Serum gamma INF inducing factor [IL18] levels in patients with chronic liver disease

Interleukin 18 [IL18] is likely to play a role in inflammatory liver disease, it is currently regarded as the primary inducer of INF gamma in inflammatory reaction, in chronic hepatitis C a significant up regulation of IL 18 in the inflammatory infiltrate has been demonstrated. The study aimed to evaluate the serum levels of IL18 in patients with chronic liver disease and to assess its role in the clinical outcome of patients with liver injury. The cohort consisted of 60 subjects age ranged from 32-65 ys, they were stratified into 4 groups; G1: 15 patients with chronic liver diseases. G2: 15 patients with liver cirrhosis G3: 15 patients with Hepatoma. G4: 15 healthy subjects serving as control Beside full routine laboratory tests. The patients were tested for autoantibodies [ANA,SMA, AMA] ,viral markers and determination of IL18 serum by ELISA. At presentation a significant increase of serum IL18 was found in all groups compared to control in addition IL18 was significantly higher in G3 than G2, furthermore it was significantly higher in G2 than G1. Moreover IL18 showed also a significant positive correlation with AST, ALT,TB,DB. in contrast a negative correlation was detected with albumin and PT It can be concluded that IL18 is likely to be involved in the pathogene-sisof human liver diseases

Role of Gastroesophageal reflux in the pathogenesis of otitis media with effusion

This prospective comparative study was designed to define the presence of Helicobacter pylori [H. pylori] in middle ear effusion [MEE] and to compare pepsin levels both in serum and MEE as a trial to define a possible role for them in the pathogenesis of otitis media with effusion [OME]. The study included 40 children with chronic OME, 30 patients had bilateral OME, whereas 10 patients had unilateral OME. Blood samples were taken before induction of anesthesia and MEEs were collected at the time of myringotomy and was divided into two parts; the first was used for determination of the presence of H. pylori and the second part for determination of pepsin-like activity. H. pylori could be detected in 48 effusion samples [71.6%] obtained from 21 patients with bilateral OME [21/30; 70%] and 6 patients with unilateral OME [6/10; 60%]. Twenty-seven [56.3%] samples were obtained from right ear and 21 samples [43.7%] were obtained from the left ear. There was a negative significant correlation, [r=-0.662, P<0.05] between age and the presence of H. pylori. Pepsin-like activity was detected in 35 samples [52.2%], at pH 2.2 in 26 samples [74.3%] and at pH 8 in 9 samples [25.7%]. There was a significant increase [P<0.05] of total pepsin-like activity in effusion compared to levels detected in serum. Furthermore, mean pepsin-like activity detected at pH 2.2 showed a significant increase compared to activity level detected both in serum and to that detected in effusion at pH 8, moreover, mean pepsin-like activity detected at pH 8 showed a significant increase compared to activity level detected in serum. There was a positive significant correlation between the presence of H. pylori and the activity level of pepsin, [r=0.81, P<0.05]. We could conclude that gastric reflux with its acidity and contents of H. pylori and pepsin plays a role in pathogenesis of otitis media with effusion

Role of granulocyte-colony stimulating factor [G-CSF] as early marker in diagnosis of neonatal sepsis

Neonatal sepsis is a life-threatening disease with an incidence of 1 to 10 per 1000 live births, and a mortality rate of 15% to 50% [Remington and Klein 1990]. The clinical signs of neonatal sepsis are nonspecific and indistinguishable from those caused by a variety of neonatal noninfective disorders, such as aspiration syndrome, maladaptation. and respiratory distress syndrome [RDS]. It is therefore recommended for all neonates who develop these signs to start empirical antimicrobial therapy [Remington and Klein, 1995]. Our work was carried out on 56 neonates [37 males and 19 females] selected from Benha University Hospitals and from "Center EI Gameeia El Shareya for neonates at Nasr City" in the period from March 2002 to January 2003. For each case we performed G-CSF serum level and the preliminary laboratory tests [CBC, CRP, blood cultures] and accordingly our patients were classified into 3 groups: Group I: [Proven sepsis with +ve blood culture result]. Group II: [Suspected sepsis with -ve blood culture result and suspected clinical and laboratory sepsis] and Group III: [Non-septic neonates with -ve blood culture and - ve CRP]. Our results were tabulated, statistically analyzed and recommendations were put

Plasma alpha glutathione S - transferase in chronic hepatitis C infection in Egypt

Chronic hepatitis C [CHC] infection is a progressive disease whose activity must be regularly assessed. alpha -Glutathione S-transferase [alpha -GST] has been suggested as a better marker of hepatocellular damage than aminotransferases in toxic and autoimmune hepatitis. The present study assessed alpha -GST as a biochemical marker of hepatocellular damage in 50 Egyptian patients with CHC [seropositive for anti-hepatitis C virus [HCV] and HCV-RNA]. They were evaluated for conventional liver biochemistry, plasma alpha -GST, serum HCV-RNA levels and liver biopsy. Plasma alpha -GST was significantly higher in CHC patients than the reference values [p < 0.01] Sixteen patients [32%] had normal values for alanine aminotransferase [ALT], plasma alpha -GST was elevated in 11 of them [3 with minimal hepatitis; 6 mild and 2 moderate hepatitis]. Elevated plasma alpha -GST levels may indicate a hepatocellular damage even when ALT level is normal in CHC infection. Plasma alpha -GST was significantly higher in cirrhotic than non-cirrhotic patients [p < 0.01] suggesting that alpha -GST measurement is probably a sensitive test detecting liver damage occurring in association with cirrhosis. Plasma alpha -GST was significantly correlated with ALT [r = 0.67, p < 0,01] and aspartate aminotransferase [AST] [r = 0.62, p < 0.01] suggesting that alpha -GST may be a potential indicator of chronic hepatocellular damage due to HCV. Furthermore, plasma alpha -GST was significantly correlated with histologic grading score of hepatitis activity [r = 0.94, p < 0.01] and staging score of architectural alterations [r = 0.65, p < 0.01] indicating that plasma alpha -GST may be a sensitive and non invasive marker for detecting hepatitis activity and hepatocellular damage in CHC patients. There was a non-significant correlation between alpha -GST and serum HCV-RNA level indicating that plasma alpha -GST could not reflect the degree of viremia in these patients. The present data showed that alpha-GST has the highest sensitivity, specificity and accuracy [84%, 90% and 90%, respectively] for the diagnosis of parenchymal disintegrity and hepatocellular damage associated with chronic HCV infection followed by ALT [68%, 85% and 80%, respectively] then AST [62%, 75% and 68%, respectively]. This may indicate that alpha -GST gives better results than ALT and AST and may be preferred to them for monitoring hepatocellular damage associated with HCV infection. In conclusion, plasma alpha-GST determination appeared to be a sensitive, specific and non-invasive biochemical marker for detecting hepatocellular damage and may have a role in the follow up of CHC patients