Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have assessed the levels of interleukin-1b (IL-1b) and interleukin-1 receptor antagonist (IL-1RA) in both serum and peritoneal dialysate effluents (PDE) from nineteen continuous ambulatory peritoneal dialysis patients (CAPD) without peritonitis and three CAPD patients with peritonitis. IL-1 beta and IL-1RA were tested using a specific ELISA immuno-assay. Fifteen normal healthy volunteers severed as control. The serum levels of IL-1RA in CAPD patients were significantly increased comparatively to their levels in healthy volunteers (p < 0.001). CAPD patients without peritonitis (stable patients) showed relatively low levels of IL-1RA in peritoneal dialysate effluents (114.4 +/- 85.1 pg/ml). Patients with peritonitis showed very high serum levels of IL-1RA at the onset of acute infection (4710 +/- 50 pg/ml). The levels of IL-1RA in PDE were very high during the onset of bacterial peritonitis (5744 +/- 254 pg/ml). The clinical recovery from peritonitis was characterized by a fall in IL-1RA in both serum and dialysate. Serum levels IL-1 beta showed a different pattern, it was not detectable in stable CAPD patients as well as in normal healthy volunteers. It was detectable only in serum of patients with peritonitis (10 +/- 0.8 pg/ml). Likewise, in most stable patients, IL-1 beta-PDE levels were not detectable, but substantial amounts can be detected in PDE during bacterial infection (80 +/- 15 pg/ml). The increase in serum and PDE levels of IL-1 beta during bacterial infection was very rapid, this cytokine disappeared in serum and PDE, 2 or 3 days before the clinical recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Interleukin-1 and its naturally occurring antagonist in peritoneal dialysis patients. 760 78

Selective bowel decontamination with the orally administered quinolone antibiotic, norfloxacin, has been shown to suppress gut gram-negative bacteria and help prevent gram-negative infections in cirrhotic patients who are at high risk of bacterial infection. Because this drug does not eradicate gram-positive organisms, it is conceivable that gram-positives could replace the suppressed gram-negatives in the gut and lead to subsequent infection. Also the effect of norfloxacin on translocation (as defined by culture positivity of mesenteric lymph nodes) has received little attention. In this study, the effect of oral norfloxacin on translocation, bacterial peritonitis, and survival was investigated in an animal model of carbon tetrachloride-induced cirrhosis and ascites. Treated rats received daily doses of orally administered norfloxacin from the onset of cirrhosis until they died or were killed. Controls received no antibiotic. Norfloxacin led to a reduction in bacterial peritonitis from 70% in untreated cirrhotic controls to 28% in treated cirrhotic rats; these data were statistically significant (P = .012). There was no effect on overall translocation rate (28% with norfloxacin vs. 50% without norfloxacin) (P > .1). Gram-positives were isolated in 100% of the bacterial peritonitis episodes and in 71.4% of culture-positive mesenteric lymph nodes in treated animals compared with only 25% of peritonitis episodes and 10% of culture-positive mesenteric lymph nodes of untreated cirrhotic controls (P < .01 for peritonitis and P < .05 for translocation). The survival rate was not different between groups (P > .1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of selective bowel decontamination with norfloxacin on spontaneous bacterial peritonitis, translocation, and survival in an animal model of cirrhosis. 776 17

Spontaneous bacterial peritonitis in liver cirrhosis is due to the passage of intestinal bacteria into intestinal lymph vessels, systemic circulation and ascitic fluid. It may occur in patients with severe portal hypertension and hepatic failure, impaired reticuloendothelial phagocytic activity and low ascitic fluid opsonic activity. Spontaneous bacterial peritonitis is a monomicrobial infection usually caused by gram-negative bacteria. The treatment of choice of spontaneous bacterial peritonitis is cefotaxime. Several subgroups of cirrhotic patients have been shown to be predisposed to develop spontaneous bacterial peritonitis, including cases with gastrointestinal hemorrhage, patients with high serum bilirubin and low ascitic fluid protein concentration (< 1 g/dl), and patients who had recovered from an episode of spontaneous bacterial peritonitis. Since spontaneous bacterial peritonitis is associated with a relatively high in-hospital mortality rate (20-40%), prophylactic measures to prevent this infection are required. Short-term and long-term selective intestinal decontamination with oral norfloxacin has proved highly effective in preventing bacterial infection and spontaneous bacterial peritonitis in bleeding cirrhotic patients as well as recurrence of spontaneous bacterial peritonitis.
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PMID:Spontaneous bacterial peritonitis in liver cirrhosis: treatment and prophylaxis. 784 26

Fifty-seven patients with decompensated cirrhosis were studied prospectively to assess the sensitivity and specificity of early clinical or biological signs of bacterial infection. Among them, 19 had proven infection on admission (7 spontaneous bacterial peritonitis, 5 bacteraemia, 3 urinary tract infections, 2 pneumonia, 1 dental abscess and 1 cholangitis). Fever, polymorphonuclear cell count, fibrinogen and C-reactive protein levels were found to be of little or no help in diagnosing bacterial infection on admission. Interleukin-6 plasma levels were, however, significantly different between infected (median: 1386 pg/ml, range: 237-20,000) and non-infected patients (median: 34 pg/ml, range: 0-4500, p < 0.00001). Levels above 200 pg/ml were always found in infected patients, giving a sensitivity of 100% and a specificity of 74%. C-reactive protein correlated weakly with interleukin-6 levels, indicating a defective acute-phase response in cirrhosis. Tumor necrosis factor alpha plasma levels were less sensitive (95%) and specific (68%) for the diagnosis of bacterial infection at a threshold of 50 pg/ml, but were more closely related to a poor patient outcome. In decompensated cirrhosis, interleukin-6 plasma levels on admission provided the most sensitive and specific tool for the diagnosis of bacterial infection.
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PMID:Interleukin-6: an early marker of bacterial infection in decompensated cirrhosis. 793 Apr 84

The reticuloendothelial system plays an important role in the prevention of bacterial infection in patients with cirrhosis. Few data are available, however, on its activity in such patients. The aim of this study was to evaluate the maximum removal capacity of hepatic reticuloendothelial system in patients with cirrhosis on the basis of study of the removal kinetics of increasing amounts of 99mTc millimicrospheres and to verify its value as a prognostic factor for death and development of spontaneous bacterial peritonitis. Common clinical and biochemical parameters, Pugh score, maximum removal capacity, aminopyrine metabolic capacity and galactose elimination capacity were measured in 43 patients with cirrhosis (33 with alcoholic cirrhosis, 8 with posthepatitic cirrhosis and 2 with cryptogenic cirrhosis). Hepatic plasma flow and indocyanine green plasma clearance were also measured in 16 of these patients. Reference range of maximum removal capacity was determined in seven normal subjects. Maximal removal capacity below the normal range was found in 24 patients (56%). In the whole series maximum removal capacity averaged 16 +/- 12 micrograms/kg body wt/min (mean +/- S.D.). Maximal removal capacity was significantly correlated with serum albumin, prothrombin index, Pugh score, aminopyrine breath test, galactose elimination capacity and indocyanine green plasma clearance but not with hepatic plasma flow. During follow-up of up to 48 mo, spontaneous bacterial peritonitis developed in six patients, all with impaired maximum uptake capacity, and 11 patients died. Survival was significantly shorter in patients with impaired maximum removal capacity than in those with normal maximum removal capacity (log-rank test: p = 0.024).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical significance of the evaluation of hepatic reticuloendothelial removal capacity in patients with cirrhosis. 811 87

Patients with decompensated liver cirrhosis have a high risk of bacterial infection and a worse prognosis. They have defects of the humoral defence mechanism; impaired antibody production and depressed serum complement levels. The cellular defence mechanism is also defective. The function of neutrophil and reticuloendothelial system is depressed. The clearance of enteric organisms from the portal circulation is impaired by portosystemic shunt and impaired Kupffer cell function. Patients with massive ascites are prone to spontaneous bacterial peritonitis due to gram negative enteric organisms.
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PMID:[Defects of defence mechanisms against bacterial infections in patients with liver cirrhosis]. 812 92

One hundred and seventy hospitalized patients with cirrhosis were included in a prospective and sequential study, to verify the prevalence and most frequent causes of bacterial infection. The differences in clinical and laboratory data between the two groups were analyzed: group I--80 patients who developed bacterial infection and group II--90 patients without bacterial infection. The prevalence or cumulative frequency of the development of bacterial infection during one hospitalization was 47.06%. Among these, the most frequent types of infection were: spontaneous bacterial peritonitis (SBP): 31.07%, urinary tract infection (UTI): 25.24% and pneumonia: 21.37%. Community infections were more frequent (56.25%) than nosocomial infections (32.50%) and they occurred sequentially in 11.25% of the cases. The agents responsible were gram negative bacteria in 72.34% of the cases. Clinical and biochemical parameters in bacterial infection were generally correlated with the severity of liver disease. Child-Pugh classification showed a predominance of class C in infected cirrhotic patients compared to non-infected ones. During hospitalization, the mortality rate of group I was 30% whereas in group II it was 5.55% (P = 0.0001). SBP and pneumonia were the most severe types of infection, with high mortality rates, 31.25% and 40.91%, respectively. These results indicate that bacterial infection is a severe complication in the course of cirrhosis.
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PMID:A prospective study of bacterial infections in patients with cirrhosis. 822 17

We describe a case of spontaneous bacterial peritonitis in a 53 year old man affected by cryptogenic micro-macronodular cirrhosis, portal hypertention, splenomegaly and hypersplenism, who was admitted with hepatic failure and septic shock and successfully treated with antibiotics (combination of clindamycin and netilmycin), surgical abdominal drainage and splenectomy. This case gave reason for a literature review and an update on the therapeutic options in these high risk patients, especially concerning the role of surgery. Spontaneous Bacterial Peritonitis (SBP) is defined as a bacterial infection of ascitic fluid in the absence of any septic focus. It is a typical life-threatening complication of hepatic cirrhosis with ascites. Mortality is very high and ranges from 75% to 97% of patients, due to septic shock and hepatic failure (hepatorenal syndrome, hepatic encephalopathy, gastrointestinal bleeding). Infection with a single organism is found in most cases. Gram negative bacilli are present in about 70% of cases and E. coli (less frequently Klebsiella, Serratia, Pseudomonas) is principally found. Gram positive cocchi comprise an additional 30% of cases. Anaerobic and microaerophilic organisms seem to be rare causes of SBP (2.7-6%); this finding is probably due to the intrinsic bacteriostatic activity of ascites, which contains high oxygen tension (70 mmHg) and is an inhospitable environment for bacteroides and Clostridia. The prevalent isolation of enteric organism suggest that the gut is the most frequent source of infection, even if the pathogenetic mechanism is not yet well known. The right treatment depends on differentiating primary (SBP) from secondary peritonitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Is the surgical treatment of spontaneous bacterial peritonitis still up-to-date?]. 824 98

Deficient production of nitric oxide may be responsible for the defective defense barrier and persistence of bacterial infection. To gain insight into amino acid-metabolism and L-arginine-nitric oxide system, we studied 34 end-stage renal disease (ESRD) patients on peritoneal dialysis (PD) (20 males, 14 females, with a mean age of 53.5 years and a mean duration on PD of 29.7 months). The concentrations of amino acids, including L-arginine, were measured in peritoneal dialysate and in the serum. The data demonstrated that patients with ESRD on PD have normal serum amino-acid profiles, whereas those with acute peritonitis develop L-arginine deficiency (from 99 +/- 9 to 52 +/- 9 mumol/L). In addition, levels of asparagine, glycine, proline (nonessential) as well as valine, threonine, and lysine (essential) were reduced in patients with peritonitis. The majority of patients with acute bacterial peritonitis have increased nitric oxide production as judged by the level of nitrites in the dialysate (36 +/- 2 vs 57 +/- 6 mumol/L). The recovery from peritonitis was associated with a decline in nitric-oxide generation. There was a smaller subgroup of these patients that showed paradoxically low nitrite levels during acute peritonitis. The nitrite: L-arginine ratio in the peritoneal dialysate was increased in patients with peritonitis, further suggesting the development of substrate deficiency. These findings implicate L-arginine as a conditionally essential amino acid in PD patients with acute peritonitis. Further studies are needed to address the issue of L-arginine supplementation in such patients.
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PMID:Decreased L-arginine during peritonitis in ESRD patients on peritoneal dialysis. 936 Jun 82

Mast cells are thought to contribute significantly to the pathology and mortality associated with anaphylaxis and other allergic disorders. However, studies using genetically mast cell-deficient WBB6F1-KitW/KitW-v and congenic wild-type (WBB6F1-+/+) mice indicate that mast cells can also promote health, by participating in natural immune responses to bacterial infection. We previously reported that repetitive administration of the c-kit ligand, stem cell factor (SCF), can increase mast cell numbers in normal mice in vivo. In vitro studies have indicated that SCF can also modulate mast cell effector function. We now report that treatment with SCF can significantly improve the survival of normal C57BL/6 mice in a model of acute bacterial peritonitis, cecal ligation and puncture (CLP). Experiments in mast cell-reconstituted WBB6F1-KitW/KitW-v mice indicate that this effect of SCF treatment reflects, at least in part, the actions of SCF on mast cells. Repetitive administration of SCF also can enhance survival in mice that genetically lack tumor necrosis factor (TNF)-alpha, demonstrating that the ability of SCF treatment to improve survival after CLP does not solely reflect effects of SCF on mast cell- dependent (or -independent) production of TNF-alpha. These findings identify c-kit and mast cells as potential therapeutic targets for enhancing innate immune responses.
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PMID:The c-kit ligand, stem cell factor, can enhance innate immunity through effects on mast cells. 985 20


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