased morbidity and mortality.Ascites is a consequence of the loss of compensatory mechanisms to maintain the overall effective arterial blood volume due to worsening splanchnic arterial vasodilation as a result of clinically significant portal hypertension.In order to maintain effective arterial blood volume,vasoconstrictor and antinatriuretic pathways are activated,which increase overall sodiumand fluid retention.As a result of progressive splanchnic arterial vasodilation,intestinal capillary pressure increases and results in the formation of protein-poor fluid within the abdominal cavity due to increased capillary permeability from the hepatic sinusoidal hypertension.In some patients,the fluid can translocate across diaphragmatic fenestrations into the pleural space,leading to hepatic hydrothorax.In addition,infectious complications such as spontaneous bacterial peritonitis can occur.Eventually,as the liver disease progresses related to higher portal pressures,loss of a compensatory cardiac output and further splanchnic vasodilation,kidney function becomes compromised fromworsening renal vasoconstriction as well as the development of impaired solute-free water excretion and severe sodium retention.Thesemechanisms then translate into significant clinical complications,such as refractory ascites,hepatorenal syndrome and hyponatremia,and all are linked to increased short-termmortality.Currently,liver transplantation is the only curative option for this spectrumof clinical manifestations but ongoing research has led to further insight on alternative approaches.This review will further explore the current understanding on the pathophysiology andmanagement of ascites as well as expand on two advanced clinical consequences of advanced liver disease,refractory ascites and hyponatremia.