Patients with Spontaneous Bacterial Peritonitis: DISCUSSION

Patients with Spontaneous Bacterial Peritonitis disscus

SBP is a major problem encountered in patients with liver cirrhosis, with an incidence of 5-30% of all infections, and hospital mortality constitutes about 50% of all SBP cases. Obviously, a positive bacteriological culture of ascitic fluid is the “gold standard” and prerequisite for the diagnosis of SBP. The value of ascitic leukocyte count has been studied in detail and is still accepted as a “silver standard” diagnostic criterion for SBP.

Cytokines, such as IL-6, IL-1 and TNF-oc, are parts of a network in the regulation of cellular immune response and in the induction of acute-phase protein synthesis and, thus, they play a crucial role in inflammatory reactions. High plasma levels of TNF-oc were found in patients with infectious diseases and in patients with fulminant hepatic failure and alcoholic hepatitis. In the patients with SBP, levels of TNF-oc in ascitic fluid decreased during the first 48 hours of antibiotic treatment. All these data suggest that the inflammatory response to infection, as estimated by the levels of cytokines in plasma or ascitic fluid, is increased in cirrhotic patients and that cytokines may have prognostic significance in patients with liver failure. Cialis Jelly

The liver is an important site of synthesis and the major organ for clearance of several cytokines. The source of cytokines found in the ascitic fluid of the patients is unknown. Cytokines in ascitic fluid in SBP probably derive from the peritonea macrophages and mesothelial cells. High mean ascitic fluid-to-plasma ratios of TNF-oc levels could suggest that the elevated TNF-oc concentration may reflect not only increased peritoneal permeability but also increased local synthesis of the cytokines.

Cytokines play a key role in the regulation of cells of the immune system and also have been implicated in the pathogenesis of malignant diseases. Bacterial products may induce TNF-oc and soluble TNF-r elevation from the leukocytes in the infected ascites. The elevated TNF-oc levels in the circulation cause a increase in TNF-r levels. TNF-r levels were elevated 100-500 times when compared with TNF-oc. The diagnostic capability of ascitic fluid and serum cytokines levels were controversial. Вас et al. reported serum and ascitic fluid TNF-oc levels were not significantly different between the cirrhotic and the malignant ascitic patients. In a few studies, ascites from patients with malignancy had significantly elevated levels of TNF-oc compared with liver diseases and normal peritoneal fluid. Moradi et al. reported that the patients with ovarian cancer have elevated levels of TNF-oc in serum and ascitic fluid. Patients with infected or malignancy-related ascites also showed higher soluble TNF-r concentrations in plasma than did patients with hepatic ascites. In addition, this study demonstrated no difference between infected and malignant ascites. The sensitivity and specificity of TNF-r p55 in differentiating malignant and infected ascites from uncomplicated ascites of chronic liver disease were 86%) and 95%o, respectively, and 79%o and 86% for TNF-r p75. In our study, we detected elevated levels of ascitic fluid TNF-oc in the SBP and malignant groups when compared with uncomplicated sterile cirrhotic ascites group. Serum TNF-oc was detected to be higher in SBP when compared with the malignant and chronic liver disease groups. In our study, sensitivity and specificity of ascitic fluid TNF-oc in discriminating malignant were 77%) and 60%) and infected ascites from sterile ascites were 82% and 66%, respectively. In addition, sensitivity and specificity of TNF-r p60 in discriminating malignant were 74% and 70% and infected ascites from sterile ascites were 80% and 76%, respectively. viagra jelly online

The concentration of CRP in serum has been found to be helpful in the diagnosis and management of patients with a wide variety of inflammatory conditions. An abnormal serum CRP level was found in 78% of patients with hepatocellular carcinoma, 8% of patients with asymptomatic hepatitis В surface antigen carriers, 5% of patients with chronic hepatitis, and 9% of cirrhotic patients without complications. It was also discovered in 72% of cirrhotic patients complicated with bacterial infections, gastrointestinal bleeding, hepatic encephalopathy or massive ascites, 67% of nine common bile duct stone patients, and 79% of patients with malignancies other than hepatocellular carcinoma. The application of this test to serous body fluids has been less extensive. As an adjunct to the diagnosis of bacterial meningitis, cerebrospinal fluid CRP was initially reported to have sensitivity of 100% and a specificity of 94%. The serum CRP concentration was found to separate patients into infected (peritonitis) and noninfected categories better than the ascitic fluid CRP concentrations. Presumably, the reason for these unexpected results is that the CRP is not produced in the inflamed body cavity but is produced in the liver and only enters a body cavity by leakage of serum protein into the body fluid. Runyon reported the ascitic fluid CRP concentrations of patients with sterile portal-hypertension-related ascites were not significantly different from those of infected specimens. However, the serum CRP values were significantly higher in patients with peritonitis than in patients with sterile portal-hypertension-related ascites. In our study, mean ascitic fluid CRP levels were detected to be higher in the SBP and malignant groups than the sterile cirrhotic ascites group. Serum CRP levels were higher in the SBP group than the malignant and sterile cirrhotic ascites group. In our study, sensitivity and specificity of ascites fluid CRP in discriminating malignant were 84% and 67% and SBP from sterile ascites were 90% and 76%, respectively. CRP levels may be elevated in the ascitic fluid due to increased capillary permeability in SBP group and peritonitis carcinomatosis. The half-life of CRP will increase up to 18 hours in actively infected cases. Moreover, the clearance of CRP in the ascitic fluid was unknown. CRP may also accumulate in the local inflammatory events as well.
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