Comparative study of the urinary level of aflatoxin M1 in patients with hepatitis C virus (HCV) and healthy people

Abstract Background: Aflatoxins are the secondary metabolites produced by the flavi section of Aspergillus. Aflatoxin B1 (AFB1) is hepatocarcinogen, teratogen and mutagen. Aflatoxin M1 (AFM1) is the hydroxylated metabolite of AFB1. The liver protects the body by lowering the toxicity of AFB1 to form different hydroxylates like AFM1. According to the synergistic effect of hepatitis and also AFB1 as the parent molecule of AFM1, the main purpose of this study was to assess the relationship between the mean levels of AFM1, in the hepatitis-C-virus (HCV)-positive patients compared to healthy individuals. Methods: After the tests of liver function enzymes, the level of AFM1 was measured and compared in the urine sample of 71 patients with HCV and 71 healthy individuals. The AFM1 of urine samples were tested using enzyme-linked immunosorbent assay (ELISA) method. Besides, the levels of serum glutamic-oxaloacetic transaminase (SGOT), serum glutamic-pyruvic transaminase (SGPT), alkaline phosphatase, total bilirubin and direct bilirubin were assessed in the blood samples. Findings: The urine of 29.7% of HCV-positive patients and 19.71% of healthy individuals consisted of some amount of AFM1. The mean level of AFM1 was 2.45 and 1.66 pg/ml in patients and controls, respectively; which was significantly different (P = 0.005). The mean levels of SGPT and alkaline phosphatase were significantly more among HCV-positive patients with AFM1 compared to those without AFM1 (P = 0.012). But, there was not any significant difference between the mean levels of SGOT and total and direct bilirubin between the HCV-positive patients with and without AFM1. Conclusion: The mean levels of SGPT and Alkaline phosphatase, which are more exclusive to survey of liver function, were significantly different between HCV-positive patients with and without AFM1. Consequently, progression of the chronic liver disease is caused by the existence of AFB1 in HCV-positive patients; therefore, the reduction of AFM1 via improving the food consumption pattern can prevent this progression. Keywords: Aflatoxin M1, Hepatitis C virus (HCV), Liver dysfunction

Comparison of Standard Triple Therapy Regimen with Sequential Therapy Regimen Containing Levofloxacin Used for The Eradication of Helicobacter Pylori in Patients with Gastrointestinal Infection Caused by Helicobacter Pylori

Objectives: The aim of this study was to compare standard triple therapy regimen with sequential therapy regimen containing levofloxacin used for the eradication of H. pylori in patients with gastrointestinal infection caused by H. pylori. Methods: This single blind clinical trial study was conducted on 96 patients with positive Rapid Urease Test (RUT) who were referred to the Endoscopy center of Hajar Hospital in Shahrekord city, located in southwest of Iran. The patients were randomly assigned into two treatment groups: sequential therapy regimen and triple therapy regimen. The patients in the first group received sequential therapy regimen including omeprazole, amoxicillin, levofloxacin, and tinidazole; the second group of patients received a triple therapy regimen consisting of omeprazole, amoxicillin, and clarithromycin. Four weeks after the end of the treatment, using H. pylori Stool Antigen (HpSA), a test was performed to prove the eradication of H. pylori. The influences of patients’ age, gender and eradication level were also investigated. Results: There were significant differences between the two groups in terms of age and education. While H. pylori eradication rate was 67.3% in the sequential therapy regimen, it was 66% in standard triple therapy regimen. In addition, among patients receiving triple therapy regimen, being aged older than 40 years had a significant relationship with eradication. Moreover, in patients receiving sequential therapy regimen, education level had a significant relationship with eradication. Conclusion: There was no statistically significant difference between the two therapy groups in terms of H. pylori eradication rate. However, given the low rates of H. pylori eradication in both sequential and triple therapy regimens observed in the present study, it seems that it is necessary to conduct further research on the bacterial resistance to the prescribed antibiotic

A COMPARATIVE STUDY OF P53 PROTEIN IMMUNOREACTIVITY IN DIFFERENTIATED AND UNDIFFERENTIATED TRANSITIONAL CELL CARCINOMA OF URINARY BLADDER

Abstract: INTRODUCTION: Transitional cell carcinoma (TCC) of the urinary bladder is one of the most common cancers, the incidence of which has been on the rise during the last few years. Histological criteria based on H & E staining are not always sufficient for determining the clinical course of an individual patient with bladder cancer. The aim of this study was to assess p53 protein Immunoreactivity in differentiated and undifferentiated TCC of urinary bladder. METHODS: The accumulation of p53 was investigated immunohistochemically in ..

A comparative study of one minute versus five seconds endoscopic biliary balloon dilation after small sphincterotomy in choleducolithiasis.

BACKGROUND Limited sphincterotomy and endoscopic papillary balloon dilation (EPBD) is a low-risk method for the treatment of choleducolithiasis. Traditionally one minute ballooning time (BT) is applied; however, the effective BT is not clear. In this study, we compare five seconds and one minute ballooning time. MATERIALS AND METHODS In this single-blind, randomized, clinical trial 60 patients with common bile duct (CBD) stones documented in ultrasonography or magnetic resonance cholangiopancreatography (MRCP), with no severe hepatic, biliary or systemic diseases, enrolled in the study. The patients were randomly assigned to receive EPBD with either five seconds (n = 31) or one minute (n = 29) ballooning time (BT) after endoscopic retrograde cholangiopancreatography (ERCP) and small sphincterotomy. Then stones were retrieved with an extractor balloon. The patients were followed for 48 hours to check the possible complications. RESULTS Successful CBD stone removal was the same in the five-second and one-minute BT groups (93.5% vs. 96.6%; P = 0.594). Pancreatitis occurred in three (9.7%) patients in the five-second BT group and in six (20.7%) patients in the one-minute BT group (P = 0.233). No hemorrhage or perforation was noted. CONCLUSIONS After a small sphincterotomy, EPBD in the five-second and one-minute BT groups had a similar efficacy. Small sphincterotomy combined with very short BT is a safe and effective method for CBD stone removal

Up-regulated CCL18, CCL28 and CXCL13 Expression is Associated with the Risk of Gastritis and Peptic Ulcer Disease in Helicobacter Pylori infection

Background: Helicobacter pylori (H. pylori) infection causes inflammation and increases the risk of developing peptic ulcer disease (PUD); however, the exact molecular mechanisms of PUD development remain unclear. The aim of this study was to investigate the expression of CCL18, CCL28, and CXCL13 in H. pylori-positive subjects in comparison with H. pylori-negative subjects, and to determine its association with different clinical outcomes and virulence factors. Methods: In total, 55 H. pylori-positive subjects with gastritis, 47 H. pylori-positive subjects with PUD, and 48 H. pylori-negative subjects were enrolled in this study. CCL18, CCL28, and CXCL13 expression were determined using real time polymerase chain reaction (PCR). The virulence factors of H. pylori such as cytotoxin-associated gene A (cagA), outer inflammatory protein A (oipA), blood group antigen-binding adhesin (babA), and vacuolating cytotoxin A (VacA) genes were evaluated using PCR. Results: CCL18, CCL28, and CXCL13 expression in H. pylori-positive subjects were significantly higher than H. pylori-negative subjects. CCL18 and CXCL13 expression in H. pylori-positive subjects with oipA+ and babA2+were significantly higher than H. pylori-positive subjects with oipA¯ and babA2¯. CCL18 and CXCL13 expression were found to be significantly elevated in H. pylori-positive subjects with gastritis compared with H. pylori-positive subjects with PUD. CCL28 expression was significantly higher in H. pylori-positive subjects with PUD compared with H. pylori-positive subjects with gastritis. Conclusions: The increased of CCL18 and CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis, while the increased of CCL28 may be involved in the pathogenesis of H. pylori-associated PUD

Up-regulated CCL18, CCL28 and CXCL13 Expression is Associated with the Risk of Gastritis and Peptic Ulcer Disease in Helicobacter Pylori infection

Background: Helicobacter pylori (H. pylori) infection causes inflammation and increases the risk of developing peptic ulcer disease (PUD); however, the exact molecular mechanisms of PUD development remain unclear. The aim of this study was to investigate the expression of CCL18, CCL28, and CXCL13 in H. pylori-positive subjects in comparison with H. pylori-negative subjects, and to determine its association with different clinical outcomes and virulence factors. Methods: In total, 55 H. pylori-positive subjects with gastritis, 47 H. pylori-positive subjects with PUD, and 48 H. pylori-negative subjects were enrolled in this study. CCL18, CCL28, and CXCL13 expression were determined using real time polymerase chain reaction (PCR). The virulence factors of H. pylori such as cytotoxin-associated gene A (cagA), outer inflammatory protein A (oipA), blood group antigen-binding adhesin (babA), and vacuolating cytotoxin A (VacA) genes were evaluated using PCR. Results: CCL18, CCL28, and CXCL13 expression in H. pylori-positive subjects were significantly higher than H. pylori-negative subjects. CCL18 and CXCL13 expression in H. pylori-positive subjects with oipA+ and babA2+were significantly higher than H. pylori-positive subjects with oipA¯ and babA2¯. CCL18 and CXCL13 expression were found to be significantly elevated in H. pylori-positive subjects with gastritis compared with H. pylori-positive subjects with PUD. CCL28 expression was significantly higher in H. pylori-positive subjects with PUD compared with H. pylori-positive subjects with gastritis. Conclusions: The increased of CCL18 and CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis, while the increased of CCL28 may be involved in the pathogenesis of H. pylori-associated PUD

Up-regulated CCL18, CCL28 and CXCL13 Expression is Associated with the Risk of Gastritis and Peptic Ulcer Disease in Helicobacter Pylori infection

Background: Helicobacter pylori (H. pylori) infection causes inflammation and increases the risk of developing peptic ulcer disease (PUD); however, the exact molecular mechanisms of PUD development remain unclear. The aim of this study was to investigate the expression of CCL18, CCL28, and CXCL13 in H. pylori-positive subjects in comparison with H. pylori-negative subjects, and to determine its association with different clinical outcomes and virulence factors. Methods: In total, 55 H. pylori-positive subjects with gastritis, 47 H. pylori-positive subjects with PUD, and 48 H. pylori-negative subjects were enrolled in this study. CCL18, CCL28, and CXCL13 expression were determined using real time polymerase chain reaction (PCR). The virulence factors of H. pylori such as cytotoxin-associated gene A (cagA), outer inflammatory protein A (oipA), blood group antigen-binding adhesin (babA), and vacuolating cytotoxin A (VacA) genes were evaluated using PCR. Results: CCL18, CCL28, and CXCL13 expression in H. pylori-positive subjects were significantly higher than H. pylori-negative subjects. CCL18 and CXCL13 expression in H. pylori-positive subjects with oipA+ and babA2+were significantly higher than H. pylori-positive subjects with oipA¯ and babA2¯. CCL18 and CXCL13 expression were found to be significantly elevated in H. pylori-positive subjects with gastritis compared with H. pylori-positive subjects with PUD. CCL28 expression was significantly higher in H. pylori-positive subjects with PUD compared with H. pylori-positive subjects with gastritis. Conclusions: The increased of CCL18 and CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis, while the increased of CCL28 may be involved in the pathogenesis of H. pylori-associated PUD

Up-regulated CCL18, CCL28 and CXCL13 Expression is Associated with the Risk of Gastritis and Peptic Ulcer Disease in Helicobacter Pylori infection

Background: Helicobacter pylori (H. pylori) infection causes inflammation and increases the risk of developing peptic ulcer disease (PUD); however, the exact molecular mechanisms of PUD development remain unclear. The aim of this study was to investigate the expression of CCL18, CCL28, and CXCL13 in H. pylori-positive subjects in comparison with H. pylori-negative subjects, and to determine its association with different clinical outcomes and virulence factors. Methods: In total, 55 H. pylori-positive subjects with gastritis, 47 H. pylori-positive subjects with PUD, and 48 H. pylori-negative subjects were enrolled in this study. CCL18, CCL28, and CXCL13 expression were determined using real time polymerase chain reaction (PCR). The virulence factors of H. pylori such as cytotoxin-associated gene A (cagA), outer inflammatory protein A (oipA), blood group antigen-binding adhesin (babA), and vacuolating cytotoxin A (VacA) genes were evaluated using PCR. Results: CCL18, CCL28, and CXCL13 expression in H. pylori-positive subjects were significantly higher than H. pylori-negative subjects. CCL18 and CXCL13 expression in H. pylori-positive subjects with oipA+ and babA2+were significantly higher than H. pylori-positive subjects with oipA¯ and babA2¯. CCL18 and CXCL13 expression were found to be significantly elevated in H. pylori-positive subjects with gastritis compared with H. pylori-positive subjects with PUD. CCL28 expression was significantly higher in H. pylori-positive subjects with PUD compared with H. pylori-positive subjects with gastritis. Conclusions: The increased of CCL18 and CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis, while the increased of CCL28 may be involved in the pathogenesis of H. pylori-associated PUD

Up-regulated CCL18, CCL28 and CXCL13 Expression is Associated with the Risk of Gastritis and Peptic Ulcer Disease in Helicobacter Pylori infection

Background: Helicobacter pylori (H. pylori) infection causes inflammation and increases the risk of developing peptic ulcer disease (PUD); however, the exact molecular mechanisms of PUD development remain unclear. The aim of this study was to investigate the expression of CCL18, CCL28, and CXCL13 in H. pylori-positive subjects in comparison with H. pylori-negative subjects, and to determine its association with different clinical outcomes and virulence factors. Methods: In total, 55 H. pylori-positive subjects with gastritis, 47 H. pylori-positive subjects with PUD, and 48 H. pylori-negative subjects were enrolled in this study. CCL18, CCL28, and CXCL13 expression were determined using real time polymerase chain reaction (PCR). The virulence factors of H. pylori such as cytotoxin-associated gene A (cagA), outer inflammatory protein A (oipA), blood group antigen-binding adhesin (babA), and vacuolating cytotoxin A (VacA) genes were evaluated using PCR. Results: CCL18, CCL28, and CXCL13 expression in H. pylori-positive subjects were significantly higher than H. pylori-negative subjects. CCL18 and CXCL13 expression in H. pylori-positive subjects with oipA+ and babA2+were significantly higher than H. pylori-positive subjects with oipA¯ and babA2¯. CCL18 and CXCL13 expression were found to be significantly elevated in H. pylori-positive subjects with gastritis compared with H. pylori-positive subjects with PUD. CCL28 expression was significantly higher in H. pylori-positive subjects with PUD compared with H. pylori-positive subjects with gastritis. Conclusions: The increased of CCL18 and CXCL13 may be involved in the pathogenesis of H. pylori-associated gastritis, while the increased of CCL28 may be involved in the pathogenesis of H. pylori-associated PUD