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Antoine Alvarez,1 Kristin Benjaminsen Borch,2 Charlotta Rylander2 1Faculty of Medicine, Paris-Sud University, Paris, France; 2Department of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, NorwayCorrespondence: Charlotta RylanderDepartment of Community Medicine, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, 9037, NorwayTel +47-77-644-831Email charlotta.rylander@uit.noIntroduction: The incidence of pancreatic cancer is increasing worldwide and characterized by a particularly low survival rate. Studies have reported weak and inconsistent evidence for associations among reproductive factors, use of exogenous hormones, and pancreatic cancer incidence in women.Purpose: To investigate relationships between reproductive factors, exogenous hormones, and the rate of pancreatic cancer incidence in a large population-based prospective cohort of women in Norway.Methods: We used data from the Norwegian Women and Cancer study on 588 incident cases of pancreatic cancer diagnosed among 165,419 women, with mean follow-up of 18.7 years. Cox proportional-hazard models were used to estimate HRs and 95% CIs for associations of interest.Results: Cumulative breastfeeding duration > 24 months was associated with 63% decreased incidence of pancreatic cancer compared to no breastfeeding. We observed an inverse linear dose–response trend between cumulative breastfeeding duration and pancreatic cancer incidence, which was confirmed in parous women and ever-smokers. Higher age at first birth and menopause were inversely associated with pancreatic cancer incidence, though with less precise effect estimates. Current use of oral contraceptives was associated with a doubling of pancreatic cancer incidence, but the analysis was hampered by a small number of cases. There was no evidence of any associations between age at menarche, parity or use of menopausal hormone therapy, and incidence of pancreatic cancer.Conclusion: Our results suggest a potential protective effect of breastfeeding duration against pancreatic cancer incidence. Inconsistent results for the other reproductive factors suggested no important role of estrogens in pancreatic cancer etiology.Keywords: pancreatic neoplasms, incidence, women, prospective study, breastfeeding, age at first birth

Helicobacter pylori (H. pylori) infection is very common worldwide. A reliable diagnosis is crucial for patients with H. pylori-related diseases. At followup, it is important to confirm that eradication therapy has been successful. There is no established gold standard for the diagnosis of H. pylori infection. Material and Methods. A sample of 304 volunteers from the general population was screened for H. pylori infection with serology, 13C-urea breath test (UBT), rapid urease test (RUT) on fresh biopsy, culture from biopsy, and histological examination. Culture was used as gold standard. Results. The sensitivity was 0.99 for serology, 0.90 for UBT, 0.90 for RUT, and 0.90 for histological examination. Corresponding specificities were 0.82, 0.99, 0.98, and 0.97, respectively. The accuracy was 0.86 for serology, 0.96 for UBT, 0.95 for RUT, 0.93 for culture, and 0.95 for histology. There was a strong correlation between the results of UBT and the histological scores of H. pylori colonisation as well as between the results of UBT and the scores of RUT. Conclusion. There were only minor differences in accuracy between the three invasive tests for H. pylori infection in this population. RUT may be recommended as the first choice since a result is obtained within hours. The accuracy of UBT was comparable to the invasive tests, and it is recommended for situations when endoscopy is not needed. [ABSTRACT FROM AUTHOR]

Background: Gastrin exerts trophic effects on the gastric mucosa by mechanisms not yet completely elucidated. Our aim was to localize the cholecystokinin-2 (CCK[sub 2]) receptor in epithelial cells of foetal and adult rat stomachs in order to determine the cell types that are directly affected by gastrin. Methods: Gastric tissue was subjected to indirect double immunofluorescence staining with antiserum against the C-terminal decapeptide of the CCK[sub 2] receptor and antibodies against 5′ bromo-2-deoxyuridine, which had been injected into the rats 1 h before they were killed, the acid pump H,K-ATPase, the membranecytoskeletal linker ezrin, pepsin/pepsinogen or histidine decarboxylase. Results: Undifferentiated foetal gastric epithelial cells expressed CCK[sub 2] receptors, whereas stem cells of adult gastric glands did not exhibit immunoreactivity. However, other epithelial cells in the progenitor zone of adult gastric glands did express CCK[sub 2] receptors. Some of these cells were faintly stained for H,K-ATPase; pepsin/pepsinogen was also detected in this region. Parietal cells in the isthmus/pit region of the glands contained ezrin, and some showed weak immunoreactivity for the CCK[sub 2] receptor. As expected, enterochromaffin-like cells also expressed CCK[sub 2] receptors. Conclusion: Our findings are consistent with the hypothesis that a CCK[sub 2] receptor mediates direct effects of gastrin on gastric epithelial cells during both stomach organogenesis and adult life. [ABSTRACT FROM AUTHOR]

Background: Gastric intestinal metaplasia (IM) is seen mostly in association with chronic gastritis, induced either by Helicobacter pylori infection or autoimmune mechanisms. IM can be categorized into three subtypes, where type III is associated with gastric carcinoma of intestinal type. Methods: Gastric biopsies from 475 subjects randomly selected from the general population and from 27 patients with autoimmune gastritis associated with pernicious anaemia were used. The criteria of Filipe & Jass were applied using different histochemical techniques in combination with haematoxylin and eosin stained material. Results: Twenty-three percent (109/475) of the subjects from the general population and 88% (24/27) in the group with autoimmune gastritis had IM. Type III IM occurred in 4% in both populations. Type III IM was located in the antrum in 90% in the general population. In the group with autoimmune gastritis, only one patient had type III IM, which was located in the corpus. Conclusions: This study reveals for the first time the prevalence and distribution of subtypes of IM in a general population from the Western world. The comparatively high prevalence of type III IM in the general population (4%) indicates that its role as a precursor of gastric carcinoma may have been overemphasized. A similar prevalence of type III IM in patients with autoimmune gastritis may be considered low and suggests that mechanisms for gastric carcinogenesis other than the atrophy - metaplasia-dysplasia sequence could also operate in this condition. [ABSTRACT FROM AUTHOR]

Some benign and malignant diseases develop on the background of chronic gastritis or duodenitis. The present study was performed in order to determine the magnitude of these background changes with relations to symptomatology and life style in the general population. Examinations were performed in 501 volunteers (age 35-85 years). Fifty percent had gastritis; this was associated with H. pylori in 87%. H. pylori-negative gastritis was associated with regular use of NSAIDs [odds ratio 3.8 (1.6-9.9)]. Duodenitis, observed in 32%, was associated with H. pylori infection [odds ratio 2.3 (1.3-4.6)], previous cholecystectomy [odds ratio 3.6 (1.1-16.1)], and regular use of NSAIDs [odds ratio 3.0 (1.4-7.1)]. Neither gastritis nor duodenitis was associated with smoking or alcohol consumption. The rate of digestive symptoms did not differ between subjects with and without uncomplicated gastritis or duodenitis. In conclusion, half of this adult population had gastritis strongly associated with H. pylori infection. Gastritis without H. pylori infection was frequently associated with regular NSAID intake. One third had duodenitis, which was associated with H. pylori infection as well as with regular use of NSAIDs and previous cholecystectomy. Digestive symptoms were not overrepresented in uncomplicated gastritis or duodenitis. [ABSTRACT FROM AUTHOR]

Background: β-Microseminoprotein is a 94-kDa protein present on most mucosal surfaces in the body. It is produced in mucin cells but is also found in a particular type of cells (E-cells) in the gastric antral mucosa. Most of these cells also contain gastrin. In atrophic corpus gastritis the gastrin-producing cells become hyperplastic, and the patients have hypergastrinemia. We wanted to ascertain whether there is a similar effect on the E-cells and on the concentration of β-microseminoprotein in serum. Methods: Antral biopsy specimens from 10 patients with atrophic corpus gastritis and 10 controls were stained immunohistochemically for β-microseminoprotein and gastrin. β-Microseminoprotein and gastrin were measured by radioimmunoassay in serum from 15 women with atrophic corpus gastritis and 31 healthy female blood donors. Results: There was a 3.5-fold increase of the number of E-cells (which also were hypertrophic) and a 2.1 times higher serum concentration of β-microseminoprotein in the patients with atrophic corpus gastritis than in the control subjects. Gastrin was seen in 28% of the E-cells in patients with atrophic corpus gastritis, compared with 87% in normal antral mucosa. There was no correlation between the serum concentrations of β-microseminoprotein and gastrin. Conclusions: In atrophic corpus gastritis antrum E-cells undergo hyperplasia and hypertrophy, and the proportion of E-cells containing gastrin decreases. Increased amounts of β-microseminoprotein are secreted to the blood but uncorrelated with gastrin. [ABSTRACT FROM AUTHOR]

In order to examine the effect of cholecystokinin on spontaneous and induced pancreatic carcinogenesis in the hamster, two sets of experiments were carried out, one involving long-term hypercholecystokininemia and one involving cancer induction during hypercholecystokininemia. The effect of hypercholecystokininemia, induced by pancreaticobiliary diversion (PBD), was studied for 8 months. Neither PBD animals nor sham-operated controls developed premalignant or malignant pancreatic lesions. However, in the PBD group the mean pancreatic weight, total protein content and DNA content were increased by 30, 29 and 27% respectively. No such increases were found in PBD animals receiving a cholecystokinin-A receptor antagonist during the last 24 days of the experiment. In the cancer induction study, the effect of PBD on N-nitrosobis(2-oxopropyl)amine-induced pancreatic carcinogenesis was studied for 3 months. Putative premalignant pancreatic lesions were diagnosed in all PBD hamsters and in four of 15 sham-operated controls. Pancreatic ductular carcinoma in situ was only found in PBD animals. The [3H]thymidine labeling index of the pancreatic lesions was significantly higher in the PBD group than in the controls. No such increase was observed in PBD animals receiving a cholecystokinin-A receptor antagonist during the last 5 days of the experiment. It is concluded that chronic endogenous hypercholecystokininemia promotes early phase pancreatic carcinogenesis, but does not per se cause development of premalignant or malignant pancreatic lesions in the hamster. [ABSTRACT FROM PUBLISHER]