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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous bacterial peritonitis (SBP) is a bacterial infection of ascitic fluid in patients with decompensated cirrhosis. The modifier 'spontaneous' distinguishes this from surgical peritonitis. The infecting organisms are usually enteric gram-negatives which have translocated from the bowel. Symptoms of infection occur in most patients with SBP, including fever, abdominal pain, mental status changes, and ileus. A high index of suspicion should exist for SBP in patients with cirrhosis and ascites. Diagnostic abdominal paracentesis can be undertaken with minimal risk and should be performed in all patients admitted to the hospital, during times of worsening clinical appearance, or when gastrointestinal bleeding occurs. The ascitic fluid polymorphonuclear cell count is the most sensitive test in evaluating for infection. Cultures of the ascitic fluid are helpful in identifying the organism and are best performed by bedside injection of blood culture bottles. Ascites total protein, lactate dehydrogenase, and glucose levels can assist in distinguishing SBP from secondary peritonitis. Empirical therapy is recommended after paracentesis if suspicion for infection exists. Cefotaxime is the best-studied antibiotic for this purpose and has excellent penetration into ascites with no nephrotoxicity. Prophylaxis should be limited to high-risk settings. Mortality rates in SBP have declined dramatically, largely due to earlier detection and improved therapy.
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PMID:Spontaneous bacterial peritonitis. 1592 Mar 24

Spontaneous bacterial peritonitis is a major cause of mortality after liver cirrhosis. Altered permeability of the mucosa and deficiencies in host immune defenses through bacterial translocation from the intestine due to intestinal bacterial overgrowth have been implicated in the development of this complication. Molecular mechanisms underlying the process are not well known. In order to understand mechanisms involved in translocation of bacteria, this study explored the role of oxidative stress in mediating changes in intestinal mucosal glycosylation and luminal bacterial content during cirrhosis. CCl4-induced cirrhosis in rats led to prolonged oxidative stress in the intestine, accompanied by increased sugar content of both intestinal brush border and surfactant layers. This was accompanied by changes in bacterial flora in the gut, which showed increased hydrophobicity and adherence to the mucosa. Inhibition of xanthine oxidase using sodium tungstate or antioxidant supplementation using vitamin E reversed the oxidative stress, changes in brush border membrane sugar content, and bacterial adherence. In conclusion, oxidative stress in the intestine during cirrhosis alters mucosal glycosylation, accompanied by an increased hydrophobicity of luminal bacteria, enabling increased bacterial adherence onto epithelial cells. This might facilitate translocation across the mucosa, resulting in complications such as spontaneous bacterial peritonitis.
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PMID:Intestinal mucosal alterations in rats with carbon tetrachloride-induced cirrhosis: changes in glycosylation and luminal bacteria. 1655 55

Spontaneous bacterial peritonitis (SBP) is one of the main infectious complications of cirrhosis and occurs in 8-30% of hospitalized patients with ascites. SBP is characterized by infection of the ascitic fluid (AF) in the absence of any primary focus of intra-abdominal infection. The main route by which the AF becomes infected is the hematogenous route. The pathogenic mechanism by which infection develops is bacterial translocation from the intestinal flora to the mesenteric lymph nodes and from there to the bloodstream. Contributing factors are an increased growth of Gram-negative aerobic bacilli in the jejunum, changes in the intestinal barrier and in addition factors which could reduce the local flow of blood. For clinical diagnosis, patients with SBP may present signs of peritoneal irritation and pain, together with changes in gastrointestinal motility, sometimes with nausea, vomiting, diarrhea or ileus. Many patients, however, may not present any symptoms or signs as a result of the presence of SBP. Diagnostic paracentesis of the AF must be performed for every patient with cirrhosis, hospitalized with ascites. Laboratory diagnosis of SBP is carried out by polymorphonuclear count in the AF, together with a positive culture from the AF, which is characteristically monomicrobial. Escherichia coli has been the main bacterium isolated from AF as well as other Gram-negative bacteria from the Enterobacteriaceae family and Streptococcus genus. A more rapid diagnosis of SBP can be obtained via the use of leukocyte esterase, which is present in biological fluids and reacts with a component of the dipstick, changing its color. During the acute phase of SBP, antibiotics should be initiated promptly once the clinical and laboratory diagnosis of SBP has been made, before the result of AF culture. Cefotaxime or other third-generation cephalosporins have been considered the first-choice empirical antibiotics in the treatment of cirrhotic patients with SBP, and is efficacious in approximately 90% of cases. Broad-spectrum quinolones, which are almost completely absorbed after oral administration and diffuse rapidly through the AF, are currently used for oral treatment of uncomplicated SBP. Patients who have already had a previous episode of SBP, with a 69% probability of recurrence within a year, will benefit from prophylactic treatment. Cirrhotic patients with a high risk of SBP and other infections, such as those with gastrointestinal bleeding, also benefit from primary prophylaxis and norfloxacin has been used with success.
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PMID:Spontaneous bacterial peritonitis: a therapeutic update. 1659 6

Spontaneous bacterial peritonitis (SBP) is an acute bacterial infection usually associated with ascites and cirrhosis or is a complication of peritoneal dialysis. There are very few case reports of cancer patients who developed this disease. Furthermore, there have been no published case reports of successfully treated gynecological cancer patients who later developed SBP. We present a case involving a 41-year-old woman who was treated for cervical carcinoma in 1992. She underwent radical surgery and adjuvant chemoradiation therapy. Two years later, the patient presented with streptococcal group B cellulitis associated with left leg lymphedema. She recovered following antibiotic treatment but had recurrent episodes of streptococcal cellulitis in her leg over the past 10 years. In 2003, the patient was admitted to the hospital because of sepsis, acute renal failure, and SBP. She was treated and recovered following treatment. SBP is usually associated with cirrhosis. Although SBP is rarely seen in successfully treated gynecological cancer patients, oncologists should be aware of this clinical entity. Timely treatment is essential to maximize chances of survival.
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PMID:Spontaneous bacterial peritonitis following treatment for cervical carcinoma. 1668 83

Liver cirrhosis is a frequent phenomenon in chronic liver diseases such as hepatitis B, hepatitis C, alcohol-related liver damage, autoimmune hepatitis and hemochromatosis. Ascites is the most frequent complication of cirrhosis. We discuss pathogenesis, diagnosis and state-of-the-art clinical management of ascites with emphasis on recent promising developments, such as covered transjugular intrahepatic portosystemic shunt (TIPS). Spontaneous bacterial peritonitis occurs in up to 10% of patients with ascites because of bacterial overgrowth with translocation through the increased permeable small intestinal wall and impaired defence mechanisms. The addition of albumin to standard antibiotic therapy may decrease mortality of spontaneous bacterial peritonitis by decreasing the incidence of renal insufficiency. Patients with coexistent marked hyperbilirubinaemia or pre-existent renal impairment could benefit from adjuvant albumin. Probiotics (bacterial food supplements) have been claimed to improve the state of underlying liver disease and may be useful in the primary and secondary prevention of spontaneous bacterial peritonitis.
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PMID:Ascites and spontaneous bacterial peritonitis in patients with liver cirrhosis. 1678 26

Portal hypertension is the main complication of cirrhosis and is responsible for its most common complications: variceal hemorrhage, ascites, and portosystemic encephalopathy. Portal hypertension is the result of increased intrahepatic resistance and increased portal venous inflow, which in turn is the result of splanchnic vasodilatation. Vasodilatation (splanchnic and systemic) and hyperdynamic circulation are hemodynamic abnormalities typical of cirrhosis and portal hypertension. Gastroesophageal varices result almost solely from portal hypertension, although the hyperdynamic circulation contributes to variceal growth and hemorrhage. Ascites results from sinusoidal hypertension and sodium retention, which is, in turn, secondary to vasodilatation and activation of neurohumoral systems. The hepatorenal syndrome represents the result of extreme vasodilatation with an extreme decrease in effective blood volume that leads to maximal activation of vasoconstrictive systems, renal vasoconstriction, and renal failure. Spontaneous bacterial peritonitis is a potentially lethal infection of ascites that occurs in the absence of a local source of infection. Portosystemic encephalopathy is a consequence of both portal hypertension (shunting of blood through portosystemic collaterals) and hepatic insufficiency that result in the accumulation of neurotoxins in the brain. This paper reviews the recent advances in the pathophysiology and management of the complications of portal hypertension.
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PMID:Portal hypertension. 1703 Nov 70

Portal hypertension is the main complication of cirrhosis and is responsible for its most common complications: variceal hemorrhage, ascites, and portosystemic encephalopathy. Portal hypertension is the result of increased intrahepatic resistance and increased portal venous inflow. Vasodilatation (splanchnic and systemic) and the hyperdynamic circulation are hemodynamic abnormalities typical of cirrhosis and portal hypertension. Gastroesophageal varices result almost solely from portal hypertension, although the hyperdynamic circulation contributes to variceal growth and hemorrhage. Ascites results from sinusoidal hypertension and sodium retention, which is in turn secondary to vasodilatation and activation of neurohumoral systems. Hepatic hydrothorax results from the passage of ascites across the diaphragm and into the pleural space. The hepatorenal syndrome represents the result of extreme vasodilatation with an extreme decrease in effective blood volume that leads to maximal activation of vasoconstrictive systems, renal vasoconstriction, and renal failure. Spontaneous bacterial peritonitis is a potentially lethal infection of ascites that occurs in the absence of a local source of infection. Portosystemic encephalopathy is a consequence of both portal hypertension (shunting of blood through portosystemic collaterals) and hepatic insufficiency resulting in the accumulation of neurotoxins in the brain.
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PMID:Portal hypertension. 1703 6

Spontaneous bacterial peritonitis (SBP) is a known complication of ascites due to cirrhosis; it has also been reported in some non-cirrhotic conditions with ascites. We report a 50-year-old lady with isolated splenic vein thrombosis who developed SBP due to E. coli .
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PMID:Spontaneous bacterial peritonitis in isolated splenic vein thrombosis with portal hypertension. 1709 Aug 53

Spontaneous bacterial peritonitis (SBP) occurs as a direct consequence of bacteria entering ascitic fluid (AF) from the intestinal lumen trough in several ways, including the hematogenous and mesenteric lymph nodes route. There are few studies on the cytokine profile of ascitic-derived mononuclear cells of patients with SBP, particularly on granzyme B (GZB). The aim of the present study was to verify whether patients with SBP have GZB-positive cells, whether they are increased in patients with aseptic ascites, and their trend after antibiotic treatment. We enrolled 36 consecutive patients (24 males and 12 females) with SBP on histologically-proven hepatitis C virus cirrhosis (group A) and 20 patients (11 males and nine females with ascites, but without evidences of SBP (group B). The diagnosis of SBP was made according to the following criteria: positive colture in AF or blood (at least two cultures) and neutrophils in AF (>250 mL polymorphonuclear leukocytes). For these patients we used ELISpot to assay GZB production on purified mononuclear cells in ascitesand peripheral blood, coupled with tumor necrosis factor-alpha tested using ELISA. A non-parametric statistical analysis was used to assess significant differences and correlations. We found positive culture in all of the patients with SBP (80% Escherichia coli; 20% Enterococcus faecium). Furthermore, the patients in group A had a higher number of GZB spot-forming colonies than the patients in group B (P < 0.001). GZB-positive cells were lower in the peripheral blood than those found in the AF of patients with SBP, while no differences were found between blood and AF in group B. Furthermore, after antibiotic treatment, GZB was reduced in the patients with SBP (P < 0.05). In conclusion, GZB may be an important mediator of the immune response towards bacteria in AF and could be used as a diagnostic tool.
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PMID:Increase of granzyme B-positive cells in ascitic fluid of patients with spontaneous bacterial peritonitis. 1802 Dec 32

Spontaneous bacterial peritonitis (SBP) is a severe complication in patients with cirrhosis and ascites. It is predominantly caused by Escherichia coli. The phylogenetic group and virulence genotype of E. coli isolates causing SBP were investigated, and the association of these characteristics with host factors and prognosis was examined. Seventy-six episodes of E. coli SBP that occurred over a 9-year period were studied. The phylogenetic group of the isolates and the presence of 36 virulence factor genes were investigated. The influence of bacterial and host factors on in-hospital mortality was assessed by multiple logistic regression. Phylogenetic groups A, B1, B2 and D were found in 26%, 4%, 46% and 24% of the isolates, respectively. Virulence factor genes were more frequent in B2 isolates than in non-B2 isolates (mean virulence score 15.4 vs. 7.3, p <10(-4)). Ciprofloxacin resistance was significantly associated with non-B2 groups and a low virulence score. Host factors independently associated with a shift from B2 to non-B2 isolates were norfloxacin prophylaxis (OR 13.01, p 0.0213) and prothrombin ratio (OR 1.04 for a 10% decrease, p 0.0211). The model for end-stage liver disease (MELD) score (OR 1.83, p 0.0007) and hospital-acquired SBP (OR 4.13, p 0.0247) were independent predictors of in-hospital mortality. In contrast, outcome was not influenced by the phylogenetic group or the virulence profile. These findings indicate that the characteristics of E. coli isolates causing SBP vary with the severity of liver disease and with fluoroquinolone prophylaxis. Host factors are more important than bacterial factors in predicting in-hospital mortality.
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PMID:Genetic background of Escherichia coli isolates from patients with spontaneous bacterial peritonitis: relationship with host factors and prognosis. 1904 Apr 75


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