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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 is a common complication in patients with cirrhosis and ascites. However, spontaneous peritonitis caused by Cryptococcus neoformans is uncommon. Delayed diagnosis of cryptococcal peritonitis often results in death. We describe three cases of spontaneous cryptococcal peritonitis in patients with decompensated cirrhosis. One case had associated symptomatic human immunodeficiency virus infection. Clinical awareness of this entity may lead to the early diagnosis and proper treatment.
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PMID:Spontaneous cryptococcal peritonitis in cirrhotic patients. 1243 96

Nitric oxide (NO) is a powerful vasodilator agent that has been found to be elevated in patients with cirrhosis, and that plays a key role in the pathogenesis of the hemodynamic abnormalities found in these patients. The reasons for this increased NO synthesis are not entirely known, but at least two main mechanisms are involved: shear stress and bacterial-induced NO synthesis. This review focuses on bacterial-induced NO synthesis. Induction of NO synthesis by different cellular populations occurs when proinflammatory cytokines act synergistically, and also by endotoxin. Spontaneous bacterial peritonitis (SBP) is the most dangerous infectious complication arising in patients with cirrhosis and ascites, and it is associated with high serum and ascitic fluid levels of proinflammatory cytokines. A subset of patients in this situation show high levels of serum and ascitic fluid NO levels when SBP is diagnosed, and these patients seem to be predisposed to the development of renal impairment. The increased NO synthesis and associated aggravated vasodilatation may be the reason why patients with SBP show high levels of plasma renin activity, in an attempt to counterbalance this new situation, and that the administration of albumin during the SBP episode significantly reduces the episode-related mortality.
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PMID:Nitric oxide in patients with cirrhosis and bacterial infections. 1260 7

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

Ascites is the most common complication of cirrhosis and occurs in more than half of all patients with cirrhosis. The development of ascites indicates progression of the underlying cirrhosis and is associated with a 50% 2-year survival rate. Conventional therapies used for the treatment of ascites include sodium restriction (<88 mmol/d), diuretics, and large volume paracentesis (LVP) (>5 L). The most effective diuretic combination is that of a potassium-sparing, distal-acting diuretic (eg, spironolactone) with a loop diuretic (eg, furosemide). LVP provides rapid resolution of symptoms with minimal complications and is well tolerated by most patients. Post-paracentesis circulatory dysfunction (PPCD) may occur after LVP and is characterized by hyponatremia, azotemia, and an increase in plasma renin activity. PPCD is associated with an increased mortality and may be prevented by administration of albumin intravenously (6 to 8 g/L of ascites removed) along with LVP. The development of either diuretic-resistant or diuretic-intractable ascites occurs in approximately 5% to 10 % of all cases of ascites. This is a poor prognostic sign, as 50% of such patients die within 6 months of its development. The only definitive therapy for refractory ascites with cirrhosis is orthotopic liver transplantation. The other options that are available include LVP, peritoneovenous shunts, and transjugular intrahepatic portosystemic shunts (TIPS). The TIPS procedure has not been shown to have any influence on survival in patients with cirrhosis and refractory ascites, and TIPS is contraindicated in patients who have advanced liver failure because it can hasten death in such individuals. Peritoneovenous shunts are associated with a high incidence of complications and frequent occlusion. They are, therefore, rarely used for refractory ascites. Spontaneous bacterial peritonitis (SBP) is a common complication of cirrhotic ascites. It may precipitate hepatorenal syndrome. The overall mortality rate from an episode of SBP is approximately 20%. Following an episode of SBP, the 1-year mortality rate approaches 70%. Hospitalized patients should be treated with intravenous third-generation cephalosporins (eg, cefotaxime), and patients at risk should receive prophylaxis with either orally administered quinolones (eg, norfloxacin) or cotrimoxazole.
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PMID:Treatment of Ascites. 1458 37

Brucella infection is a systemic disease, but the microorganism rarely causes infections in the gastrointestinal system such as hepatitis, cholecystitis, colitis and pancreatitis. Spontaneous bacterial peritonitis due to Brucella is extremely rare. Herein, we report a case of cirrhosis complicated with nongranulomatous hepatitis and peritonitis, both due to Brucella. A 63 year-old man with diabetes mellitus was admitted to hospital with complaints of weakness, backache, abdominal pain and abdominal swelling. On the basis of physical examination and laboratory findings, cryptogenic cirrhosis and spontaneous bacterial peritonitis were diagnosed. Due to persistent fever and backache, serum Brucella agglutination test was performed and found to be positive. Brucella melitensis was isolated from ascitic fluid culture. Liver biopsy findings revealed cirrhosis and a nongranulomatous hepatitis which was thought might be due to Brucella infection. Doxycycline and rifampicin, in addition to diuretics were administered for spontaneous ascites infection due to Brucella. A week later, the patient's condition improved and he became afebrile. After two months of therapy, the ascites had almost disappeared.
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PMID:Spontaneous bacterial peritonitis due to Brucella infection. 1461 44

Pasteurella species cause zoonotic infections in humans. Human pasteurella infections usually manifest as local skin or soft tissue infection following an animal bite or scratch. Systemic infections are less common and are limited to patients at the extremes of age or those who have serious underlying disorders, including cirrhosis. Most human pasteurella infections are caused by the multocida species. We report a case of Pasteurella dagmatis peritonitis and septicaemia in a patient with cirrhosis. The infection followed a scratch inflicted by a pet dog. Despite appropriate antibiotic treatment the infection proved fatal. Spontaneous bacterial peritonitis caused by P dagmatis has not been reported previously. Pasteurella dagmatis is a relatively recently described species, which is rarely reported as a human pathogen. This species may be misidentified unless commercial identification systems are supplemented by additional biochemical tests.
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PMID:Fatal Pasteurella dagmatis peritonitis and septicaemia in a patient with cirrhosis: a case report and review of the literature. 1474 55

Spontaneous bacterial peritonitis occurs in 30% of patients with ascites due to cirrhosis leading to high morbidity and mortality rates. The pathogenesis of spontaneous bacterial peritonitis is related to altered host defenses observed in end-stage liver disease, overgrowth of microorganisms, and bacterial translocation from the intestinal lumen to mesenteric lymph nodes. Clinical manifestations vary from severe to slight or absent, demanding analysis of the ascitic fluid. The diagnosis is confirmed by a number of neutrophils over 250/mm3 associated or not to bacterial growth in culture of an ascites sample. Enterobacteriae prevail and Escherichia coli has been the most frequent bacterium reported. Mortality rates decreased markedly in the last two decades due to early diagnosis and prompt antibiotic treatment. Third generation intravenous cephalosporins are effective in 70% to 95% of the cases. Recurrence of spontaneous bacterial peritonitis is common and can be prevented by the continuous use of oral norfloxacin. The development of bacterial resistance demands the search for new options in the prophylaxis of spontaneous bacterial peritonitis; probiotics are a promising new approach, but deserve further evaluation. Short-term antibiotic prophylaxis is recommended for patients with cirrhosis and ascites shortly after an acute episode of gastrointestinal bleeding.
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PMID:[Spontaneous bacterial peritonitis]. 1504 12

Spontaneous bacterial peritonitis, urinary tract infections, respiratory infections and bacteremia are the most frequent infective complications in cirrhosis. These infections are due to the concomitant presence of different facilitating mechanisms including changes in the intestinal flora and in the intestinal barrier, depression of activity of the reticuloendothelial system, decreased opsonic activity of the ascitic fluid, neutrophil leukocyte dysfunction and iatrogenic factors among others. The fact, that the probability of having a microorganism responsible for the infection quinolone resistant is higher than 30% should be taken into account when treating any infection in a cirrhotic patient receiving selective intestinal decontamination with quinolones, and therefore, quinolones as empiric treatment are not indicated.
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PMID:Bacterial infections in cirrhosis. 1528 49

Bacterial translocation is the passage of viable bacteria from the intestinal lumen to mesenteric lymph nodes and other extraintestinal sites. Spontaneous bacterial peritonitis is the main clinical consequence of bacterial translocation in cirrhosis. Translocation of bacterial products of viable or non-viable bacteria, such as endotoxin and/or bacterial DNA, through the intestinal wall could stimulate the immune system and the hyperdynamic circulatory state in cirrhosis with clinical consequences that are under evaluation. Bacterial translocation is currently considered the passage of viable gut flora across the intestinal barrier to extraluminal sites. Aerobic Gram-negative bacilli are the most common translocating bacteria. Intestinal bacterial overgrowth, impairment in permeability of the intestinal mucosal barrier, and deficiencies in local host immune defences are the major mechanisms postulated to favour bacterial translocation in cirrhosis. Bacterial translocation is a key step in the pathogenesis of spontaneous bacteraemia and spontaneous bacterial peritonitis in cirrhosis. Translocation of intestinal bacterial products from viable or non-viable bacteria, such as endotoxin and bacterial DNA, has recently been associated with pathophysiological events, such as activation of the immune system and derangement of the hyperdynamic circulatory status in cirrhosis. Clinical consequences of these effects of bacterial products are presently under investigation.
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PMID:Bacterial translocation and its consequences in patients with cirrhosis. 1564 40

Portal hypertension, the main complication of cirrhosis, 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, in turn, is 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 review covers the recent advances in the pathophysiology and management of the complications of portal hypertension.
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PMID:Portal hypertension. 1570 65


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