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Background: This study was designed to assess the relative contribution of H pylori (Hp) infection and NSAID in the pathogenesis of perforation and bleeding of peptic ulcer (PU)., Material/methods: Total of 91 PU perforations and 135 active bleeding were examined during last 5 years. At the same time, 1384 age- and gender-matched PU patients without such complications were examined. Furthermore, the effects of various concentrations of aspirin on the growth of Hp isolated from antral mucosa of these PU were examined in vitro., Results: The average rates of Hp prevalence in PU patients with perforation or bleeding in NSAID intake were, respectively, only 50% and 62% as compared to 70.7 and 74% in PU patients non-using NSAID. The Hp prevalence in perforated and bleeding PU at all ages, particularly those at age of 60 years or higher, were significantly lower compared to that found below this age, while no such difference in Hp infection rate was seen in PU not using NSAID. In vitro studies on CagA and VacA positive Hp subjected to culture medium containing aspirin showed a dose dependent reduction in bacterial growth with complete bacteria killing occurring at 500 microg/ml of aspirin., Conclusions: The Hp prevalence, especially in older PU patients using NSAID, is significantly lower in perforated and bleeding PU compared to that in non-complicated PU, and this could be explained by direct suppression of Hp by NSAID used by these patients.

Background: Previous studies have shown that sensory nerves and calcitonin gene-related peptide (CGRP) affect caerulein-induced pancreatitis. The aim of this study was to examine the role of capsaicin-sensitive nerves and the impact of CGRP administration on necrotizing pancreatitis induced by ischemia/reperfusion., Material/methods: Ablation of sensory nerves was made by capsaicin 10 days before induction of pancreatitis. Acute pancreatitis was induced in rats by limitation of pancreatic blood flow (PBF) followed by reperfusion. Treatment with saline or CGRP (10 g/kg s.c.) or stimulation of sensory nerves by low doses of capsaicin (0.5 mg/kg s.c.) was performed 1 h before ischemia. After 1 h reperfusion we examined pancreatic blood flow (PBF), plasma amylase and lipase activity, plasma interleukin-1beta (IL-1beta) concentration, pancreatic DNA synthesis and morphological signs of pancreatitis., Results: Ischemia followed by 1 h reperfusion led to induction of necrotizing pancreatitis, manifested by morphological signs of pancreatic damage, decrease in pancreatic DNA synthesis and PBF, as well as an increase in plasma amylase and lipase activity and plasma IL-1beta concentration. Both, treatment with CGRP and stimulation of sensory nerves attenuated pancreatic damage. Ablation of sensory nerves enhanced I/R evoked pancreatic damage. The deleterious effect of deactivation of sensory nerves on I/R-induced pancreatitis was partly reversed by administration of CGRP prior to I/R., Conclusions: Stimulation of sensory nerves protects the pancreas against damage evoked by I/R, whereas ablation of these nerves aggravates tissue damage in the pancreas exposed to I/R. The beneficial effect of sensory nerves is partly dependent on CGRP release.

Background: Helicobacter pylori (Hp) infection represents a crucial factor in pathogenesis of gastric cancer (GC). Factors emanating from bacterium as well as from environmental contributions such as salt diet and inadequate supply of antioxidants, affect the risk for GC development., Results: Atrophic gastritis is considered to be a precursor lesion of intestinal type GC that is accompanied by hypergastrinemia with subsequent induction of cyclooxygenase-2 (COX-2), whose products are responsible for slowing apoptosis and for angiogenesis in GC tumor. The involvement of proinflammatory cytokines (especially IL-1 and IL-8) and reactive oxygen species (ROS) due to NF kappa B activation, increased cell proliferation combined with inhibition of apoptosis as well as upregulation of peroxisome proliferation activated receptor gamma (PPAR gamma) and inducible nitric oxide synthase (iNOS) appear to be major molecular biology alterations in pathogenesis of GC., Conclusions: These results suggest the therapeutic usefulness of inhibitors of gastrin expression and release such as powerful somatostatin analogs (Sandostatin) or blockers of COX-2 (coxibs) in the control of GC development and progression as chemopreventive agents. Comparative genomic and proteomic is the key in identifying biomarkers in host and bacterium for the prediction of gastric cancer in Hp-infected patients.

Background: Infection by Helicobacter pylori (Hp) has been linked to extradigestive pathologies including ischemic cerebral disease. The aim of our study was to assess the relationship between chronic Hp infection and ischemic stroke risk factors., Material/methods: 80 patients (pts) aged 60-75 years with ischemic stroke confirmed by CT scans (group I) and 80 age- and gender-matched healthy controls (group II) were included into trial. Atherosclerotic plaques from 20 Hp positive pts were obtained at carotid endarterectomy for Hp DNA assessment by PCR. In all groups following parameters were determined; 1) the prevalence of Hp infection using (13)C-Urea Breath Test (UBT), 2) plasma anti-Hp and anti-CagA IgG and interleukin-8 (IL-8), and 3) plasma lipids and fibrinogen. Hp positive pts and controls received one-week anti-Hp therapy and after six months total cholesterol, low-density lipoprotein (LDL)-cholesterol, fibrinogen and IL-8 levels were re-examined., Results: Hp infection was detected by UBT in 83.75% of stroke pts but only in 65% of controls. CagA seropositivity was also significantly higher in stroke pts (57.5%) than in controls (33.75%). Plasma levels of cholesterol, LDL-cholesterol and fibrinogen as well as IL-8 were significantly higher in Hp positive subjects, especially in pts with ischemic stroke. Six months following successful anti-Hp therapy, the plasma levels of total cholesterol, LDL-cholesterol, fibrinogen and IL-8 were significantly lower than those in Hp positive stroke pts and controls., Conclusions: Hp infection represents risk factor of ischemic stoke via an interaction of Hp cytotoxins or cytokines with atherosclerotic plaques in carotic arteries.

Hp and NSAID are the most common pathogens in the stomach, but their interaction on gastro-duodenal mucosa has been little studied. Hp infection in humans does not interfere with NSAID-induced gastric ulcer healing by omeprazole, therefore, there is no rationale to eradicate the germ. Hp infection induces COX-2 expression resulting in excessive biosynthesis of gastroprotective prostaglandin (PG), which should in turn counteract NSAID-induced gastropathy and contribute to healing of existing ulcers. Some investigators claim that Hp infection acts synergistically with NSAID on ulcerogenesis and propose that Hp should be eradicated, particularly at the onset of long-term NSAID therapy. Our studies in about 6500 dyspeptic patients undergoing upper endoscopy and 13C-urea breath test revealed that about 70% of these patients are Hp positive and 31% of these develop gastro-duodenal ulcers. Of these ulcers, 66% were Hp positive and NSAID negative, 3%--NSAID positive and Hp negative, 8% were both Hp positive and NSAID positive, while 23% ulcers were Hp and NSAID negative. An evidence was obtained for negative interaction between Hp infection and NSAID on risk of gastro-duodenal ulcers suggesting that Hp may attenuate the peptic ulcerogenesis. Our results support the concept 1) the interaction between Hp infection and NSAID on gastro-duodenal ulcerations is antagonistic, 2) the Hp and NSAID are independent risk factors for peptic ulcerations in humans, 3) there is no need for the Hp eradication in NSAID-treated patients, and 4) the rate of ulcer complications (hemorrhage and perforation) remains constant despite the decrease in Hp and ulcer prevalence.

Background: Zollinger-Ellison syndrome is a very rare disease caused by tumor with gastrin producing cells accompanied by hypergastrinemia leading to gastric hypersecretion and peptic ulcers and their complications., Case Study: Female case of gastrinoma (Zollinger-Ellison syndrome; Z-E) with a record of 38 yrs of survival. Acute gastro-duodenal ulcers started at 28 yr of age and Z-E was diagnosed by using gastrin assays. Basal and maximal acid outputs and ratio of basal/maximal outputs were away over normal limits. Because of ulcer recurrence and complications, patient was subjected to several gastric surgeries but refused total gastrectomy. She was also treated with many H2-receptor (R) antagonists and proton-pump inhibitors (PPI), each new drug being initially highly effective but then showing declining efficacy except when PPI, lansoprazole was used. The gastrin level rose in the course of disease from initial high value of 2000 pg/mL to the extreme 4500 ng/mL at present. During the last 2 yrs, metastasis mainly to liver developed and they were successfully treated by synthetic octapeptide derivative of somatostatin and, as a result, metastatis partly reduced and plasma gastrin drasticly decreased. Biopsy taken from liver metastasis showed the presence of typical gastrinoma cells with gastrin and chromogranin, while that from oxyntic mucosa revealed the ECL-cell hyperplasia with carcinoid tumors and unexpected gastric atrophy., Conclusions: This phenomenal case described in this article might be the new proven evidence needed by gastroenterologists to overturn the traditional treatment using total gastrectomy as a treatment of choice to the partial gastrectomy combined with proton pump inhibitors.