肝硬化患者胃生长素、瘦素水平的研究

检测肝硬化患者胃生长素(ghrelin)、瘦素的水平,探讨其与营养状态、肝硬化并发症的关系。测定45例肝硬化患者ghrelin、瘦素水平。病例组ghrelin水平显著性高于正常(P<0.05)。病例组瘦素水平显著性高于正常(P<0.01),并随Ch ild-Pugh分级而递增,其中B、C级与对照组相比,差异显著(P<0.05)。肝硬化患者ghrelin升高;瘦素参与了肝硬化时的营养不良。     

血清前白蛋白、胆碱酯酶对判断肝硬化患者肝储备功能及预后的临床价值

目的　评价血清前白蛋白 (PA)和胆碱酯酶 (ChE)与肝硬化患者的肝储备功能及其预后的关系。方法　测定 41例肝硬化患者和 19例健康人的PA和ChE活性 ,并按Child分级进行比较。结果　肝硬化组PA含量、ChE活性均较正常组显著降低 ;按Child分级比较 ,肝硬化组PA含量在A级与对照组、B级与A级之间差异无显著性 ,在C级与B级之间差异有显著性 (P <0 0 5 ) ;ChE活性在ChildA级与对照组、B级与A级、C级与B级之间差异有显著性 ;合并肝性脑病者 ,其ChE活性较合并上消化道出血者和腹水者显著下降。结论　血清PA含量和ChE活性可作为反映肝储备功能、判断肝病严重程度和预后的有意义的指标     

对肝肺综合征诊治的76例临床分析

目的:探讨肝肺综合征(HPS)的临床特点及诊断方法,提高对其认识。方法:回顾性分析76例HPS患者的临床资料,并与无HPS的133例肝硬化患者在肺功能、血气分析等方面进行比较。结果:在HPS组中除4例为慢性酒精性肝损害基础上的急性药物性肝炎外,72例均为肝硬化患者。临床表现为呼吸困难、紫绀、杵状指及蜘蛛痣。据Child-Pugh分级标准,肝功能B级和C级者59例(77.6%),平均PaO2为(79.93±11.29)mm Hg(1 mm Hg=0.133 kPa),对照组为(92.48±13.53)mm Hg,2组比较有统计学意义(P0.01)。HPS组中76例中有48例直立性缺氧10%(63.1%)。不同门静脉内径、有无蜘蛛痣、不同肝功能分级的PaO2和SaO2值比较,均有统计学意义(P0.01)。影像学检查结果示肺内血管扩张。结论:肝肺综合征的发生与肝功能不全有明显的关系,该病患者常有呼吸困难、紫绀、杵状指、蜘蛛痣及直立性缺氧等典型表现,患者低氧血症发生率高,而肺功能存在弥散功能障碍,肺血管有明显的扩张。     

肝硬化106例心电图改变

肝硬化失代偿期可出现许多并发症,其中心脏的损害为人们关注不多,这些病变可以影响患者的生活质量甚至危及生命。我们总结了106例在我院住院的肝硬化失代偿期患者,就其心电图改变总结报告如下。1对象和方法1.1对象选择2003年6月至2004年10月在我院消化内科住院的肝硬化患者共106(男68,女38)例。年龄31~78(平均52.6)岁。排除并发有高血压病、肺心病、冠心病、先天性心脏病、心肌炎、心肌病等心脏疾病。其中乙肝肝硬化85例,酒精性肝硬化18例,血吸虫性肝硬化2例,不明原因肝硬化1例。按肝功能Ch ild-Pugh分级;A级19例,B级41例,C级46例。伴有腹…     

肝硬化患者血氧水平的变化和意义

目的　探讨肝硬化合并低氧血症的发病机制、发生率及临床治疗效果。方法　用自动血气分析仪检测 2 0例正常者、5 0例肝硬化患者动脉血氧水平。结果　肝硬化组肺泡 动脉氧分压差 (AaDpO2 )显著高于对照组 ,动脉血氧分压 (PaO2 )明显低于对照组。肝性低氧血症的发生率是 5 4% ( 2 7/ 5 0 ) ,在肝功能ChildC级患者最为明显 ,肝性低氧血症与门脉高压、蜘蛛痣、杵状指 (趾 )密切相关。肝硬化ChildA级、B级患者常规治疗前后动脉血氧水平有显著差异。结论　肝硬化合并低氧血症与门脉高压和肺内血管扩张有关 ,检测动脉血氧水平有助于肝硬化预后判断和肝肺综合征(HPS)的诊断。相当一部分HPS患者的临床治疗效果欠佳。     

老年肝硬化患者血清恶性肿瘤生长因子和巨噬细胞抑制因子-1的水平

目的探讨老年肝硬化患者血清恶性肿瘤生长因子(TSGF)和巨噬细胞抑制因子(MIC)-1水平及其在肝硬化严重程度中的意义。方法选择老年乙型肝炎肝硬化患者120例作为肝硬化组(B组),根据肝功能Child-Pugh分级分为肝功能A级(48例)、肝功能B级(46例)、肝功能C级(26例)三个亚组;根据是否合并腹水分为肝硬化合并腹水(54例)和肝硬化不合并腹水(66例)两个亚组。选择同期120例健康体检者为对照组(A组)。采用Child-Pugh分级法进行肝功能分级。采用速率法测定血清TSGF水平。采用酶联免疫吸附试验(ELISA)测定血清MIC-1水平。结果 B组血清TSGF和MIC-1水平明显高于A组(P0.05)。与肝功能A级比较,肝功能B级和肝功能C级患者血清TSGF和MIC-1水平明显升高(均P0.05);与肝功能B级比较,肝功能C级患者血清TSGF和MIC-1水平明显升高(均P0.05)。有腹水组患者血清TSGF和MIC-1水平明显高于无腹水组(P0.05)。结论老年乙型肝炎肝硬化患者血清TSGF和MIC-1水平升高,升高水平与肝硬化的肝功能分级和是否存在腹水关系密切。     

肝硬化患者血清总胆汁酸测定的临床意义

目的 探讨肝硬化患者血清总胆汁酸测定的临床意义.方法 75例肝硬化患者Child-Pugh分级,A级28例,B级31例,C级16例,检测血清总胆汁酸水平,与49例正常体检者进行组间比较.结果 肝硬化各级(组)血清总胆汁酸水平均明显高于正常对照组(P<0.01),且其增高程度随Child-Pugh分级差异而不同.结论 总胆汁酸是评价肝硬化患者肝功能的重要指标.与Child-Pugh分级密切相关.     

肝脏瞬时弹性成像技术及血清肝纤维化指标在肝硬化中的评估作用

目的探讨肝脏瞬时弹性成像技术及血清肝纤维化指标在肝硬化中的评估价值。方法研究对象为青海省人民医院2017年9月～2018年3月收治的125例病毒性肝炎肝硬化患者,根据肝硬化Child-Pugh分级分为A级67例,B级32例,C级26例,另选取30例健康体检者作为对照组。检测所有研究对象的血清肝纤维化4项指标[透明质酸(HA)、层黏连蛋白(LN)、Ⅲ型前胶原(PCⅢ)、Ⅳ型胶原(Ⅳ-C)],并对所有肝硬化患者进行肝脏瞬时弹性成像检查。比较不同肝硬化Child-Pugh分级患者的肝纤维化4项指标及肝脏硬度值(LSM)。结果肝硬化Child-Pugh分级A、B、C级组患者血清HA、LN、PCⅢ、Ⅳ-C水平均显著高于对照组(P0.05),且肝纤维化4项指标血清水平随着肝硬化Child-Pugh分级的增加而明显升高,各组间比较差异均有统计学意义(P0.05)。肝硬化Child-Pugh分级A级患者LSM显著低于肝硬化Child-Pugh分级B级与C级,肝硬化Child-Pugh分级B级患者LSM又显著低于肝硬化Child-Pugh分级C级,三组比较有显著差异(P0.05)。通过对血清肝纤维化指标、LSM与Child-Pugh分级总分的Pearson相关分析得出,血清HA、LN、PCⅢ、Ⅳ-C、LSM水平与Child-Pugh分级总分呈正相关(P0.05)。结论肝硬化患者的肝硬化Child-Pugh分级越高,肝纤维化4项指标血清水平越高,LSM越大,肝脏瞬时弹性成像技术及血清肝纤维化指标可作为肝硬化严重程度评估的有效手段。     

肝硬化患者血清胆固醇、胆碱酯酶、总胆汁酸的变化及临床意义探讨

目的探讨肝硬化患者血清总胆固醇(Tch)、胆碱酯酶(ChE)、总胆汁酸(TBA)变化的临床意义。方法检测92例肝硬化患者及68例健康者的Tch、ChE及TBA水平。结果肝硬化组Tch、ChE水平低于对照组(P<0.05),TBA水平显著高于对照组(P<0.01),Tch、ChE在肝功能Child-Pugh分级C级中最低,TBA在C级中最高,与A级和B级相比存在显著性差异(P<0.01)。结论血清Tch、ChE、TBA能较准确地提示肝细胞的损害程度,判断肝硬化病情,估计预后。     

肝硬化患者血清转化生长因子β1 水平与Child-pugh分级的关系

为探讨肝硬化患者血清转化生长因子(TGF-β1)水平变化及与Child-Pugh分级的关系。用ELISA法测定了93例肝硬化患者及50例健康人血清TGF-β1水平。结果显示,肝硬化患者血清TGF-β1较对照组显著升高(P<0．01)且由Child A级到Child C级逐渐升高,各组间均有显著性差异(P<0．01)。提示血清TGF-β1是反映肝硬化患者肝功能损害程度的指标之一,可用于判断肝硬化患者肝功能损害程度及评价预后。     

肝肺综合征23例临床分析

目的提高对肝肺综合征(HPS)的临床认识,减少漏诊、误诊。方法回顾我院确诊的23例肝肺综合征病例,分析肝肺综合征的临床特点。结果肝肺综合征男、女发病比例为1.3∶1,平均年龄(42±21)岁,除1例急性重症肝炎外,其余22例均为肝硬化,门静脉高压发生率为82.6%。根据Child-Pugh分级标准,肝功能B、C级为78.2%。主要临床表现:呼吸困难发生率为91.3%,发绀为91.3%,肝掌为69.5%,杵状指(趾)为65.1%,面部血管扩张为56.5%,蜘蛛痣为56.5%。动脉血氧分压(PaO2)平均值为(50.8±14.1)mmHg(1mmHg=0.133kPa),直立性低氧血症发生率为85.7%(12/14),肺一氧化碳弥散量百分比(DLCO%)平均值为43.1%。39.1%(9/23)患者胸部X线检查表现为HPS而出现双下肺斑点状、小结节影或网状结节影。23例HPS均进行了99m锝-大颗粒聚合白蛋白(99mTc-MAA)核素首次通过肺灌注显像,平均分流率为36.3%。结论HPS主要发生于肝硬化Child-Pugh分级较重和(或)门静脉高压的患者。临床上对不能解释的低氧血症,同时有门静脉高压、蜘蛛痣(面部血管扩张)和(或)杵状指(趾)表现者应高度怀疑肝肺综合征。直立性低氧血症是HPS较特异性表现。HPS可有肺弥散功能降低、胸部影像学异常改变,但不具有特异性。99mTc-MAA核素首次通过肺灌注显像有助于确定肺血管扩张,明确HPS的诊断。     

Prognostic significance of the hepatopulmonary syndrome in patients with cirrhosis

BACKGROUND AND AIMS: The hepatopulmonary syndrome (HPS) has been defined by chronic liver disease, arterial deoxygenation, and widespread intrapulmonary vasodilation. Mortality of patients with HPS is considered to be high, but the effect of HPS on survival in patients with cirrhosis remains unclear. METHODS: A total of 111 patients with cirrhosis were studied prospectively by using transthoracic contrast echocardiography for detection of pulmonary vasodilation, blood gas analysis, and pulmonary function test. Twenty different clinical characteristics and survival times were noted. RESULTS: Twenty-seven patients (24%) had HPS. Their mortality was significantly higher (median survival, 10.6 months) compared with patients without HPS (40.8 mo, P < 0.05), even after adjusting for liver disease severity (2.9 vs. 14.7 months in Child-Pugh class C with [n = 15] and without HPS [n = 35, P < 0.05]; 35.3 vs. 44.5 months in Child-Pugh class B with [n = 7] and without HPS [n = 23, P = NS]), and exclusion of patients who underwent liver transplantation during follow-up (median survival 4.8 vs. 35.2 months, P = 0.005). Causes of death were mainly nonpulmonary and liver-related in the 19 patients with and the 35 patients without HPS who died. In multivariate analysis, HPS was an independent predictor of survival besides age, Child-Pugh class, and blood urea nitrogen. Mortality correlates with severity of HPS. CONCLUSIONS: The presence of HPS independently worsens prognosis of patients with cirrhosis. This should influence patient management and scoring systems and accelerate the evaluation process for liver transplantation.     

Hepatopulmonary syndrome - past to present

Hepatopulmonary syndrome (HPS) is the one of the complication of liver cirrhosis with portal hypertension, irrespective of etiology, age and sex. It has also been observed in non cirrhotic portal hypertension and in acute hepatic conditions. Presence of hypoxemia or abnormal alveolar arterial oxygen tension with intrapulmonary vasodilation in liver cirrhosis is termed as HPS. Contrast echocardiogram is the better screening tool to demonstrate intrapulmonary shunt. Clinicians should be aware of other common chronic pulmonary and cardiac comorbid conditions, in particular COPD, tuberculosis, bronchial asthma and idiopathic pulmonary fibrosis, etc. which may coexist with HPS. There is no specific clinical finding to diagnose but digital clubbing, cyanosis, dyspnoea, platypnoea, and spider naevi are more common among cirrhosis with HPS. The presence of HPS independently worsens prognosis of cirrhosis. Even though number of mechanisms have been proposed to explain arterial hypoxemia in HPS, role of nitric oxide is the major one along with cytokines. Liver transplantation is the choice of treatment though mortality is comparatively high. There is no still effective recommended medical therapy to reverse this condition and anti cytokine/ nitric oxide inhibitors, etc are under preliminary stage.     

Hepatopulmonary syndrome: prevalence and clinical profile.

BACKGROUND: The hepatopulmonary syndrome (HPS) is defined as a triad of liver dysfunction, intrapulmonary vascular dilatations (IPVD) and arterial hypoxemia. There is paucity of Indian studies regarding the prevalence of IPVD and arterial hypoxemia particularly amongst patients with non-cirrhotic portal fibrosis (NCPF) and extrahepatic portal vein obstruction (EHPVO), where liver dysfunction is not a feature. METHODS: All patients with portal hypertension and esophageal varices seen at a tertiary care hospital during 1995-98 were studied. Ultrasonography of abdomen, contrast-enhanced echocardiography (CEE), arterial blood gas analysis and assessment of alveolar-arterial oxygen gradient were done. RESULTS: Of 138 patients with portal hypertension seen during the study period, 88 fulfilled the inclusion and exclusion criteria. These included 63 with cirrhosis, 15 with NCPF and 10 with EHPVO. CEE showed IPVD in 17 (27%) patients with cirrhosis, of which 11 (17.5%) fulfilled the criteria for HPS. IPVD were also noted in 4 (26.6%) cases of NCPF and 3 (30%) of EHPVO, though only 2 (13.3%) and 1 (10%) respectively had elevated alveolar-arterial gradient and liver dysfunction in addition. Age and sex distribution and duration of symptoms were not different in patients with HPS. Patients with HPS had higher incidence of dyspnea, platypnea, clubbing and spider nevi. CONCLUSIONS: Hepatopulmonary syndrome is present in 17.5% of cirrhotics, 13.3% of patients with NCPF and 10% with EHPVO. Patients with HPS had significantly higher incidence of dyspnea, platypnea, clubbing and spider nevi.     

肝硬化患者门脉系统血流动力学指标与Child-Pugh分级的相关性研究

研究肝硬化患者脾静脉和门静脉血流量及其比值(Qsv/QPv)与肝脏储备功能Child-Pugh分级的关系.采用彩色多普勒超声仪对168例肝炎后肝硬化患者(ChildA级43例,B级67例,C级58例)和59例健康成年人检测了门静脉、脾静脉的内径、流速,再计算出相关的血流量,并进行了比较分析.结果显示,随着Qsv/Qpv的升高,肝硬化患者的肝功能不断下降,各组之间比较有非常显著性差异(P＜0.01).肝硬化患者肝功能损害越重,脾静脉血流量占门静脉血流量的比值越高.如果将Qsv/Qpv的截断值定于40%,则其提示肝硬化患者肝功能下降至B级或以下的敏感性、特异性、准确性分别达80.80%、74.42%和79.17%.彩色多普勒超声测量门静脉系统及其血流动力学指标用于判断肝硬化患者的肝功能状态是一个较好的临床手段.     

对肝肺综合征诊治的探讨

目的提高对肝肺综合征（ＨＰＳ）的认识。方法回顾性分析了６例ＨＰＳ的临床资料，所有患者均经动态肺灌注显像检查。结果６例ＨＰＳ的病因均为肝炎后肝硬化。除有肝病的临床表现外，还有进行性呼吸困难、紫绀（６／６）、杵状指（５／６）和低氧血症，平均动脉血氧分压为６．８７ｋＰａ（１ｋＰａ＝７．５ｍｍＨｇ），动脉血氧饱和度为８５．２％。此外，还有立位性缺氧或平卧呼吸。６例患者经动态肺灌注显像均异常，有肺内血管扩张。结论有门脉高压、皮下蜘蛛痣和杵状指体征时，提示ＨＰＳ的存在。早期诊断和治疗有助于缓解低氧血症，改善患者的预后。     

Clinical characteristics,predictors, and survival among patients with hepatopulmonary syndrome

Background. Hepatopulmonary syndrome (HPS) is a complication of advanced liver disease. The impact of HPS on survival is not clearly understood.Material and methods. A prospective study was carried out at Department of Medicine, King Edward Medical University Lahore from June 2011 to May 2012. Patients with cirrhosis of liver were evaluated for presence of HPS with arterial blood gas analysis and saline bubble echocardiography. All patients were followed for 6 months for complications and mortality. Cox regression analysis was done to evaluate role of HPS on patient survival.Results. 110 patients were included in the study. Twenty-nine patients (26%) had HPS. MELD score was significantly higher (p < 0.01) in patients with HPS (18.93 ± 3.51) as compared to that in patients without HPS (13.52 ± 3.3). Twenty two (75.9%) patients of Child class C, 5 (17.2%) patients of Child class B and 2 (6.9%) patients of Child class A had HPS (P 0.03). The clinical variables associated with presence of HPS were spider nevi, digital clubbing, dyspnea, and platypnea. HPS significantly increased mortality during six month follow up period (HR: 2.47, 95% CI: 1.10-5.55). Child-Pugh and MELD scores were also associated with increased mortality. HPS was no longer associated with mortality when adjustment was done for age, gender, Child-Pugh, and MELD scores (HR: 0.44, 95% CI: 0.14-1.41). Both the Child-Pugh and MELD scores remained significantly associated with mortality in the multivariate survival analysis.Conclusions. HPS indicates advanced liver disease. HPS does not affect mortality when adjusted for severity of cirrhosis.     

Correlations of MMP-2 and MMP-9 gene polymorphisms with the risk of hepatopulmonary syndrome in cirrhotic patients: A case-control study

Hepatopulmonary syndrome (HPS) increases the mortality of patients who suffered from liver cirrhosis, especially patients plagued by severe hypoxemia. Gene polymorphisms are reported to be related to the risk of HPS in cirrhotic patients. Thus, our study aims to elucidate the correlation between MMP-2 and MMP-9 gene polymorphisms and HPS in cirrhotic patients. A total of 152 cirrhotic patients suffering from HPS as well as another 152 cirrhotic patients without HPS were recruited. Polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) was performed for MMP-2 and MMP-9 gene polymorphisms and logistic regression analysis for the relationship between clinicopathological features and HPS occurrence in cirrhotic patients. There were significant differences in genotype and allele frequency of MMP-2 rs243865 and MMP-9 rs3918242 polymorphisms between the HPS and control groups. CC/CT genotype and C allele of MMP-2 rs243865 polymorphism as well as CC/TT genotype and T allele of MMP-9 rs3918242 polymorphism increased the risk of HPS in cirrhotic patients. Genotypes of rs243865 and rs3918242 polymorphisms had remarkable correlations with spider nevi, clubbed fingers (toes), transaminase elevation, portal vein width, esophageal varices, Child-Pugh classification and partial pressure of arterial oxygen (PaO₂). Logistic regression analysis showed that rs243865 and rs3918242 polymorphisms, spider nevi, clubbed fingers (toes), esophageal varices, and Child-Pugh classification were closely associated with the occurrence of HPS in cirrhotic patients. Our findings demonstrate that MMP-2 rs243865 polymorphism and MMP-9 rs3918242 polymorphism can increase the risk of HPS occurrence in cirrhotic patients, which provides a potential target for prevention of HPS in cirrhotic patients.     

肝硬化门脉高压症患者的十二指肠损害

目的探讨肝硬化门脉高压症患者十二指肠损害的发生率及其与肝硬化病程、门脉高压性胃病、肝功能分级的关系。方法对72例肝硬化门脉高压症患者进行胃镜检查,观察十二指肠粘膜病变,同时检测14C呼气试验。另选72例接受胃镜检查的非肝硬化门脉高压患者为对照组。结果肝硬化门脉高压症患者十二指肠糜烂发生率为41.7%,随肝硬化病程延长和肝功能分级差而增高,而幽门螺杆菌感染率与对照组无显著性相差(P>0.05)。糜烂主要发生于十二指肠降部,糜烂轻重程度与肝功能分级无关(P>0.05)。结论肝硬化门脉高压症患者十二指肠糜烂与非特异性十二指肠炎不同,是门脉高压导致十二指肠的一种病变。