Gastrointestinal Hemorrhage ; drug therapy ; etiology ; prevention & control ; Humans ; Hypertension, Portal ; complications

A major cause of cirrhosis related morbidity and mortality is the development of variceal bleeding, a direct consequence of portal hypertension. Less common causes of gastrointestinal bleeding are peptic ulcers, malignancy, angiodysplasia, etc. Upper gastrointestinal bleeding has been classified according to the presence of a variceal or non-variceal bleeding. Although non-variceal gastrointestinal bleeding is not common in cirrhotic patients, gastroduodenal ulcers may develop as often as non-cirrhotic patients. Ulcers in cirrhotic patients may be more severe and less frequently associated with chronic intake of non-steroidal anti-inflammatory drugs, and may require more frequently endoscopic treatment. Portal hypertensive gastropathy (PHG) refers to changes in the mucosa of the stomach in patients with portal hypertension. Patients with portal hypertension may experience bleeding from the stomach, and pharmacologic or radiologic interventional procedure may be useful in preventing re-bleeding from PHG. Gastric antral vascular ectasia (GAVE) seems to be different disease entity from PHG, and endoscopic ablation can be the first-line treatment.
Gastric Antral Vascular Ectasia/complications ; Gastric Mucosa/pathology ; Gastrointestinal Hemorrhage/*etiology ; Humans ; Hypertension, Portal/*complications/prevention & control ; Liver Cirrhosis/complications ; Peptic Ulcer/complications

INTRODUCTIONHepatic venous pressure gradient (HVPG) measurement is recommended for prognostic and therapeutic indications in centres with adequate resources and expertise. Our study aimed to evaluate the quality of HVPG measurements at our centre before and after introduction of a standardised protocol, and the clinical relevance of the HVPG to variceal bleeding in cirrhotics.

METHODSHVPG measurements performed at Singapore General Hospital from 2005-2013 were retrospectively reviewed. Criteria for quality HVPG readings were triplicate readings, absence of negative pressure values and variability of ≤ 2 mmHg. The rate of variceal bleeding was compared in cirrhotics who achieved a HVPG response to pharmacotherapy (reduction of the HVPG to < 12 mmHg or by ≥ 20% of baseline) and those who did not.

RESULTS126 HVPG measurements were performed in 105 patients (mean age 54.7 ± 11.4 years; 55.2% men). 80% had liver cirrhosis and 20% had non-cirrhotic portal hypertension (NCPH). The mean overall HVPG was 13.5 ± 7.2 mmHg, with a significant difference between the cirrhosis and NCPH groups (p < 0.001). The proportion of quality readings significantly improved after the protocol was introduced. HVPG response was achieved in 28 (33.3%, n = 84) cirrhotics. Nine had variceal bleeding over a median follow-up of 29 months. The rate of variceal bleeding was significantly lower in HVPG responders compared to nonresponders (p = 0.025).

CONCLUSIONThe quality of HVPG measurements in our centre improved after the introduction of a standardised protocol. A HVPG response can prognosticate the risk of variceal bleeding in cirrhotics.

Esophageal and Gastric Varices ; complications ; physiopathology ; Female ; Follow-Up Studies ; Gastrointestinal Hemorrhage ; etiology ; physiopathology ; prevention & control ; Humans ; Hypertension, Portal ; complications ; physiopathology ; Liver Cirrhosis ; complications ; physiopathology ; Male ; Middle Aged ; Portal Pressure ; physiology ; Prognosis ; Retrospective Studies

OBJECTIVETo determine the effectiveness of timolol in preventing first variceal hemorrhage in portal hypertensive patients with esophageal varices.

METHODSA total of 42 cirrhotic patients with esophageal varices were enrolled in this study and received timolol or band ligation therapy randomly,with 21 patients in each group. The diameters of portal vein (PV), superior mesenteric vein (SMV), and splenic vein (SPV) as well as the portal venous flow and the splenic venous flow were measured. The first esophageal variceal bleeding of the two groups was recorded.

RESULTSThe diameters of PV, SMV, and SPV as well as the flow of PV and SPV showed no significant difference before and after treatment in band ligation group (P>0.05). In timolol group,however,the diameter of portal vein significantly decreased after treatment [(14.11±2.96) mm vs. (12.15±1.61)mm, P<0.05], and the average blood flow of portal vein also significantly decreased after treatment [(1277.33±495.19) ml/min vs. (719.17±245.16)ml/min, P<0.05]. Both timolol and band ligation effectively prevented esophageal variceal bleeding, and the risk of first esophageal variceal bleeding in these two groups were not significantly different (15% vs. 10%, P<0.05).

CONCLUSIONSTimolol is safe and effective in preventing the first variceal bleeding in portal hypertensive patients with esophageal varices.

Adult ; Aged ; Female ; Gastrointestinal Hemorrhage ; etiology ; prevention & control ; Humans ; Hypertension, Portal ; complications ; Ligation ; Male ; Middle Aged ; Timolol ; therapeutic use ; Young Adult

OBJECTIVETo investigate reason and the management of portal vein thrombosis in patients with portal hypertension postoperatively.

METHODS329 patients with portal hypertension in liver cirrhosis who had splenectomy was reviewed from 1992 to 2001. In whom 43 (13.1%) patients with portal vein thrombosis postoperative were analyzed.

RESULTSIn these patients, except 1 died for portal vein phlebitis, all patients were recovered. There are 138 patients who underwent splenectomy or splenectomy and devascularization, 26 (18.8%) of them had thrombosis. 191 patients underwent splenectomy and portacaval or portasplenic shut, 17 (8.9%) of them had thrombosis. The data of these two groups have significant difference (chi(2) = 8.44, P < 0.01).

CONCLUSIONSThrombocytosis postsplenectomy as well as the changes of portal hemodynamics is the main reason of portal vein thrombosis. Portal vein thrombosis is also in association with the operative ways. Operation standardization, dynamic examining platelet count, routine color ultrasonography examining and early anticoagulation therapy are the effective methods in preventing and managing portal thrombosis postoperation for portal hypertension.

Adult ; Budd-Chiari Syndrome ; etiology ; prevention & control ; therapy ; Female ; Follow-Up Studies ; Humans ; Hypertension, Portal ; surgery ; Male ; Middle Aged ; Portal Vein ; pathology ; Postoperative Complications ; Vascular Surgical Procedures ; adverse effects ; methods

Adrenergic beta-Antagonists ; therapeutic use ; Antiviral Agents ; therapeutic use ; Esophageal and Gastric Varices ; etiology ; prevention & control ; Gastrointestinal Hemorrhage ; diagnosis ; etiology ; prevention & control ; Gastroscopy ; Hemostasis, Endoscopic ; methods ; Hemostatic Techniques ; Hemostatics ; therapeutic use ; Humans ; Hypertension, Portal ; complications ; Liver Cirrhosis ; complications

Esophageal and Gastric Varices ; complications ; Gastrointestinal Hemorrhage ; etiology ; surgery ; Hepatic Encephalopathy ; epidemiology ; etiology ; prevention & control ; Hepatorenal Syndrome ; etiology ; surgery ; Humans ; Hypertension, Portal ; complications ; surgery ; Portasystemic Shunt, Transjugular Intrahepatic ; adverse effects ; methods ; Postoperative Complications ; Treatment Outcome

Animals ; Antihypertensive Agents ; therapeutic use ; Esophageal and Gastric Varices ; complications ; prevention & control ; Gastroscopy ; Hepatic Stellate Cells ; metabolism ; Humans ; Hypertension, Portal ; diagnosis ; etiology ; therapy ; Liver Cirrhosis ; complications ; Portasystemic Shunt, Transjugular Intrahepatic

OBJECTIVE: To investigate variations of plasma endothelin (ET) and its clinical significance in portal hypertensive patients with esophageal variceal hemorrhage. METHODS: Sixty-six patients with portal hypertension were randomly divided into 2 groups. Group I (32 patients) received general therapy and Group II (34 patients) received general therapy and UTI after hemorrhage. The plasma ET concentration and liver function were determined at 1, 2, 4, 7, 10, and 14 d after the hemorrhage. Another 20 patients without the hemorrhage were elected as the control group. RESULTS: At 7 and 14 d after the hemorrhage, the levels of TBIL, ALT and AST were elevated at first and then decreased in Groups I and II. The decrease of TBIL, ALT and AST levels was significantly faster in Group II than in Group I (P < 0.05, P < 0.01, P < 0.05, respectively) on 14 d after the hemorrhage. At 1 d after the hemorrhage the ET concentration was markedly increased in Group I and II as compared with the control group (P < 0.01). Then it was gradually decreased on 10 d after the hemorrhage. The ET concentration in Group II was decreased more rapidly than that in Group I on 2, 4 and 7 d after the hemorrhage (P < 0.05; P < 0.01; P < 0.05, respectively). The ET concentration was positively correlated to TBIL levels in groups I and II (r = 0.734, P < 0.01). And the decreased index of ET concentration was negatively correlated to the increased index of TBIL (r = -0.486, P < 0.05). CONCLUSION The increased plasma ET in portal hypertensive patients with hemorrhage may contribute to liver injury. UTI can protect the liver function by inhibiting ALT, AST, TBIL and ET level.
Adult ; Aged ; Endothelin-1 ; blood ; Esophageal and Gastric Varices ; blood ; etiology ; Female ; Glycoproteins ; therapeutic use ; Humans ; Hypertension, Portal ; blood ; complications ; Liver Failure ; prevention & control ; Male ; Middle Aged ; Trypsin Inhibitors ; therapeutic use