Journal articles on the topic 'Gastriti'
To see the other types of publications on this topic, follow the link: Gastriti.
Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles
Consult the top 50 journal articles for your research on the topic 'Gastriti.'
Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.
You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.
Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.
1
Güney, Güven, Yılmaz Baş, Murat Kekilli, and Emre Demir. "Is History of Adenotonsillectomy a Protective Factor for Helicobacter pylori Gastritis?" Flora the Journal of Infectious Diseases and Clinical Microbiology 24, no. 1 (March 1, 2019): 27–31. http://dx.doi.org/10.5578/flora.67193.
Full text
2
Lupu, V. V., Gabriela Păduraru, Ancuţa Ignat, Eliza Tighici-Saizu, Claudia Olaru, Nicoleta Gimiga, Angelica Cristina Marin, Cornelia Săvescu, Ioana Florea, and Marin Burlea. "GASTRITELE ŞI HELICOBACTER PYLORI LA COPIL – DIAGNOSTICUL ENDOSCOPIC PRIMAR ŞI SECUNDAR." Romanian Journal of Pediatrics 64, no. 3 (September 30, 2015): 326–29. http://dx.doi.org/10.37897/rjp.2015.3.19.
Full textAbstract:
Infecţia cu Helicobacter pylori (H. pylori) este o problemă comună şi semnificativă de sănătate publică. Obiectiv. Determinarea prevalenţei infecţiei cu H. pylori la copiii cu simptomatologie sugestivă şi conturarea cazurilor în funcţie de tipul şi felul gastritei prin efectuarea de endoscopii digestive superioare. Material şi metodă. Studiu retrospectiv realizat pe o perioadă de 5 ani pe 1.269 de copii cu simptomatologie gastrică, la care s-au efectuat endoscopii cu biopsie, stabilindu-se rata de infecţie cu H. pylori prin examen direct sau testul ureazei. Rezultate. Frecvenţa H. pylori în cazul gastritei acute a fost semnificativ mai mică (34,78%) comparativ cu frecvenţa acesteia în cazul gastritei cronice (54,94%). În cadrul celor 10 tipuri de gastrită, cele mai frecvente sunt formele purpurice (43,66%), nodular purpurică (25,93%) şi nodular antrală (15,84%), la polul opus situându-se gastrita atrofi că şi hipertrofică. Asocierile cele mai frecvente decelate endoscopic sunt cu esofagita gr I în 51,6%, duodenita în 45,07% şi forma purpurică în 24,74%. Concluzii. Infecţia cu H. pylori este cel mai frecvent asociată gastritei cronice (54,94%). Identificarea precoce a infecţiei este esenţială pentru eradicarea bacteriei şi prevenirea apariţiei diferitelor tipuri de gastrită identifi cate endoscopic.
3
KUTLAR, Mehmet Can, Gülser DOĞAN, Lara GÜLKAYA, Aynur Sema DERİNYOL, Kübra Nur YEĞİN, Fatma TEKİN, Melis Nur ÖZDEMİR, et al. "Bir Kanıta Dayalı Tıp Uygulaması: Helicobacter Pylori Gastriti Tedavisinde Uygun Yaklaşım Nasıl Olmalı?" Yüksek İhtisas Üniversitesi Sağlık Bilimleri Dergisi 3, no. 1 (April 29, 2022): 6–14. http://dx.doi.org/10.51261/yiu.2022.00042.
Full textAbstract:
ABSTRACT Introduction: Evidence-Based Medicine Program, which is a part of Phase III education program of Yüksek İhtisas University Faculty of Medicine, was held between 12.10.2021 and 16.11.2021 in six divided sessions, as a total of 13 hours. Material and Method: Our study group students, together with the facilitator lecturer, divided the work among ourselves for the problems of the case chosen and obtained literature information to find out the solution by using the evidence pyramid. Results: By working on the information obtained in the practice of evidence-based medicine, the students developed solutions for the problems of a patient diagnosed with Helicobacter pylori gastritis, who was given traditional triple therapy (clarithromycin, amoxicillin, lansoprazole) and had problems during the treatment. Conclusion: It was thought that the patient was not treated appropriately. Quadruple bismuth or dual amoxicillin therapy has been suggested. Proton pump inhibitor should be given bid and the patient should comply with the 14-day treatment period. In addition to drug treatment, probiotic supplement (Lactobacillus derivatives) may also be recommended to the patient. Keywords: Evidence-based medicine, Helicobacter pylori, gastritis, treatment, dietary supplement
4
Franic, Teo V., Louise M. Judd, Nhung V. Nguyen, Linda C. Samuelson, Kate L. Loveland, Andy S. Giraud, Paul A. Gleeson, and Ian R. van Driel. "Growth factors associated with gastric mucosal hypertrophy in autoimmune gastritis." American Journal of Physiology-Gastrointestinal and Liver Physiology 287, no. 4 (October 2004): G910—G918. http://dx.doi.org/10.1152/ajpgi.00469.2003.
Full textAbstract:
A prominent pathological feature of murine autoimmune gastritis is a pronounced mucosal hypertrophy. Here, we examined factors that may be responsible for inducing this hypertrophy. Because gastrin is known to be both an inducer of gastric mucosal cell proliferation and is elevated in autoimmune gastritis, mice deficient in gastrin were thymectomised at day 3 and assessed for autoimmune gastritis. Gastrin-deficient mice showed all the characteristic features of murine autoimmune gastritis, including gastric unit hypertrophy due to hyperproliferation and accumulation of immature epithelial cells, decreases in the number of zymogenic and parietal cells, and autoantibodies to the gastric H+/K+-ATPase. Hence, gastrin is not required for either the establishment of chronic gastritis or development of the typical pathological features of this disease. We also examined mRNA levels of a number of gastric mucosal growth factors in RNA samples from mice with hypertrophic autoimmune gastritis. Members of the Reg family, RegIIIβ and RegIIIγ, were greatly elevated in mice with hypertrophic gastritis, whereas RegI and amphiregulin (an EGF receptor ligand) were more modestly and/or inconsistently induced. These data demonstrate that induction of gastric mitogenic factors, such as members of the Reg family, can be achieved in inflammatory situations by gastrin-independent pathways. Members of the Reg family, in particular RegIIIβ and RegIIIγ, are good candidates to be involved in inducing the mucosal hyperproliferation in autoimmune gastritis. These findings are likely to be of relevance to other gastric inflammatory conditions.
5
Sablina, Anastasiya O., Sergej S. Aleksanin, and Oleg A. Sablin. "Anti-parietal cell antibodies seroconversion in patients with autoimmune atrophic gastritis: a prospective study." HERALD of North-Western State Medical University named after I.I. Mechnikov 12, no. 1 (May 28, 2020): 71–78. http://dx.doi.org/10.17816/mechnikov202012171-78.
Full textAbstract:
The purpose of the study was to evaluate the atrophic changes of body and antrum gastric mucosa, the occurrence of Helicobacter pylori infection and the possibility of seroconversion in patients with autoimmune gastritis throughout 10 years.
Material and methods. 203 Chernobyl nuclear power plant accident recovery workers were included in the prospective study. Blood levels of anti-parietal cell antibodies, basal gastrin-17, pepsinogens I and II were evaluated in all the patients to diagnose autoimmune gastritis and to assess gastric mucosa non-invasively.
Results. Anti-parietal cell antibodies were found in 34.5% of the patients. Eradication rates were low (32.850.0%) in the patients with atrophy of gastric mucosa in the first 3 years of observation. Statistically significant decrease in pepsinogen I and gastrin-17 serum levels was observed in the patients with H. pylori-associated autoimmune gastritis throughout first 46 years. In the next 710 years pepsinogen I and gastrin-17 serum levels were increasing possibly due to positive effect of H. pylori eradication therapy. Successful eradication leads to disappearance of anti-parietal cell antibodies in 33.4% of the patients by the 10th year of the observation.
Conclusion. The obtained results show that H. pylori eradication therapy is effective in reducing atrophic changes of gastric mucosa in the patients with autoimmune gastritis. Against the background of successful treatment the levels of pepsinogen I and gastrin-17, the markers of body and antrum gastric mucosa atrophy, were increasing. In the patients with autoimmune gastritis but without H. pylori infection the following trend was not noticed.
6
Elsebaey, Mohamed A., Mohamed A. Tawfik, Samah A. Elshweikh, Manal Saad Negm, Mohammed H. Elnaggar, Ghada Mahmoud Alghazaly, and Sherief Abd-Elsalam. "Impact of Helicobacter pylori Infection on Gastric Variceal Bleeding among Patients with Liver Cirrhosis." Gastroenterology Research and Practice 2019 (February 10, 2019): 1–6. http://dx.doi.org/10.1155/2019/6529420.
Full textAbstract:
Background and Aims. Currently, it is well known that Helicobacter pylori- (H. pylori-) related peptic ulcer is one of the main causes of nonvariceal bleeding in cirrhotic patients. However, there is a lack of data to identify the exact effect ofH. pyloriinfection on variceal bleeding. This study was conducted to identify the impact ofH. pyloriinfection on gastric variceal bleeding in cirrhotic patients.Patients and Methods. 76 cirrhotic patients with gastric varices were included in this prospective study and divided into 2 groups: nonbleeding gastric varices (32 patients) and bleeding gastric varices (44 patients). The fasting serum gastrin level was measured. Mucosal biopsies from the gastric body and antrum were examined to determine the patterns of gastritis and the presence ofH. pylori.Results. The frequency ofH. pyloriinfection in the studied patients was 59.2%. There were significant differences between both groups regarding liver decompensation (P=0.001), red color sign over gastric varices (P=0.0011), prevalence ofH. pyloriinfection (P=0.0049), histological patterns of gastritis (P=0.0069), and serum gastrin level (P=0.0200). By multivariate analysis, Child C cirrhosis, red color sign over gastric varices, andH. pylori-induced follicular gastritis were independent risk factors for bleeding from gastric varices.Conclusion.H. pylori-induced follicular gastritis is considered as an additional risk factor for bleeding from gastric varices.
7
Feldman, Mark, Byron Cryer, and Edward Lee. "Effects of Helicobacter pylorigastritis on gastric secretion in healthy human beings." American Journal of Physiology-Gastrointestinal and Liver Physiology 274, no. 6 (June 1, 1998): G1011—G1017. http://dx.doi.org/10.1152/ajpgi.1998.274.6.g1011.
Full textAbstract:
Helicobacter pylori gastritis is common, but effects on gastric secretion are not well understood. We measured basal and pentagastrin-stimulated gastric acidity, pepsin activity, and fluid output, as well as serum gastrin concentrations and H. pylori antibody levels, before and after treatment of H. pylori gastritis in 28 men and women. Subjects were studied before and 1 and 3 mo after a course of bismuth, metronidazole, and tetracycline. Elimination of H. pylori gastritis, accomplished in 14 subjects, increased basal and pentagastrin-stimulated gastric acidity (by 15 meq/l) and basal acid output significantly (by 2.1 meq/h 1 mo after therapy). Elimination of H. pylori had an opposite effect on pepsin secretion, significantly decreasing pepsin output by 30%. Elimination of H. pylori significantly reduced nonparietal fluid output by 35%, without affecting fluid output from parietal cells. Serum gastrin and H. pylori antibody levels declined significantly after elimination of H. pylori. None of these changes was observed in 14 subjects whose H. pylori gastritis was resistant to antimicrobial therapy. In summary, eradication of H. pylori infection increases gastric acidity by reducing nonparietal gastric secretion from peptic and other cells.
8
Varro, Andrea, and Joy ES Ardill. "Gastrin: an analytical review." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 40, no. 5 (September 1, 2003): 472–80. http://dx.doi.org/10.1258/000456303322326380.
Full textAbstract:
The gastric hormone gastrin is produced in multiple forms that vary in their biological properties. In this analytical review, the strategies available for the assay of different gastrins in plasma are considered. Except for research purposes, it is seldom necessary or even desirable to employ assays that are specific for an individual molecular form of gastrin. Instead, routine clinical assays of plasma gastrin should ideally react equally with the sulphated and unsulphated forms of the COOH-terminally amidated peptides, the most important of which are peptides of 17 and 34 amino acid residues (i.e. G17 and G34), and should not react with the related hormone cholecystokinin. Methods appropriate for the use of such assays are reviewed. These assays are important in the diagnosis of gastrinoma. Although it is recognized that circulating concentrations of gastrin are elevated in other conditions, including chronic atrophic gastritis, Helicobacter pylori infection and long-term administration of proton pump inhibitors, it is not clear whether gastrin radioimmunoassay is important for the clinical management in these conditions.
9
Sequenza, M. J., M. R. Loi, F. Londrino, P. Sale, S. Andrulli, A. Noce, O. Durante, et al. "Sicurezza nella scelta dell'Inibitore di Pompa Protonica nel nefropatico cronico." Giornale di Clinica Nefrologica e Dialisi 24, no. 3 (January 26, 2018): 11–15. http://dx.doi.org/10.33393/gcnd.2012.1152.
Full textAbstract:
Il paziente nefropatico cronico facilmente presenta alterazioni morfologiche e funzionali dell'apparato gastroenterico. I segni più comuni e precoci nella sindrome uremica cronica sono rappresentati dai disturbi gastrointestinali. Da alcuni decenni abbiamo a disposizione dei farmaci con potente azione inibente la secrezione acida gastrica: gli inibitori di pompa protonica (IPP) hanno una struttura chimica affine, uno stesso meccanismo d'azione e sono molto importanti per il trattamento delle patologie acido correlate, per l'eradicazione dell'Helicobacter Pylori, per la prevenzione e la cura della gastropatia da farmaci antinfiammatori non steroidei (FANS). Somministriamo ai nostri pazienti questa classe di farmaci, con terapie che continuano nel tempo, nonostante la risoluzione della malattia (gastroprotezione). Ma gli IPP possono essere utilizzati indistintamente nei nefropatici cronici oppure sarebbe utile conoscere il profilo del farmaco per una corretta scelta? In questo articolo si argomenta che i loro effetti collaterali non sono molto rilevanti e sono abbastanza simili: il loro impiego nel lungo termine è sicuro. La potenza e l'efficacia dei vari IPP, dall'analisi comparativa dei vari trial clinici, risulta essere molto simile sulla base dei milligrammi di sostanza utilizzata. L'unica eccezione illustrata in questo lavoro è rappresentata da 6 pazienti in emodialisi, trattati con lansoprazolo (15 mg), che presentavano gastriti e ulcere peptiche complicate da gravi episodi di ematemesi e melena con conseguente anemia. Tutti gli IPP hanno dimostrato un'efficacia clinica sovrapponibile, tuttavia vanno valutati di volta in volta i vantaggi (relativi) di ciascun IPP. I criteri di scelta di un IPP sembrano basati, principalmente sulle indicazioni autorizzate, sulle formulazioni disponibili, sul profilo di sicurezza del farmaco.
10
Antico, Antonio, Marilina Tampoia, Danilo Villalta, Elio Tonutti, Renato Tozzoli, and Nicola Bizzaro. "Clinical Usefulness of the Serological Gastric Biopsy for the Diagnosis of Chronic Autoimmune Gastritis." Clinical and Developmental Immunology 2012 (2012): 1–5. http://dx.doi.org/10.1155/2012/520970.
Full textAbstract:
Aim. To assess the predictive value for chronic autoimmune gastritis (AIG) of the combined assay of anti-parietal-cell antibodies (PCA), anti-intrinsic-factor antibodies (IFA), anti-Helicobacter pylori(Hp) antibodies, and measurement of blood gastrin.Methods. We studied 181 consecutive patients with anemia, due to iron deficiency resistant to oral replacement therapy or to vitamin B12 deficiency.Results. 83 patients (45.8%) tested positive for PCA and underwent gastroscopy with multiple gastric biopsies. On the basis of the histological diagnosis, PCA-positive patients were divided into 4 groups: (1) 30 patients with chronic atrophic gastritis; they had high concentrations of PCA and gastrin and no detectable IFA; (2) 14 subjects with metaplastic gastric atrophy; they had high PCA, IFA, and gastrin; (3) 18 patients with nonspecific lymphocytic inflammation with increased PCA, normal gastrin levels, and absence of IFA; (4) 21 patients with multifocal atrophic gastritis with “borderline” PCA, normal gastrin, absence of IFA and presence of anti-Hp in 100% of the cases.Conclusions. The assay of four serological markers proved particularly effective in the diagnostic classification of gastritis and highly correlated with the histological profile. As such, this laboratory diagnostic profile may be considered an authentic “serological biopsy.”
11
Parhusip, Dumawan Harris, Gontar Alamsyah Siregar, and Leonardo Basa Dairi. "The Difference of Serum Gastrin-17 Level Based on Gastritis Severity and Helicobacter Pylori Infection." Open Access Macedonian Journal of Medical Sciences 7, no. 8 (April 29, 2019): 1266–69. http://dx.doi.org/10.3889/oamjms.2019.325.
Full textAbstract:
BACKGROUND: Gastritis was defined as the histological presence of gastric mucosal inflammation. One of the most common aetiology was H. pylori. Gastrin-17 was a hormone that was secreted by G cells. H. pylori infection induced increased in gastrin-17 in gastritis. Therefore, this study was to investigate the relationship of gastrin-17 with gastritis severity and H. pylori infection.
AIM: To determine the difference in serum Gastrin-17 level based on gastritis severity and H. pylori infection.
METHODS: A cross-sectional study enrolling 45 patients with gastritis was conducted in Haji Adam Malik General Hospital between April and July 2018. Endoscopy and biopsy examinations were performed to confirm the diagnosis of gastritis. Gastritis severity was assessed using the Updated Sydney System. The presence of H. pylori infection was detected by a Campylobacter-like organism (CLO) examination. Gastrin-17 level and demographic data were also gathered. The analysis was done using Mann Whitney and Kruskal-Wallis test. P-value of < 0.05 was considered statistically significant.
RESULTS: Serum Gastrin-17 level was significantly different based on gastritis severity (P = 0.001 according to neutrophils infiltration and P = 0.023 according to degree of atrophy), H. pylori infection (P = 0.038), and combined gastritis severity and H. pylori infection (P < 0.001). Serum Gastrin-17 level was higher in subjects with severe neutrophils infiltration, without atrophy, and with H. pylori infection.
CONCLUSION: There was a significant difference in serum Gastrin-17 level based on gastritis severity and H. pylori infection.
12
Fukayama, M., Y. Hayashi, T. Takizawa, M. Koike, S. Endo, and H. Okumura. "Glycoprotein hormone alpha-subunit in human stomach." Journal of Histochemistry & Cytochemistry 34, no. 8 (August 1986): 995–1001. http://dx.doi.org/10.1177/34.8.3525666.
Full textAbstract:
To demonstrate the immunoreactive alpha-subunit of human chorionic gonadotropin (hCG) or glycoprotein hormones in non-neoplastic gastric mucosa, and to clarify the nature and significance of alpha-subunit-immunoreactive cells, immunohistochemical studies were performed on gastric mucosa using polyclonal antibodies for hCG alpha and beta, hLH beta, hFSH beta, hTSH beta, and gastrin, and a monoclonal antibody for hCG alpha. Surgically resected stomachs were classified as follows: nearly normal (Group A); antral gastritis (Group B); fundic gastritis with pseudopyloric glands (Group C); and intestinal metaplasia (Group D). Cells immunoreactive for the alpha-subunit were present in the pyloric glands and to a lesser extent in the fundic glands (Groups A and B). Almost all alpha-subunit-immunoreactive cells were nonreactive for the beta-subunits of the four glycoprotein hormones. alpha-subunit-immunoreactive cells corresponded to gastrin-containing cells in the pyloric glands, but were unrelated to gastrin in the fundic glands. In fundic gastritis, alpha-subunit-immunoreactive cells appeared to increase (Group C), and many hyperplastic foci were observed in atrophic glands with hyperplasia of the argyrophilic cells (Groups C and D). Isolated hCG alpha or the alpha-subunit of glycoprotein hormones may be present in the endocrine cells of gastric mucosa, and alpha-subunit-immunoreactive cells in the fundic glands seem to proliferate in fundic gastritis.
13
Judd, Louise M., Paul A. Gleeson, Ban-Hock Toh, and Ian R. van Driel. "Autoimmune gastritis results in disruption of gastric epithelial cell development." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 1 (July 1, 1999): G209—G218. http://dx.doi.org/10.1152/ajpgi.1999.277.1.g209.
Full textAbstract:
We have investigated the underlying basis of the lesion in murine autoimmune gastritis, a model of the human disease pernicious anemia. The disease is mediated by T lymphocytes and characterized by selective depletion of parietal and zymogenic cells from the gastric unit (gland) together with gastric epithelial cell hyperplasia. The gastric units of gastritic stomachs contained 2.3-fold more cells than normal and accumulated rapidly dividing, short-lived gastric epithelial stem cells and mucous neck cells. Most of these immature cells failed to differentiate into end-stage cells but rather appeared to die by apoptosis. We also found no correlation between anti-parietal cell autoantibody titers and the degree of gastric pathology, providing further evidence that autoantibodies do not play a direct role in the pathogenesis of gastritis. Taken together, the normal developmental pathways of the gastric mucosa are disrupted in autoimmune gastritis, resulting in an amplification of immature cell types. The differentiation of these immature cells appears to be blocked, contributing to depletion of end-stage cells. This scenario provides an explanation for depletion of not only parietal cells but also zymogenic cells even though they are not directly targeted by the immune system.
14
Tsukanov, V. V., O. V. Smirnova, E. V. Kasparov, A. A. Sinyakov, A. V. Vasyutin, and Yu L. Tonkikh. "Changes in the indices of prooxidant and antioxidant systems in blood plasma in men with atrophic gastritis and gastric cancer." Terapevticheskii arkhiv 90, no. 2 (February 15, 2018): 24–27. http://dx.doi.org/10.26442/terarkh201890224-27.
Full textAbstract:
Aim. To study changes in the indices of prooxidant and antioxidant systems in plasma in men with atrophic gastritis and gastric cancer. Materials and methods. The study included 60 healthy men, 42 patients with atrophic gastritis and 50 men, nicardipine patients with gastric cancer stage II according to TNM. All patients underwent serological diagnosis of diffuse atrophic gastritis (definition of pepsinogens and gastrin-17) and Helicobacter pylori infection. The diagnosis of "atrophic gastritis" was verified by morphological examination of biopsy specimens obtained during fibroesophagogastroduodenoscopy. Diagnosis of gastric cancer was carried out in the Krasnoyarsk regional oncologic dispensary on the basis of a comprehensive instrumental and morphological examination. All patients spectrophotometric methods in plasma was determined the content of diene conjugates (DC), malonic dialdehyde (MDA), glutathione-S-transferase (GST), glutathione peroxidase (GPO), superoxide dismutase (SOD) and catalase. Results. The concentration of SOD, GST, GPO and catalase had no significant differences in patients with atrophic gastritis and gastric cancer and prevailed in comparison with healthy persons. Patients with cancer of the stomach content in the blood plasma DK 2.7 times and MDA at 35.2 times higher than healthy individuals, indicating severe oxidative stress in patients with cancer. In patients with atrophic gastritis was observed similar but less pronounced pattern. Conclusion. The results indicate the presence of oxidative stress in men with atrophic gastritis and gastric cancer.
15
Feldman, Mark, Byron Cryer, Doug Sammer, Edward Lee, and Stuart J. Spechler. "Influence of H. pylori infection on meal-stimulated gastric acid secretion and gastroesophageal acid reflux." American Journal of Physiology-Gastrointestinal and Liver Physiology 277, no. 6 (December 1, 1999): G1159—G1164. http://dx.doi.org/10.1152/ajpgi.1999.277.6.g1159.
Full textAbstract:
Gastric acid secretion, gastrin release, gastric emptying, and gastroesophageal acid reflux were measured in asymptomatic individuals before and after elimination of Helicobacter pylorigastritis. After basal gastric acid secretion and serum gastrin concentrations were measured, meal-stimulated gastric acid secretion and gastrin release were assessed during in vivo intragastric titration to pH 3. Experiments were repeated 4 wk after treatment with lansoprazole, amoxicillin, and clarithromycin. Esophageal pH was also monitored for 24 h before and after therapy. Basal gastric acidity increased ∼20 mmol/l in subjects whose infection was eradicated ( P < 0.05) but not in those with persistent infection. Basal and meal-stimulated gastric acid secretion did not change after H. pylorieradication, despite a 41% reduction in meal-stimulated gastrin release ( P < 0.05). Gastroesophageal acid reflux increased two- to threefold after successful treatment ( P < 0.05) but did not change in subjects with persistent infection. Thus elimination of H. pylori gastritis increases gastric acidity, probably by reducing nonparietal alkaline secretion, and this may facilitate gastroesophageal acid reflux.
16
Lee, San Min, Dae Young Cheung, Jin Il Kim, and Soo-Heon Park. "Lower risk of gastric atrophy and intestinal metaplasia in MALT lymphoma patients despite of H. pylori infection." Journal of Clinical Oncology 37, no. 4_suppl (February 1, 2019): 33. http://dx.doi.org/10.1200/jco.2019.37.4_suppl.33.
Full textAbstract:
33 Background: Atrophic gastritis and intestinal metaplasia are sequential consequences of chronic H. pylori infection. H. pylori infection is a well-known risk factor for gastric adenocarcinoma and MALT lymphoma of stomach. Atrophic gastritis and intestinal metaplasia increase the risk of gastric adenocarcinoma development. The relationship between gastric MALT lymphoma and atrophic gastritis-intestinal metaplasia has not been on the spot of interest. We investigated the clinical characteristics of gastric MALT lymphoma and co-presence of atrophic gastritis and intestinal metaplasia. Methods: Study was conducted by review of electronic medical record of patients who were diagnosed with gastric MALT lymphoma at an academic institute, the Yeouido St. Mary's Hospital, Seoul, Korea, from January 2001 to March 2018. Results: A total of 51 subjects were enrolled consecutively during the study period and analyzed retrospectively. The mean age was 57.5-year-old. The male to female ratio was 1.04 (26/25). On histologic examination, background atrophic gastritis was accompanied in 64.7% (33/51). Serum pepsinogen I, II and gastrin level, as serological marker for atrophy, were evaluated in 21 subjects. Thirteen out of 21 (61.9%) were compatible with serological atrophic gastritis (pepsinogen I / II ratio of less than three or pepsinogen I < 70 ng/mL). Conclusions: Prevalence of background mucosal atrophy or intestinal metaplasia was around 60% in patients with gastric MALT lymphoma. This is comparable to that of general population and lower than that of patients with gastric adenocarcinoma. Even though age can be a confounding factor, this result suggests different carcinogenic pathway of gastric MALT lymphoma from adenocarcinoma.
17
Tsuboi, Mayo, Ryota Niikura, Yoku Hayakawa, Yoshihiro Hirata, Tetsuo Ushiku, and Kazuhiko Koike. "Distinct Features of Autoimmune Gastritis in Patients with Open-Type Chronic Gastritis in Japan." Biomedicines 8, no. 10 (October 14, 2020): 419. http://dx.doi.org/10.3390/biomedicines8100419.
Full textAbstract:
In Asia, the incidences of Helicobacter pylori infection and gastric cancer are high, but their association with autoimmune gastritis (AIG) is unclear. This was a retrospective cohort study of patients endoscopically diagnosed with chronic gastritis between 2005 and 2017. AIG was diagnosed according to anti-parietal cell antibody positivity. Laboratory, histological findings, and gastric cancer incidence were compared between AIG and non-AIG patients. The AIG group had more females and a higher rate of thyroid disease. Serum levels of gastrin were significantly higher in AIG patients (mean 1412 and 353 pg/mL, p < 0.001). The endoscopic findings included a significantly higher percentage of corpus-dominant atrophy in AIG (31.67%) than in non-AIG (7.04%) patients (p < 0.001). Clusters of ECL cells were observed in 28% of AIG patients and 7% of non-AIG patients (p = 0.032). The cumulative incidence of gastric cancer at 5 and 10 years was 0% and 0.03% in the AIG group and 0.03% and 0.05% in the non-AIG group, and no significant difference in gastric cancer incidence was observed. Despite significant differences in gastrin levels between AIG and non-AIG patients, there was no evidence of an impact of AIG on the incidence of gastric cancer.
18
Kolesnikova, I. Yu, and A. S. Novikova. "Gastric Polyps and Atrophic Gastritis." Russian Journal of Gastroenterology, Hepatology, Coloproctology 31, no. 2 (June 2, 2021): 27–33. http://dx.doi.org/10.22416/1382-4376-2021-31-2.
Full textAbstract:
Aim. A study of atrophic gastritis severity and rate in patients with gastric polyps (GP).Materials and methods. The study enrolled 61 patients with hyperplastic (HGP) and 41 — with adenomatous GP (AGP). All patients had 24-h gastric pH-metry, control of the pepsinogen I, II and gastrin-17 levels, in addition to a general clinical, endoscopic, histological examination and testing for Helicobacter pylori.Results. GP patients had benign manifestations prevailed with epigastric heaviness and overflow, and a scarce history of H. pylori testing at no control of rendered eradication therapy. A symptomatic proton pump inhibitor treatment in GP was either prescribed or voluntary. Focal atrophic gastritis in endoscopy was revealed in 12 (19.7 %) HGP and 16 (39.0 %) AGP patients, diffused atrophic gastritis — in 49 (80.3 %) HGP and 25 (60.9 %) AGP patients. Low-grade chronic gastritis in histology prevailed in HGP, moderate — in AGP, and severe — in 21.9 % cases. Moderate (27.9 %) to severe (65.6 %) atrophy of gastric mucosa was registered in HGP, with 53.7 and 39.0 % respective AGP cases. Polyp dysplasia was detected in 20 % HGP and 75.6 % AGP cases. Pepsinogen I <25 µg/L at a pepsinogen I/II ratio ><3 was observed in 38 (62.3 %) HGP and 18 (43.9 %) AGP patients. Hypo- and anacidic were 65.6 % HGP and 31.7 % AGP patients. >H. pylori-positive were 52.5 % HGP and 70.7 % AGP cases.Conclusion. A largely similar aetiopathogenesis of gastric polyps and chronic atrophic gastritis warrants the H. pylori diagnosis and a more detailed patient control for chronic gastritis grading and staging, functional insufficiency of gastric mucosa and the severity of hyperplastic and dysplastic change. The H. pylori eradication, in contrast to anti-secretory therapy, allows the containment of chronic gastritis and is a critical measure in gastric cancer prevention.
19
Zavros, Y., G. Rieder, Amy Ferguson, and J. L. Merchant. "Gastritis and Hypergastrinemia Due to Acinetobacter lwoffii in Mice." Infection and Immunity 70, no. 5 (May 2002): 2630–39. http://dx.doi.org/10.1128/iai.70.5.2630-2639.2002.
Full textAbstract:
ABSTRACT In mouse models and humans, Helicobacter pylori is associated with an increase in serum gastrin and gastrin-expressing (G) cells with a concomitant decrease in somatostatin-expressing D cells. Inflammation of the gastric mucosa can progress to metaplastic changes in the stomach and to decreased colonization by H. pylori and increased colonization by non-H. pylori organisms. In addition, about 20% of individuals with chronic gastritis are H. pylori negative, suggesting that other organisms may induce gastritis. Consistent with this hypothesis, we report here that Acinetobacter lwoffii causes the same histologic changes as does H. pylori. Gastric epithelial cells were isolated from the entire stomach by an enzymatic method for quantitation by both flow cytometry and morphometric analysis. Two months after mice were inoculated with H. pylori or A. lwoffii, the mucosal T- and B-cell numbers significantly increased. After 4 months of infection, there was a threefold increase in the number of G cells and a doubling in the number of parietal cells. A threefold decrease in the number of D cells occurred in H. pylori- and A. lwoffii-infected mice. Plasma gastrin levels increased after both H. pylori and A. lwoffii infection. Histology revealed the presence of inflammation in the gastric mucosa with both A. lwoffii and H. pylori infection. A periodic acid-Schiff stain-alcian blue stain revealed mucous gland metaplasia of the corpus. Collectively, the results demonstrate that gastritis and hypergastrinemia are not specific for H. pylori but can be induced by other gram-negative bacteria capable of infecting the mouse stomach.
20
Kishino, Maiko, Kenshi Yao, Hiroshi Hashimoto, Hiroki Nitta, Rie Kure, Ayako Yamamoto, Kana Yamamoto, Kouichi Nonaka, Shinichi Nakamura, and Katsutoshi Tokushige. "A case of early autoimmune gastritis with characteristic endoscopic findings." Clinical Journal of Gastroenterology 14, no. 3 (February 10, 2021): 718–24. http://dx.doi.org/10.1007/s12328-021-01351-4.
Full textAbstract:
AbstractSignificant atrophic gastritis in the fundic gland region is a well-known endoscopic finding observed in autoimmune gastritis (AIG). The endoscopic features of early AIG have not been reported. Iron deficiency, vitamin B12 deficiency, anemia, or neurological symptoms may not be observed in the early stages of AIG, and it may thus be difficult to diagnose early AIG based on clinical findings. We treated a 50-year-old Japanese female whose condition was suspected to be early AIG. The endoscopic findings showed normal gastric pyloric gland mucosa, and diffuse reddened and edematous gastric fundic gland mucosa. Pathologically, local infiltration of lymphocytes and decrease of parietal cells was present in a deep part of the gastric fundic gland mucosa. Blood tests showed that the titer of parietal cell antibody (PCA) was 1:320 and the gastrin level was 820 pg/ml. We determined that the patient had AIG because she also had Hashimoto’s disease, the PCA titer was high, the serum gastrin level was slightly increased, and inflammation was observed only in the gastric body on the endoscopic images. To the best of our knowledge, this is the first case report of endoscopic findings that suggest early AIG, before atrophic changes were observed.
21
AL-Ezzy, Ali Ibrahim Ali. "Immunopathological and Modulatory Effects of Cag A+ Genotype on Gastric Mucosa, Inflammatory Response, Pepsinogens, and Gastrin-17 Secretion in Iraqi Patients infected with H. pylori." Open Access Macedonian Journal of Medical Sciences 6, no. 5 (May 14, 2018): 794–802. http://dx.doi.org/10.3889/oamjms.2018.178.
Full textAbstract:
OBJECTIVE: To determine the immunopathological correlation between Cag A+ H. pylori-specific IgG; pepsinogen I&II (PI&PII); gastrin-17 (G-17); status of gastric and duodenal mucosa and inflammatory activities on different gastroduodenal disorders.METHODOLOGY: Eighty gastroduodenal biopsies were taken from patients with gastroduodenal disorders for histopathological evaluation and H. pylori diagnosis. Serum samples were used for evaluation of gastric hormones and detection of H. pylori-specific IgG antibodies. The tissue expression of H. pylori Cag A gene was detected by in situ hybridisation.RESULTS: H. pylori IgG antibodies were detected in (88.8%) of enrolled patients. According to Cag A gene expression, Significant difference (P value ˂ 0.05) was detected in levels of PG I; PGII, PG I/PG II among patients with gastric disorders. Serum G-17 level was negatively correlated with Cag A gene expression (P-value = 0.04). There was a significant correlation between H. pylori IgG and PG I; PG II; G-17. The current study revealed that corpus atrophic gastritis was diagnosed histologically with (5%) gastric ulcer cases; (3.75%) of duodenal ulcer cases; (3.75%) of duodenitis cases; (1.25%) of gastropathy cases and (8.75%) of gastritis cases. At the same time H. pylori gastritis diagnosed concurrently with (8.75%) of gastric ulcer cases; (11.25%) of duodenal ulcer cases; (17.5%) of gastropathy cases; (3.75%) of duodenitis cases and (2.5%) of prepyloric ulcer cases. A significant correlation was reported between the Immunopathological status of gastric mucosa and endoscopic mucosal finding among duodenal ulcer cases and gastritis cases only. A positive correlation was reported between serum levels of PGI; PGII; PGI/PGII; G-17; PMNs grade and Immunopathological status of the gastroduodenal mucosa of H. pylori Infected patients. A significant difference was reported in lymphocyte grades among gastric disorders without correlation with immunohistopathological changes in the mucosa (P-value = 0.002). A significant difference was reported in lymphocyte grades among different disorders according to H. pylori IgG. A significant difference was reported in serum level of PG I; PG II; PG I/PG II; G-17 according to PMN and lymphocyte grades (P-value ˂ 0.01). PMNs grades positively correlated with gastric Cag A expression; H. pylori IgG; PG II; G-17 levels. PG I; PG I/ PG II correlated with lymphocyte grades (P-value ˂ 0.05); while PGII has a negative correlation (P-value = 0.039).CONCLUSION: Endoscopic mucosal finding does not reflect exactly the actual immunopathological changes of gastric mucosa during H. pylori infection. Secretion of gastrin was not affected by the presence of Cag A in gastric tissue. Instead, the fluctuation in the hormone level appears to be due to the presence of H. pylori infection in gastric tissue. Gastric tissue infiltration with PMNs & lymphocytes inflammatory infiltrates has a direct effect on PGs and gastrin levels in serum of infected patients. The level of PG I; PG II; G-17 secretion correlated with the development of immune response against H. pylori and production of specific H. pylori IgG. Finally, H. pylori can modulate gastric secretions through Cag A dependent and independent pathways.
22
Dondov, Ganchimeg, Dashmaa Amarbayasgalan, Batbold Batsaikhan, Tegshjargal Badamjav, Batchimeg Batbaatar, Baljinnyam Tuvdenjamts, Nasanjargal Tumurbat, et al. "Diagnostic performances of pepsinogens and gastrin-17 for atrophic gastritis and gastric cancer in Mongolian subjects." PLOS ONE 17, no. 10 (October 17, 2022): e0274938. http://dx.doi.org/10.1371/journal.pone.0274938.
Full textAbstract:
In Mongolia, gastric cancer morbidity and mortality are high, and more than 80 percent of cases are diagnosed at an advanced stage. This study aimed to evaluate pepsinogens (PGIs) and gastrin-17 (G-17) levels and to determine the diagnostic performances for gastric cancer and chronic atrophic gastritis among Mongolian individuals. We enrolled a total of 120 subjects, including gastric cancer (40), atrophic gastritis (40), and healthy control (40), matched by age (±2) and sex. Pepsinogen I (PGI), Pepsinogen II (PGII), G-17, and H. pylori IgG levels were measured using GastroPanel ELISA kit (Biohit, Helsinki, Finland). Also, PGI to PGII ratio (PGR) was calculated. For atrophic gastritis, when the optimal cut-off value of PGI was ≤75.07 ng/ml, the sensitivity and specificity were 75% and 50%, respectively; when the optimal cut-off value of PGR was ≤6.25, sensitivity and specificity were 85% and 44.7%, respectively. For gastric cancer, when the optimal cut-off value of PGI was ≤35.25 ng/ml, the sensitivity and specificity were 47.2% and 86.8%, respectively; when the optimal cut-off value of PGR was ≤5.27, sensitivity and specificity were 75% and 60.5%, respectively. Combinations of biomarkers with risk factors could improve diagnostic accuracy (AUC for atrophic gastritis 74.8, 95% CI 64.0–85.7, p<0.001; AUC for gastric cancer 75.5, 95% CI 64.2–86.8, p<0.001). PGI, PGR biomarkers combined with the risk of age, family history of gastric cancer, and previous gastric disease could not be an alternative test for upper endoscopy but might be a supportive method which is identifying individuals at medium- and high risk of gastric cancer and precancerous lesions who may need upper endoscopy.
23
Loor, Alexandra, and D. L. Dumitraşcu. "Helicobacter pylori Infection, Gastric Cancer and Gastropanel." Romanian Journal Of Internal Medicine 54, no. 3 (September 1, 2016): 151–56. http://dx.doi.org/10.1515/rjim-2016-0025.
Full textAbstract:
Abstract Gastric cancer (GC) is one of the most widespread types of cancer worldwide. Helicobacter pylori infection has been clearly correlated with gastric carcinogenesis. At present and in the near future, the most important challenge is and will be the significant reduction of mortality due to GC. That goal can be achieved through the identification of higher-risk patients, such as those with atrophic gastritis, intestinal metaplasia and dysplasia. In this review we intend to discuss the importance of diagnosing H. pylori infection and chronic atrophic gastritis in preventing gastric cancer, using a new non-invasive test called GastroPanel. This test is a classification algorithm including four biochemical parameters pepsinogen I and II (PGI and PGII), gastrin-17 (G17), and anti-Helicobacter pylori antibodies (Ig G anti-Hp) measured in fasting sera, which allows to classify patients as having atrophic or non-atrophic gastritis and to find whether gastritis is associated or not with H. pylori infection. GastroPanel is not a “cancer test”, but it can and should be used in the screening and diagnosis of subjects with a high cancer risk; still, a careful diagnostic made by superior digestive endoscopy is compulsory to find possible precancerous or cancerous lesions at an early and curable stage.
24
Yasunaga, Yuichi, Juan José Bonilla-Palacios, Yasuhisa Shinomura, Shuji Kanayama, Yoshiji Miyazaki, and Yuji Matsuzawa. "High Prevalence of Serum Immunoglobulin G Antibody toHelicobacter pyloriand Raised Serum Gastrin and Pepsinogen Levels in Enlarged Fold Gastritis." Canadian Journal of Gastroenterology 11, no. 5 (1997): 433–36. http://dx.doi.org/10.1155/1997/437467.
Full textAbstract:
To clarify the prevalence ofHelicobacter pyloriinfection in enlarged fold gastritis, serum immunoglobulin (Ig) G antibody toH pyloriwas determined in 19 patients with severely enlarged gastric body folds (the widest fold greater than 10 mm on the radiograph), 55 patients with moderately enlarged folds (6 to 10 mm) and 44 control subjects (5 mm or less). The prevalence of serum IgG antibody toH pyloriin the severe (100%) and moderate groups (100%) was significantly higher than that in controls (34.1%) (PÃ0.01). There were significant differences among the three groups in serum gastrin, pepsinogen I and pepsinogen II levels (severe had the highest levels, followed by moderate and then controls, PÃ0.001).H pyloricolonization in the gastric mucosa was confirmed by culture, urease test or both, and inflammation by hematoxylin and eosin stain in the 25H pyloriseropositive patients who underwent endoscopy and biopsy. Results suggest thatH pyloriinfection is highly prevalent in enlarged fold gastritis. Further studies on enlarged fold gastritis andH pyloriinfection are needed.
25
Mkrtumyan, Ashot Musaelovich, I. V. Maev, and K. I. Bairova. "Morphofunctional characteristic of gastric adipocytes in patients with type 2 diabetes mellitus." Diabetes mellitus 12, no. 2 (June 15, 2009): 46–50. http://dx.doi.org/10.14341/2072-0351-5397.
Full textAbstract:
Aim. To measure gastrointestinal hormones in plasma, evaluate morphofunctional state of G- and beta-cells in patients with gastric pathology and concomitanttype 2 diabetes mellitus (DM2). Materials and methods. A total of 84 patients with gastric ulcer (GU) and chronic gastritis (CG) were available for observation including 46 with DM2.Semi-quantitative evaluation of stomach infection by H.pylori. was performed by a histological method. Stained G- and beta-cells were counted under 400xmagnification in 10 fields of vision for each medicinal preparation used in the study. Chromogranin A, somatostatin, and gastrin were detected by immunohistochemicalmethods, gastrin-17 and somatostatin-14 by the respective immunoassays. Control group comprised 10 practically healthy volunteers. Results. Patients with combined GU (or CG) and DM2 pathology had smaller density of G- and beta-cells, lower plasma gastrin and somatostatin levelsthan those without DM2 (p
26
Lopez-Diaz, Lymari, Karen L. Hinkle, Renu N. Jain, Yana Zavros, Cynthia S. Brunkan, Theresa Keeley, Kathryn A. Eaton, Juanita L. Merchant, Catherine S. Chew, and Linda C. Samuelson. "Parietal cell hyperstimulation and autoimmune gastritis in cholera toxin transgenic mice." American Journal of Physiology-Gastrointestinal and Liver Physiology 290, no. 5 (May 2006): G970—G979. http://dx.doi.org/10.1152/ajpgi.00461.2005.
Full textAbstract:
The stimulation of gastric acid secretion from parietal cells involves both intracellular calcium and cAMP signaling. To understand the effect of increased cAMP on parietal cell function, we engineered transgenic mice expressing cholera toxin (Ctox), an irreversible stimulator of adenylate cyclase. The parietal cell-specific H+,K+-ATPase β-subunit promoter was used to drive expression of the cholera toxin A1 subunit (CtoxA1). Transgenic lines were established and tested for Ctox expression, acid content, plasma gastrin, tissue morphology, and cellular composition of the gastric mucosa. Four lines were generated, with Ctox-7 expressing ∼50-fold higher Ctox than the other lines. Enhanced cAMP signaling in parietal cells was confirmed by observation of hyperphosphorylation of the protein kinase A-regulated proteins LASP-1 and CREB. Basal acid content was elevated and circulating gastrin was reduced in Ctox transgenic lines. Analysis of gastric morphology revealed a progressive cellular transformation in Ctox-7. Expanded patches of mucous neck cells were observed as early as 3 mo of age, and by 15 mo, extensive mucous cell metaplasia was observed in parallel with almost complete loss of parietal and chief cells. Detection of anti-parietal cell antibodies, inflammatory cell infiltrates, and increased expression of the Th1 cytokine IFN-γ in Ctox-7 mice suggested that autoimmune destruction of the tissue caused atrophic gastritis. Thus constitutively high parietal cell cAMP results in high acid secretion and a compensatory reduction in circulating gastrin. High Ctox in parietal cells can also induce progressive changes in the cellular architecture of the gastric glands, corresponding to the development of anti-parietal cell antibodies and autoimmune gastritis.
27
Zavros, Yana, John Y. Kao, and Juanita L. Merchant. "Inflammation and Cancer III. Somatostatin and the innate immune system." American Journal of Physiology-Gastrointestinal and Liver Physiology 286, no. 5 (May 2004): G698—G701. http://dx.doi.org/10.1152/ajpgi.00529.2003.
Full textAbstract:
In the stomach, somatostatin is secreted from D cells and is a potent inhibitor of gastrin-induced acid secretion. During bacterial infection, somatostatin expression and release are suppressed. As a result, gastric infection often induces hypergastrinemia that, in turn, stimulates gastric acid secretion, the stomach's most important antimicrobial agent. There are an abundance of data showing that inflammatory cytokines regulate somatostatin in immune and neural cells. However, it was not until recently that the immunoregulation of gastric somatostatin was studied in vivo. This theme article discusses the role of somatostatin as an immunoregulatory peptide during gastritis.
28
Kovac, Suzana, Gregory J. Anderson, Warren S. Alexander, Arthur Shulkes, and Graham S. Baldwin. "Gastrin-Deficient Mice Have Disturbed Hematopoiesis in Response to Iron Deficiency." Endocrinology 152, no. 8 (June 7, 2011): 3062–73. http://dx.doi.org/10.1210/en.2010-1474.
Full textAbstract:
Gastrins are peptide hormones important for gastric acid secretion and growth of the gastrointestinal mucosa. We have previously demonstrated that ferric ions bind to gastrins, that the gastrin-ferric ion complex interacts with the iron transport protein transferrin in vitro, and that circulating gastrin concentrations positively correlate with transferrin saturation in vivo. Here we report the effect of long-term dietary iron modification on gastrin-deficient (Gas−/−) and hypergastrinemic cholecystokinin receptor 2-deficient (Cck2r−/−) mice, both of which have reduced basal gastric acid secretion. Iron homeostasis in both strains appeared normal unless the animals were challenged by iron deficiency. When fed an iron-deficient diet, Gas−/− mice, but not Cck2r−/−mice, developed severe anemia. In iron-deficient Gas−/−mice, massive splenomegaly was also apparent with an increased number of splenic megakaryocytes accompanied by thrombocytosis. The expression of the mRNA encoding the iron-regulatory peptide hepcidin, Hamp, was down-regulated in both Cck2r−/− and Gas−/−mice on a low-iron diet, but, interestingly, the reduction was greater in Cck2r−/− mice and smaller in Gas−/− mice than in the corresponding wild-type strains. These data suggest that gastrins play an important direct role, unrelated to their ability to stimulate acid secretion, in hematopoiesis under conditions of iron deficiency.
29
Dunn, Andrew L. J., Michael G. Drage, Christa L. Whitney-Miller, Loralee A. McMahon, and Raul S. Gonzalez. "Gastrin Staining in Inflamed Stomach Biopsies Labeled as “Antral” Rarely Detects Atrophic Gastritis." American Journal of Clinical Pathology 154, no. 6 (July 7, 2020): 761–66. http://dx.doi.org/10.1093/ajcp/aqaa098.
Full textAbstract:
Abstract Objectives Autoimmune metaplastic atrophic gastritis (AMAG) is an underrecognized entity, especially in its early stage. This study assessed whether the use of gastrin immunohistochemistry would increase sensitivity for diagnosing early AMAG. Methods Three-hundred gastric biopsies were prospectively stained for gastrin by immunohistochemistry. Inclusion criteria included well-oriented gastric mucosa with mucus glands and minimal plasma cell infiltrate not suspected to represent pyloric metaplasia. Patient age, sex, designated location of biopsy, presence or absence of intestinal metaplasia, and clinical information were not criteria. Any case with absence of gastrin-positive endocrine cells reflexed to chromogranin immunohistochemistry. Maloriented biopsies or cases with current Helicobacter infection were excluded. Results The 298-patient study cohort comprised 222 females (mean age, 47 years; range, 16-80 years) and 76 males (mean age, 49 years; range, 7-80 years). Biopsies were designated as “antral/antral nodules” (61%), and the rest were labeled “gastric/random stomach” (39%). Nine cases (3%) exhibited absence of gastrin-positive endocrine cells; one of those showed endocrine cell hyperplasia by chromogranin staining. Conclusions Pathologists should be aware of the histologic features of early AMAG and meticulously analyze tissue regardless of specimen labeling. Gastrin immunostain is a supplemental diagnostic tool when encountering inflamed antral-appearing specimens.
30
Simpson, Kenneth W., Dalit Strauss-Ayali, Eugenio Scanziani, Reinhard K. Straubinger, Patrick L. McDonough, Alix F. Straubinger, Yung-Fu Chang, Cynzia Domeneghini, Naila Arebi, and John Calam. "Helicobacter felis Infection Is Associated with Lymphoid Follicular Hyperplasia and Mild Gastritis but Normal Gastric Secretory Function in Cats." Infection and Immunity 68, no. 2 (February 1, 2000): 779–90. http://dx.doi.org/10.1128/iai.68.2.779-790.2000.
Full textAbstract:
ABSTRACT The relationship of Helicobacter felis, a bacterium observed in the stomachs of cats, to gastric disease is unclear. The objective of this study was to determine if H. felisinfection alters gastric histopathology, proinflammatory cytokine expression, and secretory function and evokes a humoral immune response in cats. Five specific-pathogen-free (SPF)Helicobacter-free cats were studied before and for 1 year after oral inoculation with H. felis (ATCC 49179). Four SPFH. felis-uninfected cats served as controls. The stomachs of all five H. felis-inoculated cats became colonized, as determined by urease activity, histopathology, PCR, culture, and transmission electron microscopy of serial gastric biopsies at 0, 3, 5, 8, and 12 months. Uninoculated cats remained Helicobacterfree. Lymphoid follicular hyperplasia, atrophy, and fibrosis were observed primarily in the pylorus of infected cats. Mild mononuclear inflammation was detected in both infected and uninfected cats, but was more extensive in infected cats, with pangastric inflammation, eosinophilic infiltrates, and cardia gastritis observed only in infected cats. No upregulation of antral mucosal interleukin 1α (IL-1α), IL-1β, or tumor necrosis factor alpha was detected by reverse transcription-PCR in any cat. The gastric secretory axes, assessed by fasting plasma gastrin, antral mucosal gastrin and somatostatin immunoreactivity, and pentagastrin-stimulated gastric acid secretion, were similar in both infected and uninfected cats. Gradual seroconversion (immunoglobulin G) was observed in four of five infected cats, with enzyme-linked immunosorbent assay values reaching 4× to 12× baseline 12 months postinfection. These findings indicate thatH. felis infection in cats induces lymphoid follicular hyperplasia, mild gastritis, and seroconversion, but is associated with normal gastric secretory function.
31
Chen, Shujie, Jing Zhong, Qunyan Zhou, Xiaofeng Lu, Liangjing Wang, and Jianmin Si. "The Regenerating Gene IαIs Overexpressed in Atrophic Gastritis Rats with Hypergastrinemia." Gastroenterology Research and Practice 2011 (2011): 1–7. http://dx.doi.org/10.1155/2011/403956.
Full textAbstract:
The role of gastrin on the development of atrophic gastritis (AG) and its relationship with the expression of RegIα in vivoremain unclear. We established experimental AG in rats by combination administration with sodium salicylate, alcohol, and deoxycholate sodium. The mean score of inflammation in gastric antrum in AG rats was significantly elevated (P<0.05), while the number of glands dramatically decreased (P<0.05). In addition, the cell proliferation in gastric glands was increased in experimental AG rats, as determined by immunohistochemistry staining of PCNA and GS II. The level of serum gastrin in AG rats was significantly elevated relative to that of normal rats (P<0.01). Moreover, the expression of RegIα protein and its receptor mRNA was increased in gastric tissues in AG rats (P<0.05). Taken together, we demonstrated that the overexpression of Reglα is related with hypergastrinemia in AG rats.
32
McWilliams, D. F., S. A. Watson, D. M. Crosbee, D. Michaeli, and R. Seth. "Coexpression of gastrin and gastrin receptors (CCK-B and ΔCCK-B) in gastrointestinal tumour cell lines." Gut 42, no. 6 (June 1, 1998): 795–98. http://dx.doi.org/10.1136/gut.42.6.795.
Full textAbstract:
Background—The peptide hormone gastrin is a recognised growth factor for gastrointestinal (GI) tumour cells. Carboxyamidated gastrins bind to the cell surface gastrin/cholecystokinin B (CCK-B) receptor which can be expressed as either a normal or a truncated isoform (ΔCCK-B).Aims—To compare gastrin gene expression with ΔCCK-B and total CCK-B (both isoforms) gene expression in both GI and non-GI tract derived human tumour cell lines.Methods—Total RNA was extracted and gene expression was assayed by the reverse transcription-polymerase chain reaction followed by Southern blotting and hybridisation with specific oligo probes.Results—Gastrin was expressed by 5/5 gastric and 7/8 colorectal cell lines. Coexpression of gastrin CCK-B isoform was found in 80% of gastric and 75% of colorectal cell lines. Non-GI cell lines, with the exception of a lymphoblastic leukaemia cell line, showed no coexpression. The truncated receptor, ΔCCK-B, was shown in 3/5 gastric and 5/8 colorectal cell lines and was always coexpressed with gastrin.Conclusions—The truncated gastrin receptor, ΔCCK-B, is coexpressed with gastrin in 8/13 GI tumour cell lines. Gastrin and CCK-B receptor isoforms may be involved in maintaining autocrine/paracrine growth pathways in GI cancer cells.
33
Pritchard, D. M., D. Berry, S. M. C. Przemeck, F. Campbell, S. W. Edwards, and A. Varro. "Gastrin increases mcl-1 expression in type I gastric carcinoid tumors and a gastric epithelial cell line that expresses the CCK-2 receptor." American Journal of Physiology-Gastrointestinal and Liver Physiology 295, no. 4 (October 2008): G798—G805. http://dx.doi.org/10.1152/ajpgi.00015.2008.
Full textAbstract:
Elevated serum concentrations of the hormone gastrin are associated with the development of gastric carcinoid tumors, but the mechanisms of tumor development are not fully understood. We hypothesized that the antiapoptotic effects of gastrin may be implicated and have therefore investigated the role of antiapoptotic members of the bcl-2 family of proteins. AGS-GR human gastric carcinoma cells stably transfected with the CCK-2 receptor were used to assess changes in the expression of bcl-2 family members following gastrin treatment and the function of mcl-1 during apoptosis was investigated by use of small-interfering RNA (siRNA). Treatment of AGS-GR cells with 10 nM gastrin for 6 h caused maximally increased mcl-1 protein abundance. Gastrin-induced mcl-1 expression was inhibited by the transcription inhibitor actinomycin D and by the protein synthesis inhibitor cycloheximide. Downstream signaling of mcl-1 expression occurred via the CCK-2 receptor, protein kinase C, and MAP kinase pathways, but not via PI 3-kinase. Transfection with mcl-1 siRNA significantly suppressed mcl-1 protein expression and abolished the antiapoptotic effects of gastrin on serum starvation-induced apoptosis. Mcl-1 protein expression was also specifically increased in the type I enterochromaffin-like cell carcinoid tumors of 10 patients with autoimmune atrophic gastritis and hypergastrinemia. Gastrin therefore signals via the CCK-2 receptor, protein kinase C, and MAP kinase to induce expression of antiapoptotic mcl-1 in AGS-GR cells, and mcl-1 expression is also increased in human hypergastrinemia-associated type I gastric carcinoid tumors. Gastrin-induced mcl-1 expression may therefore be an important mechanism contributing toward type I gastric carcinoid development.
34
Xue, Huiguang, Aihua Yang, Fuguo Liu, Xueguo Sun, and Xishuang Liu. "Clinical significance of Serum Pepsinogen I/II and gastrin-17 determination in gastric cancer diagnosis and prognosis." European Journal of Inflammation 16 (January 1, 2018): 205873921878129. http://dx.doi.org/10.1177/2058739218781291.
Full textAbstract:
Currently, the diagnosis of atrophic gastritis and gastric cancer are mainly made by endoscopy and histopathology. Our study aimed to explore the practical value of Serum Pepsinogen I/II and gastrin-17 in gastric cancer diagnosis and prognosis. We collected 60 cases of gastric ulcer from February 2015 to November 2016 as gastric ulcer group, and 40 cases of gastric cancer treated in the same period as gastric cancer group. In 3 years after gastric cancer, 20 patients were served as postoperative gastric cancer group, and 70 healthy subjects as control group. The results showed that serum Pepsinogen I/II, gastrin-17, and other serum gastric function indexes were tested by enzyme-linked immunosorbent assay (ELISA). The serum PGI level of gastric ulcer group was higher than control group ( P < 0.05). The serum G-17 concentrations in gastric ulcer group, gastric cancer group, and postoperative gastric cancer group were all higher than control group ( P < 0.05). The area under receiver operating characteristic (ROC) curve of PGI screening was 0.905 and the best cutoff point was PGI < 75 µg/L. Their sensitivity and specificity were 87.2% and 75.1%; the area under ROC curve of PGI/PGII rate screening was 0.761 and the best cutoff point was PGI/PGII < 4. Their sensitivity and specificity were 88.9% and 62.3%. Multi logistical regression showed that the level of serum PGI, PGI, and G-17 and the odds ratio (OR) level of gastric cancer risk were 2.093, 2.653, and 0.494 ( P < 0.05). The examination of Serum Pepsinogen I/II, gastrin-17, and other serum gastric function indexes can be used in the diagnosis and prognosis of gastric cancer and has a rather high practical value in monitoring recurrence in postoperative gastric cancer patients.
35
Matsumoto, M., J. Park, and T. Yamada. "Gastrin receptor characterization: affinity cross-linking of the gastrin receptor on canine gastric parietal cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 252, no. 1 (January 1, 1987): G143—G147. http://dx.doi.org/10.1152/ajpgi.1987.252.1.g143.
Full textAbstract:
We applied affinity cross-linking methods to label the gastrin receptor on isolated canine gastric parietal cells in order to elucidate the nature of its chemical structure. 125I-labeled Leu15-gastrin and 125I-labeled gastrin2(-17) bound to intact parietal cells and their membranes with equal affinity, and half-maximal inhibition of binding was obtained at an incubation concentration of 3.2 X 10(-10) M unlabeled gastrin. 125I-gastrin2(-17) was cross-linked to plasma membranes or intact parietal cells by incubation in disuccinimidyl suberate. The membrane pellets were solubilized with or without dithiothreitol and applied to electrophoresis on 7.5% sodium dodecyl sulfate polyacrylamide gels. Autoradiograms revealed a band of labeling at Mr 76,000 and labeling of this band was inhibited in a dose-dependent fashion by addition of unlabeled gastrin to the incubation mixture. Dithiothreitol in concentrations as high as 100 mM did not alter the electrophoretic mobility of the labeled band. After taking into account the molecular weight of 125I-gastrin2(-17), our results suggest that the gastrin receptor on parietal cells is a single protein of Mr 74,000 without disulfide-linked subunits.
36
Sablina, A. O., O. A. Sablin, S. S. Aleksanin, G. G. Rodionov, I. I. Shantyr', and I. E. Ushal. "Amoxicillin secretion by gastric mucosa in Chernobyl nuclear power plant accident recovery workers with atrophic and nonatrophic gastritis undergoing eradication therapy." Medicо-Biological and Socio-Psychological Problems of Safety in Emergency Situations, no. 3 (November 11, 2020): 36–42. http://dx.doi.org/10.25016/2541-7487-2020-0-3-36-42.
Full textAbstract:
Relevance. Today gastric cancer is still one of the oncologic diseases most often leading to death. H. pylori eradication reduces risk of gastric cancer, but its efficacy depends on gastric mucosa state. Atrophy of gastric mucosa is more common in Chernobyl nuclear power plant (CNPP) accident recovery workers than in patients who have not been involved in CNPP accident recovery works. It seems especially important to investigate the features of antibiotics transport to H. pylori colonization area in this contingent.Intention – to determine the features of amoxicillin secretion by gastric mucosa in CNPP accident recovery workers with atrophic and nonatrophic gastritis undergoing H. pylori eradication.Methodology. 65 CNPP accident recovery workers were divided into groups depending on state of gastric mucosa according to endoscopic and histological examination, immunosorbent assay of pepsinogens I and II and gastrin-17 basal serum levels. On the first day of eradication therapy, gastric secretion samples were obtained via nasogastric probe 30, 60, 120, 180 and 240 minutes after oral amoxicillin administration. Drug concentrations in gastric secretion were assessed via liquid chromatography-mass spectrometry.Results and discussion. Amoxicillin concentrations in gastric secretion samples were lower (р < 0.01) in patients with atrophic antral gastritis than in patients with normal gastric mucosa and atrophic fundal gastritis. Patients with fundal atrophy were characterized by lower amoxicillin concentrations 30 and 60 (p = 0.02) minutes after drug intake than in patients with normal gastric mucosa, and higher concentration in the 120th (p < 0.01) and 180th (p = 0.02) minute than in patients with antral atrophy. Amoxicillin concentrations in patients with antral atrophy were lower (p < 0.01) than in non-atrophy group in the 30th, 60th and 120th minute. In the 240th minute, amoxicillin concentrations in patients with fundal atrophy exceeded concentrations in both other groups (p < 0.01). Amoxicillin concentration peak was registered in patients with fundal and antral atrophy in the 180th minute, in patients without atrophy – from the 30th to 120th minute.Conclusion. Atrophy of gastric mucosa is characterized by decreased transport of orally administered amoxicillin from bloodstream to gastric lumen. Depending on gastric mucosa state, amoxicillin concentrations in gastric secretion should be evaluated at different time points after drug administration: in patients with atrophic gastritis – in the 180th minute, in patients without atrophy – in the 120th minute. While predicting the efficacy and choosing H. pylori eradication regimen, morphological and functional state of gastric mucosa should be taken into account.
37
Faller, G., H. Steininger, J. Kränzlein, H. Maul, T. Kerkau, J. Hensen, E. G. Hahn, and T. Kirchner. "Antigastric autoantibodies in Helicobacter pyloriinfection: implications of histological and clinical parameters of gastritis." Gut 41, no. 5 (November 1, 1997): 619–23. http://dx.doi.org/10.1136/gut.41.5.619.
Full textAbstract:
Background—It has recently been shown that humoral antigastric autoreactivities occur in a substantial number ofHelicobacter pylori infected patients.Aims—To analyse the relevance of such antigastric autoantibodies for histological and serological parameters of the infection as well as for the clinical course.Methods—Gastric biopsy samples and sera from 126 patients with upper abdominal complaints were investigated for evidence of H pylori infection using histology and serology. Autoantibodies against epitopes in human gastric mucosa were detected by immunohistochemical techniques. Histological and clinical findings of all patients were then correlated with the detection of antigastric autoantibodies.Results—H pylori infection was significantly associated with antigastric autoantibodies reactive with the luminal membrane of the foveolar epithelium and with canalicular structures within parietal cells. The presence of the latter autoantibodies was significantly correlated with the severity of body gastritis, gastric mucosa atrophy, elevated fasting gastrin concentrations, and a decreased ratio of serum pepsinogen I:II. Furthermore the presence of anticanalicular autoantibodies was associated with a greater than twofold reduced prevalence for duodenal ulcer.Conclusion—The data indicate that antigastric autoantibodies play a role in the pathogenesis and outcome of H pylori gastritis, in particular in the development of gastric mucosal atrophy.
38
Dimaline, R., and C. M. Lee. "Chicken gastrin: a member of the gastrin/CCK family with novel structure-activity relationships." American Journal of Physiology-Gastrointestinal and Liver Physiology 259, no. 5 (November 1, 1990): G882—G888. http://dx.doi.org/10.1152/ajpgi.1990.259.5.g882.
Full textAbstract:
The biological activity of natural chicken gastrins isolated from the "antrum"-like region of the chicken gut have been studied on gastric secretion in chickens, turkeys, and rats, pancreatic secretion in turkeys and rats, and gallbladder contraction in chickens and guinea pigs. Natural chicken gastrin was shown to be approximately 85% sulfated on the tyrosine that occurs at position 7 from the COOH-terminus. In both avian and mammalian systems, chicken gastrins were found to be potent stimulants of acid secretion but were virtually inactive as stimulants of pancreatic secretion and gallbladder contraction. Peptides with the COOH-terminal tetrapeptide amide of CCK and a sulfated tyrosine at position 7 from the COOH-terminus are usually potent stimulants of pancreas and gallbladder. However, although chicken gastrin has a CCK-like structure, it has a gastrin-like spectrum of biological actions. A proline immediately adjacent to the sulfated tyrosine may produce a steric effect that lowers the activity of chicken gastrin on pancreas and gallbladder. Evidently, then, the factors that determine specificity of action of CCK and gastrin are different in birds and mammals.
39
Ignat, Ancuţa, Gabriela Păduraru, Angelica Cristina Marin, Anamaria Ciubară, Valeriu V. Lupu, and Marin Burlea. "ULCERUL GASTRIC DUPĂ ADMINISTRAREA PE TERMEN SCURT DE ANTIINFLAMATOARE NESTEROIDIENE LA UN COPIL MIC – PREZENTARE DE CAZ." Romanian Journal of Pediatrics 64, no. 4 (December 31, 2015): 458–60. http://dx.doi.org/10.37897/rjp.2015.4.21.
Full textAbstract:
Agenţii antiinflamatori nesteroidieni (AINS) produc leziuni gastrice prin intermediul a două mecanisme: iritaţia locală şi acţiunea sistemică. Un copil în vârstă de 2 ani şi 10 luni, sex feminin, a primit AINS timp de 2 zile pentru o infecţie acută a tractului respirator superior şi a prezentat vărsături în „zaţ de cafea“ o zi mai târziu. Endoscopia digestivă superioară a evidenţiat o leziune de ulcer gastric. Biopsia gastrică a fost negativă pentru infecţia cu H. pylori, iar pacienta a fost diagnosticată cu ulcer gastric acut indus de consumul de AINS în absenţa altor cauze de ulcer gastric. Ulcerele gastrice se dezvoltă foarte rar după o administrare pe termen scurt de AINS, fapt ce a determinat raportarea acestui caz. Luând în considerare atât riscurile cât şi beneficiile terapiei cu AINS, este indicat ca în cazul fiecărui pacient care trebuie să urmeze un tratament cronic cu medicamente antiinflamatorii să fie căutaţi posibilii factori de risc asociaţi.
40
Patil, Amruta P., and Prashant A. Shirure. "Effect of add-on proton pump inhibitors on parameters of glycemic control in type-2 diabetic patients." International Journal of Basic & Clinical Pharmacology 6, no. 6 (May 23, 2017): 1233. http://dx.doi.org/10.18203/2319-2003.ijbcp20172219.
Full textAbstract:
Proton pump inhibitors (PPIs) block the parietal cell H+/K+ ATPase, are superior at suppressing acid secretion & promoting peptic ulcer healing, wildly used clinically for the therapy of gastro-esophageal reflex disease, gastritis due to excess stomach acid, and gastric ulcers. After blocking the production of gastric acid, the proton-pump inhibitors indirectly elevate serum gastrin levels via a negative feedback effect. Evidences are reported that gastrin promotes β cell neogenesis in pancreatic ductal complex, modest pancreatic β cell replication and improvement of glucose tolerance in animal models. Some recent clinical studies have shown improved glucose tolerance in type-2 diabetes mellitus (T2DM). Although PPIs may be possible candidates for a new approach in the therapy of diabetes, a prospective, long-term, randomized, double-blind, placebo-controlled study is needed to establish the effect of PPIs on glycemic control in a large number of patients with T2DM.
41
Schott, Matthias, Cornelia Sagert, Holger S. Willenberg, Sven Schinner, Uwe Ramp, Andrea Varro, Andreas Raffel, et al. "Carcinogenic Hypergastrinemia: Signet-Ring Cell Carcinoma in a Patient with Multiple Endocrine Neoplasia Type 1 with Zollinger-Ellison’s Syndrome." Journal of Clinical Endocrinology & Metabolism 92, no. 9 (September 1, 2007): 3378–82. http://dx.doi.org/10.1210/jc.2007-0283.
Full textAbstract:
Abstract Context: Gastric neuroendocrine tumors are rare neoplasms that originate from gastric enterochromaffin-like (ECL) cells in the oxyntic mucosa. Gastrin and its derivates have been reported to regulate epithelial cell proliferation, migration, and differentiation. Mutations in the epithelial cadherin (E-cadherin) gene have been shown to be associated with the occurrence of diffuse gastric carcinomas in affected families. Objective: In this study we investigated the histopathological and molecular findings in the gastrointestinal wall of a patient with multiple endocrine neoplasia type 1 with malignant duodenal gastrinoma and multiple gastric ECL cell tumors, who additionally developed a signet-ring cell carcinoma of the stomach. Design and Patient: Biopsies from the gastrointestinal tract of a patient with multiple endocrine neoplasia type 1 were immunostained for vesicular monoamine transporter-2 and E-cadherin. Nonamidated gastrin products were measured in the serum of the patient using antibodies that react with progastrin, Gly-extended, and amidated gastrins. Genetic analyses were performed to exclude germ-line mutations within the E-cadherin gene. Results: Immunohistochemical studies of gastric ECL cell tumors showed a largely diminished E-cadherin expression in comparison to gastric surface mucosa cells and a loss of E-cadherin expression in the cells of the signet-ring carcinoma. Detailed biochemical measurements revealed progastrin concentrations that were approximately 20%, and Gly-gastrin concentrations that were approximately 10% the amidated gastrin concentrations in plasma. Molecular analyses revealed no E-cadherin germ-line mutation. Conclusion: Our immunohistochemical studies might suggest that the gastrinoma-associated excessive progastrin tissue concentrations led to diminished expression of E-cadherin within the gastric mucosa and promoted tumor development of a signet-ring cell carcinoma.
42
Nørsett, Kristin G., Islay Steele, Cedric Duval, Stephen J. Sammut, Senthil V. M. Murugesan, Susan Kenny, Lucille Rainbow, et al. "Gastrin stimulates expression of plasminogen activator inhibitor-1 in gastric epithelial cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 301, no. 3 (September 2011): G446—G453. http://dx.doi.org/10.1152/ajpgi.00527.2010.
Full textAbstract:
Plasminogen activator inhibitor (PAI)-1 is associated with cancer progression, fibrosis and thrombosis. It is expressed in the stomach but the mechanisms controlling its expression there, and its biological role, are uncertain. We sought to define the role of gastrin in regulating PAI-1 expression and to determine the relevance for gastrin-stimulated cell migration and invasion. In gastric biopsies from subjects with elevated plasma gastrin, the abundances of PAI-1, urokinase plasminogen activator (uPA), and uPA receptor (uPAR) mRNAs measured by quantitative PCR were increased compared with subjects with plasma concentrations in the reference range. In patients with hypergastrinemia due to autoimmune chronic atrophic gastritis, there was increased abundance of PAI-1, uPA, and uPAR mRNAs that was reduced by octreotide or antrectomy. Immunohistochemistry revealed localization of PAI-1 to parietal cells and enterochromaffin-like cells in micronodular neuroendocrine tumors in hypergastrinemic subjects. Transcriptional mechanisms were studied by using a PAI-1-luciferase promoter-reporter construct transfected into AGS-GR cells. There was time- and concentration-dependent increase of PAI-1-luciferase expression in response to gastrin that was reversed by inhibitors of the PKC and MAPK pathways. In Boyden chamber assays, recombinant PAI-1 inhibited gastrin-stimulated AGS-GR cell migration and invasion, and small interfering RNA treatment increased responses to gastrin. We conclude that elevated plasma gastrin concentrations are associated with increased expression of gastric PAI-1, which may act to restrain gastrin-stimulated cell migration and invasion.
43
Winter, Christina, Sonja Hartl, Dagmar Kolb, Gerd Leitinger, and Eva Roblegg. "Investigations to Evaluate Gastric Mucoadhesion of an Organic Product to Ameliorate Gastritis." Pharmaceutics 12, no. 4 (April 7, 2020): 331. http://dx.doi.org/10.3390/pharmaceutics12040331.
Full textAbstract:
Gastritis is an inflammatory disease leading to abdominal pain, nausea, and diarrhea. While therapy depends on etiology, adhesive agents protecting the gastric tissue represent a promising treatment option. Caricol®-Gastro is an organic product that significantly decreased gastritic abdominal pain in a recent clinical study. To investigate whether this beneficial effect can be attributed to the formation of a protective layer covering the gastric mucosa after oral application, several methods were used to determine adhesion. These include macro-rheological measurements and gastric mucin interactions, which were correlated to network formation, examined by Cryo-scanning electron microscopy technique, wettability via sessile drop method on human gastric adenocarcinoma cell layers, and ex vivo adhesion studies on gastric porcine tissue with the falling liquid film technique considering physiological conditions and Franz diffusion cells for quantification. The results showed that Caricol®-Gastro formed a stable viscoelastic network with shear thinning properties. It exhibited high wettability and spreadability and adhered to the excised gastric mucosa. We found that oat flour, as the main ingredient of Caricol®-Gastro, supports the gel network regarding viscoelasticity and, to a lesser extent, adhesion in a concentration dependent manner. Moreover, our data highlight that a variety of coordinated methods are required to investigate gastric adhesion.
44
Taniguchi, Masahiro, Gota Sudo, Yuzufumi Sekiguchi, and Hiroshi Nakase. "Autoimmune gastritis concomitant with gastric adenoma and subacute combined degeneration of the spinal cord." BMJ Case Reports 14, no. 5 (May 2021): e242836. http://dx.doi.org/10.1136/bcr-2021-242836.
Full textAbstract:
A 62-year-old woman was referred to our department for further investigation of anaemia. Blood test showed macrocytic anaemia. Oesophagogastroduodenoscopy (OGD) revealed proximal-predominant gastric atrophy and flat elevated lesion in the gastric body. Several days after OGD, she complained of gait disturbance and was diagnosed with subacute combined degeneration of the spinal cord. Furthermore, laboratory tests showed positive for both anti-parietal cell and anti-intrinsic factor antibodies, as well as increased serum gastrin level and decreased pepsinogen I level, which confirmed the diagnosis of autoimmune gastritis (AIG). Anaemia and neurological symptoms were improved after vitamin B12 supplementation. Subsequently, the patient underwent gastric endoscopic submucosal dissection; histopathological examination revealed gastric adenoma. AIG can cause gastric neoplasms and vitamin B12 deficiency, with the latter resulting in pernicious anaemia and neurological disorders. These diseases are treatable but potentially life-threatening. This case highlights the importance of early diagnosis of AIG and proper management of its comorbidities.
45
Maya Syari, Dina, and Hotna Sari. "EVALUASI PENGGUNAAN OBAT PROTON PUMP INHIBITOR PADA PASIEN RAWAT JALAN DENGAN GANGGUAN LAMBUNG (GASTRITIS) DI RUMAH." JIFI (Jurnal Ilmiah Farmasi Imelda) 5, no. 1 (September 30, 2021): 1–4. http://dx.doi.org/10.52943/jifarmasi.v5i1.623.
Full textAbstract:
Gastritis is an inflammatory process in the gastric mucosa and gastric mucosa. Gastritis is a state of inflammation or bleeding off the gastric mucosa that is acute, chronic, diffuse, or local. Gastritis or heartburn is an inflammation of the stomach wall, this disease is often found to arise suddenly which is usually characterized by nausea or vomiting, bleeding pain, weakness, decreased appetite or headache. The purpose of this study was to determine the PPI class of drugs most widely used by outpatients with gastric gastritis disorders. Knowing the factors that most often influence of gastric gastritis disorders.To find out the age most often affected by gastric gastritis. This research method used an observational method with the research design used was data collection carried out retrospectively, namely by tracing records at the outpatient installation of Imelda Hospital Medan from January 1 to December 31, 2019. The data obtained at the installation is descriptive and evaluate the use of PPIs with the treatment of gastritis aimed at improving the patient's quality of life, relieving complaints, curing gastritis, preventing recurrences and complications. Besed on the results of the study, the most outpatients with gastritis at the Imleda Hospital Medan were 15 women (17%), 6 men (29%), And the most commonlyused PPI drugs for gastritis patients were lansoprazole in 18 patients (86%), Omeprazole 3 patients (14%).
46
Rivas-Ortiz, Claudia Ivette, Stephanie Euridice Morales-Guerrero, Sergio Ponce-de-León-Rosales, Armando Gamboa-Domínguez, Claudia Rangel-Escareño, Luis Federico Uscanga-Domínguez, Germán Rubén Aguilar-Gutiérrez, David Kershenobich-Stalnikowitz, Yolanda López-Vidal, and Gonzalo Castillo-Rojas. "Overview of Gene Expression Analysis in Gastric Disease Infected with Helicobacter pylori: CLDN1 and MMP9 Could Be Biomarkers for Early Diagnosis of Gastric Cancer." Processes 10, no. 2 (January 20, 2022): 196. http://dx.doi.org/10.3390/pr10020196.
Full textAbstract:
Chronic Helicobacter pylori infection produces several lesions in the human stomach, which can progress to chronic atrophic gastritis and gastric cancer. To date, there is very little information on gene expression in chronic atrophic gastritis and its relationship with progression to gastric cancer. In this study, we performed a gene expression analysis during chronic atrophic gastritis in order to identify possible biomarkers that allow an early diagnosis of gastric cancer. We studied biopsies from patients with chronic atrophic gastritis and gastric cancer. The biopsies were analyzed by a gene expression microarray and corroborated by qPCR and validated through immunohistochemistry. Our results revealed that gene expression profiles in patients with chronic atrophic gastritis showed molecular changes of the gastric mucosa, leading to gastric cancer. The gene expression profiles of CLDN1, CLDN7, OLFM4, C-MYC and MMP9 were more notable from the chronic atrophic gastritis. The gene expression patterns observed in this study allowed the identification of CLDN1 and MMP9 proteins as promising biomarkers of early stages of gastric cancer development.
47
Dockray, G. J., R. Dimaline, E. R. Forster, D. Evans, A. Sandvik, and A. Varro. "Gastrin cell responses to acidification of the achlorhydric rat stomach." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 3 (September 1, 1993): G440—G444. http://dx.doi.org/10.1152/ajpgi.1993.265.3.g440.
Full textAbstract:
In the rat, gastrin cells are normally exposed to the stimulatory effects of food and the inhibitory influences of acid in the gastric lumen. We have studied the effects of intragastric acid on gastrin cell function in animals in which the tonic inhibitory action of acid was removed by prior treatment with the proton pump blocker omeprazole. In fasted rats with gastric fistula treated with omeprazole, instillation of acid into the stomach produced a prompt decrease in plasma gastrin, but gastrin mRNA abundance showed a modest transient increase over a period of 2 h and thereafter no change; there was also a transient increase in tissue concentrations of the gastrin precursor progastrin that was compatible with increased gastrin synthesis. Concentrations of tissue gastrins, in general, increased after acid instillation, which can be attributed to continued synthesis in the presence of suppressed gastrin release. In rats fed ad libitum, a single dose of omeprazole (which produces achlorhydria for 24-30 h) produced an increase in plasma gastrin that peaked after 24 h and declined to control levels over the following 48 h; in contrast, gastrin mRNA abundance peaked 48 h after omeprazole before declining to control levels. The results indicate that whereas gastrin release might be promptly inhibited by intragastric acid, the changes in gastrin mRNA abundance are much slower: achlorhydria increases gastrin mRNA within 24 h, but acid takes longer to depress gastrin mRNA abundance. Over periods of a few hours, gastrin release and synthesis need not, therefore, change in parallel.
48
Eaton, K. A., M. J. Radin, and S. Krakowka. "An Animal Model of Gastric Ulcer Due to Bacterial Gastritis in Mice." Veterinary Pathology 32, no. 5 (September 1995): 489–97. http://dx.doi.org/10.1177/030098589503200506.
Full textAbstract:
Conventional female BalbC mice were inoculated with Gastrospirillum-like bacteria in mouse gastric homogenate or in 5.0-μm filtrate of gastric homogenate. The bacteria were originally isolated from cheetahs with gastritis. The mice were killed 6 months, 7 months, or 1 year after inoculation. All mice became infected with Gastrospirillum-like bacteria that were confined to the gastric mucosa. Control mice, given either sterile Brucella broth, 0.22-μm filtrate of infected gastric homogenate, or uninfected gastric homogenate did not become infected with bacteria. Lesions in infected mice included severe lymphoplasmacytic gastritis (26/26 infected mice), gastric epithelial hyperplasia (25/26 infected mice), and gastric ulceration (11/26 infected mice). Neutrophilic inflammatory cell infiltrates were inconsistent. None of the uninfected control mice had Gastrospirillum-like bacteria, gastritis, gastric epithelial hyperplasia, or gastric ulceration. These results implicate Gastrospirillum-like bacteria from cheetahs in the pathogenesis of gastric ulceration. This model will be useful in investigating the mechanisms of gastric ulceration associated with bacterial gastritis.
49
Keskin, Onur, Mehmet Bektas, Caglar Keskin, and Irfan Soykan. "A Comparison of Baseline Clinical Characteristics of Autoimmune Gastritis Patients with and without Type-1 Gastric Carcinoid Tumor." Acta Medica 51, no. 2 (June 25, 2020): 17–24. http://dx.doi.org/10.32552/0.actamedica.462.
Full textAbstract:
Objectives : Autoimmune gastritis (AIG) is an antibody-mediated autoimmune disease and characterized by gastric parietal cell loss. Type-1 gastric carcinoid tumor (GCT) is a disease that mostly develops on the basis of AIG. The aim of this study is to determine similarities and differences of baseline clinical parameters between these two disorders.
Methods: Patients diagnosed as AIG both without gastric carcinoid tumor (n:197) and with GCT (n:40) between 2004 and 2015 at Ankara University Faculty of Medicine, Department of Gastroenterology, were included in this analysis. Data of initial signs and symptoms, basal blood count-anemia parameters, laboratory investigations, serum gastrin levels, anti parietal cell antibody (APCA) status, serological helicobacter pylori (Hp) markers and serum chromogranine A (CgA) levels of patients were obtained, and baseline parameters of these disorders were compared
Results: Patient groups were similar in age and gender. Hemoglobin, iron, total iron binding capacity (TIBC), ferritin, vitamin B12 levels, APCA and HpIgG positivity rates and concomitant autoimmune thyroid disease prevalence were also similar. Median gastrin level in AIG+GCT patients was significantly higher compared to the AIG without GCT (807 vs. 1307 pg/ml; p:0.006). ROC analysis revealed that a 1000 pg/ml threshold value for serum gastrin level is able to distinguish these two disorders with 65% sensitivity and 65% specificity rates (area under the curve: 0.65;p:0.006). The serum CgA level did not significantly differ between patient groups.
Conclusion: High serum gastrin but not CgA levels may be useful in deciding which patients should be followed closely in AIG.
50
Macukanovic-Golubovic, Lana, Vuka Katic, Gorana Rancic, Mladen Milenovic, Goran Marjanovic, and Zoran Golubovic. "Study on histogenesis of enterochromaffin-like carcinoid in autoimmune atrophic gastritis associated with pernicious anemia." Vojnosanitetski pregled 64, no. 8 (2007): 543–48. http://dx.doi.org/10.2298/vsp0708543m.
Full textAbstract:
Background/Aim. Autoimmune atrophic fundic gastritis induces the pernicious anemia (PA), as well as the changes in both epithelium and endocrine cells of gastric mucosa. The most important complications are: achlorhydria, hypergastrinemia, gastric cancer and enterochromaffin-like ( ECL) carcinoid. The aim of this study was to examine ECL carcinoid histogenesis in A-gastritis associated with PA. Methods. During the period from 2000?2006, 65 patients with PA and 30 patients of the control group were examined. Histopathological examination was done in endoscopical biopsies of gastric mucosa fixed in 10% formaldehyde. Paraffin sections were stained with classic hematoxylin-eosin (HE); histochemical AB-PAS (pH 2.5), cytochemical argyrophilic Servier-Munger?s and immunocytochemical PAP methods for G cell identification and chromogranin A antibodies - specific marker for neuroendocrine ECL cells. Both G and ECL cells were counted per 20 fields, of surface 0.0245312 mm2 by a field. Basal gastrin serum levels were also examined by using radioimmunoassay (RIA) method. The obtained results were statisticaly calculated by using Student?s t test. Results. Marked antral G cell hyperplasia associated with corporal ECL hyperplasia was found. ECL cell hyperplasia was of simplex, linear, adenomatoid type to the pattern of intramucous ECL cell carcinoid. An average number of G cells was statistically significant in the patients with PA as compared to the control group (p < 0.05) as well as an average number of ECL cells. Conclusion. We concluded that antral G cell hyperplasia accompanied by gastrinemia induces ECL hyperplasia and ECL corporal carcinoid in A-gastritis and that their histogenesis develops trough simple, linear and adenomatoide hyperplasia. .