摘要:

We have observed 4 cases of extraintestinal cancer complicating Crohn’s disease (CD). They included renal cancer, urinary bladder cancer, ovarian cancer and myeloma. A review of the literature showed a considerable number of reports of extraintestinal cancer complicating CD with a total of 75 further cases. The significance of those and our cases is discussed. The possibility of extraintestinal cancer must be kept in mind following patients with CD. Our report suggests there may be a nonnegligible risk of extraintestinal cancer, particularly genitourinary tumor, in CD. The causal relationship, if any, remains undetermine

ISSN:0012-2823    

DOI:10.1159/000200468

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Since their introduction in 1976, and until recently, the H2-receptor antagonists have been the ‘state-of-the-art’ gastric acid inhibitors, but the advent of omeprazole, the acid pump inhibitor, has necessitated a reassessment of therapy for acid-related diseases. In making this reassessment, the following therapeutic goals should be considered: rapid and reliable therapeutic effect, safety, simple treatment regimen, resolution of recurrence, and cost-effectiveness. Extensive clinical evidence indicates that omeprazole offers an advance over the H2-receptor antagonists in achieving these goals. A series of meta-analyses shows that omeprazole gives more rapid symptom relief and more reliable healing than the H2-receptor antagonist, ranitidine, in uncomplicated duodenal ulcer (DU), in uncomplicated gastric ulcer (GU) and in reflux oesophagitis (RO). By contrast with the H2-receptor antagonists, refractoriness leading to failure to heal is virtually unknown with omeprazole. Omeprazole also fulfils the goal of therapeutic safety, and this has been documented in extensive short- and long-term clinical and laboratory studies. Omeprazole has a simple treatment regimen: 20 mg once daily is recommended in the routine treatment of DU, GU and RO. As a result of its high therapeutic success rate, omeprazole is also cost-effective. Taking all these factors into account, it is concluded that omeprazole approaches the therapeutic targets set for the treatment of acid-related disord

ISSN:0012-2823    

DOI:10.1159/000200507

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

We investigated the effects of cimetidine and omeprazole on angiogenesis in granulation tissue and on the healing of gastric ulcers induced by acetic acid in rats. Either cimetidine (50 or 100 mg/kg) or omeprazole (10 or 20 mg/kg) was orally administered once daily for 9 consecutive days from the day following ulcer production. The ulcer index on the 10th and 30th days after ulcer production, and the extent of angiogenesis on the 10th day were examined. Cimetidine dose-dependently decreased the extent of angiogenesis on the 10th day, whereas the ulcer index on the 10th days was not significantly different between cimetidine-treated and control rats. The ulcer index of the groups treated with cimetidine during the initial 9-day period was increased compared with the control group on the 30th day. In contrast, oral omeprazole did not affect angiogenesis on the 10th day and decreased the ulcer index on both the 10th and 30th days. These results suggest that oral cimetidine may inhibit angiogenesis in ulcer granulation tissue possibly via the blocking of histamine H2 receptors and this may be one cause of delayed ulcer healing.

ISSN:0012-2823    

DOI:10.1159/000200469

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Gastrin has two principal biological effects: stimulation of acid secretion from gastric parietal cells and stimulation of mucosal growth in the acid-secreting part of the stomach. Circulating gastrin regulates the increase in acid secretion that occurs during and after meals. Gastrin also stimulates mucosal growth in the stomach. Exogenously administered gastrin causes increased cell division in the proliferative zone that lies between the surface cells and the gastric glands in the acid-secreting mucosa. The newly formed cells undergo differentiation into surface epithelial cells, parietal cells and gastric enterochromaffin-like cells. Furthermore, the increased mucosal proliferation that occurs with refeeding after a period of fasting may be mediated by gastrin since refeeding stimulates gastrin production and a parallel increase in mucosal DNA synthesis. Both food and gastrin cause a rapid increase in cell division and an increase in gastric ornithine decarboxylase mRNA in fasting rats. In preliminary immunoneutralization experiments, the stimulation of ornithine decarboxylase produced by food was inhibited by gastrin antibody. The sustained inhibition of gastric acid secretion obtained by surgery or with antisecretory drug therapy results in hypergastrinaemia associated with increased gastric mucosal cell proliferation. A good correlation between gastric enterochromaffin-like cell density and circulating gastrin concentrations has been found under these conditions as well as during infusions of exogenous gastrin. Trophic effects of gastrin have also been reported for the colon, duodenum and pancreas, but chronic hypergastrinaemia does not appear to produce hyperplasia of these organs. It can be concluded, therefore, that gastrin acts as a physiological stimulant of both gastric acid secretion and gastric mucosal growth and mediates the gastric mucosal proliferation that occurs in response to feeding and hypochlorhydria.

ISSN:0012-2823    

DOI:10.1159/000200509

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Acute edematous pancreatitis was induced in conscious rats by intravenous infusion of cerulein at a supramaximal dose of 7.5 μg/kg/h during 6 h. The most important finding of our study was a marked decrease in the protein and non-protein content of sulfhydryl groups parallel to an evident elevation in the malondialdehyde concentration in pancreatic tissue. The presented data suggest that in cerulein-induced acute pancreatitis in rats, oxygen radicals mediate increased peroxidation reactions which are accompanied by depletion of nonenzymatic sulfhydryl-containing free radical scavengers. The above phenomenon contributes to a disturbance in thiol metabolism resulting in serious diminution of pancreatic protein sulfhydryl compounds

ISSN:0012-2823    

DOI:10.1159/000200470

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Life-long administration (≥2 years) of a number of long-acting gastric acid inhibitors (including H2-receptor antagonists, omeprazole and ciprofibrate) has been associated with the development of gastric enterochromaffin-like cell (ECL cell) carcinoids in rats. It has been postulated that they are a consequence of some unique property of the longer-acting acid inhibitors. There is, however, a great deal of evidence to support the hypothesis that these gastric ECL cell carcinoids develop as a result of life-long hypergastrinaemia in rats. Several lines of investigation reported here show that gastric ECL cell hyperplasia occurs when gastrin levels are increased without the use of acid-inhibiting drugs. In rats, hypergastrinaemia developed after 4 weeks’ administration of exogenous gastrin (4 μg/kg/h). The number of gastric ECL cells per visual field had increased to 250 compared with 180 in the controls. Long-term hypergastrinaemia, induced by partial gastric corpectomy, increased plasma gastrin levels from 200 to 800 pg/ml and the density of gastric ECL cells increased from 190 to 310 cells/visual field 10 weeks after the operation. Importantly, gastric ECL cell hyperplasia, which was produced in rats by administration of omeprazole, 14 mg/kg/day for 1 year, was fully reversible following normalization of gastrin levels. Until now, gastric ECL cell carcinoids have not been reported in studies of shorter-acting, reversible H2-receptor antagonists such as ranitidine, perhaps because the correct staining techniques (i.e. Grimelius and Sevier-Munger silver stains) have not been used. We now report that in female rats, 2 years’ administration of ranitidine, 2 g/kg/ day, in the diet is associated with hypergastrinaemia and histological changes similar to those reported with omeprazole, 14 mg/kg/day, which gave the same degree of acid inhibition. Moreover, ranitidine, 2 g/kg/day, in the diet for 2 years was also associated with the development of gastric ECL cell carcinoids in 19 out of 100 rats. The results presented in this paper provide support for the hypothesis that the development of gastric ECL cell carcinoids in the rat gastric mucosa is a consequence of prolonged hypergastrinaemia achieved surgically or pharmacologically and is not a unique effect of any individual acid-inhibitor

ISSN:0012-2823    

DOI:10.1159/000200510

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

In 134 patients with celiac disease the compliance with a gluten-free diet (GFD) and the presence of antigliadin antibodies (AGA) were evaluated. Compliance with the GFD was good in 71 %, moderate in 11 % and poor in 18 %. High levels of AGA (IgA and IgG) were found in 24.2% of patients with good GFD, in 40% of those with moderate GFD and in 75 % of those with poor GFD compliance. Our data suggest that the presence of AGA is correlated with the degree of adherence to the GFD, and that AGA measurement may be of some value in the monitoring of GFD in patients with celiac disease.

ISSN:0012-2823    

DOI:10.1159/000200471

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The effect of the radical removing agents, allopurinol and dimethyl sulphoxide (DMSO), on the healing rate of ethanol (1 ml of 40% solution) induced gastric mucosal injury was studied in the rat. One millilitre of 1 2 or 5 % allopurinol or DMSO were instilled into the stomach 1 24 and 48 h after giving ethanol by gavage. One hour after administration of ethanol, gastric mucosal injury was produced in all animals (20.4 ± 1.2 mm2, mean ± SEM, n = 10). Treatment for 24 h with 2% allopurinol or DMSO significantly (p < 0.01) reduced the extent of the ethanol injury (11.1 ± 0.8 and 11.9 ± 0.9 mm2, respectively, vs. 19.2 ± 1.1 mm2, n= 10) and this was similarly achieved by the 5% solutions (10.4 ± 0.9 and 10.2 ± 0.8 mm2, respectively, vs. 19.2 ± 1.1 mm2, n= 10). After treatment for 48 h, 30%of animals having 1 % allopurinol or DMSO remained with injury significantly (p < 0.001) less than that seen with ethanol alone (4.1 ± 0.4 and 3.9 ± 0.5 mm2, respectively, vs. 12.1 ± 0.9 mm2, n = 10); however, none treated with 2 or 5% solutions remained with any injury. Healing of this injury was confirmed microscopically and was achieved by regeneration. Thus, removing oxygen-derived free radicals stimulates the healing of ethanol-induced acute gastric mucosal injury

ISSN:0012-2823    

DOI:10.1159/000200472

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Two hundred consecutive patients suffering from non-ulcer dyspepsia were studied for the presence of Helicobacter pylori in antral gastritis and normal antral mucosa, using the combination of culture, modified Giemsa stain and a sensitive immunoperoxidase stain as means of detection. H. pylori gastritis was present in 56% of the cases. The bacterium was present in 75% of cases of normal antral mucosa, however, in low numbers. It is concluded that 87% of patients with non-ulcer dyspepsia are H. pylori-positive implying a larger role for the micro-organism as initially thought.

ISSN:0012-2823    

DOI:10.1159/000200473

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

It has been claimed that the in vivo incubation of rat gastric mucosa with a test drug, followed by labelling with tritiated thymidine and selective in vitro digestion is a suitable method for evaluating genotoxic potential. However, the method rests on the assumptions that the radiolabel released on digestion has been incorporated into damaged DNA which has undergone repair (i.e. unscheduled DNA synthesis, UDS) and that the results are not confounded by the presence of dividing cells (scheduled DNA synthesis). This study examined the method by repeating the digestion procedure on rat gastric mucosa which had been labelled with bromodeoxyuridine in vivo, to mimic the 3H-TdR experiments previously reported. Results showed that the cell digest contained a mixture of cells, including parietal cells, and that there was a 6.9 ± 0.69% (n = 43) contamination with dividing cells over a 2-hour period of labelling. This represents a 10-fold enrichment of dividing cells as compared to intact tissue. It is concluded that measurements of total radioactivity in DNA made using this digestion method cannot be related solely to UDS, but are related to a variety of unrecognized artifacts

ISSN:0012-2823    

DOI:10.1159/000200512

出版商:S. Karger AG    

年代:1990

数据来源: Karger