الفهرس 
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Abstract
SBP is one of the most serious complications of liver cirrhosis. SBP is diagnosed when there is an elevated ascitic fluid absolute PMN count (at least 250/mm3) and a positive ascitic fluid culture and without evidence of an intra-abdominal surgically treatable source of infection.
Spontaneous forms of ascitic fluid infection are the result of overgrowth of a specific organism in the intestine, translocation of that microbe from the intestine to mesenteric lymph nodes and resulting spontaneous bacteremia and colonization of susceptible ascitic fluid. Empirical antibiotic therapy must be initiated immediately after the diagnosis of SBP. In the 1990s, cefotaxime, a third generation cephalosporin, was extensively investigated in patients with SBP because at that time it covered most causative organisms and because of its high ascitic fluid concentrations during therapy.
Ascitic TREM 1 and Serum Hs CRP are useful serum marker for SBP can be used as marker of diagnosis. TREM‐1 is a 30‐kDa glycoprotein of the Ig family, consisting of a single extracellular Ig‐like domain of the V‐type, a transmembrane region, and a short intracytoplasmic tail.
C-reactive protein (CRP), named for its capacity to precipitate C-polysaccharide of Streptococcus pneumoniae, is a well-known marker of inflammation and is also used as a marker of infection in different settings. High sensitive CRP (hs-CRP) is more sensitive than CRP as an inflammatory marker. High sensitive CRP has been known to be elevated in chronic liver diseases and SBP. Hs-CRP is synthesized primarily by the liver in response to tissue damage; because its half-life is constant, the only determinant of the serum level is the rate of hs-CRP production in the liver.
The present study was held to study the changes in ascitic TREM 1 and serum hs CRP in liver cirrhosis and SBP and to evaluate its role as an emerging novel biomarker of SBP.
The study was conducted on 80 subjects in Alexandria Main University Hospital, Tropical Medicine Department, the subjects were divided into two groups. The first two groups consisted of 40 patients each. group I contained patients with liver cirrhosis with ascites with SBP while group II contained patients with liver cirrhosis with ascites without SBP.
Patients receiving antibiotics during the past week, Patients with infections other than SBP, Patients with secondary bacterial peritonitis, Peritonitis carcinomatosis, Pancreatic peritonitis, Malignancy, Tuberculosis and Patients with history of abdominal surgery were excluded from the study.
All patients were subjected to the following:
1. Detailed history and thorough clinical examination.
2. Laboratory investigations including
a. Routine investigations :
• Complete blood picture and ESR
• Blood urea and serum creatinine.
• Serum electrolytes (sodium, potassium)
b. Liver function tests and liver enzymes including serum alanine transaminase (ALT), serum aspartate transaminase (AST), serum albumin, serum bilirubin, prothrombin time, INR and alkaline phosphatase (ALP)
c. Ascitic fluid Chemistry (Protein, glucose, lactate dehydrogenase) and cytology (white blood cells, neutrophils, Lymphocytes, red blood cells).
d. Ascitic fluid culture and sensitivity.
e. Urine analysis, urine and blood culture.
3. Diagnosis of HCV by positive assays for HCV Ab by ELISA.
4. Diagnosis of hepatitis B by HbsAg and anti HBcore Abs.
5. Measurement of ascitic TREM 1 using ELISA.
6. Measurement of serum hs-CRP using BN II and BN ProSpec system.
7. Chest x- ray.
8. Abdominal and Pelvic ultrasonography.
9. Triphasic CT abdomen was performed for exclusion of HCC in cases of FHL by ultrasound.
Statistical analysis of data obtained from the present study revealed the following results:
• As regards haematological findings, total leucocytic counts were higher in groups I than group II.
• As regard ESR was higher in group I than in group II.
• Liver function tests showed lower serum albumin in groups I than group II.
• As regards ascitic fluid parameters, lower ascitic protein, higher ascitic LDH, higher ascitic neutrophils, higher ascitic lymphocytes were higher in group I than group II.
• No significant difference was found regarding Child Pugh score of groups I and II.
• Ascitic TREM 1 was found to be significantly higher in patients with liver cirrhosis and ascites with SBP than in patients with liver cirrhosis and ascites without SBP.
• Serum hs CRP was found to be significantly higher in patients with liver cirrhosis and ascites with SBP than in patients with liver cirrhosis and ascites without SBP.
• Ascitic TREM 1 was found to be significantly higher in patients with massive ascites than patients with moderate and mild ascites.
• The ROC curve for ascitic TREM 1 was significant (p <0.001) and showed that the cutoff point discriminating SBP from other group was 546 pg/ml, with sensitivity of 85%, specificity of 62.5%, positive predictive value of 69.4% and negative predictive value of 80.6%.
• The ROC curve for serum hs CRP was significant (p <0.001) and showed that the cutoff point discriminating SBP from other group was 18.8 mg/l with sensitivity of 90%, specificity of 70%, positive predictive value of 75% and negative predictive value of 87.5%.
• The ROC curve for combined ascitic TREM 1 and serum hs CRP were significant (p <0.001) and showed that the cutoff point discriminating SBP from other group was 546 pg/ml and 18.8 mg/l respectively with sensitivity of 70%, specificity of 80%, positive predictive value of 77.78% and negative predictive value of 72.73 %.