Impact of helicobacter pylori on gastric mucosal cell proliferation

The interaction of H. Pylori and gastric mucosal proliferation was measured by means of flow cytometry. This study included 40 patients proved to have gastritis by upper GI endoscopy and also had H. Pylori positive in histopathological examination of gastric biopsies. The patients were divided into two groups. The first group [lansoprazole group] included 20 patients who received 30 mg lansoprazole twice daily to remove HCl effect on gastric mucosal cell proliferation. While, the second group [triple therapy group] included 20 patients who received two weeks H. pylori eradication regimen in the form of twice daily 30 mg lansoprazole, clarithromycine [500 mg] and amoxycillin [1 gm]. The flow cytometric analysis showed that H. pylori inhibits gastric mucosal cell proliferation in the proliferation index [PI] and in the S-phase independently on the gastric luminal HCl. The cell cycle analysis has reflected that H. pylori inhibits a crucial event in the cell cycle of gastric mucosa occurring at the GI/S border independently on the HCl production

Relationship of autonomic neuropathy and helicobacter pylori infection in dyspeptic patients with type-2 diabetes mellitus

To evaluate the prevalence of Helicobacter pylori [HP] and its relationship with autonomic neuropathy [AN], this work studied 200 patients with type-2 diabetes mellitus [DM type-2] matched for sex, age [ +/- 5 years] and body weight [ +/- 5 Kg] as well as 200 nondiabetic subjects, all affected by dyspepsia of unknown origin. The results documented that the prevalence of peptic ulcer was similar in both groups of patients [20% Vs 25%], chronic gastritis was 36% in diabetic group and 55% in the control group. Non-ulcer and non- gastritis dyspepsia was significantly more frequent in diabetic group than in control group [44% Vs 20%]. Also, in this study, two other tests have been compared with the histological evidence of HP [used as golden standard] i.e. the urease test [CP-test] and the assay of anti- HPG immunoglobulins. Both were positive in a significantly higher percentage in neuropathic diabetic patients in comparison with non- neuropathic diabetic ones

Prognostic utility of soluble E-cadherin and CD14 in sepsis-induced multiorgan failure

Inflammatory cytokines, endothelial activation and endothelialleucocyte interaction are fundamental participants in the development of organ failure secondary to systemic inflammatory response. The adhesion molecules, cadherins, are ideally suited markers of cell-cell adhesion as they are essential for maintaining tissue architecture and consequently organ function. CD[14] is a 55KD glycoprotein, lipopolysaccharides [LPS] binding to its soluble form which plays a harmful role by transmitting LPS damaging effects to endothelial cells. The aim of the present study is to assess the diagnostic and prognostic value of both E-cadherin and CD[14] in sepsis induced multiorgan failure [MOF] compared to septic patients not fulfilling the picture of MOF. This study was conducted on 51 patients admitted in Pediatric ICU [36 patients had sepsisinduced MOF and 15 patients had sepsis] and 20 healthy infants as a control group. The age of the studied group ranged from 2-24 months [mean age 6.5 +/- 3.8 months]. Serum E-cadherin and CD[14] were measured by enzyme linked immunosorbent assay [ELISA] in all patients and controls: Both E cadherin and CD[14] were significantly higher [P < 0.001] in MOF patients [X +/- SD = 12.3 +/- 3.8 microg/ml and 7 +/- 1.2 microg/ml respectively] compared to septic patients [X +/- SD =6.6 +/- 1.2 microg and 4.7 +/- 1.4 microg/ml, respectively] and to the control group [X +/- SD = 4.6 +/- 1.1 microg/ ml and 2.3 +/- 0.5microg/ml, respectively]. Both E-cadherin and CD[14] were significantly higher in non-survivors compared to survivors in sepsis group [P < 0.001], while in MOF patients only E cadherin was significant [P < 0.05]. E cadherin was significantly correlated with the Sepsis-Related Organ Failure [SOFA] score [r: 0.75] and the number of failing organs [r: 0.63] within the group of MOF patients. Meanwhile, CD[14] was not correlated with them. Nonsurvivors had highly significant higher levels of E cadherin and CD[14] compared to the survivors [P < 0.001]. Examining the diagnostic performance of both markers applying Receiver Operator Characteristic [ROC] curve analysis showed that the best diagnostic cut-off level for E-cadherin is 8.lmicrog/ml [sensitivity 83.3%, specificity 90% and efficacy 78.4%] and for CD[14] is 6.2 microg/ml [sensitivity 75%, specificity 90% and efficacy 73%]. E-cadherin proved to be a better prognostic marker for MOF patients on the basis of Z scoring analysis. Both E-cadherin and CD[14] can be considered as markers of sepsis and sepsis induced MOF. They both have high diagnostic efficacy. However, E-cadherin is a better marker of organ failure severity and prognosis within the MOF patients