血吸虫性门脉纤维化及肝实质纤维化程度与门脉内径的关系

在湖南省洞庭湖血吸虫病重度流行区以B超检测高频率暴露渔民的门脉及肝实质纤维化程度以及门脉内径，分析其相关性。结果表明血吸虫性门脉纤维化及肝实质纤维化程度与门脉内径大小成正相关，相关系数分别为0.375和0.332，具有显著性意义。作者认为门脉内径可以作为评估血吸虫病患者肝损程度的指标。     

Long-term Follow-up of a Patient with Portal Hypertension and Hepatic Failure Due to Hepatic Hydatid Disease

We observed liver failure with a presumed etiology of echinococcosis in an 89-year-old woman. Our patient had been born and then resided on Rebun Island until she was 12 years old. At 46 years old, she had been referred to our hospital due to right abdominal pain. Ultrasound had revealed multilocular cysts in the right lobe of the liver. At 84 years old, the hepatic cyst occupied nearly the entire liver with ring-shaped calcification along the cyst wall. The patient was diagnosed with decompensated cirrhosis and hepatic hydatid disease based on typical imaging and the long-term natural clinical course.     

Portal Hypertension and Esophageal Varices in Cystic Fibrosis: Unreliability of Echo-Doppler Flowmetry

To investigate the role of echo-Doppler flowmetry in evaluating patients with cystic fibrosis and portal hypertension at risk of esophageal varices, we studied 26 subjects divided in 3 groups: 9 with portal hypertension and esophageal varices, 8 with chronic liver disease without varices, and 9 without chronic liver disease. Spleen size, diameter, blood velocity, and flow rate of portal, splenic, and superior mesenteric veins were recorded. In patients without chronic liver disease Doppler measurements were repeated on 2 different days to assess intraobserver variability. Significant differences among the three groups were found for mean values of spleen size and diameters of portal, splenic, and superior mesenteric veins. Nevertheless, a considerable overlapping of individual data was observed. No differences were observed in mean hemodynamic measurements, except for blood velocity in portal vein and flow rate in splenic vein. The intraobserver variability for repeated Doppler measurements was clinically unacceptable for most of the variables studied. Echo-Doppler assessment of splanchnic flow seems to be an unreliable tool in the management of cystic fibrosis patients with portal hypertension at risk of esophageal varices.     

肝硬化门脉高压患者血浆SS、VIP及MTL变化的临床意义

目的　研究生长抑素(SS)、血管活性肠肽(VIP)、胃动素(MTL)在门脉高压症中的水平及其作用。方法　应用放射免疫学方法对 62例肝硬化门脉高压症患者、51例正常对照者血浆及 43份门脉高压性腹水进行SS、VIP与MTL的检测。结果　门脉高压症组血浆SS、VIP与MTL水平分别为 58 23±13 5pg/ml, 18 68±4 22pg/ml及 362 95±32 82pg/ml;正常对照组分别为 81 23±31 89pg/ml, 11 96±3 27pg/ml及 202 95±26 42pg/ml,二者差异有显著性(P<0 05)。腹水组分别为 148 03±28 41pg/ml, 14 12±3 64pg/ml及 267 43±29 04pg/ml。腹水SS、MTL高于对照组血浆含量(P<0 05)。腹水VIP与对照组血浆含量差异无显著性。肝硬化腹水患者血浆SS低于无腹水者,而VIP与MTL水平高于无腹水者(P<0 05)。VIP、MTL随着肝功能分级的发展而逐步增加。结论　血浆SS、VIP与MTL在肝硬化门脉高压症的病理生理机制中起着重要作用。     

Correlation of hepatic venous pressure gradient with variceal bleeding, size of esophageal varices, etiology, ascites and degree of liver dysfunction in cirrhosis of liver

An elevated hepatic venous pressure gradient (HVPG) has been associated with risk of variceal bleeding, and outcome and survival after variceal bleeding. In this pilot study, we measured HVPG in 40 patients with liver cirrhosis and studied its relationship with etiology of liver disease, esophageal variceal size, history of variceal bleeding or ascites, biochemical liver tests and Child-Pugh class. There was no procedurerelated complication. The mean (SD) HVPG was similar in patients who had history of variceal bleeding as compared to those who did not (15.4 [2.8] mmHg vs. 13.9 [2.7] mmHg, p=0.1); HVPG had no significant association with etiology of cirrhosis (p=0.4). HVPG levels were significantly higher in patients with larger esophageal varices (grade III/IV vs. I/II: 15.2 [2.7] mmHg vs.13.1 [2.8] mmHg, p=0.04), poorer Child-Pugh class (B or C versus A), and presence of ascites (p=0.04). Thus, HVPG correlated with variceal size, Child-Pugh class, and presence of ascites, but not with variceal bleeding status.     

Portal vein thrombosis,mortality and hepatic decompensation in patients with cirrhosis: A meta-analysis

AIM: To determine the clinical impact of portal vein thrombosis in terms of both mortality and hepatic decompensations (variceal hemorrhage, ascites, portosystemic encephalopathy) in adult patients with cirrhosis.METHODS: We identified original articles reported through February 2015 in MEDLINE, Scopus, Science Citation Index, AMED, the Cochrane Library, and relevant examples available in the grey literature. Two independent reviewers screened all citations for inclusion criteria and extracted summary data. Random effects odds ratios were calculated to obtain aggregate estimates of effect size across included studies, with 95%CI.RESULTS: A total of 226 citations were identified and reviewed, and 3 studies with 2436 participants were included in the meta-analysis of summary effect. Patients with portal vein thrombosis had an increased risk of mortality (OR = 1.62, 95%CI: 1.11-2.36, P = 0.01). Portal vein thrombosis was associated with an increased risk of ascites (OR = 2.52, 95%CI: 1.63-3.89, P < 0.001). There was insufficient data available to determine the pooled effect on other markers of decompensation including gastroesophageal variceal bleeding or hepatic encephalopathy.CONCLUSION: Portal vein thrombosis appears to increase mortality and ascites, however, the relatively small number of included studies limits more generalizable conclusions. More trials with a direct comparison group are needed.     

Portal hypertensive gastropathy: A systematic review of the pathophysiology,clinical presentation,natural history and therapy

AIM: To describe the pathophysiology, clinical presentation, natural history, and therapy of portal hypertensive gastropathy(PHG) based on a systematic literature review.METHODS: Computerized search of the literature was performed via Pub Med using the following medical subject headings or keywords: "portal" and "gastropathy"; or "portal" and "hypertensive"; or "congestive" and "gastropathy"; or "congestive" and "gastroenteropathy". The following criteria were applied for study inclusion: Publication in peer-reviewed journals, and publication since 1980. Articles were independently evaluated by each author and selected for inclusion by consensus after discussion based on the following criteria: Well-designed, prospective trials; recent studies; large study populations; and study emphasis on PHG. RESULTS: PHG is diagnosed by characteristic endoscopic findings of small polygonal areas of variable erythema surrounded by a pale, reticular border in a mosaic pattern in the gastric fundus/body in a patient with cirrhotic or non-cirrhotic portal hypertension. Histologic findings include capillary and venule dilatation, congestion, and tortuosity, without vascular fibrin thrombi or inflammatory cells in gastric submucosa. PHG is differentiated from gastric antral vascular ectasia by a different endoscopic appearance. The etiology of PHG is inadequately understood. Portal hypertension is necessary but insufficient to develop PHG because many patients have portal hypertension without PHG.PHG increases in frequency with more severe portal hypertension, advanced liver disease, longer liver disease duration, presence of esophageal varices, and endoscopic variceal obliteration. PHG pathogenesis is related to a hyperdynamic circulation, induced by portal hypertension, characterized by increased intrahepatic resistance to flow, increased splanchnic flow, increased total gastric flow, and most likely decreased gastric mucosal flow. Gastric mucosa in PHG shows increased susceptibility to gastrotoxic chemicals and poor wound healing. Nitrous oxide, free radicals, tumor necrosis factor-alpha, and glucagon may contribute to PHG development. Acute and chronic gastrointestinal bleeding are the only clinical complications. Bleeding is typically mild-to-moderate. Endoscopic therapy is rarely useful because the bleeding is typically diffuse. Acute bleeding is primarily treated with octreotide, often with concomitant proton pump inhibitor therapy, or secondarily treated with vasopressin or terlipressin. Nonselective β-adrenergic receptor antagonists, particularly propranolol, are used to prevent bleeding after an acute episode or for chronic bleeding. Iron deficiency anemia from chronic bleeding may require iron replacement therapy. Transjugular-intrahepaticportosystemic-shunt or liver transplantation is highly successful ultimate therapies because they reduce the underlying portal hypertension.CONCLUSION: PHG is important to recognize in patients with cirrhotic or non-cirrhotic portal hypertension because it can cause acute or chronic GI bleeding that often requires pharmacologic therapy.     

Transjugular Intrahepatic Portosystemic Shunt does not affect the efficacy and safety of direct-acting antivirals in patients with advanced cirrhosis: A real-life,case-control study

BackgroundTransjugular Intrahepatic Portosystemic Shunt (TIPS) is a well-established treatment for complications of portal hypertension.AimsTo analyze the impact of TIPS on virologic response and safety profile in patients treated with direct-acting antivirals (DAAs).MethodsWe analyzed data from HCV-positive cirrhotic patients treated with DAAs. Twenty-one patients with previous TIPS placement were compared with 42 matched subjects without TIPS. Logistic regression was used to identify predictors of hepatic function worsening and adverse events.ResultsNo differences were found between the two groups in particular regarding sustained virologic response (92.5 and 97.6% in TIPS vs no-TIPS, p = 0.559). Model for End-stage Liver Disease (MELD) of both TIPS and no-TIPS groups declined from baseline to week 24 of follow-up (from 12.5 ± 3.5 to 10.8 ± 3.4 and from 11.1 ± 3.5 to 10.3 ± 3.4, p = 0.044 and 0.025). There were no differences in adverse event rates. At univariate analysis, age was associated with MELD increase from baseline to week 24 (OR 1.111, 95% CI 1.019-1.211, p = 0.017), and patients with higher baseline MELD developed serious adverse events more frequently (OR 0.815, 95% CI 0.658–1.010, p = 0.062). Patients with or without TIPS did not show differences in transplant-free survival.ConclusionTIPS placement does not affect virologic response and clinical outcome of patients receiving DAAs.     

Distinctive aspects of peptic ulcer disease,Dieulafoy's lesion,and Mallory-Weiss syndrome in patients with advanced alcoholic liver disease or cirrhosis

AIM: To systematically review the data on distinctive aspects of peptic ulcer disease (PUD), Dieulafoy’s lesion (DL), and Mallory-Weiss syndrome (MWS) in patients with advanced alcoholic liver disease (aALD), including alcoholic hepatitis or alcoholic cirrhosis. METHODS: Computerized literature search performed via PubMed using the following medical subject heading terms and keywords: “alcoholic liver disease”, “alcoholic hepatitis”,“ alcoholic cirrhosis”, “cirrhosis”, “liver disease”, “upper gastrointestinal bleeding”, “non-variceal upper gastrointestinal bleeding”, “PUD”, ‘‘DL’’, ‘‘Mallory-Weiss tear”, and “MWS’’. RESULTS: While the majority of acute gastrointestinal (GI) bleeding with aALD is related to portal hypertension, about 30%-40% of acute GI bleeding in patients with aALD is unrelated to portal hypertension. Such bleeding constitutes an important complication of aALD because of its frequency, severity, and associated mortality. Patients with cirrhosis have a markedly increased risk of PUD, which further increases with the progression of cirrhosis. Patients with cirrhosis or aALD and peptic ulcer bleeding (PUB) have worse clinical outcomes than other patients with PUB, including uncontrolled bleeding, rebleeding, and mortality. Alcohol consumption, nonsteroidal anti-inflammatory drug use, and portal hypertension may have a pathogenic role in the development of PUD in patients with aALD. Limited data suggest that Helicobacter pylori does not play a significant role in the pathogenesis of PUD in most cirrhotic patients. The frequency of bleeding from DL appears to be increased in patients with aALD. DL may be associated with an especially high mortality in these patients. MWS is strongly associated with heavy alcohol consumption from binge drinking or chronic alcoholism, and is associated with aALD. Patients with aALD have more severe MWS bleeding and are more likely to rebleed when compared to non-cirrhotics. Pre-endoscopic management of acute GI bleeding in patients with aALD unrelated to portal hypertension is similar to the management of aALD patients with GI bleeding from portal hypertension, because clinical distinction before endoscopy is difficult. Most patients require intensive care unit admission and attention to avoid over-transfusion, to correct electrolyte abnormalities and coagulopathies, and to administer antibiotic prophylaxis. Alcoholics should receive thiamine and be closely monitored for symptoms of alcohol withdrawal. Prompt endoscopy, after initial resuscitation, is essential to diagnose and appropriately treat these patients. Generally, the same endoscopic hemostatic techniques are used in patients bleeding from PUD, DL, or MWS in patients with aALD as in the general population. CONCLUSION: Nonvariceal upper GI bleeding in patients with aALD has clinically important differences from that in the general population without aALD, including: more frequent and more severe bleeding from PUD, DL, or MWS.     

The Sequential Application of Baveno VII Criteria and VITRO Score Improves Diagnosis of Clinically Significant Portal Hypertension

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Two-Step Strategy,FIB-4 Followed by Magnetic Resonance Elastography,for Detecting Advanced Fibrosis in NAFLD

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Mortality Outcomes by Fibrosis Stage in Nonalcoholic Fatty Liver Disease: A Systematic Review and Meta-analysis

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Liver Stiffness by Magnetic Resonance Elastography Predicts Future Cirrhosis,Decompensation, and Death in NAFLD

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