Evaluation of Non Invasive versus Invasive Methods for Diagnosis of Helicobacter pylori Infection among Patients with Gastroduodenal Disorders.

H. pylori, a spiral gram-negative bacterium, is associated with gastroduodenal diseases. All H. pylori diagnostic assays have limitations. Cytotoxin-associated gene A (cag A), a virulence marker, can be identified by PCR. We evaluated H. pylori diagnostic methods, invasive: rapid urease test (RUT), and histopathological examination (HE), and serology as non-invasive method. Positive cases were studied for presence of cag A gene. Upper endoscopies and gastric biopsies were performed on 67 dyspeptic patients for RUT, HE and PCR. Anti H. pyloriIgG were measured by ELISA. Of 67 dyspeptic patients, 23 (34%) had more than one endoscopic finding, 46 (68.7%) were H.pylori positive by HE, and 21(31.3%) were negative with variable grades of mucosal antral neutrophil infiltration. Of the 46 HE positives, PCR detected CagA in 22 (47.8%). Using HE as the gold standard test, the sensitivity of ELISA and RUT was 93.48% and 86.96%, respectively; and the specificity was 85.71% and 47.62%, respectively. In conclusion, IgG detection by ELISA is a suitable screening test for diagnosis of H. pylori associated gastroduodenal diseases. Histopathology should be performed in ELISA negative cases to exclude infection.

Haematological side effect of Helicobacter pylori eradication.

The effect of Helicobacter pylori infection on systemic disorders is not well understood. This study was to evaluate the effect of H. pylori eradication on blood count, differential leucocytic count and RBCs indices. In this study, a total of 115 H. pylori positive patients underwent eradication triple therapy for one week, with cured 100 patients. Complete blood count, RBCs indices and differential leucocytic count were analyzed before 2 & 12 weeks after eradication for the cured patients. The results showed that two weeks after H. pylori eradication, platelets count significantly increased but total leucocytic counts and neutrophils were significantly reduced. After three months, RBCs count, Hb concentration, MCV and MCHC were significantly increased, but lymphocytic counts was significantly reduced.

The role of plasma transforming growth factor beta-1 in the development of fibrosis in patient with HCV related steatohepatitis.

Hepatitis C virus (HCV) is a major public health problem worldwide, which causes high rate of chronic liver disease such as liver cirrhosis and hepatocellular carcinoma. Plasma transforming growth factor Beta-1 (TGFB-1) is a member of large family of peptides, which has a major regulatory role in hepatic fibrosis and cirrhosis. The study evaluated the role of transforming growth factor Beta-1 (TGFB-1) in induction of fibrosis in liver parasites-free HCV patients with related steatohepatitis. Thirty HCV patients who were clinically and serologically positive were selected. They were diagnosed as fatty liver by abdominal ultrasonography; steatohepatitis and confirmed by histopathological biopsies examination. ELISA evaluated plasma transforming growth factor Beta-1 (TGFB-1) level. Also, 12 cross-matched subjects clinically, parasitologically and serologically free were used as a controls. The level of plasma transforming growth factor Beta-1 (TGFB-1) was highly elevated in the patients versus controls with mean +/- SD 18739.86 +/- 18539.46 and 6465 +/- 1142 respectively (P < 0.001). The TGFB-1 level in HCV related steato-hepatitis was elevated in all grades in contrast to controls (P < 0.05), without relation between the TGFB-1 levels and steatohepatitis severity. The TGFB-1 level showed high significant difference in all stages of fibrosis in patients in contrast to controls and the TGFB-1 level was very high when fibrosis started in stage I (P < 0.01) and tended to decrease in fibrosis of stage 2 & 3 (P < 0.05). There was highly significant positive correlation between TGFB-1 and body mass index (BMI) r = 0.774.