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Query: UMLS:C0341503 (bacterial peritonitis)
1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In cirrhotic patients under pharmacologic treatment for portal hypertension, a reduction in hepatic venous pressure gradient (HVPG) of >or=20% of baseline or to <or=12 mm Hg markedly reduces the risk of variceal rebleeding. This study was aimed at evaluating whether these hemodynamic targets also prevent other complications of portal hypertension and improve long-term survival. One hundred five cirrhotic patients included in prospective trials for the prevention of variceal rebleeding were studied. Seventy-three of the patients had 2 separate HVPG measurements, at baseline and under pharmacologic therapy with propranolol +/- isosorbide mononitrate. Patients were followed for up to 8 years. Survival and risk of developing portal hypertension-related complications were compared between responders and nonresponders. Twenty-eight patients showed a reduction of HVPG >or=20% of baseline or to <or=12 mm Hg (responders), and 45 patients were nonresponders. Nonresponders had a significantly greater risk of developing variceal rebleeding (P =.013), ascites (P =.025), spontaneous bacterial peritonitis (P =.003), hepatorenal syndrome (P =.026), and hepatic encephalopathy (P =.024) than responders. Eight-year cumulative probability of survival was significantly lower in nonresponders than in responders (52% vs. 95%, respectively, P =.003). At multivariate analysis, being a nonresponder was independently associated with the risk of developing rebleeding, ascites, spontaneous bacterial peritonitis, and lower survival. In conclusion, in cirrhotic patients receiving pharmacologic treatment for prevention of variceal rebleeding, a decrease in HVPG >or=20% or to <or=12 mm Hg is associated with a marked reduction in the long-term risk of developing complications of portal hypertension and with improved survival.
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PMID:Hemodynamic response to pharmacological treatment of portal hypertension and long-term prognosis of cirrhosis. 1266 85

The aim of the study was to determine the prevalence and detailed data concerning the incidence of spontaneous bacterial peritonitis in the Czech Republic. Ninety-nine patients with liver cirrhosis and ascites were examined. Spontaneous bacterial peritonitis was diagnosed in 35 patients (35.4%). It was revealed more often in patients with alcoholic aetiology of cirrhosis whose anamnesis involved sub-febrile or febrile states and the deterioration of ascites. Elevated serum leucocyte counts and increased levels of C-reactive protein can contribute to the diagnosis. A low level of total protein and albumin in ascites predisposes to the increase of this infection. The reduction of the platelet count in a set of patients with spontaneous bacterial peritonitis indicates the influence of portal hypertension in the aetiology of the disease.
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PMID:Spontaneous bacterial peritonitis in the Czech Republic: prevalence and aetiology. 1281 4

Portal hypertension as a consequence of liver cirrhosis is responsible for its most common complications: ascites, spontaneous bacterial peritonitis, hepatorenal syndrome, hepatic encephalopathy and the most important one--variceal hemorrhage. Variceal bleeding results in considerable morbidity and mortality. This review covers all areas of importance in the therapy of acute variceal hemorrhage--endoscopic and pharmacological treatment, transjugular intrahepatic portosystemic shunt, surgery and balloon tamponade. Indications and limitations of these therapeutic modalities are widely discussed.
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PMID:Management of acute variceal bleeding. 1283 94

Patients with cirrhosis of the liver are at high risk of a large variety of complications. Especially the development of portal hypertension, followed by gastroesophageal varicosis and ascites are potentially life threatening problems. In the treatment of gastroesophageal varicosis primary prophylaxis to prevent a first bleeding episode, acute therapy for bleeding varices, and secondary prophylaxis to prevent patients from rebleeding have to be considered. While treating patients with ascites the high frequency of side effects induced by diuretics has to be taken into account. In addition, the diagnosis of spontaneous bacterial peritonitis must not be missed. Hepatorenal syndrome, a typical complication of advanced cirrhosis is especially difficult to treat and is considered an indication for liver transplantation.
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PMID:[Complications of liver cirrhosis: portal hypertension, gastroesophageal varices and ascites]. 1452 28

The gut flora plays an important role in the pathogenesis of the complications of cirrhosis. Cirrhotic patients are prone to develop bacterial infections, mainly the 'spontaneous' infection of ascites or spontaneous bacterial peritonitis. Other complications of cirrhosis, such as variceal haemorrhage and ascites, occur mostly or solely as a consequence of portal hypertension. Portal pressure increases initially as a consequence of an increased intrahepatic resistance but, once collaterals have formed, high portal pressure is maintained by an increased splanchnic blood inflow secondary to vasodilatation. Splanchnic vasodilatation is the initiating event in the hyperdynamic circulatory state that aggravates the complications of cirrhosis. The gut flora plays a role in both the development of infections and in the hyperdynamic circulatory state of cirrhosis and, although less prominently, it also plays a role in the pathogenesis of hepatic encephalopathy. This chapter presents evidence regarding gut flora and its modification in the pathogenesis and management of these complications of cirrhosis.
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PMID:Gut microflora in the pathogenesis of the complications of cirrhosis. 1512 75

Patients with cirrhosis and ascites show systemic and splanchnic arterial vasodilation, which causes a reduction in effective arterial blood volume and the activation of hormonal anti-natriuretic systems. Renal impairment is the most important predictor of hospital mortality in cirrhotic patients with SBP. In patients with SBP, the inflammatory response to the infection (TNF-alpha, IL-6) may be an important mechanism of renal dysfunction. Ascitic-fluid NO metabolites are related independently to the development of renal impairment. Treatment of SBP with intravenous albumin in addition to cefotaxime prevents renal impairment and reduces mortality in comparison with treatment with cefotaxime alone. As soon as ascites develops, liver transplantation should be considered in eligible patients, especially when local mean waiting times exceed life expectancy. Nitric oxide (NO), tumour necrosis factor alpha (TNF-alpha) and interleukin-6 (IL-6) have been implicated in the pathogenesis of circulatory alterations observed in cirrhotic patients with ascites. Kidney failure is one of the main factors associated with mortality in patients with end-stage liver disease developing complications, particularly severe infections and variceal haemorrhage. Renal impairment occurs in patients with the highest concentration of cytokines in plasma and ascitic fluid and is associated with marked activation of the renin-angiotensin system. In patients with spontaneous bacterial peritonitis (SBP), serum and ascitic fluid levels of NO metabolites (nitrites and nitrates) were higher than those of patients with sterile ascites, and renal impairment is considered to be caused by a decrease in effective arterial blood volume as a result of the infection. The administration of albumin prevents deterioration of renal function and reduces mortality in these patients. However, SBP and renal dysfunction are late complications in the course of liver cirrhosis. As soon as ascites develops, liver transplantation should be considered in eligible patients, especially when local mean waiting times exceed life expectancy. A better knowledge of metabolic disorders associated with the early stage of cirrhosis is essential for the development of optimal therapeutic strategies for the prophylaxis and treatment of portal hypertension and its complications.
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PMID:Nitric oxide and renal function in cirrhotic patients with ascites: from physiopathology to practice. 1516 58

Gastrointestinal dysfunction in patients with cirrhosis may contribute to complications such as malnutrition and spontaneous bacterial peritonitis. To determine whether cirrhotic patients with ascites have altered intestinal function, we compared intestinal permeability and absorption in patients with liver disease and normal subjects. Intestinal permeability and absorption were investigated in 66 cirrhotic patients (48 with ascites, 18 without ascites) and 74 healthy control subjects. Timed recovery of 3-O-methyl-D-glucose, D-xylose, L-rhamnose, and lactulose in urine following oral administration was measured in order to assess active and passive carrier-mediated, and nonmediated, absorptive capacity, as well as intestinal large-pore/small-pore (lactulose/rhamnose) permeability. Test sugars were measured by quantitative thin-layer chromatography and results are expressed as a percentage of test dose recovered in a 5-h urine collection. Sugar excretion ratios relating to small intestinal permeability (lactulose/rhamnose) and absorption (rhamnose/3-O-methyl-D-glucose) were calculated to avoid the effects of nonmucosal factors such as renal clearance, portal hypertension, and ascites on the recovery of sugar probes in urine. Compared with normal subjects, the mean lactulose/rhamnose permeability ratio in cirrhotic patients with ascites was significantly higher (0.058 vs. 0.037, P < 0.001) but not in cirrhotic patients without ascites (0.041 vs. 0.037). Cirrhotic patients with ascites had significantly lower mean recoveries of 3-O-methyl-D-glucose (23.0 vs. 49.1%; P < 0.001), D-xylose (18.8 vs. 34.5%; P < 0.001), L-rhamnose (4.0 vs. 9.1%; P < 0.001), and lactulose (0.202 vs. 0.337%; P < 0.001) than normal subjects. However, the mean rhamnose/3-O-methyl-D-glucose ratio was the same in cirrhotic patients with ascites as normal subjects (0.189 vs. 0.189), indicating that the reduction in probe recovery was due to nonmucosal factors. Compared with normal subjects, cirrhotic patients with ascites have abnormal intestinal permeability, measured by urinary lactulose/rhamnose excretion, and normal small intestinal absorption, assessed by the urinary rhamnose/3-O-methyl-D-glucose ratio. Low urine recovery of sugar probes found in cirrhotic patients appears to be the result of nonintestinal factors affecting clearance rather than reduced intestinal absorption.
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PMID:Assessment of intestinal permeability and absorption in cirrhotic patients with ascites using combined sugar probes. 1518 67

Portal hypertension is an unavoidable complication of liver cirrhosis, which usually limits the survival (bleeding from esophageal varices, ascites). Increase in portal pressure is not only due to mechanical obstruction of portal circulation, but there is also a dynamic component (endothelial dysfunction of hepatic microcirculation) and increased blood flow through the splanchnic circulation. For the long-term treatment of portal hypertension two groups of medicaments are available at present: non-selective betablockers (vasoconstriction in splanchnic bed) and nitrates (lowering of intrahepatic resistance). Long-term treatment is necessary in these situations: Primary prophylaxis of bleeding from esophageal varices (in patients, who never bled, but with "risk" varices)--non-selective betablockers; secondary prophylaxis (in patients after variceal bleeding)--non-selective betablockers (possibly with nitrates) or endoscopic treatment. It is clearly documented, that this treatment lowers the risk of the first or repeated bleeding from varices and hence lowers the mortality and morbidity due to this complication in patients with liver cirrhosis. Another serious complication of liver cirrhosis is the spontaneous bacterial peritonitis. All patients after that infection have to receive prophylactic treatment with antibiotics. This treatment should be long life, till the disappearance of ascites or till the liver transplantation.
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PMID:[Long-term pharmacological treatment of portal hypertension]. 1598 90

Onset of ascites in cirrhosis of the liver is associated with worsened quality of life, increased risk of spontaneous bacterial peritonitis, and renal failure. Portal hypertension produces splanchnic vasodilation that triggers the cascade of events leading to release of Na retentive vasoconstrictor hormones. Management of ascites caused by cirrhosis is based on improving the Na excretion with diuretics and Na restriction in diet. Refractory ascites and hepatorenal syndrome are the complications of ascites that carry a very high mortality. Large volume paracentesis and transjugular intrahepatic porto-systemic shunts are useful in managing patients with refractory ascites. Liver transplant is the only way to improve survival in ascites caused by cirrhosis.
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PMID:Management of ascites in cirrhosis. 1620 72

Conditions that necessitate surgery frequently arise in patients with chronic liver disease and cirrhosis. Because cirrhosis has the ability to cause physiologic derangements in every organ system in the body, clinicians face significant challenges in preoperative preparation of the patient with cirrhosis in order to decrease postoperative morbidity and mortality. Emergent operations add an extra dimension of complexity to the clinical picture, due to limited preoperative time to prepare the patient with cirrhosis for surgery. In cases of severely decompensated cirrhosis, clinicians should have in their armamentarium possible alternatives to surgery that can be used to temporize the emergent nature of the disease and improve patient outcomes. The classification of cirrhotic liver disease by Child and Turcotte was initially utilized to predict mortality in patients undergoing surgically placed shunts for portal hypertensive bleeding. Subsequent studies have pointed to the fact that other general and thoracic surgery procedures can be assigned predicted mortality rates according to a similar classification scheme, the modified Child-Pugh score. Patients with cirrhosis facing surgery should undergo a careful history and physical examination and should be accurately placed into a designated Child-Pugh category. Because the modified Child-Pugh class is the most reliable determinant of postoperative morbidity and mortality, every attempt should be made to upgrade a patient's class in a favorable direction prior to surgery. Patients should be carefully evaluated for the presence of ascites and dietary alterations. In addition, medical management with diuretics should be employed to prevent postoperative ascites leak and possible infectious complications including bacterial peritonitis. Perhaps one of the most feared complications in the patient with cirrhosis facing surgery is hemorrhage. Because the liver is vital in maintenance of coagulation homeostasis, several pharmacologic adjuncts may be administered to correct any coagulopathy in the peri-operative period. Several diseases such as cholelithiasis and peptic ulcer disease are known to be more prevalent in the cirrhotic patient, and clinicians treating these diseases should have a thorough understanding of the pathophysiology of cirrhosis and portal hypertension. Patients with cirrhosis and portal hypertensive bleeding that are considered good surgical candidates (ie, Child-Pugh class A) may benefit from surgical portasystemic shunt in contrast to angiographically placed portacaval shunt (ie, transjugular intrahepatic portosystemic shunt ) due to the lack of durable patency and cost effectiveness in the latter. In patients with cirrhosis awaiting orthotopic liver transplantation, TIPS may be a lifesaving temporizing technique that is utilized as a bridge to transplantation.
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PMID:Management of the cirrhotic patient that needs surgery. 1631 65


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