37 research outputs found

    Helicobacter Pylori related Gastritis in Adults a Clinical, Endoscopic Histopathological and Rapid Urease Test Study.

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    The Understanding Of Etiopathogenesis Of Peptic Ulcer, Expressed As Gastritis, Gastric Ulcer, Duodenitis, Duodenal Ulcer Has Been Revolutionised During Last Decade With The Discovery In 1983, Of A New Pathogen Categorized As Helicobacter Pylori By Warren And Marshall. 67.68 Several Reports Have Subsequently Supported The Association Of H.Pylori As A Major Etiological Factor In The Development Of Peptic Ulcer Disease 50, 78 And Recent Reports Also Suggest Its Association With Gastric Carcinoma And Lymphoma.82,88 Bacterium Has Been Classified As Class I Definite Gastric Carcinogen To Human 77,83,97 A Prospective Study Of Adult Presenting With Upper Abdominal Pain,20 Dyspepsia, Vomiting, Haematemesis Is Undertaken To Evaluate The Relationship Of This Symptomcomplex To Inflammatory Gastroduodenal Lesions With Special Reference To H.Pylori Infection. The Clinical Endoscopic Findings, Rapid Urease Test And Histopathological Evaluation Of Gastric Antral Specimen With Special Stains 16 To Demonstrate The Organism Are Presented And Analysed. Regarding The Histopathology, Previous Studies On The Pathologic Changes Of Gastric Mucosa, Colonized By H.Pylori Have Markedly Focused On Inflammatory Reaction. In Addition To More Common Inflammatory Cell Infiltration It Is Only Recently The Histopathologic Effect Of H.Pylori On Gastric Epithelium At Light Microscopic Level Has Been Stressed And This Has Been Studied Systematically, Describing Striking Changes In Surface Epthelium And Attributing Them As Specific For H.Pylori Colonization And Correlating Them With Type Of Cytotoxin 30,17,18 ,Production And Risk Of Peptic Ulcer.50,53 H.Pylori Infection Can Be Diagnosed By Invasive 12,14,66 (Requiring Endoscopy) And Non Invasive Technique. 22,29,64 In This Study The Various Methods Of Identification Of H.Pylori And Histopathological Features Associated H.Pylori In Gastric Mucosa In Patients, Presenting With Dyspepsia Are Discussed And Described In Detail Paying Particular Attention To Histopathological Effects Of H.Pylori On Epithelial Cells And Evaluate The Gastric Mucosa As Per Updated Sydney System.23,24,70,88 In Addition, The Recent Literature Regarding Epidemiology, Clinical Features, Pathogenesis Of Infection Is Also Reviewed

    Adenoma de las glándulas de Brunner. Reporte de un caso y revisión de literatura

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    Se reporta el caso de un paciente varón de 69 años con un gran adenoma de las glándulas de Brunner que se presentó con anemia severa sintomática y pérdida de peso significativa. El estudio endoscópico alto detectó una gran tumoración duodenal que se extendía del bulbo hasta la segunda porción y la biopsia fue informada como duodenitis crónica inespecífica con cambios metaplásicos gástricos. El paciente fue sometido a una duodenopancreatectomía y la histología de la pieza quirúrgica fue un tumor de glándulas de Brunner. El adenoma de glándulas de Brunner se considera un tumor benigno del duodeno; sin embargo, la resección endoscópica está limitada a lesiones menores

    The Urease Activity of Helicobacter pylori and Duodenal Ulcer Disease

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    Helicobacter pylori, a spiral shaped bacterium has recently been identified as one of the most important acquired factors in the development of duodenal ulcer disease. This organism colonises the gastric antral mucosa, the body of the stomach and areas of gastric metaplasia in the duodenum. Infection of the gastric mucosa by H pylori is associated with the development of type B gastritis, but also with the development of gastric ulcers, and more strongly with the development of duodenal ulcers. Almost 100% of individuals who have a duodenal ulcer have infection with H pylori. Eradication of H pylori infection of the antral mucosa is associated with a fall in basal plasma gastrin concentration, the meal stimulated gastrin response and gastric acid output suggesting that infection with H pylori could lead to increased gastric acidity and cause the development of duodenal ulcer disease. H pylori possesses unusually high urease enzyme activity. It has been suggested that the organism's urease activity could enable it to survive at low gastric pH by producing a cloud of ammonium which markedly raises the pH of the organism's environment and of the antral mucosal surface. The production of an alkaline microenvironment above the antral gastrin producing G cells could block the normal inhibition of gastrin release by gastric acid. An increased antral pH could also promote the uptake of amines which promote gastrin release. To examine the effects of infection on gastric ammonium concentration, plasma gastrin concentration and the creation of an alkaline microenvironment a series of studies were undertaken. The effect of infection by H pylori on the concentrations of ammonium and urea in gastric juice was investigated. The effect of stimulating and inhibiting urease activity on gastrin release was investigated. The effect of the alkalinisation of the gastric antrum on gastrin release was also investigated. The effect of urease activity on the survival of H pylori was also studied in a series of in vitro environments. Characteristic changes in the concentrations of ammonium and urea in gastric juice samples were demonstrated. In 27 subjects with duodenal ulcer disease the median (range) ammonium concentration was 3.4 mmol/L (1.0-13.0 mmol/L) when H pylori was present compared with 0.64 mmol/L (0.02-1.4 mmol/L) following eradication. In 16 subjects with chronic renal failure the median gastric juice ammonium concentration when infection was present was 20.0 mmol/L (13.9-43.1 mmol/L) compared with 4.8 mmol/L (0.5-12.3 mmol/L) when infection was absent. Gastric juice urea concentrations were lower when infection with the organism was present, median 0.8 mmol/L (0.5-2.9 mmol/L) compared with 2.1 mmol/L (1.0-3.7 mmol/L) after it had been eradicated. In subjects with chronic renal failure with infection the median gastric juice urea concentration was 2.2 mmol/L (0.5-8.7 mmol/L) compared with 13.8 mmol/L (5.4-20.8 mmol/L) when the organism was not present. The concentrations of urea and ammonium in the gastric juice samples did not clearly distinguish between the presence or absence of infection. When the urea/ammonium ratio was calculated all subjects with H pylori had a ratio of less than 0.8 while those free of infection had a ratio greater than 0.9. The urea/ammonium ratio could therefore be used to detect the presence of infection. The effect of stimulating and inhibiting urease activity, on the plasma gastrin concentration was studied. Urease activity was stimulated by the intragastric infusion of dextrose solution containing urea. Subjects with duodenal ulcer disease who had proven infection with H pylori were studied. The same subjects acted as their own controls following eradication of H pylori. The intragastric infusion of 50 mmol/L urea in a dextrose solution increased the median gastric juice ammonium concentration from 2.3 mmol/L (1.3-5.9 mmol/L) to 6.1 mmol/L (4.2-11.9 mmol/L). There was no change in plasma gastrin concentration observed during infusion of urea either before or after eradication of the organism. Inhibition of H pylori urease activity was also attempted. The specific urease inhibitor, acetohydroxamic acid was administered as a single 750 mg oral dose to 6 subjects who had duodenal ulcer disease. Inhibition of enzyme activity was demonstrated by the suppression of a 14C-urea breath test administered shortly after the dose of acetohydroxamic acid and reversion of the urea/ammonium ratio to that of non-infected subjects. No change in the basal plasma gastrin concentration or meal stimulated gastrin response occurred following inhibition of urease activity. Some investigators have failed to observe a rise in plasma gastrin concentration in response to alkalinisation of the gastric antrum. This could explain why stimulating and inhibiting urease activity failed to alter plasma gastrin concentrations. (Abstract shortened by ProQuest.)

    The role of gastrin in the development of gastric preneoplastic and neoplastic changes

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    The hormone gastrin regulates gastric acid secretion and through its effects on cell proliferation, apoptosis and angiogenesis also regulates gastric epithelial and enterochromaffin-like (ECL) cell growth. The influence of various factors (host, bacterial and environmental) upon fasting serum gastrin concentrations and to what extent these factors interact to influence the progression of gastric preneoplastic pathology is not fully understood. Long standing hypergastrinaemia secondary to hypochlorhydria resulting from autoimmune gastritis can result in the development of ECL-cell hyperplasia. In some patients this progresses to type-1 gastric neuroendocrine tumour formation. The factors that influence this progression have not been fully characterised. The management of type-1 gastric neuroendocrine tumours is dependent on their size. However, there is still controversy regarding the optimal management of larger (> 1cm) tumours. Antrectomy is one option and the results of an octreotide suppression test (to determine gastrin dependency of type-1 gastric neuroendocrine tumours in order to predict response to antrectomy) have been reported in a single patient. This aims of this thesis were to assess: 1. The interaction between various factors (host, bacterial and environmental) that may influence fasting serum gastrin concentrations and the development of gastric preneoplastic pathology. 2. The roles of certain factors in the progression of ECL-cell hyperplasia to type-1 gastric neuroendocrine tumours. 3. The role of an octreotide suppression test in identifying patients with type-1 gastric neuroendocrine tumours who may benefit from antrectomy. In a large cohort of >1000 prospectively recruited patients, we demonstrated that in addition to H. pylori infection, the presence of a host factor (advancing age), a bacterial virulence factor (cagA) and elevated fasting serum gastrin concentrations (>100pM) were significantly associated with the presence of gastric preneoplastic pathology. Concurrent proton pump inhibitor therapy was however not associated with the presence of gastric preneoplastic pathology. The interactions between H. pylori infection, proton pump inhibitor use and the presence of gastric preneoplastic pathology in determining fasting serum gastrin concentrations were found to be complex. In addition, other host and environmental factors also influenced fasting serum gastrin concentrations. Although results from our study did not demonstrate any statistically significant associations, there did appear to be correlations between the presence of factors such as hypothyroidism, positive anti-gastric parietal and intrinsic factor antibodies and extent of gastric atrophy with the presence of more advanced degrees of gastric ECL-cell hyperplasia. Although a positive octreotide suppression test was associated with tumour regression following antrectomy in four patients with type-1 gastric neuroendocrine tumours, a fifth patient who had a positive test did not show tumour regression and needed additional surgery. In conclusion, gastrin appears to act as an important co-factor in the pathogenesis of epithelial and neuroendocrine neoplasia in the stomach, but interactions with other factors are complex

    Bowel Histology of CVID Patients Reveals Distinct Patterns of Mucosal Inflammation

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    Diarrhea is the commonest gastrointestinal symptom in patients with common variable immunodeficiency (CVID). Different pathologies in patients’ bowel biopsies have been described and links with infections have been demonstrated. The aim of this study was to analyze the bowel histology of CVID patients in the Royal-Free-Hospital (RFH) London CVID cohort. Ninety-five bowel histology samples from 44 adult CVID patients were reviewed and grouped by histological patterns. Reasons for endoscopy and possible causative infections were recorded. Lymphocyte phenotyping results were compared between patients with different histological features. There was no distinctive feature that occurred in most diarrhea patients. Out of 44 patients (95 biopsies), 38 lacked plasma cells. In 14 of 21 patients with nodular lymphoid hyperplasia (NLH), this was the only visible pathology. In two patients, an infection with Giardia lamblia was associated with NLH. An IBD-like picture was seen in two patients. A coeliac-like picture was found in six patients, four of these had norovirus. NLH as well as inflammation often occurred as single features. There was no difference in blood lymphocyte phenotyping results comparing groups of histological features. We suggest that bowel histology in CVID patients with abdominal symptoms falls into three major histological patterns: (i) a coeliac-like histology, (ii) IBD-like changes, and (iii) NLH. Most patients, but remarkably not all, lacked plasma cells. CVID patients with diarrhea may have an altered bowel histology due to poorly understood and likely diverse immune-mediated mechanisms, occasionally driven by infections

    Infección por Helicobacter pylori y su relación con patologías gástricas en pacientes de Latinoamérica.

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    Helicobacter pylori infection is one of the most common human infections, affecting more than 50% of the world's population. In addition, this pathogen is responsible for gastrointestinal disorders around the world. In this context, the general objective of this study was to analyze Helicobacter pylori infection and its relationship with gastric pathologies in Latin American patients. The design of the documentary study is descriptive, since a bibliographic review was carried out in scientific databases such as PubMed, SciELO, Elsevier, Google Scholar, Redalyc and Springer, and search equations were used with the terms "H. pylori", "gastrointestinal disorders", "prevalence", "Latin America" and the Boolean operators 'AND' and 'OR'. In the preliminary search 215 documents or articles were found, with the inclusion and exclusion criteria, the abstracts were evaluated independently by critical reading to eliminate duplicate documents or articles, leaving 56 articles for the research. The results showed that Colombia has one of the highest infection rates of all countries, since studies report 86% prevalence of Helicobacter pylori in adults and 80% in children, in gastric pathology studies report 83.3% chronic gastritis, 12.5% gastric ulcer and 4.2% gastric cancer. It is concluded that the mentioned infection is associated with different gastric pathologies among which gastritis stands out with the highest prevalence followed by peptic ulcers, duodenal ulcers and gastric neoplasms.La infección por Helicobacter pylori es una de las infecciones humanas más comunes dado que afecta a más del 50% de la población mundial. Adicionalmente, este patógeno es responsable de afecciones gastrointestinales alrededor del mundo. Bajo este contexto, el objetivo general del presente trabajo fue analizar la infección por Helicobacter pylori y su relación con patologías gástricas en pacientes de Latinoamérica. El diseño del estudio documental es de tipo descriptivo, puesto que se realizó una revisión bibliográfica en bases de datos científicas como PubMed, SciELO, Elsevier, Google Scholar, Redalyc y Springer, además, se emplearon ecuaciones de búsqueda con los términos “H. pylori”, “afecciones gastrointestinales”, “prevalencia”, “Latinoamérica” y los operadores booleanos ‘AND’ y ‘OR’.. En la búsqueda preliminar se encontraron 113 documentos o artículos, con los criterios de inclusión y exclusión, fueron evaluados de forma independiente mediante lectura crítica los resúmenes para eliminar los documentos o artículos duplicados, quedando como resultados 45 artículos para la realización de la investigación. Se obtuvieron los resultados que Colombia tiene una de las tasas de infección más altas que otros países, puesto que los estudios reportan un 86% de prevalencia de Helicobacter pylori en adultos y un 80% en niños, en la patología gástrica en los estudios reportan el 83,3% gastritis crónica, el 12,5% úlcera gástrica y el 4,2% cáncer gástrico. Se concluye que la infección mencionada está asociada a distintas patologías gástricas entre las cuales se destaca la gastritis con mayor prevalencia seguida de las úlceras pépticas, duodenales y neoplasias gástricas

    Verlaufsbeobachtung von Patienten mit funktionellen Oberbauchbeschwerden. Untersuchung zur klinischen Symptomatik, Gastritis und Komplikationen über einen Zeitraum von 20 Jahren.

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    Hintergrund: Unter dem Begriff der funktionellen Dyspepsie werden postprandiale Beschwerden des oberen Gastrointestinaltraktes ohne fassbares morphologisches Korrelat zusammengefaßt. Die Pathogenese dieses heterogenen Beschwerdebildes ist vielfältig und insbesondere der Einfluss einer Infektion mit Helicobacter pylori ist unklar. Auch sind evidenzbasierte Prognosefaktoren und der klinische Langzeitverlauf unzureichend bekannt. Patienten und Methoden: In der vorliegenden Untersuchung wurden 105 Patienten (61 männliche, 44 weibliche, mittleres Alter 60 10 Jahre), bei denen zwischen 1974 und 1980 die Diagnose einer funktionellen Dyspepsie gestellt wurde, mit Hilfe einer ausführlichen standardisierten Befragung im Hinblick auf aktuelle Beschwerden, den Krankheitsverlauf seit Beginn der Ausgangsuntersuchung befragt. Alle Patienten wiesen primär eine endoskopisch unauffällige Magenschleimhaut auf. Bei allen Patienten wurde ein histologischer Ausgangsbefund der Magenschleimhaut erhoben. Der Einfluss der funktionellen Dyspepsie auf die Lebensqualität wurde mit Hilfe des gastrointestinalen Lebensqualitätsindex durchgeführt. Im Rahmen der Nachuntersuchung wurde eine Ösophagogastroduodenoskopie mit entsprechenden Biopsien, ein CLO-Test, ein 13C-Urease Atemtest zum Nachweis von Helicobacter pylori, sowie eine Gastrinspiegelbestimmung im Serum durchgeführt. Die Ergebnisse sind mit der Kaplan-Meier Schätzungs-Kurve dargestellt und wurden mit dem Breslow-Test oder dem Log-rank Test auf statistische Signifikanz untersucht. Ergebnisse: Nach einer mittleren Nachbeobachtungszeit von 20,5 2,7 Jahren konnte bei 99 Patienten (58 männlich, 41 weiblich) eine ausführliche standardisierte Befragung im Hinblick auf aktuelle Beschwerden, den Krankheitsverlauf seit Beginn der Ausgangsuntersuchung und auf den Einfluss auf die Lebensqualität durchgeführt werden. 57 Bei allen 99 Patienten wurde eine Ösophagogastroduodenoskopie und ein 13C-Urease Atemtest zum Nachweis von Helicobacter pylori durchgeführt. Bei 97 Patienten erfolgte eine Gastrinspiegelbestimmung im Serum. Von den nachuntersuchten Patienten lag bei 32,3% bei der Erstuntersuchung vor 20,5 2,7 Jahren ein histologisch unauffälliger Befund der Magenschleimhaut vor, 57,7% des gesamten Patientenkollektives wiesen eine Oberflächengastritis auf. Bei 10,1% wurde zusätzlich eine intestinale Metaplasie beschrieben. Zum Zeitpunkt der Nachuntersuchung wurden 39% der Patienten mit Hilfe des 13C-Urease Atemtest Helicobacter pylori-positiv getestet. Bei 3 weiteren Patienten, deren Atemtest negativ ausfiel, erfolgte ein positiver Helicobacter pylori Nachweis in der Magenbiopsie (Urease-Schnelltest). Bei 8 Patienten, die Helicobacter pylori negativ waren, war bereits eine Eradikationstherapie erfolgreich durchgeführt worden. Somit waren insgesamt 50 der nachuntersuchten Patienten initial Helicobacter pylori positiv. Zum Zeitpunkt der Nachbeobachtungszeit klagten 56,4% Patienten über eine Persistenz, bzw. eine Verschlechterung und 43,6% der Patienten berichteten über eine Besserung bzw. Verschwinden der Beschwerden. Bei den männlichen Patienten blieb der Befund in 45,8 % der Fälle stabil oder verschlechterte sich, bei den weiblichen Patienten hingegen in 71,4 % der Fälle. Eine Verbesserung bzw. Verschwinden der klinischen Beschwerden wurde bei 53,5% der Helicobacter pylori negativen und bei 46,5% der Helicobacter pylori positiven Patienten beobachtet. 53,6% der Helicobacter pylori positiven Patienten berichteten, dass die Symptome der funktionellen Dyspepsie weiterhin persistierten oder sich sogar verschlechtert hatten. Bei Patienten mit Helicobacter pylori negativen Status war dies in 46,4% der Fall. Diese Unterschiede waren nicht statistisch signifikant. Im Verlauf von 20,5 2,7 Jahren traten bei 34 Patienten seit der Erstuntersuchung gastrointestinale Komplikationen auf, wobei bei den Helicobacter pylori positiven Patienten die Komplikationsrate bei 38%, bei den Helicobacter pylori-negativen Patienten hingegen nur bei 26% lag. Die gastrointestinalen Komplikationen traten bei Frauen und Männer gleich häufig auf. Die Lebensqualität, gemessen mit dem gastrointestinalen Lebensqualitätsindex (GLQ-Index) betrug zum Zeitpunkt der Nachuntersuchung bei Patienten mit gastrointestinalen Komplikationen 101 Punkte, während der Wert der Lebensqualität bei den Patienten ohne Komplikationen 111 Punkte betrug. Diese Unterschiede waren nicht signifikant. 58 Die psychischen Faktoren im GLQI Test, wie Leidensdruck und Angst, korrelieren tendenziell positiv mit dem häufigen Auftreten von Komplikationen in der Vergangenheit. Patienten mit guter Streßbewältigung zeigten im Vergleich zu den Patienten mit schlechter Streßbewältigung keinen Unterschied hinsichtlich des Auftretens von Komplikationen. Die Helicobacter pylori-positiven Patienten wiesen am Ende der Nachbeobachtungszeit einen statistisch signifikant höheren mittleren Serumgastrinspiegel auf (154,7 101,2 pg/l) als die Helicobacter pylori-negativen Patienten (91,1 81,6 pg/l). Schlussfolgerung: Die Prognose der funktionellen Dyspepsie ist bezüglich der subjektiven Beschwerdesymptomatik im Langzeitverlauf nicht befriedigend. Das weibliche Geschlecht ist mit einer schlechteren Prognose vergesellschaftet. Die Infektion mit Helicobacter pylori korreliert mit einem erhöhten Gastrinspiegel im Serum. Diese Patienten weisen im Verlauf tendenziell häufiger Komplikationen auf

    Dyspepsia

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    This textbook is specifically written for clinicians involved in managing patients with dyspepsia. It is a practical guide with up-to-date suggestions on evaluation, diagnosis, and management from experts from around the world. Each chapter is a succinct review of current topics that play a role in the pathogenesis and management of this disorder. Special populations such as pediatrics, those with cardiovascular disease and womens health are specifically examined
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