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

Bacterial infection coincides with migration of leucocytes from the circulation into the bacterium-infected tissue. Recently, we have shown that endothelial cells, upon binding and ingestion of Staphylococcus aureus, exhibit proinflammatory properties including procoagulant activity and increased intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression on the cell surface, resulting in hyperadhesiveness, mainly for monocytes. The enhanced extravasation of monocytes to bacterium-infected sites is facilitated by the local production of chemotactic factors. From another study we concluded that the locally produced chemokine MCP-1 is important in the recruitment of monocytes to the peritoneal cavity in a model of bacterial peritonitis. In the present study we investigated whether cultured human endothelial cells after infection with bacteria produce and release MCP-1, which in turn stimulates monocyte chemotaxis. We observed that endothelial cells released significant amounts of MCP-1 within 48 h after ingestion of S. aureus. This was dependent on the number and the virulence of the bacteria used to infect the endothelial cells. The kinetics as well as the amount of MCP-1 released by S. aureus-infected endothelial cells differed markedly from that released by endothelial cells upon stimulation with IL-1beta. Supernatant from S. aureus-infected or IL-1beta-stimulated cells promoted monocyte chemotaxis which was almost entirely abrogated in the presence of neutralizing anti-MCP-1 antibody, indicating that most of the chemotactic activity was due to the release of MCP-1 into the supernatant. Our findings support the notion that endothelial cells can actively initiate and sustain an inflammatory response after an encounter with pathogenic microorganisms, without the intervention of macrophage-derived proinflammatory cytokines.
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PMID:Infection of human endothelial cells with Staphylococcus aureus induces the production of monocyte chemotactic protein-1 (MCP-1) and monocyte chemotaxis. 1046 52

The incidence of bacterial infections in cirrhotic patients admitted to hospital is very high. In several studies, 30% to 50% of cirrhotics presented bacterial infections at admission, or developed this type of complication during hospitalization. Most bacterial infections in cirrhotic patients are hospital-acquired. Between 15% to 35% of cirrhotics admitted to hospital develop nosocomial infections; these figures contrast sharply with the hospital-acquired infection rate in the general hospital population (5% to 7%). Urinary tract infections (12% to 29%), spontaneous bacterial peritonitis (7% to 23%), respiratory tract infections (6% to 10%) and bacteraemia (4% to 9%) are the most frequent bacterial infectious complications seen in cirrhotic patients. However, since spontaneous bacterial peritonitis is the most characteristic bacterial infection in cirrhosis, this report will focus (mainly) on this infectious complication.
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PMID:Bacterial infections in liver cirrhosis. 1060 6

The pathophysiology of circulatory and renal dysfunction in cirrhosis and the treatment of ascites and related conditions (hepatorenal syndrome and spontaneous bacterial peritonitis) have been research topics of major interest during the last two decades. However, many aspects of these problem remain unclear and will constitute major areas of investigation in the next millennium. The pathogenesis of sodium retention, the most prevalent renal function abnormality of cirrhosis, is only partially known. In approximately one third of patients with ascites, sodium retention occurs despite normal activity of the renin-aldosterone and sympathetic nervous systems and increased circulating plasma levels of natriuretic peptides and activity of the so-called natriuretic hormone. These patients present an impairment in circulatory function which, although less intense, is similar to that of patients with increased activity of the renin-aldosterone and sympathetic nervous systems, suggesting that antinatriuretic factors more sensitive to changes in circulatory function that these systems may be important in the pathogenesis of sodium retention in cirrhosis. The development of drugs that inhibit the tubular effect of antidiuretic hormone and increase renal water excretion without affecting urine solute excretion has opened a field of great interest for the management of water retention and dilutional hyponatremia in cirrhosis. Two families of drugs, the V2 vasopressin receptor antagonists and the kappa-opioid agonists, have been shown to improve free water clearance and correct dilutional hyponatremia in human and experimental cirrhosis with ascites. The first type of drugs blocks the tubular effect of antidiuretic hormone and the second inhibits antidiuretic hormone secretion by the neurohypophysis. On the other hand, two new treatments have also been proved to reverse hepatorenal syndrome in cirrhosis. The most interesting one is that based on the simultaneous administration of plasma volume expansion and vasoconstrictors. The second is transjugular intrahepatic porto-systemic shunt. The long-term administration (1-3 weeks) of analogs of vasopressin (ornipressin or terlipressin) or other vasoconstrictors together with plasma volume expansion with albumin is associated with a dramatic improvement in circulatory function and normalization of serum creatinine concentration in patients with severe hepatorenal syndrome. Of interest is the observation that in many of these patients, hepatorenal syndrome does not recur following discontinuation of the treatment, thus raising important questions about the mechanism by which hepatorenal syndrome follows a progressive course in most untreated cases. The pathogenesis of circulatory dysfunction in cirrhosis and the role of local mechanisms in the development of the splanchnic arteriolar vasodilation associated with portal hypertension will continue as important topics in clinical and basic research in Hepatology. Of special interest is the study of the mechanism by which circulatory function further deteriorates following complications such as severe bacterial infection or therapeutic interventions such as therapeutic paracentesis, and the adverse consequences of the impairment in circulatory function on renal and hepatic hemodynamics. Finally, although major advances have been made concerning the treatment and secondary prophylaxis of spontaneous bacterial peritonitis in cirrhosis, many aspects of the pathogenesis of this infection remain unclear. The mechanism of bacterial translocation and of the colonization of bacteria in the ascitic fluid are particularly important to design adequate measures for primary prophylaxis of this severe bacterial infection.
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PMID:Complications of cirrhosis. II. Renal and circulatory dysfunction. Lights and shadows in an important clinical problem. 1072 2

Studies by other laboratories have shown that angiotensin II (AII) can affect the function of cells which comprise the immune system. In the present study, the effect of AII on the function of peritoneal macrophages and peripheral blood monocytes was assessed. In vitro exposure (4 h prior to assay) of peritoneal macrophages from mice and rats to AII increased the percentage of cells that phagocytosed opsonized yeast and the number of yeast per macrophage. Furthermore, AII increased the respiratory burst capacity of peritoneal macrophages from mice and rats and peripheral blood mononuclear cells from humans. Because of these observations, the effect of AII on host resistance to bacterial infection was assessed. Intraperitoneal administration of AII was shown to increase host resistance (reduced abscess formation) in an animal model of bacterial peritonitis. Studies were then conducted to assess whether parenteral administration of AII, a clinically relevant route, could affect peritoneal host resistance in a manner similar to that observed after peritoneal administration. These studies showed that subcutaneous administration of AII throughout the postinfection interval increased the level of host resistance to bacterial peritonitis. Furthermore, in a study which compared AII and Neupogen, an agent approved for use for the reduction of febrile neutropenia after myeloablative therapy, daily subcutaneous administration of AII reduced abscess size and incidence, whereas Neupogen did not have any therapeutic benefit in this model. These data suggest that AII may be of therapeutic benefit as an immunomodulatory agent.
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PMID:Angiotensin II increases host resistance to peritonitis. 1088 64

Phlegmonous colitis (PC) is an acute infectious entity caused by bacteria. In this study, we reviewed 8,822 autopsy cases and found 13 cases of PC (0.15%). PC affected 2.43% of patients with hepatic cirrhosis or subacute liver atrophy, both of which were considered to be due to hepatitis viral infection. Before autopsy, none of the cases studied was suspected to involve PC, irrespective of the immediate cause of patient death. Thirteen autopsy cases showed some or all of the following pathohistologic characteristics: (1) involvement of the cecum (9 cases, 76.9%), (2) phlegmonous inflammatory changes and edema in the submucosa (100%), (3) bacterial infection (100%), (4) no microscopically detectable mucosal injuries (12 cases, 92.3%), and (5) acute serositis (peritonitis) (2 cases, 15.4%). These results suggest that PC is an unrecognized, but fatal complication of patients with some hepatic diseases and that PC has pathohistologic characteristics in common with previously reported spontaneous bacterial peritonitis in animal models. PC probably arises due to spontaneous infection in patients with hepatic cirrhosis.
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PMID:Phlegmonous colitis: a specific and severe complication of chronic hepatic disease. 1119 78

Our article concentrates on two acute states, which develop less dramatically but their after-effects may be very serious: Spontaneous bacterial peritonitis and Ogilvie's syndrome. Spontaneous bacterial peritonitis is a bacterial infection of the ascitic fluid without any intraperitoneal source of infection. Ascites is a condition of the disease but need not be clinically manifested. Spontaneous bacterial peritonitis comes usually during heavy hepatic impairment. Diagnosis can be set according: 1. Positive cultivation of ascitic fluid, 2. PMN levels higher than 250/mm3, 3. No infection, which may require a surgical intervention is apparent. Liver disease, which brings about the spontaneous bacterial peritonitis can be: 1. Chronic (e.g. alcoholic cirrhosis), 2. Subacute (e.g. alcoholic hepatitis), 3. Acute (e.g. fulminant hepatic failure). Mortality of this form of peritonitis can reach up to 46%. The most frequent etiological factor is alcohol and viral hepatitis, the most frequent agents are E. coli and Klebsiella pneumoniae. The disease is most effectively cured by cefalosporins of the third generation. With inadequate treatment, prognosis may be poor. Intestinal pseudoobstruction syndrome has clinical symptomatology of a serious impairment with ileus without signs of any mechanical intestinal obstruction. Syndrome can be classified according to its development: 1. Acute form--acute intestinal pseudoobstruction syndrome--Ogilvie's syndrome, 2. Chronic form--chronic intestinal pseudoobstruction syndrome. Pathogenic mechanism of the syndrome is not known. The disease is related to immobility, administration of some drugs, electrolyte imbalance and concomitant diseases (most frequently malignant tumors). Clinical symptomatology dominates nausea, vomiting, diffuse abdominal pain, constipation or diarrhoea. For diagnostics the first step should be termination of all medication, which could have causing affects, then taking native abdominal X-ray picture where gaseous intestinal distension can be prominent (coecum distended up to 9-12 cm). Identification of fluid surfaces is not usual. Endoscopic examination can exclude obstruction in the distal part of gut minimally. The most frequent complication is perforation of coecum. Pharmacological treatment relays on prokinetics. The basic intervention remains decompression by a rectal catheter or an effective coloscopic decompression with subsequent introduction of a cannula. Mortality of the disease fluctuates between 43 and 46%.
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PMID:[Acute states in gastroenterology: spontaneous bacterial peritonitis and the acute intestinal pseudoobstruction syndrome]. 1150 91

Hosts after severe burn injury are known to have a defect in the Th1 immune response and are susceptible to bacterial infections. We herein show that liver NK cells are potent IFN-gamma producers early after burn injury. However, when mice were injected with LPS 24 h after burn injury, IFN-gamma production from liver mononuclear cells (MNC; which we previously showed to be NK cells) was suppressed, and the serum IFN-gamma concentration did not increase, while serum IL-10 conversely increased compared with control mice. Interestingly, a single injection of IL-18 simultaneously with LPS greatly restored the serum IFN-gamma concentration in mice with burn injury and also increased IFN-gamma production from liver MNC. Nevertheless, a single IL-18 injection into mice simultaneously with LPS was no longer effective in the restoration of serum IFN-gamma and IFN-gamma production from the liver MNC at 7 days after burn injury, when mice were considered to be the most immunocompromised. However, IL-18 injections into mice on alternate days beginning 1 day after burn injury strongly up-regulated LPS-induced serum IFN-gamma levels and IFN-gamma production from liver and spleen MNC of mice 7 days after burn injury and down-regulated serum IL-10. Furthermore, similar IL-18 therapy up-regulated serum IFN-gamma levels in mice with experimental bacterial peritonitis 7 days after burn injury and greatly decreased mouse mortality. Thus, IL-18 therapy restores the Th1 response and may decrease the susceptibility to bacterial infection in mice with burn injury.
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PMID:IFN-gamma production from liver mononuclear cells of mice in burn injury as well as in postburn bacterial infection models and the therapeutic effect of IL-18. 1237 Mar 78

Bacterial infection is a common complication in cirrhotic patients. The portal hypertension as well as the immune depression observed in these patients can explain this high incidence of bacterial infection. Because of the high probability of cirrhotic patients to develop infections, antibiotic prophylaxis is warranted in some conditions, such as upper gastrointestinal bleeding or after spontaneous bacterial peritonitis. Nevertheless, antibiotic prophylaxis is not widely recommended for cirrhotic patients.
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PMID:Current aspects of antibiotic prophylaxis for upper gastrointestinal bleeding in cirrhosis patients. 1249 10

Patients with liver cirrhosis have an impaired function of reticuloendothelial system; moreover they exhibit several defects of cellular and humoral immunity. These deficiencies enhance their susceptibility to bacterial infections. The prognosis is better if the infection is detected as early as possible and treated adequately. Except in cases of septicemia, empirical monotherapy is effective. Broad-spectrum beta-lactam antibiotics have proved efficient for the treatment of severe infections; a limitation of third-generation cephalosporins is their ineffectiveness against Enterococci; the acylureidopenicillins may be a good choice since they are active against Enterococci and most enteric, pulmonary and urinary pathogens, including Escherichia coli and Streptococcus pneumoniae which are the pathogens most frequently isolated from cirrhotic patients with severe infection. Similarly, the combination of a beta-lactamase inhibitor with a penicillin may offer an adequate antibacterial spectrum. Piperacillin, like other beta-lactam antibiotics, can induce leukopenia in patients with cirrhosis; the more severe the hepatic dysfunction, the greater the risk; a reduction in dosages is necessary. Meropenem monotherapy is effective and safe for the initial therapeutic regimen of bacterial infection. The fluoroquinolones may be useful for the treatment of infections in liver cirrhosis; however, the marginal activity against S. pneumoniae is a drawback. Oral long-term fluoroquinolone administration is utilized for the prevention of spontaneous bacterial peritonitis recurrence; selective intestinal decontamination with fluoroquinolones is useful in preventing bacterial infections in cirrhosis with gastrointestinal hemorrhage. Given the high risk of nephrotoxicity due to aminoglycosides in liver cirrhosis, these antibiotics should be used only in cases of severe infection with septicemia, in which beta-lactam-aminoglycoside combination is indicated for rapid bactericidal effect and enhanced killing afforded by synergism. Perhaps a short course (no more than 3 days) and a once-daily schedule of administration would minimize the risk of aminoglycoside-induced nephrotoxicity.
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PMID:[The choice of antibiotic therapy for bacterial infections in patients with cirrhosis of the liver]. 1496 93

Incidence of bacterial infections in hospitalised patients with liver disease is high. Due to a liver dysfunction immune reactivity is significantly impaired and bacterial infections are more frequent. Also incidence of nosocomial infections is higher in patients with liver disease compared to patients hospitalised for other conditions. To make a differential diagnosis of infectious and non-infectious aetiology of an inflammation is very difficult. Characteristic laboratory tests for bacterial infection include test of a number of leucocytes in peripheral blood, differential count of leucocytes, erythrocyte sedimentation, procalcitonin, C-reactive protein, tumor necrosis factor alpha, interleukin-1, interleukin-6, interleukin-8, and complement fragment C3a. Clinically the most significant are C-reactive protein test and procalcitonin test. Procalcitonin is a protein, a calcitonin precursor, which is in healthy individuals produced by cells of thyroid gland. A half-life of procalcitonin in serum is 20-24 hours which makes it suitable for daily monitoring and enables to control a course of treatment and to distinguish bacterial infection from other types of inflammations. Procalcitonin levels rise in bacterial, parasite, and yeast infections. Elevated procalcitonin levels appear only in inflammations of an infectious etiology with systemic signs. In patients with liver cirrhosis bacterial infections are more frequent. They usually include spontaneous bacterial peritonitis, infection of the respiratory system, urinary infections, and bacteremia. A timely proof of a bacterial infection and an appropriate and effective antibiotic therapy lead to an improvement of the general state of a patient and to his/her better prognosis. Procalcitonin determination is appropriate for diagnosing infections and control of treatment.
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PMID:[Procalcitonin as an indicator of infection in patients with liver cirrhosis]. 1507 92


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