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Objectives: The present study examined the cross-talk between prostanoids and nitric oxide (NO) in human gastric biopsies during Helicobacter pylori infection., Subjects and Methods: A pool of 1 or 2 biopsies per patient (11 H. pylori positive and 9 H. pylori negative) were incubated in the medium with/without drugs, 1400W and NS-398, inhibitors of inducible nitric oxide synthase (iNOS) and cyclooxygenase 2 (COX-2), respectively. Levels of NO and prostaglandin E(2) (PGE(2)), predominant products of activity of NOS and COX enzymes, were measured in the medium whereas the expressions of iNOS and COX protein, examined by Western blotting, were measured in the biopsies., Results: The 11 patients with H. pylori infection showed a marked expression of COX-2 and iNOS proteins and high levels of PGE(2) and NO, as a consequence of iNOS and COX-2 activation, while proteins were absent and the level of nitrite and PGE(2) was low in the 9 noninfected patients. The COX-2 inhibitor decreased both NO and PGE(2). The iNOS-specific inhibitor decreased NO but did not have any effect on the increase in gastric mucosal PGE(2). Both inhibitors had no effect on the protein level of these two enzymes., Conclusions: The data showed that COX-2 inhibitor might modulate the iNOS pathway, suggesting that COX-2 activity and/or its products may be related to the functional activation of iNOS but not to the expression of iNOS protein., (Copyright 2009 S. Karger AG, Basel.)

Objective: To evaluate clinical utility of rapid urease test (RUT), brash cytology and histology for detecting Helicobacter pylori., Study Design: Brush cytology materials were obtained from the antrum of the stomach in 109 patients who suffered from dyspepsia and were candidates for endoscopy. RUT and histology with hematoxylin-eosin staining were performed. Infection status was established by observation of typical HP in cytology or biopsy., Results: A total of 78% ofpatients were diagnosed as positivefor HP organisms using brush cytology; 66% had histologic results positive for HP and 59% for RUT. Observation of typical organism by cytology or histology was the gold standard; 3 tests results were compared. Sensitivity of brush cytology (95%) was higher than that of histology (80.5%) and RUT (72%)., Conclusion: Gastric brushing cytology provides a sensitive, inexpensive, accurate and easy technique for rapid detection of HP infection. When additional information on severity of mucosal damage or presence of cell atypias is not necessary, histologic examination can be omitted; a cost-effective strategy for assessing HP status might consist of taking antral biopsies, the former for RUT, and performing brush cytology slides, which should be stained and examined only when the RUT result is negative.

The LDH isoenzyme pattern of the uninvolved mucosa of gastric cancer patients differs as regards the LDH isoenzyme pattern from that of similar tissue of patients with benign gastric disease; the former tissue is characterised by a high M/H ratio of the LDH isoenzymes (M and H sub-units). A high M/H ratio characterises antral mucosa when the latter is compared with fundic mucosa. Mucosa showing superficial and atrophic gastritis also has a higher M/H ratio, whereas the presence of intestinal metaplasia does not appear to influence the M/H ratio. These observations are consistent with the concept that the tissue from which the cancer arose may possess a pre-malignant biochemical lesion.

A correlation was sought between changes in enzymes involved in gastric acid secretion (Mg-, NaK-, K- and HCO3-stimulated ATPases) and histological changes in gastric biopsies. Alkaline phosphatase was also studied. Mg- and NaK-stimulated ATPase activities increased significantly in biopsies from the pylorus and antrum which showed moderate or severe gastritis. NaK ATPase levels increased and HCO3 ATPase decreased in incisural, body and fundic mucosa which had intestinal metaplasia and atrophic gastritis. No K+ ATPase was found in normal mucosa. The total activity of alkaline phosphatase did not vary with histological changes in the gastric mucosa. Results indicate that the ATPase enzyme systems are sensitive indicators of gastric mucosal disease.

Adenylate cyclase (AC) in response to prostaglandin E2 (PGE2) and histamine was studied in morphologically different biopsy specimens from human gastric mucosa. The activities of the enzyme were log-normally distributed and did not differ between males and females. PGE2 activated AC in a concentration-dependent manner in normal gastric mucosa (n = 57), chronic superficial gastritis (GI, 18), chronic gastritis with beginning atrophy (GII, 10), chronic atrophic gastritis (GIII, 24), gastric ulcer (GU, 39), duodenal ulcer (DU, 32), and biopsies of patients operated according to Billroth II (BII, 20) and was most efficacious in GIII and BII. Histamine, which was studied in normal gastric mucosa (n = 27), DU (n = 20), GU (n = 13), and BII (n = 18), stimulated AC most efficaciously and potently in DU, was less effective in normal gastric mucosa and GU, and had no effect at all in BII. Cimetidine treatment of DU patients did not change the PGE2 action, while the degree of stimulation by histamine was reduced. The data indicate characteristic differences of the PGE2- and histamine-sensitive AC in the mucosal samples of these patients.