Base de dados : MEDLINE
Pesquisa : A06.224.365 [Categoria DeCS]
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[PMID]:28417934
[Au] Autor:Arin RM; Vallejo AI; Rueda Y; Fresnedo O; Ochoa B
[Ad] Endereço:Department of Physiology, Faculty of Medicine and Nursing, University of the Basque Country UPV/EHU, Sarriena s/n, 48940 Leioa, Bizkaia, Spain. rosamaria.arin@ehu.eus.
[Ti] Título:Expression of Adenosine A Receptor and Adenosine Deaminase in Rabbit Gastric Mucosa ECL Cells.
[So] Source:Molecules;22(4), 2017 Apr 12.
[Is] ISSN:1420-3049
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:Adenosine is readily available to the glandular epithelium of the stomach. Formed continuously in intracellular and extracellular locations, it is notably produced from ATP released in enteric cotransmission. Adenosine analogs modulate chloride secretion in gastric glands and activate acid secretion in isolated parietal cells through A adenosine receptor (A2BR) binding. A functional link between surface A2BR and adenosine deaminase (ADA) was found in parietal cells, but whether this connection is a general feature of gastric mucosa cells is unknown. Here we examine whether A2BR is expressed at the membrane of histamine-producing enterochromaffin-like (ECL) cells, the major endocrine cell type in the oxyntic mucosa, and if so, whether it has a vicinity relationship with ADA. We used a highly homogeneous population of rabbit ECL cells (size 7.5-10 µm) after purification by elutriation centrifugation. The surface expression of A2BR and ADA proteins was assessed by flow cytometry and confocal microscopy. Our findings demonstrate that A2BR and ADA are partially coexpressed at the gastric ECL cell surface and that A2BR is functional, with regard to binding of adenosine analogs and adenylate cyclase activation. The physiological relevance of A2BR and ADA association in regulating histamine release is yet to be explained.
[Mh] Termos MeSH primário: Adenosina Desaminase/genética
Celulas Tipo Enterocromafim/metabolismo
Mucosa Gástrica/citologia
Mucosa Gástrica/metabolismo
Expressão Gênica
Receptor A2B de Adenosina/genética
[Mh] Termos MeSH secundário: Adenosina Desaminase/metabolismo
Animais
Biomarcadores
Citometria de Fluxo
Coelhos
Receptor A2B de Adenosina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Receptor, Adenosine A2B); EC 3.5.4.4 (Adenosine Deaminase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170531
[Lr] Data última revisão:
170531
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170419
[St] Status:MEDLINE


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[PMID]:28276835
[Au] Autor:Villanacci V; Casella G; Lanzarotto F; Di Bella C; Sidoni A; Cadei M; Salviato T; Dore MP; Bassotti G
[Ad] Endereço:a Pathology Section, Department of Molecular and Translational Medicine , Spedali Civili and University of Brescia , Brescia , Italy.
[Ti] Título:Autoimmune gastritis: relationships with anemia and Helicobacter pylori status.
[So] Source:Scand J Gastroenterol;52(6-7):674-677, 2017 Jun - Jul.
[Is] ISSN:1502-7708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Autoimmune gastritis (AIG) is a gastric pathologic condition affecting the mucosa of the fundus and the body and eventually leading to hypo-achlorhydria. AIMS: We report our clinical and pathological experience with AIG. METHODS: Data from patients with a diagnosis of AIG seen in the period January 2002-December 2012 were retrieved. Only patients with complete sets of biopsies were analyzed. RESULTS: Data from 138 patients were available for analysis. Pernicious anemia was present in 25% of patients, iron deficiency anemia was found in 29.7% of patients, hypothyroidism in 23% of patients, type 1 diabetes in 7.9% of patients, and vitiligo in 2.8% of patients. Parietal cell antibodies were positive in 65% of patients, and no patient had serology positive for celiac disease. All gastric biopsies showed glandular atrophy associated with enterochromaffin-like (ECL)-cells hyperplasia, features limited to the mucosa of the fundus and body, and focal glandular intestinal metaplasia. Helicobacter pylori was negative in all cases. CONCLUSIONS: AIG was strongly associated with anemia; atrophy, intestinal metaplasia and ECL hyperplasia in the gastric fundus and body are hallmarks of this condition.
[Mh] Termos MeSH primário: Anemia Ferropriva/epidemiologia
Anemia Perniciosa/epidemiologia
Doenças Autoimunes/complicações
Gastrite/complicações
Helicobacter pylori/isolamento & purificação
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Idoso de 80 Anos ou mais
Atrofia
Autoanticorpos/sangue
Diabetes Mellitus Tipo 1/epidemiologia
Células Enterocromafins/patologia
Celulas Tipo Enterocromafim/patologia
Feminino
Fundo Gástrico/patologia
Gastrite/patologia
Seres Humanos
Hiperplasia
Hipotireoidismo/epidemiologia
Intestinos/patologia
Itália
Masculino
Metaplasia/patologia
Meia-Idade
Células Parietais Gástricas/imunologia
Estudos Retrospectivos
Vitiligo/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170310
[St] Status:MEDLINE
[do] DOI:10.1080/00365521.2017.1288758


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[PMID]:27309188
[Au] Autor:Sagatun L; Fossmark R; Jianu CS; Qvigstad G; Nordrum IS; Mjønes P; Waldum HL
[Ad] Endereço:a Department of Gastroenterology and Hepatology , St Olav's Hospital , Trondheim , Norway ;
[Ti] Título:Follow-up of patients with ECL cell-derived tumours.
[So] Source:Scand J Gastroenterol;51(11):1398-405, 2016 Nov.
[Is] ISSN:1502-7708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: To review the presentation, treatment and outcome of patients with type 1 gastric carcinoid tumours. MATERIAL AND METHODS: We retrospectively reviewed medical records and re-evaluated histopathological specimens of 26 patients with type 1 gastric carcinoids treated at a single tertiary referral centre from 1993 to 2013, with median time of follow-up 52.5 months (IQR 90.8). RESULTS: Seven patients (27%) had single tumours and 19 patients (73%) multiple tumours at the time of diagnosis. The median number of tumours and median diameter of largest tumour were 2.5 (IQR 3.2) and 6.0 mm (IQR 9.5) respectively. Median serum gastrin was 321.0 pmol/l (IQR 604.0) and median serum chromogranin A 7.7 nmol/l (IQR 5.3). Three patients had metastatic disease at the time of diagnosis and two developed metastases during follow-up. Patients with metastatic disease had larger primary tumours than the others (20.0 mm (IQR 28.5) vs. 5.0 mm (IQR 5.5), p = 0.04). There was a positive correlation between age and tumour size (r = 0.44, p = 0.03) and between serum chromogranin A and serum gastrin at diagnosis (r = 0.76, p = 0.001). Patients were either treated with surgery (n = 8 (31%)), a long-acting somatostatin analogue and/or gastrin receptor antagonist (n = 10 (39%)) for a period of time, or were observed without treatment (n = 8 (31%) with close endoscopic follow up. CONCLUSIONS: Although gastric carcinoids have an overall good prognosis, a significant proportion develops metastatic disease. As partial and total gastrectomy is associated with major side effects, treatment with long-acting a somatostatin analogue or gastrin antagonist should be considered.
[Mh] Termos MeSH primário: Tumor Carcinoide/patologia
Tumor Carcinoide/terapia
Celulas Tipo Enterocromafim/patologia
Neoplasias Gástricas/patologia
Neoplasias Gástricas/terapia
[Mh] Termos MeSH secundário: Idoso
Antineoplásicos Hormonais/uso terapêutico
Tumor Carcinoide/mortalidade
Cromogranina A/sangue
Comorbidade
Feminino
Seguimentos
Gastrectomia
Mucosa Gástrica/patologia
Gastrinas/sangue
Seres Humanos
Estimativa de Kaplan-Meier
Masculino
Meia-Idade
Metástase Neoplásica
Noruega
Octreotida/uso terapêutico
Receptor de Colecistocinina B/antagonistas & inibidores
Receptor de Colecistocinina B/uso terapêutico
Estudos Retrospectivos
Somatostatina/análogos & derivados
Somatostatina/uso terapêutico
Neoplasias Gástricas/mortalidade
Centros de Atenção Terciária
Tomografia Computadorizada por Raios X
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents, Hormonal); 0 (Chromogranin A); 0 (Gastrins); 0 (Receptor, Cholecystokinin B); 51110-01-1 (Somatostatin); RWM8CCW8GP (Octreotide)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160617
[St] Status:MEDLINE
[do] DOI:10.3109/00365521.2016.1169588


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[PMID]:27150581
[Au] Autor:Fossmark R; Calvete O; Mjønes P; Benitez J; Waldum HL
[Ad] Endereço:Department of Gastroenterology and Hepatology, St. Olav's Hospital, Trondheim, Norway.
[Ti] Título:ECL-cell carcinoids and carcinoma in patients homozygous for an inactivating mutation in the gastric H(+) K(+) ATPase alpha subunit.
[So] Source:APMIS;124(7):561-6, 2016 Jul.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:A family with a missense variant of the ATP4A gene encoding the alpha subunit of the gastric proton pump (H(+) K(+) ATPase) has recently been described. Homozygous siblings were hypergastrinemic (median gastrin 486 pM) and had gastric tumours diagnosed at a median age of 33 years. In the current histopathological study, we further characterized the tumours found in the gastric corpus. The tumours had the histological appearance of carcinoids (NET G1 or G2) and were immunoreactive for the general neuroendocrine markers chromogranin A (CgA) and synaptophysin as well as the ECL-cell markers vesicular monoamine transporter 2 (VMAT2) and histidine decarbozylase (HDC). One of the tumours consisted of a NET G2 component, but also had a component with glandular growth, which morphologically was classified as an intestinal type adenocarcinoma. Many glands of the adenocarcinoma contained a large proportion of cells positive for neuroendocrine markers, especially the small vesicle marker synaptophysin and the cytoplasmic enzyme HDC. In conclusion, patients homozygous for an inactivating ATP4A mutation develop gastric ECL-cell carcinoids in their 3rd or 4th decade. The adenocarcinoma may be classified as neuroendocrine with ECL-cell differentiation.
[Mh] Termos MeSH primário: Adenocarcinoma/patologia
Tumor Carcinoide/patologia
Celulas Tipo Enterocromafim/enzimologia
ATPase Trocadora de Hidrogênio-Potássio/deficiência
ATPase Trocadora de Hidrogênio-Potássio/genética
Homozigoto
Neoplasias Gástricas/patologia
[Mh] Termos MeSH secundário: Adulto
Cromogranina A/análise
Histidina Descarboxilase/análise
Histocitoquímica
Seres Humanos
Imuno-Histoquímica
Mutação de Sentido Incorreto
Sinaptofisina/análise
Proteínas Vesiculares de Transporte de Monoamina/análise
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Chromogranin A); 0 (SLC18A2 protein, human); 0 (SYP protein, human); 0 (Synaptophysin); 0 (Vesicular Monoamine Transport Proteins); EC 3.6.3.10 (ATP4A protein, human); EC 3.6.3.10 (H(+)-K(+)-Exchanging ATPase); EC 4.1.1.22 (Histidine Decarboxylase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170123
[Lr] Data última revisão:
170123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160507
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12546


  5 / 216 MEDLINE  
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[PMID]:27038741
[Au] Autor:Fossmark R; Rao S; Mjønes P; Munkvold B; Flatberg A; Varro A; Thommesen L; Nørsett KG
[Ad] Endereço:Department of Cancer Research and Molecular Medicine, NTNU, Trondheim, Norway; Department of Gastroenterology and Hepatology, St. Olav's University Hospital, Trondheim, Norway. Electronic address: reidar.fossmark@ntnu.no.
[Ti] Título:PAI-1 deficiency increases the trophic effects of hypergastrinemia in the gastric corpus mucosa.
[So] Source:Peptides;79:83-94, 2016 05.
[Is] ISSN:1873-5169
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The gastric hormone gastrin plays a role in organizing the gastric mucosa. Gastrin also regulates the expression of genes that have important actions in extracellular matrix modelling, including plasminogen activator inhibitor (PAI)-1 which is part of the urokinase plasminogen activator (uPA) system. The uPA system (including PAI-1) is associated with cancer progression, fibrosis and thrombosis. Its biological role in the stomach and molecular mechanisms of action are not well understood. The aim of this study was to examine the effect of PAI-1 on the trophic changes observed in gastric corpus mucosa in hypergastrinemia using PAI-1 and/or HK-ATPase beta subunit knockout (KO) mice. HK-ATPase beta subunit KO mice were used as a model of hypergastrinemia. In 12 month old female mice, intragastric acidity and plasma gastrin were measured. The stomachs were examined for macroscopic and histological changes. In mice null for both PAI-1 and HK-ATPase beta (double KO), there was exaggerated hypergastrinemia, increased stomach weight and corpus mucosal thickness, and more pronounced trophic and architectural changes in the corpus compared with HK-ATPase beta KO mice. Genome-wide microarray expression data for the gastric corpus mucosa showed a distinct gene expression profile for the HK-ATPase beta KO mice; moreover, enrichment analysis revealed changes in expression of genes regulating intracellular processes including cytoskeleton remodelling, cell adhesion, signal transduction and epithelial-to-mesenchymal transition (EMT). Genes differentially expressed in the double KO compared with HK-ATPase beta KO mice included the transcription factor Barx2 and the chromatin remodeler gene Tet2, which may be involved in both normal gastric physiology and development of gastric cancer. Based on the present data, we suggest that PAI-1 plays a role in maintaining gastric mucosal organization in hypergastrinemia.
[Mh] Termos MeSH primário: Mucosa Gástrica/enzimologia
Gastrinas/sangue
Serpina E2/genética
[Mh] Termos MeSH secundário: Animais
Celulas Tipo Enterocromafim/enzimologia
Celulas Tipo Enterocromafim/patologia
Feminino
Mucosa Gástrica/patologia
ATPase Trocadora de Hidrogênio-Potássio/genética
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Antro Pilórico/enzimologia
Antro Pilórico/patologia
Serpina E2/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gastrins); 0 (Serpin E2); 0 (Serpine2 protein, mouse); EC 3.6.3.10 (H(+)-K(+)-Exchanging ATPase)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160404
[St] Status:MEDLINE


  6 / 216 MEDLINE  
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[PMID]:26879837
[Au] Autor:Craven CJ
[Ad] Endereço:Queensland University of Technology, Brisbane, Australia. cj.craven@qut.edu.au.
[Ti] Título:A hypothesis of couplet molecules and couplet cells in gastric function and an association with Helicobacter pylori.
[So] Source:BMC Gastroenterol;16:16, 2016 Feb 16.
[Is] ISSN:1471-230X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Gastrin, from G-cells, and histamine, from enterochromaffin-like (ECL) cells, are two of the hormones that regulate gastric activity. DISCUSSION: It is proposed that the G-cells and the ECL cells are coupled by the couplet molecules gastrin and histamine and by a prior asymmetrical cell division. The gastrin (from G-cells) stimulates the ECL cells to produce and secrete histamine while, in a reciprocal way, this histamine (from ECL cells), stimulates the G-cells to produce and secrete gastrin. These molecules would also stimulate cell division - the gastrin would stimulate cell division of ECL cells while histamine would stimulate that of G-cells. A chemical complex of gastrin and histamine is postulated as is also the asymmetric cell divisions of precursor cells to produce the coupled G-cells and ECL cells. CONCLUSION: There is sufficient evidence to support the feasibility of the model in general, but more direct experimental evidence is required to validate the model as applied here to gastric function.
[Mh] Termos MeSH primário: Celulas Tipo Enterocromafim/metabolismo
Células Secretoras de Gastrina/metabolismo
Helicobacter pylori/metabolismo
Modelos Biológicos
Estômago/citologia
[Mh] Termos MeSH secundário: Animais
Divisão Celular/fisiologia
Digestão/fisiologia
Gastrinas/secreção
Liberação de Histamina/fisiologia
Seres Humanos
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gastrins)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160217
[St] Status:MEDLINE
[do] DOI:10.1186/s12876-016-0429-0


  7 / 216 MEDLINE  
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[PMID]:26872579
[Au] Autor:Waldum HL; Hauso Ø; Brenna E; Qvigstad G; Fossmark R
[Ad] Endereço:a Department of Cancer Research and Molecular Medicine , Norwegian University of Science and Technology , Trondheim , Norway ;
[Ti] Título:Does long-term profound inhibition of gastric acid secretion increase the risk of ECL cell-derived tumors in man?
[So] Source:Scand J Gastroenterol;51(7):767-73, 2016 Jul.
[Is] ISSN:1502-7708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Since the description of ECL cell-derived tumors in rodents after long-term profound acid inhibition inducing hypergastrinemia, there has been concern that proton pump inhibitors (PPIs) could also do that in man. The recent description of a Spanish family with gastric ECL cell tumors at the age of about 30 years secondary to a defect in the proton pump due to mutation in the ATP4A gene clearly shows that hypergastrinemia alone also is sufficient to induce ECL cell neoplasia in man. The present review aims to evaluate the risk of gastric neoplasia secondary to gastric acid inhibition. METHODS: Literature (MEDLINE) was searched for the role of the ECL cell in gastric carcinogenesis in animals and man in general and particularly secondary to long-term inhibition of acid secretion. RESULTS: An important proportion of patients treated with PPI develops hypergastrinemia causing ECL cell hyperplasia and the first descriptions of ECL cell carcinoids secondary to PPI have been reported. The role of the ECL cell has hitherto been under estimated in gastric carcinogenesis in man where for instance the signet ring cell type of gastric carcinoma seems to originate from the ECL cell. CONCLUSIONS: The first two of three steps in rodent ECL cell carcinogenesis (hyperplasia, carcinoid, and carcinoma) secondary to PPI dosing, have been described for man. It is every reason to believe that the final step, gastric carcinoma, will develop also in man. Clinical decisions should be based not only on so-called evidence based medicine, but also on physiological knowledge and animal studies.
[Mh] Termos MeSH primário: Celulas Tipo Enterocromafim
Ácido Gástrico/secreção
Inibidores da Bomba de Prótons/efeitos adversos
Neoplasias Gástricas/induzido quimicamente
[Mh] Termos MeSH secundário: Animais
Celulas Tipo Enterocromafim/patologia
Celulas Tipo Enterocromafim/fisiologia
Seres Humanos
Hiperplasia
Roedores
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Proton Pump Inhibitors)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170502
[Lr] Data última revisão:
170502
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160214
[St] Status:MEDLINE
[do] DOI:10.3109/00365521.2016.1143527


  8 / 216 MEDLINE  
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[PMID]:26177572
[Au] Autor:Lundell L; Vieth M; Gibson F; Nagy P; Kahrilas PJ
[Ad] Endereço:Gastrocentrum, Department of Clinical Sciences, Intervention and Technology (CLINTEC), Centre for Digestive Diseases, Karolinska University Hospital, Karolinska Institutet, Stockholm, Sweden.
[Ti] Título:Systematic review: the effects of long-term proton pump inhibitor use on serum gastrin levels and gastric histology.
[So] Source:Aliment Pharmacol Ther;42(6):649-63, 2015 Sep.
[Is] ISSN:1365-2036
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Proton pump inhibitors (PPIs) have a well-established safety profile. However, concerns have been raised about a potential relationship between PPI-induced hypergastrinaemia and the development of enterochromaffin-like (ECL) cell hyperplasia, neuroendocrine tumours and gastric cancer during long-term therapy. AIM: To review the effects of long-term PPI use on serum gastrin levels and gastric histopathology. METHODS: A systematic literature search was conducted in PubMed on 21 April 2015 to identify studies reporting the effects of long-term (defined as >3 years) PPI use on gastrin levels and gastric histopathology. RESULTS: A total of 16 studies (1920 patients) met the inclusion criteria. During long-term PPI therapy, mean gastrin levels rose to one to three times the upper limit of the normal range (~100 pg/mL), and an increased prevalence of ECL cell hyperplasia was observed (+7.8-52.0%). Helicobacter pylori-positive patients had a significantly increased risk of developing ECL linear/micronodular hyperplasia compared with H. pylori-negative patients [OR: 2.45 (95% CI: 1.47-4.10), P = 0.0006]; however, no evidence of neoplastic changes was found. The risk of corpus atrophy was markedly higher in H. pylori-positive patients than in H. pylori-negative patients [OR: 11.45 (95% CI: 6.25-20.99), P < 0.00001]. Not a single case of gastric adenocarcinoma was found. CONCLUSIONS: Long-term PPI therapy induced moderate hypergastrinaemia in most patients and an increased prevalence of ECL cell hyperplasia. H. pylori-positive patients receiving long-term PPI therapy were exposed to a higher risk of corpus atrophy than H. pylori-negative patients. No neuroendocrine tumours or gastric cancers were found.
[Mh] Termos MeSH primário: Celulas Tipo Enterocromafim/patologia
Gastrinas/sangue
Hiperplasia/induzido quimicamente
Inibidores da Bomba de Prótons/administração & dosagem
Inibidores da Bomba de Prótons/efeitos adversos
[Mh] Termos MeSH secundário: Esquema de Medicação
Gastrinas/biossíntese
Infecções por Helicobacter/tratamento farmacológico
Helicobacter pylori/isolamento & purificação
Seres Humanos
Tumores Neuroendócrinos/induzido quimicamente
Tumores Neuroendócrinos/patologia
Fatores de Risco
Neoplasias Gástricas/induzido quimicamente
Neoplasias Gástricas/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Gastrins); 0 (Proton Pump Inhibitors)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150817
[Lr] Data última revisão:
150817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150717
[St] Status:MEDLINE
[do] DOI:10.1111/apt.13324


  9 / 216 MEDLINE  
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[PMID]:25665655
[Au] Autor:Boyce M; Thomsen L
[Ad] Endereço:Hammersmith Medicines Research, Central Middlesex Hospital , London NW10 7NS , England.
[Ti] Título:Gastric neuroendocrine tumors: prevalence in Europe, USA, and Japan, and rationale for treatment with a gastrin/CCK2 receptor antagonist.
[So] Source:Scand J Gastroenterol;50(5):550-9, 2015 May.
[Is] ISSN:1502-7708
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Gastric carcinoids (neuroendocrine tumors) arise from enterochromaffin-like cells in the gastric mucosa. Most are caused by hypergastrinemia. The objectives were to determine if their prevalence in Europe, USA and Japan meets the criteria for an orphan disease and to justify treatment with a gastrin/CCK2 receptor antagonist. METHODS: We obtained data from European and USA cancer registries, and searched PubMed. RESULTS: Prevalence per 10,000 population obtained from cancer registries was: median 0.32 (range 0.09-0.92) for Europe; and 0.17 for the USA, equivalent to 4812 for the whole population. A PubMed search for gastric carcinoids yielded prevalence for Japan only, which was 0.05 per 10,000 population, equivalent to 665 for the entire population. A further search for gastric carcinoids in patients with pernicious anemia (PA) or autoimmune chronic atrophic gastritis (CAG), two presentations of about 80% of gastric carcinoids, produced prevalence rates of 5.2-11%. Prevalence of PA itself was 0.12-1.9%. Data on CAG epidemiology were sparse. CONCLUSION: Prevalence of gastric carcinoids varied widely. All sources probably underestimate prevalence. However, prevalence was below the limits required for recognition by drug regulatory authorities as an orphan disease: 5 per 10,000 population of Europe; 200,000 for the whole population of the USA; and 50,000 for the whole population of Japan. Because gastric carcinoids are an orphan disease, and nonclinical and healthy volunteer studies support treatment with netazepide, a gastrin/CCK2 antagonist, netazepide has been designated an orphan medicinal product in Europe and the USA for development as targeted treatment for gastric carcinoids.
[Mh] Termos MeSH primário: Benzodiazepinonas/uso terapêutico
Tumor Carcinoide/tratamento farmacológico
Tumor Carcinoide/epidemiologia
Neoplasias Gastrointestinais/tratamento farmacológico
Neoplasias Gastrointestinais/epidemiologia
Compostos de Fenilureia/uso terapêutico
Receptor de Colecistocinina B/antagonistas & inibidores
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Anemia Perniciosa/epidemiologia
Celulas Tipo Enterocromafim/metabolismo
Europa (Continente)/epidemiologia
Feminino
Mucosa Gástrica/metabolismo
Gastrite Atrófica/epidemiologia
Seres Humanos
Japão/epidemiologia
Masculino
Prevalência
Doenças Raras
Distribuição por Sexo
Estados Unidos/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Benzodiazepinones); 0 (Phenylurea Compounds); 0 (Receptor, Cholecystokinin B); 0 (YF 476)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150317
[Lr] Data última revisão:
150317
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150211
[St] Status:MEDLINE
[do] DOI:10.3109/00365521.2015.1009941


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[PMID]:25464111
[Au] Autor:Song H; Zhu J; Lu D
[Ad] Endereço:Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Box 281, Stockholm, SE- 17177, Sweden. huan.song@ki.se.
[Ti] Título:Long-term proton pump inhibitor (PPI) use and the development of gastric pre-malignant lesions.
[So] Source:Cochrane Database Syst Rev;(12):CD010623, 2014 Dec 02.
[Is] ISSN:1469-493X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Proton pump inhibitors (PPIs) are the most effective drugs to reduce gastric acid secretion. PPIs are one of the most commonly prescribed classes of medications worldwide. Apart from short-term application, maintenance therapy with PPIs is recommended and increasingly used in certain diseases, such as Zollinger-Ellison syndrome and gastro-oesophageal reflux disease, especially for people with erosive oesophagitis or Barrett's oesophagus. Although PPIs are generally safe, their efficacy and safety of long-term use remains unclear. The question of whether the long-term use of PPIs could promote the development of gastric pre-malignant lesions has been widely investigated, but results are inconsistent. Limited insight on this problem leads to a dilemma in decision making for long-term PPI prescription. OBJECTIVES: To compare the development or progression of gastric pre-malignant lesions, such as atrophic gastritis, intestinal metaplasia, enterochromaffin-like (ECL) cell hyperplasia, and dysplasia, in people taking long-term (six months or greater) PPI maintenance therapy. SEARCH METHODS: We searched the following databases (from inception to 6 August 2013): the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, and CINAHL. In addition, we searched the reference lists of included trials and contacted experts in the field. SELECTION CRITERIA: We searched for randomised controlled trials (RCTs) in adults (aged 18 years or greater) concerning the effects of long-term (six months or greater) PPI use on gastric mucosa changes, confirmed by endoscopy or biopsy sampling (or both). DATA COLLECTION AND ANALYSIS: Two review authors independently performed selection of eligible trials, assessment of trial quality, and data extraction. We calculated odds ratios (OR) for analysis of dichotomous data and mean differences for continuous data, with 95% confidence intervals (CI). MAIN RESULTS: We included seven trials (1789 participants). Four studies had high risk of bias and the risk of bias in the other three trials was unclear. In addition, it was difficult to assess possible reporting bias. We pooled 1070 participants from four RCTs to evaluate corporal atrophy development revealing an insignificantly increased OR of 1.50 (95% CI 0.59 to 3.80; P value = 0.39; low-quality evidence) for long-term PPI users relative to non-PPI users. In five eligible trials, corporal intestinal metaplasia was assessed among 1408 participants, also with uncertain results (OR 1.46; 95% CI 0.43 to 5.03; P value = 0.55; low-quality evidence). However, by pooling data of 1705 participants from six RCTs, our meta-analysis showed that participants with PPI maintenance treatment were more likely to experience either diffuse (simple) (OR 5.01; 95% CI 1.54 to 16.26; P value = 0.007; very-low-quality evidence) or linear/micronodular (focal) ECL hyperplasia (OR 3.98; 95% CI 1.31 to 12.16; P value = 0.02; low-quality evidence) than controls. No participant showed any dysplastic or neoplastic change in any included studies. AUTHORS' CONCLUSIONS: There is presently no clear evidence that the long-term use of PPIs can cause or accelerate the progression of corpus gastric atrophy or intestinal metaplasia, although results were imprecise. People with PPI maintenance treatment may have a higher possibility of experiencing either diffuse (simple) or linear/micronodular (focal) ECL cell hyperplasia. However, the clinical importance of this outcome is currently uncertain.
[Mh] Termos MeSH primário: Lesões Pré-Cancerosas/induzido quimicamente
Inibidores da Bomba de Prótons/efeitos adversos
Neoplasias Gástricas/induzido quimicamente
[Mh] Termos MeSH secundário: Celulas Tipo Enterocromafim/patologia
Gastrite Atrófica/induzido quimicamente
Seres Humanos
Hiperplasia/induzido quimicamente
Intestinos/patologia
Quimioterapia de Manutenção/efeitos adversos
Metaplasia/induzido quimicamente
Lesões Pré-Cancerosas/patologia
Ensaios Clínicos Controlados Aleatórios como Assunto
Neoplasias Gástricas/patologia
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Proton Pump Inhibitors)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:160602
[Lr] Data última revisão:
160602
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141203
[St] Status:MEDLINE
[do] DOI:10.1002/14651858.CD010623.pub2



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