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

Hepatocellular carcinoma is a primary tumor complicating liver disease, associated with cirrhosis in 80-90% of the cases. A kidney transplant recipient with chronic B and C viral hepatitis was admitted because of general malaise, renal function impairment and positive AST, ALT and alkaline phosphatase tests, and very high alpha-fetoprotein levels. Ascites, spontaneous bacterial peritonitis and renal failure developed. A CT showed multiple liver masses. Renal failure required hemodialysis. The patient died 17 days after the initial symptoms with hepatic encephalopathy. A postmortem liver biopsy confirmed the diagnosis of cirrhosis and hepatocellular carcinoma (HCC). This report, as well as a few others, shows the accelerated evolution of chronic viral hepatitis in kidney transplant patients and questions the convenience of kidney transplantation and the adequate follow up in chronic viral hepatitis.
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PMID:[Fatal acute hepatic failure with hepatocarcinoma presentation in a patient with renal transplant with asymptomatic chronic B and C hepatitis]. 1172 27

296 patients with first clinical symptoms of alcoholic liver disease were hospitalized in Probationary-Infectious Diseases Department in Kielce, between 1994-2000. In 52 (17.6%) of them, acute hepatic failure was diagnosed by detection of hepatic encephalopathy. Initial laboratory data of those patients who died (6.1%), and those who survived (11.5%) was compared. No statistically significant differences in analyzed parameters were found, except for significantly higher bilirubin concentration in the group of deceased. In both groups of patients, the frequency of hepatic failure complications, present at the admission to the hospital or those developed in the course of the disease, was also analyzed. The following complications were observed significantly more often in deceased: ascites, hepatorenal syndrome (HRS), spontaneous bacterial peritonitis (SBP), and gastrointestinal haemorrhage (GIH), while sepsis was similarly frequent in both groups.
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PMID:Acute hepatic failure in alcoholic liver disease. 1221 30

Esophageal varices develop in patients with cirrhosis once portal pressure, measured by hepatic venous pressure gradient, and exceeds 10 mm Hg. At a portal pressure of 12 mm Hg, variceal bleeding may develop that is associated with a mortality of 30% to 50% per episode. In addition to an elevated portal pressure, other risk factors for the development of variceal hemorrhage include: variceal size, endoscopic features on the variceal wall (i.e., red wales), and Child-Pugh class. In patients with suspected variceal hemorrhage, the treatment of the acute episode includes intravascular volume expansion, hemostasis through the use of pharmacological agents and endoscopy, and the prevention and treatment of potential complications associated with variceal hemorrhage such as aspiration pneumonia, spontaneous bacterial peritonitis and hepatic encephalopathy. Given a high rate of rebleeding, long-term prevention through secondary prophylaxis should be instituted in all patients who have survived an episode of variceal bleeding. Current prophylactic options include: non-selective beta-blockers alone (first line) or in combination with long-acting nitrates (isosorbide mononitrate) and/or endoscopic variceal obliteration achieved through sclerotherapy or preferably, band ligation.
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PMID:The critically ill liver patient: the variceal bleeder. 1261 Aug 53

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

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

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

Hospitalized patients with cirrhosis are at increased risk of developing bacterial infections, the most common being spontaneous bacterial peritonitis (SBP) and urinary tract infections. Independent predictors of the development of bacterial infections in hospitalized cirrhotic patients are poor liver synthetic function and admission for gastrointestinal hemorrhage. Short term (seven-day) prophylaxis with norfloxacin reduces the rate of infections and improves survival and should therefore be administered to all patients with cirrhosis and variceal hemorrhage. Cirrhotic patients who develop abdominal pain, tenderness, fever, renal failure or hepatic encephalopathy should undergo diagnostic paracentesis, and those who meet the criterion for SBP (eg, an ascites neutrophil count greater than 250/mm3) should receive antibiotics, preferably a third-generation cephalosporin. In addition to antibiotic therapy, albumin infusions have been shown to reduce the risk of renal failure and mortality in patients with SBP, particularly in those with renal dysfunction and hyperbilirubinemia at the time of diagnosis. Patients who recover from an episode of SBP should be given long term prophylaxis with norfloxacin and should be assessed for liver transplantation.
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PMID:Bacterial infections in cirrhosis. 1519 Mar 98

Bacterial infections increase morbidity and mortality in cirrhosis. Our aim was to investigate whether in alcoholic hepatitis the development of bacterial infections was also a poor prognostic factor. In the retrospective evaluation of 681 hospitalized patients with liver disease, from a single center during a six-year period, 52 (7.5%) cases of alcoholic hepatitis were well documented, 73.1% by liver biopsy with histopathological analysis and the others by well characterized clinical-biochemical data. Males were predominant (ratio 3.3:1.0), mean age of 40 years and mean alcohol intake of 193 g/day. Major complications were: Hepatic encephalopathy (n=5), renal insufficiency (n=4) and digestive bleeding (n=3). Bacterial infections were found in 11 (21%) patients, distributed into: pulmonary (n=5), spontaneous bacterial peritonitis (n=2), urinary (n=3) and dermatological (n=1). Early hospital death occurred in eight (15.4%) patients and comparative analysis between these and those who survived showed that poor prognostic factors were: presence of hepatic encephalopathy (p=0.012), total bilirubin > 20 mg% (p=0.012) and the presence of severe infections (pulmonary and spontaneous bacterial peritonitis) with statistical significance (p=0.004). In conclusion we have demonstrated that severe bacterial infections are poor prognostic factors for alcoholic hepatitis. Our recommendation, based on prophylaxis with antibiotics during digestive bleeding in cirrhosis and in acute hepatic insufficiency, is to extend this prophylaxis to alcoholic hepatitis, in its severe form, in order to prevent bacterial infections and early death.
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PMID:[Alcoholic hepatitis: bad prognosis due to concomitant bacterial infections]. 1533 56

Hepatorenal syndrome (HRS) is a complex syndrome. In addition to severe reduction of renal function due to renal vasoconstriction, there is impairment in systemic haemodynamics, activation of the renin-angiotensin and sympathetic nervous systems and antidiuretic hormone, vasoconstriction of the brain, muscle and skin, and dilutional hyponatraemia. Treatment in patients with type 2 HRS, the most frequent form of HRS, is directed towards managing refractory ascites. Paracentesis is the treatment of choice. TIPS is also effective but is more expensive, is associated with higher incidence of hepatic encephalopathy, and does not increase survival. Although a rapidly progressive renal failure is the most characteristic manifestation of type 1 HRS, there is failure in other organs such as the liver and the brain. A decrease in cardiac output develops in these patients, associated with a decrease in cardiopulmonary pressures. Since type 1 HRS mainly occurs in patients with spontaneous bacterial peritonitis and massive release of cytokines within the peritoneal cavity, it may be considered as a special form of multiorgan failure of circulatory origin. Not surprisingly, the treatment of choice in type 1 HRS is the combination of vasoconstrictors to reduce arterial vasodilation and plasma volume expansion with albumin to increase cardiac preload. TIPS is also effective in these patients and the combination of pharmacological treatment followed by TIPS may be the most effective approach.
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PMID:Review article: hepatorenal syndrome--how to assess response to treatment and nonpharmacological therapy. 1533 2

Rifaximin (4-deoxy-4'-methylpyrido[1',2'-1,2]imidazo- [5,4-c]-rifamycin SV) is a synthetic antibiotic designed to modify the parent compound, rifamycin, in order to achieve low gastrointestinal (GI) absorption while retaining good antibacterial activity. Both experimental and clinical pharmacology clearly show that this compound is a nonsystemic antibiotic with a broad spectrum of antibacterial action covering Gram-positive and Gram-negative organisms, both aerobes and anaerobes. Being virtually nonabsorbed, its bioavailability within the GI tract is rather high with intraluminal and fecal drug concentrations that largely exceed the minimal inhibitory concentration values observed in vitro against a wide range of pathogenic organisms. The GI tract represents, therefore, the primary therapeutic target and GI infections the main indication. The appreciation of the pathogenic role of gut bacteria in several organic and functional GI diseases has increasingly broadened its clinical use, which is now extended to hepatic encephalopathy, small intestine bacterial overgrowth, inflammatory bowel disease and colonic diverticular disease. Potential indications include the irritable bowel syndrome and chronic constipation, Clostridium difficile infection and bowel preparation before colorectal surgery. Because of its antibacterial activity against the microorganism and the lack of strains with primary resistance, some preliminary studies have explored the rifaximin potential for Helicobacter pylori eradication. Oral administration of this drug, by getting rid of enteric bacteria, could also be employed to achieve selective bowel decontamination in acute pancreatitis, liver cirrhosis (thus preventing spontaneous bacterial peritonitis) and nonsteroidal anti-inflammatory drug (NSAID) use (lessening in that way NSAID enteropathy). This antibiotic has, therefore, little value outside the enteric area and this will minimize both antimicrobial resistance and systemic adverse events. Indeed, the drug proved to be safe in all patient populations, including young children. Although rifaximin has stood the test of time, it still attracts the attention of both basic scientists and clinicians. As a matter of fact, with the advancement of the knowledge on microbial-gut interactions in health and disease novel indications and new drug regimens are being explored. Besides widening the clinical use, the research on rifaximin is also focused on the synthesis of new derivatives and on the development of original formulations designed to expand the spectrum of its clinical use.
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PMID:Rifaximin, a poorly absorbed antibiotic: pharmacology and clinical potential. 1585 48


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