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

Hemophilus influenzae, usually pathogenic in the pediatric population, caused septicemia and peritonitis in the cirrhotic adult described here. Susceptibility to this unusual adult pathogen was perhaps related to liver disease or corticosteroid treatment. This organism has not previously been associated with the syndrome of spontaneous bacterial peritonitis in an adult.
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PMID:Spontaneous peritonitis due to Hemophilus influenzae in an adult. 31 18

Pasteurella multocida has been the etiologic agent in at least three cases of "spontaneous" bacterial peritonitis (SBP). We report another patient with P. multocida bacteremia and SBP and suggest that there may be more than a chance association between cirrhotic liver disease and this unusual organism which rarely causes sepsis in man.
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PMID:Pasteurella multocida bacteremia associated with peritonitis and cirrhosis. 60 99

Patients with low protein ascites and deficient ascitic fluid opsonic activity have been shown to be unusually predisposed to development of spontaneous bacterial peritonitis. Survivors of spontaneous peritonitis frequently develop recurrent infection. Diuresis has been shown to increase the ascitic fluid opsonic activity of patients who have never had spontaneous bacterial peritonitis. Patients with adequate opsonic activity are protected from ascitic fluid infection. Theoretically, the subset of patients who develop spontaneous peritonitis may have such severe liver disease that (i) their ascites is refractory to diuretic therapy or (ii) their ascitic fluid opsonic activity does not increase in response to diuresis. In this study, opsonic activity and concentrations of total protein and complement components were measured in the ascitic fluid of 11 patients who were hospitalized with spontaneous bacterial peritonitis and who responded to oral diuretics. The mean values of all of these parameters were found to increase significantly comparing the end-of-diuresis samples to the specimens that were diagnostic of ascitic fluid infection. Patients who survive spontaneous bacterial peritonitis are able to increase their ascitic fluid total protein and opsonic activity in response to diuresis. This increase in endogenous antimicrobial activity may help prevent recurrence of ascitic fluid infection.
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PMID:Diuresis increases ascitic fluid opsonic activity in patients who survive spontaneous bacterial peritonitis. 150 Jun 89

We present data on 10 patients (5 men and 5 women, aged 21-56 yrs) with end-stage liver disease or tumour who underwent orthotopic liver transplantation at Groote Schuur Hospital between October 1988 and June 1991. Standard surgical techniques were used for procuring the donor liver, the recipient hepatectomy and the implantation of the liver. The venovenous bypass method was used in all but 2 patients. Postoperative immunosuppression was usually achieved with cyclosporin, azathioprine and low-dose steroids. Six patients were treated with prophylactic OKT3. Rejection episodes were treated with bolus doses of intravenous steroids. The indications for liver transplantation included chronic active hepatitis progressing to cirrhosis (5), biliary cirrhosis in association with inflammatory bowel disease (1), sclerosing cholangitis (2), alpha 1-antitrypsin deficiency (1), and tumour (1). All patients with chronic liver disease had experienced at least one complication, examples of which included encephalopathy, bacterial peritonitis, ascites, variceal bleeding and septicaemia. Serious postoperative complications included acute rejection of the transplanted liver, renal and liver failure that responded to intensive care support and medical management. One patient died on the 11th postoperative day with complications of bleeding oesophageal ulcer, shock and fungaemia. The remaining patients are alive and well 1-31 months after transplantation.
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PMID:Orthotopic liver transplantation at Groote Schuur Hospital. 150 34

To investigate the possibility that low complement concentrations in the plasma and ascites of patients with severe liver disease could be secondary to complement consumption, complement activation was studied in 32 patients with severe liver disease, 11 of whom had spontaneous bacterial peritonitis (SBP). In patients with SBP, plasma C3 and C4 were significantly lower than in uninfected patients (mean values 0.74 v 1.13 g/l, p less than 0.01 and 0.20 v 0.28 g/l, p less than 0.05 respectively). Plasma complement activation via the classical pathway, as shown by C4d/C4, was significantly increased in patients with SBP compared with uninfected patients (37.3 v 22.2, p less than 0.01) as was C3d/C3 (14.0 v 8.11, p less than 0.01), but there was no significant difference in Ba/B between SBP and uninfected patients. Ascitic C3 concentrations were higher in patients without SBP than in infected patients (0.37 v 0.08 g/l, p less than 0.05), as were factor B values (0.11 v 0.03 g/l, p less than 0.05). There was no significant difference in ascitic C4 concentrations in patients with SBP compared with uninfected patients (0.03 v 0.07 g/l). Although consumption of C3, as shown by C3d/C3 in ascites, was increased in infected patients compared with uninfected patients (79.1 v 36.1, p less than 0.05), there was no difference in ascitic complement activation between the groups for either the classical or alternative pathways. In SBP, decreased plasma C3 and C4 are primarily caused by increased activation of the classical pathway and not impaired hepatic synthesis. Activation and consumption of C3 is one factor causing the low ascitic C3 concentrations observed in SBP.
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PMID:Activation of the classical complement pathway in spontaneous bacterial peritonitis. 156 47

Bacterial peritonitis has been known to complicate severe liver disease. Aerobic organisms are responsible for the vast majority of cases, whereas anaerobic bacteria are responsible for less than 5% of all cases reported in the literature. We now report a case of Clostridium cadaveris anaerobic bacterial peritonitis in a 58-yr-old female, an organism that to our knowledge has not been previously implicated as an infectious agent in this entity.
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PMID:Clostridium cadaveris: an unusual cause of spontaneous bacterial peritonitis. 172 12

Serum concentrations of cancer antigen 125 (CA 125) were determined for 373 patients with various liver diseases: 57 with acute hepatitis, 57 with chronic hepatitis, 244 with liver cirrhosis (86 compensated and 158 decompensated), and 15 with primary liver cancer. The antigen was measured simultaneously in the serum and ascitic fluid of 46 of the patients with liver cirrhosis and sequentially in the serum and ascitic fluid of another 25 cirrhotics treated with paracentesis and (or) diuretics. Abnormal results for CA 125 were detected in sera from 4% of the patients with acute or chronic hepatitis, 60% of the patients with liver cirrhosis, and 67% of the patients with primary liver cancer. The main factor associated with abnormal serum concentrations of this antigen was the presence of ascites, with pathological CA 125 values in 94% of patients with ascites without jaundice (mean 566 +/- 528 arb. units/mL), compared with only 40% of patients with jaundice and without ascites (mean 40.1 +/- 28.5 arb. units/mL) (P less than 0.001). High concentrations of CA 125 were mainly associated with spontaneous bacterial peritonitis. The serum concentration of CA 125 decreased after treatment with paracentesis, but increased in patients treated with diuretics rather than paracentesis. The release of this antigen in liver cirrhosis appears to be independent of the liver disorder and, rather, results from peritoneal synthesis of this antigen.
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PMID:Cancer antigen 125 in serum and ascitic fluid of patients with liver diseases. 186 98

Asymptomatic bacterascites is defined as the presence of bacteria in ascitic fluid without clinical features of peritonitis or increased ascitic fluid polymorphonuclear cells. Asymptomatic bacterascites is a controversial entity, and little information is available regarding its spontaneous evolution. Clinical features, bacteriological data and outcome in 22 cirrhotic patients with asymptomatic bacterascites are reported and are compared with those of a group of 36 cirrhotic patients with spontaneous bacterial peritonitis. Eleven patients had gram-negative bacteria and 11 had one gram-positive bacteria. Only in three patients (13.6%) did peritonitis develop. Twelve patients received no antibiotic therapy, and in none did peritonitis develop. At 1 month, 27% of patients with asymptomatic bacterascites had died. Patients with asymptomatic bacterascites had less-severe liver disease; they more frequently had gram-positive bacteria in ascitic fluid and had a lower 1-mo mortality rate than did patients with spontaneous bacterial peritonitis. We conclude that asymptomatic bacterascites is usually the transient residence of bacteria in ascitic fluid. Peritonitis rarely develops in patients with asymptomatic bacterascites and, in most of them, antibiotic therapy is not required.
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PMID:Asymptomatic bacterascites: is it spontaneous bacterial peritonitis? 206 60

Tuberculous peritonitis is a rare disease, which often goes unrecognized because of the subtle clinical clues and its insidous onset. We retrospectively analyzed the records of 37 cases of tuberculous peritonitis diagnosed over a 15-year period, and compared the clinical and diagnostic features of cirrhotic and noncirrhotic patients. In cirrhotic patients, tuberculous peritonitis can simulate ascites from liver disease or spontaneous bacterial peritonitis. The diagnosis is difficult in these patients because the ascitic fluid may not be of the exudative type as a result of the low albumin level in serum, and lymphocytes do not predominate in all cases. Adenosine deaminase (ADA) activity in ascitic fluid was elevated (higher than 40 U/L) in all 11 patients (four patients with hepatic cirrhosis). The time required to achieve a correct diagnosis was significantly longer in cirrhotic than in noncirrhotic patients. The overall mortality was 13%, with deaths occurring exclusively among cirrhotic patients. We emphasize that tuberculous peritonitis in cirrhotic patients can present an atypical picture. A considerable element of suspicion is necessary.
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PMID:Tuberculous peritonitis: a study comparing cirrhotic and noncirrhotic patients. 214 14

Rational treatment of portal hypertensive complications requires a knowledge of the cause of portal hypertension and an assessment of the severity of liver disease. In the United States, chronic liver disease, usually due to alcohol, is the most common underlying cause. The history, physical examination, and laboratory analysis are usually sufficient to confirm the presence of underlying liver disease. If there is any question as to the etiology of portal hypertension, however, a more complete evaluation is required, whether the presenting complication is ascites, variceal bleeding, or hypersplenism. Usually, such an evaluation will require a liver biopsy, portal pressure measurement, and angiography. Occasionally, a noninvasive evaluation will be sufficient, but the value of these noninvasive parameters is still under investigation. Surgical mortality generally depends on the severity of the liver disease. Therefore, surgical intervention must be carefully considered in comparison to other therapeutic modalities depending on the patient's hepatic functional reserve. Secondary bacterial peritonitis due to perforation requires surgery regardless of the severity of the underlying liver disease.
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PMID:Diagnosis and hemodynamic assessment of portal hypertension. 218 5


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