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Biomedical subjects

E Brenna

Publications and source records attributed to E Brenna.

At least 19 recordsLinked to original sources
PubMed2003

Cytotoxicity of streptozotocin on neuroendocrine cells of the pancreas and the gut.

Streptozotocin has been used to induce diabetes mellitus in experimental animals and has been thought to have a selective cytotoxic effect on the beta-cells in the islets of Langerhans. The aim of the present study was to determine whether streptozotocin has any cytotoxic effect on other neuroendocrine cells of the gastrointestinal tract. Eight female Sprague-Dawley rats received intraperitoneal injections of 100 mg/kg streptozotocin in citric acid buffer; the concentration of streptozotocin was adjusted to 25 mg/ml buffer. Seven rats, serving as controls, received an equivalent volume of the vehicle. The rats were killed after three days and the fundus, antrum, small intestine and pancreas were examined for neuroendocrine cells. Our study confirms that streptozotocin is cytotoxic towards beta-cells. In addition, it is cytotoxic towards neuroendocrine cells of the oxyntic mucosa of the stomach. This finding may have clinical significance and suggests that streptozotocin may be used in the treatment of gastric neuroendocrine tumors as well as insulinomas.

Animals↗
PubMed2001

[Health costs of acute poisoning with pesticides: empirical analysis].

This work, based on an empirical analysis carried out by the Poison Centre of Milan, is an attempt to estimate the direct costs of acute intoxication due to pesticide use in Italy. From the analysis undertaken, it is possible to demonstrate that the number of incidents of acute intoxication registered every year in Italy is not negligible and that it causes a cost of nearly Lit 2,000,000,000. The investigation, supported also by empirical studies from other countries, suggests that, in order to reduce the incidence of this pathology, greater attention should be paid to prevention, regulation and education.

Acute Disease↗
PubMed2000

[Treatment of esophageal varices with banding ligation].

BACKGROUND: Randomised trials have shown that banding ligation is superior to sclerotherapy, requiring fewer treatment sessions to achieve variceal eradication, and giving lower rebleeding and complication rates. MATERIAL AND METHODS: From November 1997 through December 1999, we have treated 22 patients with bleeding oesophageal varices with endoscopic banding ligation to obliterate the varices and prevent recurrent bleeding. RESULTS: A total of 72 banding procedures have been performed using rubber bands. The varices have been obliterated in 14 patients requiring a median of 3.5 (range 2-8) procedures, which is in good agreement with other published data. Twelve of these patients have been observed for a median of six (range 1-19) months without signs of recurrent bleeding. One patient had a bleeding four months after the last ligation procedure; the varices were obliterated six weeks before. One patient had a recurrent bleeding between the first and second banding procedure. One patient bled from an oesophageal ulcer caused by a rubber band two weeks after the procedure. Otherwise no serious complications occurred. INTERPRETATION: On the basis of our own experiences and published studies, we propose that endoscopic banding ligation should be the method of choice for elective treatment of bleeding varices.

Adult↗
PubMed2000

Estimating the impact of a diffuse technology on the running costs of a hospital. A case study of a picture archiving and communication system.

OBJECTIVES: This paper considers the methodological problems that arise in conducting cost analyses in economic evaluations where only observational (rather than experimental) data are available and where the technology being evaluated is diffuse, such that the unit of analysis has to be the institution rather than the patient. METHODS: A case study is reported that concerns the application of computer technology in radiology: picture archiving and communication systems (PACS). A range of different approaches were used to estimate changes in running costs, including time series analyses of routine data and direct observation of resource use. RESULTS: The analysis illustrates some of the difficulties involved in costing the introduction of a diffuse technology. Nevertheless, it provides a firm indication that, overall, the introduction of PACS was found to be associated with a significant increase in hospital costs, suggesting that the initial expectations of financial savings were unduly optimistic. CONCLUSIONS: The research demonstrates that, using multiple methods, it is possible to estimate cost changes within a single hospital. In addition, the paper discusses the nature of the uncertainties in such analyses and possible ways of representing such uncertainty in terms of confidence intervals.

Budgets↗
PubMed2000

Detection of chromogranin A in human gastric adenocarcinomas using a sensitive immunohistochemical technique.

Neuroendocrine cells are often disclosed in human gastric adenocarcinomas and may be recognised by their immunoreactivity towards chromogranin A. However, in dedifferentiated neuroendocrine tumour cells, the chromogranin A content may be reduced making it difficult to detect with conventional immunohistochemical methods. We therefore used a sensitive signal amplification technique in order to evaluate chromogranin A immunoreactivity and thus neuroendocrine differentiation in 40 gastric adenocarcinomas. Neuroendocrine cells were visualised by means of a monoclonal chromogranin A antibody and the avidin-biotin peroxidase complex technique, without and with addition of tyramide signal amplification. Double immunohistochemistry towards chromogranin A and Ki-67 were used to disclose proliferation in the neoplastic cells. A marked increase in the number of carcinomas containing chromogranin A-immunoreactive neoplastic cells was noted when applying the tyramide signal amplification technique. In addition, the number of immunoreactive cells within each tumour increased, and in some cases almost all the neoplastic cells became immunoreactive. Chromogranin A-immunoreactive tumour cells showing signs of proliferation were found in the majority of these carcinomas. In conclusion, we have disclosed widespread immunoreactivity towards chromogranin A in a proportion of gastric adenocarcinomas when enhancing the signal with tyramide signal amplification. Neuroendocrine differentiation is thus a common finding in gastric carcinomas when using sensitive methods.

Adenocarcinoma↗
PubMed2000

Gastrin has a specific proliferative effect on the rat enterochromaffin-like cell, but not on the parietal cell: a study by elutriation centrifugation.

Gastrin has a general growth-promoting effect on gastric oxyntic mucosa, and a more pronounced one on the enterochromaffin-like (ECL) cell. Whether gastrin has a proliferative effect on the parietal cell lineage beyond the general effect is uncertain. Hypergastrinaemia was evoked in rats using pantoprazole (group II: 100 micromol kg-1, group III: 400 micromol kg-1) for 45 days. Plasma gastrin was 43 +/- 8 pmol L-1 (control), 283 +/- 54 pmol L-1 (group II) and 577 +/- 63 pmol L-1 (group III). Gastric mucosal cells were isolated and fractionated by elutriation centrifugation. Total cell number, percentage and number of ECL and parietal cells, and histamine were determined in each fraction. The number of mucosal cells increased 1.5-fold in both hypergastrinaemic groups. Enterochromaffin-like cell content was 2.6 +/- 0.5% (control), 6.0 +/- 0.6% (group II) and 9.0 +/- 0.8% (group III). Histamine concentration in oxyntic mucosal cells rose similarly. The size of the ECL cells was 8.5 +/- 0.1 microm (control), 10.8 +/- 0.2 microm (group II) and 12.1 +/- 0.2 microm (group III), and the increased size was confirmed by shifted distribution in elutriation fractions. Histamine per ECL cell increased with cell size. The number of parietal cells increased parallel to the total number of mucosal cells (1.5-fold). Parietal cell size and percentage, assessed by image analysis and distribution in elutriation fractions, were unchanged after pantoprazole dosing. Gastrin has a pronounced, concentration-dependent specific trophic effect on ECL cells and a general proliferative effect on gastric mucosa, including parietal cells.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2000

Personal review: is profound acid inhibition safe?

Inhibitors of gastric acid secretion, particular proton pump inhibitors, are effective drugs in the treatment and prophylaxis of acid-related diseases. Proton pump inhibitors are therefore prescribed widely, often for minor complaints. Gastric acidity kills swallowed microorganisms, and acid secretion must be of biological importance because it is maintained in phylogenesis. Acid secretion is controlled by feedback mechanisms, mainly via gastrin. A decrease in acidity always causes an increase in plasma gastrin. The trophic effect of gastrin leads to hyperplasia and neoplasia of the enterochromaffin-like (ECL) cell. ECL cell derived tumours in man were previously regarded as rare, and also as rather benign. It is now clear that the ECL cell gives rise to a significant proportion of gastric carcinomas. Moreover, ECL cell carcinoids secondary to hypergastrinaemia may develop into highly malignant tumours. Treatment with a proton pump inhibitor is followed by rebound acid hypersecretion and decreased efficiency of H2-blockers, thus such treatment may induce a type of physical dependence. It is therefore reasonable to be cautious and not to treat younger (< 50 years) patients for long periods of time with profound inhibitors of gastric acid secretion. Chromogranin A in the blood is a sensitive marker of the ECL cell mass, and it could be used to survey patients on long-term proton pump inhibitors.

Antacids↗
PubMed1998

Neuroendocrine differentiation in human gastric carcinoma.

BACKGROUND: Distinguishing between neuroendocrine carcinoma and adenocarcinoma may be difficult. METHODS: In the current prospective study blood and tumor tissue from patients with gastric carcinoma were collected. The tissue was fixed in different ways to allow examination for neuroendocrine markers by multiple methods such as various histochemical and immunohistochemical methods and electron microscopy. Blood and tumor homogenates were examined by radioimmunoassay for specific hormones and general neuroendocrine markers. RESULTS: Based on examination of general neuroendocrine markers such as chromogranin A (by immunohistochemistry, Northern blot analysis, and tissue concentration), neuron specific enolase (immunohistochemistry) as well as electron microscopy, it was possible to conclude that approximately 10% of the tumors were actually neuroendocrine malignant tumors. Among these tumors, the enterochromaffin-like (ECL) cell was the most preponderant cell of origin (Sevier-Munger positive and serotonin negative immunoreactive tumor cells with secretory granules resembling those observed in normal ECL-cells). As reported previously, tumors of the diffuse type (according to the classification of Laurén) most often were reclassified as neuroendocrine carcinomas. CONCLUSIONS: The current study shows that neuroendocrine and particularly ECL cell-derived tumors are more common in the stomach than previously recognized.

Adenocarcinoma↗
PubMed1998

Treatment with proton pump inhibitors induces tolerance to histamine-2 receptor antagonists in Helicobacter pylori-negative patients.

BACKGROUND: Treatment with H2 receptor antagonists (H2RAs) and proton pump inhibitors (PPIs) induces hypergastrinemia and causes rebound hypersecretion of gastric acid after treatment, and during treatment with H2RAs tolerance develops. In the present study we investigated whether a treatment period with a PPI induced tolerance to an H2RA. METHODS: Thirteen patients with esophagitis were given omeprazole for 90 days. Twenty-four-hour pH monitorings without and with ranitidine were performed before and after treatment with omeprazole. Blood samples and biopsy specimens from the oxyntic mucosa were analyzed for gastrin, histamine, and chromogranin A. RESULTS: An increase in mucosal histamine and a reduction in the effect of ranitidine on gastric pH was found 14 days after discontinuing omeprazole compared with before treatment in Helicobacter pylori-negative but not in H. pylori-positive patients. CONCLUSIONS: Treatment with omeprazole reduces the effect of ranitidine in H. pylori-negative patients. This is caused by an increase in histamine released by the enterochromaffin-like cell secondarily to hypergastrinemia, corresponding to the tolerance towards H2RAs seen in patients with Zollinger-Ellison syndrome.

Adult↗
PubMed1997

[A simple method for endoscopic placement of a nasojejunal feeding tube].

The aim of this paper is to describe a simple, nonsurgical method for endoscopic placement of a nasojejunal feeding tube. A stylet inserted in the tube facilitates nasogastric intubation. A thread on the tip of the tube is grasped with a biopsy forceps inserted through an endoscope, and the tube can be placed in the distal part of the duodenum under direct endoscopic inspection. By means of a guide wire the tube can be pushed further to the desired position in the upper part of the jejunum. The endoscope can now be removed while pressure is exerted on the stylet, thus preventing the tube from dislocating. By this method, oral-nasal transfer of the tube is avoided, the tube is placed in the upper jejunum under direct endoscopic inspection, and the stylet inserted in the tube facilitates intubation and prevents it from dislocating when the endoscope is withdrawn.

Endoscopes, Gastrointestinal↗
PubMed1997

Review article: the pharmacological inhibition of gastric acid secretion--tolerance and rebound.

During the last decade our understanding of the regulation of gastric acid secretion has changed considerably. The recognition that gastrin acts mainly by releasing histamine from the enterochromaffin-like (ECL) cell is of major importance. It is now necessary to review and seek new explanations for the development of tolerance and for the post-treatment acid hypersecretion that may be observed when treatment with acid-secretory inhibitors is discontinued. Tolerance and rebound related to H2-receptor antagonists has previously been explained as upregulation of gastrin and/or histamine H2-receptors, and/or an increased parietal cell mass. Experimental evidence for these theories is scarce. On the other hand, tolerance can now be explained by a gastrin-induced increase in ECL cell-derived histamine at the parietal cell H2-receptor competing with the antagonist. The lack of tolerance to proton pump inhibitors may be explained by their mode of action, being non-competitive and acting at the H+, K+-ATPase rather than at stimulatory receptors. Post-treatment rebound acid hypersecretion can be understood as gastrin upregulating and/or stimulating growth of the ECL cell, leading to increased amounts of releasable histamine post-treatment. Novel experimental data strongly support this view of the development of tolerance and post-treatment rebound acid hypersecretion.

Animals↗
PubMed1997

Relationship between the efficacy of amoxicillin and intragastric pH for the treatment of Helicobacter pylori infection.

BACKGROUND: Proton pump inhibitors are reported to enhance the efficacy of antibiotics in the treatment of Helicobacter pylori infection. An elevated intragastric pH is considered to be an important factor for this increased antimicrobial efficacy. The aim of this study was to assess the effect of different doses of lansoprazole on 24-hour intragastric pH and to correlate the effect of amoxicillin on the cure rate for H. pylori infection with the intragastric pH obtained during lansoprazole treatment. PATIENTS AND METHODS: Thirty-six duodenal ulcer patients who tested positively for H. pylori as assessed by a rapid urease test, culture, and histological evaluation were allocated randomly to dual treatment with amoxicillin, 3 gm/day, and lansoprazole in different doses ranging between 30 and 180 mg/day for 2 weeks. A 24-hour intragastric pH measurement was taken in all patients on the fifth day of treatment. H. pylori status was determined by culture and histological workup 6 weeks after cessation of the amoxicillin-lansoprazole medication. RESULTS: The H. pylori infection was treated successfully in 19 of 32 patients who completed the dual therapy (per protocol, 59.4%). The median intragastric pH in patients who were treated successfully was 4.4 (95% confidence interval [CI] = 3.7-4.7), as compared to 4.0 (95% CI = 3.5-4.5) in patients who were not treated successfully (p = .47, Wilcoxon's rank sum test). The median percentage of time that the intragastric pH exceeded 4 was not different in the two groups (p = .77). Administration of lansoprazole in doses exceeding 30 mg induced only a moderate additional increase in intragastric pH. CONCLUSIONS: Profound inhibition of gastric acid secretion seems not to be necessary to improve the effect of amoxicillin on the cure rate for H. pylori infection in patients with duodenal ulcers.

Adult↗
PubMed1997

Bombesin inhibits histamine release from the rat oxyntic mucosa by a somatostatin-dependent mechanism.

BACKGROUND AND METHODS: This study examines the effect of bombesin on endogenous somatostatin and the histamine-synthesizing enterochromaffin-like cells. Somatostatin and histamine were measured in the venous effluent of isolated/antrectomized vascularly perfused rat stomachs after administration of bombesin and gastrin alone or combined. Histidine decarboxylase (HDC) enzyme activity and mRNA abundance were measured in the gastric corpus after intravenous administration of bombesin to conscious rats. RESULTS: Bombesin released somatostatin from the isolated stomachs and reduced basal and gastrin-stimulated venous histamine. Somatostatin antiserum partially reversed the effect of bombesin on basal and gastrin-stimulated histamine release. In conscious fed rats, intravenous bombesin doubled serum gastrin concentrations and increased HDC activity. CONCLUSION: We conclude that endogenous (paracrine) somatostatin inhibits basal and gastrin-stimulated histamine release from the ECL cell. In intact animals this effect is surmountable by simultaneously released gastrin, suggesting that a balance between the effects of gastrin and somatostatin determines the activation of the ECL cell.

Animals↗