DOCSLIB.ORG

March-2014 Issue

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
March-2014 Issue Which is for the good of mankind remains in the earth INSTRUCTIONS TO AUTHORS All material submitted for publication should be sent exclusively to the 'Pakistan Journal of Gastroenterology'. Three copies of manuscripts should be sent by registered post three months prior to the date of next publication, addressed to: The Executive Editor Pakistan Journal of Gastroenterology Welcare Liver & G.I. Clinic, 93-B Shadman, Main Boulevard, Shadman Chowk, Lahore The authors should comply with the following policy: 1. The editorial board retains the customary rights to style, shorten or reject the article submitted for publication. 2. Original articles should normally contain research related to Gastroenterology and may be in the form of clinical research papers, unusual case reports, new ideas and innovations regarding techniques, procedures and instruments, and short reports. 3. Special articles related to medical education, new and useful statistical techniques and those related to any drug, special procedure, etc. will also be entertained. 4. Review articles should constitute critical analysis and latest developments. Prior permission of the editors should be sought before sending a review article. 5. Manuscripts should be typed double spaced on one side of the paper and the pages should be numbered. 6. Scientific articles should conform to the internationally recognized structure viz. abstract, introduction, material and method, results, discussion and references. Tables and illustrations should be submitted separately from the text. Technically incorrect articles will not be accepted. 7. The references should be presented according to the style of Index Medicus. Titles of books should be followed by place of publication, publisher and year. 8. The article once submitted will not be returned irrespective of its publication. The author is advised to retain a copy. 9. The author is requested to send their materials on floppy computer disc to minimize the typing errors. 10. All authors must give written consent for publication on the attached proforma. BIANNUAL MARCH, 2007 LAHORE - PAKISTAN To: THE EXECUTIVE EDITOR PAKISTAN JOURNAL OF GASTROENTEROLOGY WELCARE LIVER & G.I. CLINIC, 93-B SHADMAN, MAIN BOULEVARD, SHADMAN CHOWK, LAHORE FROM: NAME OF FIRST AUTHOR: ___________________________ POSTAL ADDRESS: ___________________________ ___________________________ PHONE NOS: ___________________________ SUBJECT: UNDERTAKING BY THE AUTHORS I Dr. 1. ________________________ ______________________ 2.________________________ ______________________ 3.________________________ ______________________ 4.________________________ ______________________ 5. ________________________ ______________________ 6.________________________ ______________________ solemnly declare that my / our articles entitled” __________________________________ _____________________________________________________________ has not been submitted before for publication in any other Journal and if approved for publication in Pakistan Journal for Gastroenterology, it will not be submitted again elsewhere. I / We further declare that it is review / original article / case report. *(The copies of article once submitted will not be returned irrespective of its publication). Signature of 1st Author CORRIGENDUM In the last Pakistan J. of Gastroenterology, Vol. 27 (Biannual Apr. – Sep., 2013), published and circulated last year, the volume number was printed inappropriately as Vol. 27. Actually it was Vol. 28 Biannual October 2013). Therefore, it should be read as Pakistan J. of Gastroenterology, Vol. 28 (Biannual October 2013) for future reference. 75 Pakistan J. of Gastroenterology, Vol. 29, Biannual Mar., 2014 The Pakistan Journal of G A S T R O E N T E R O L G Y Editor-in-Chief: Patron: Executive Editor: Editors: Editorial Advisory Board: Peer Review Committee: For Correspondence: Executive Editor Address: Welcare Liver & g. i. Clinic, 93-B Shadman, Main Boulevard, Shadman Chowk, Lahore Phone: 03008477287. E-mail: [email protected] Web: www.psg.org.pk EDITORIAL GASTROESOPHAGEAL REFLUX DISEASE (GERD) Gastroesophageal reflux disease (GERD) or dyspepsia of normal anti - reflux mechanism to protect against is recurrent or persistent discomfort or pain involving abnormal frequency and quantity of GER. GER itself is upper abdomen which is characterized by early satiety, not a disease process but rather a normal physiologic postprandial fullness, nausea, and bloating. In phenomenon, which occurs many times each day, Pakistan though hospital-based surveys are showing especially after large meals, without making symptoms upto 24% prevalence, actually it is more in general or mucosal damage. When acid reflux occurs, fluid or people both in the cities and villages as well due to food can be tasted in the back part of the mouth. When modernization of life style, food choices and their refluxed stomach acid meets the lining of the timings. esophagus it may result burning sensation in the Reflux of gastric juices and hiatus hernia are the throat or the chest called acid indigestion or most common causes. Adults with GERD usually heartburn. Persistent reflux that happens more than encounter the symptoms after eating a meal, lying on twice a week is labeled as GERD, and it can ultimately their backs, when bending over or if they are lifting bring about more serious health problems. People of heavy weight things. Symptoms often become very any age group can suffer GERD. Two factors distinct during the night. GERD is very commonly contribute to mucosal damage i.e., direct toxic injury noticed in pregnant women (> 50% experience acid and prolonged mucosal contact time with gastric acid reflux and/or heartburn). If symptoms and reflux or pepsin or both. episodes occur together < 25% or > 75% of time, causal Esophageal clearance occurs by primary or association is low or high respectively. In symptomatic secondary peristaltic waves. Acid neutralization by patients who are using aggressive acid suppressive swallowed saliva and esophageal mucosal resistance, therapy, demonstration of complete acid suppression acid residue at mucosal surface maintains low clearly indicates that acid reflux is not a major factor, esophageal pH immediately after peristaltic and if acid reflux is still occurring then there is a need contractions. Salivary bicarbonate neutralizes mucosal of different therapy. pH in a stepwise fashion in 8 – 10 swallows. Duration Adults with GERD, may experience any of the of time from reflux event until restoration of normal symptoms, including heartburn, belching, esophageal pH is the Esophageal Acid Clearance Time. regurgitation, bad breath (halitosis), nausea, Delayed gastric emptying leads to retention of solid dysphagia, odynophagia (painful swallowing), chest foods, secretion of food - induced acid, gastric pain, particularly after eating, water brash (increased distension and LES relaxations. In post – prandial salivation), reflux esophagitis, peptic stricture in state, possible delayed gastric emptying results in esophagus, Barrett’s esophagus, esophageal increased esophageal acid contact time. carcinoma, abdominal pain, sinusitis, asthma, Drugs may aggravate GER by decreasing LES laryngitis, pharyngitis, sensitive teeth, choking feeling, pressure e.g. beta – agonist, theophylline, chronic coughing, and damage to the esophagus itself. anticholinergic, tricyclic anti – depressants, The damaged esophagus will begin to scar, may start progesterone, diazepam & calcium channel blockers or to become narrow resulting strictures formation, direct esophageal mucosal injury e.g. tetracycline, which can lead to dysphagia. If the esophagus is quinidine, KCL, iron, NSAIDs, Aspirin, Alendronate. injured even more, it could evolve to Barrett’s Hiatus hernia is present in 50% patients having > 50 esophagus; will cause the esophagus to change in color years of age. Endoscopically 80% patients with GERD and shape, and there is a raised risk of cancer too. have hiatus hernia and > 50% patients of hiatus hernia Gastroesophageal reflux disease (GERD) is a more do have GERD. On endoscopy, majority of the patients crucial form of Gastroesophageal reflux (GER), also have no visible damage in the mucosal lining (non- called acid regurgitation or acid reflux. Here digestive erosive GERD/NERD), whereas others have reflux juices – called acids –go up along with the food esophagitis, stricture formation or Barrett's change in commonly. It occurs when the LES relax to open the esophagus. Severe esophageal mucosal disease spontaneously, for variable period of time, or does not almost guarantees presence of hiatushernia and may close properly and contents from the stomach rise up results in melena, vomiting blood or coffee ground into the esophagus. GER occurs when there is failure looking material, dysphagia, anemia (low blood count), Pakistan J. of Gastroenterology, Vol. 29, Biannual Mar., 2014 38 MUHAMMAD ARIF NADEEM un-explained weight loss. Patients with GERD and its changes or medications, then additional testing may be complications should be checked carefully by a required, where barium swallow radiograph can detect gastroenterologist. GERD may deteriorate or initiate abnormalities like hiatal hernia and other anatomical the chronic cough, asthma, and pulmonary fibrosis. or physical problems of the esophagus but will not Anatomical anti - reflux barrier is a fortress, perceive mild irritation, although strictures or ulcers of composed of LES, crural diaphragm and the esophagus can be detected. Upper
Load more

Recommended publications
  • Gastritides: Diagnostic Evaluation of Multifaceted Conditions
    Gastritides: Diagnostic Evaluation of Multifaceted Conditions Gregory Y. Lauwers, MD Senior Member H. Lee Moffitt Cancer Center & Research Institute Tampa, FL [email protected] Changing epidemiology of gastritis (Autoimmune) (Chemical Reactive) Vieith M. Bayreuth Clinic data based on 1,333 389 cases Prevalence of Reactive Gastropathy and H. Pylori Gastritis H. Pylori Reactive Gastropathy Maguilnik I. AP&T 2012;36 • Urease activity: Biopsies (CLO-test) breath test • Serology • Stool antigen IF NEGATIVE • Sampling error -- Antibiotic monotherapy (e.g., other infections) • PPI (decreased # of bacteria; shift from antrum to prox. stomach) • Focally Enhanced Gastritis (IBD) Treated H. pylori gastritis H. Heilmannii • Low prevalence • (0.3-0.7% in devped countries) • Household pets • Mild inflammation • H. felis: • severe chronic active gastritis Autoimmune Atrophic Gastritis • Autosomal dominant inheritance • Confined to corpus and fundus • Immune – mediated injury (autoantibodies) – Loss of parietal cells – Gland atrophy – Metaplasia: pseudopyloric and intestinal types Autoimmune Gastritis SYN Treponema pallidum NK-Cell enteropathy NK-Cell enteropathy CD3 CD56 Granzyme EBV Gastritis EBV gastritis EBER Russell Body Gastritis IgG Lymphocytic gastritis •0.83% of unselected biopsies •1.7% to 4.5% of inflamed biopsies >25 IELs/ 100 epith cells (N:1-9) AJSP 1999;23. •Pan gastric:76% - Fundus:18% - Antrum:6% LYMPHOCYTIC GASTRITISCD3 • H. pylori: 30-40% [pan gastric or corpus predominant] • Celiac sprue: 26.4-38% [typically antral] • Crohn disease:1.5% • non GSE autoimmune disease: 4% • Neoplasia (gastric cancer; lymphoma):4% • Drugs (Ticlopidine, Ticlid®):1% • HIV • No clinical association in 20-28% of the cases… a seasonal tendency (fall) was noted AJSP 1999;23. Personal data: 346 cases (age range 1-87 years, mean age 51 years).
    [Show full text]
  • A 51-Year-Old Man with Gastric Cancer and Lung Nodules
    T h e new england journal o f medicine case records of the massachusetts general hospital Founded by Richard C. Cabot Nancy Lee Harris, m.d., Editor Eric S. Rosenberg, m.d., Associate Editor Jo-Anne O. Shepard, m.d., Associate Editor Alice M. Cort, m.d., Associate Editor Sally H. Ebeling, Assistant Editor Christine C. Peters, Assistant Editor Case 29-2007: A 51-Year-Old Man with Gastric Cancer and Lung Nodules Edward T. Ryan, M.D., Suzanne L. Aquino, M.D., and Richard L. Kradin, M.D. Presentation of Case Dr. Allison L. McDonough (Internal Medicine): A 51-year-old man with a history of From the Division of Infectious Disease gastric cancer was admitted to the hospital because of a new pulmonary lesion. (E.T.R.) and the Departments of Radiology (S.L.A.) and Pathology (R.L.K.), Massa- The patient had been in good health until approximately 5 years before admis- chusetts General Hospital; and the De- sion, when he had a decreased appetite and epigastric discomfort; evaluation at partments of Medicine (E.T.R.), Radiology another facility revealed a hiatal hernia, gastroesophageal reflux, and a duodenal (S.L.A.), and Pathology (R.L.K.), Harvard Medical School. ulcer. Testing for Helicobacter pylori was positive. Omeprazole and metoclopramide were administered, and the hiatal hernia was surgically repaired. Pain, persistent N Engl J Med 2007;357:1239-46. gastroesophageal reflux, and weight loss developed approximately 2.5 years before Copyright © 2007 Massachusetts Medical Society. admission. A primary care physician at this hospital prescribed combination therapy (lansoprazole, amoxicillin, and clarithromycin) for 2 weeks to treat the H.
    [Show full text]
  • 1. Pathology of the Stomach. Ileus. Vascular Diseases of the Bowels and the Peritoneum
    1. Pathology of the stomach. Ileus. Vascular diseases of the bowels and the peritoneum. PATHOLOGY OF THE STOMACH Stomach mucosa • Gastric mucosa is covered by a layer of mucus. The mucosal glands comprise the cardiac glands, the fundic glands in the fundus and body of the stomach, and the pyloric glands in the antrum. • The surface mucous cells and the cardiac and pyloric glands secrete mucus which protects the stomach from self- digestion. • In fundic glands, the chief cells secrete pepsinogen; the parietal cells secrete HCl, bicarbonate, and intrinsic factor, and the endocrine cells release histamine. • Pyloric endocrine cells secrete gastrin, somatostatine, etc. Glossary • Gastritis - inflammation of the gastric mucosa associated with gastric mucosal injury • Gastropathy - epithelial cell damage and regeneration without associated inflammation • Erosion - circumscribed necrosis-induced defect of mucosa that does not cross the muscularis mucosae • Ulcer - the defect extends beyond the mucosa ACUTE GASTRITIS Pathogenesis Common condition, induced by acute damage to the gastric mucosa due to • alcohol, NSAIDs (nonsteroidal anti-inflammatory drugs, e.g., aspirin) or steroids • stress situations, e.g., severe burns, hypothermia, shock, CNS trauma, etc. • Helicobacter pylori infection Pathological features • Hemorrhagic-erosive inflammation of gastric mucosa affecting the entire stomach (pangastritis) or the antrum of stomach (antral gastritis) • Mucosal hyperemia, punctate hemorrhages, multiple erosions • + Acute ulcers: anywhere in the
    [Show full text]
  • Reactive Gastropathy: Frequency in Endoscopic Biopsies Evaluated at the Universidad Nacional De Colombia
    Original articles Reactive gastropathy: Frequency in endoscopic biopsies evaluated at the Universidad Nacional de Colombia María del Pilar Suárez Ramos, MD,1 Diana Lucía Martínez Baquero, MD,1 Martha Eugenia Cabarcas Santoya, MD,1, 2 Orlando Ricaurte Guerrero, MD.1, 2 1 Residents in Anatomical and Clinical in the Abstract Department of Pathology at the Universidad Nacional de Colombia, Bogotá, D.C, Colombia Reactive gastropathy (RG) is primarily produced by non-steroid antiinfl ammatory drugs (NSAIDs) and bile 2 Medical Pathologists and Associate Professors in the refl ux. It can occur alone or coexist with other types of chronic gastritis (CG). 5,079 histopathological reports of Molecular Pathology Group of the Medicine Faculty gastric biopsies from 4,254 patients were reviewed: 825 of them had 2 to 7 follow-up studies. 12.8% of these of the Universidad Nacional de Colombia, Bogotá D.C, Colombia patients were diagnosed with GR while 63.4% were diagnosed with chronic non-atrophic gastritis (CNAG) and 27.3% were diagnosed with chronic multifocal atrophic gastritis (CMAG). Helicobacter pylori infections were Translation from Spanish to English by T.A. Zuur and found in 61.6% of the cases with CNAG, 51.5% with CMAG, and in 18.5% of cases with GR only (p <0.0001). The Language Workshop ......................................... Among patients suffering from both RG and CNAG 43.9% had H. pylori infections. 40.7% of those suffering Received: 28-04-11 from both CMAG and RG were infected with H. pylori. During monitoring of patients RG diagnoses increased Accepted: 11-10-11 to 22.2% in the second study, 26.7% in the third study, and 28.8% in the fourth through seventh studies.
    [Show full text]
  • Diverticular Disease-Related Colitis
    Diverticular Disease-Related Colitis KEY FACTS Colon TERMINOLOGY ○ Abscess, fistula, perforation • Segmental colitis-associated diverticulosis (SCAD) ○ Exception is Crohn disease-like variant of SCAD that may show mural lymphoid aggregates ETIOLOGY/PATHOGENESIS MICROSCOPIC • Unknown, TNF-α may play role • Chronic colitis-like changes mimicking inflammatory bowel CLINICAL ISSUES disease • Presents with hematochezia, abdominal pain, diarrhea • Ulcerative colitis-like variant shows changes confined to • Median age: 64 years mucosa ○ Range: 40-86 years ○ Diverticulitis may or may not be present in these cases • Predominately involves descending and sigmoid colon (with • Crohn disease-like variant shows mural lymphoid rectal sparing) aggregates • Treatment directed toward diverticular disease suppresses • Changes in both variants confined to segment involved symptoms with diverticulosis coli MACROSCOPIC TOP DIFFERENTIAL DIAGNOSES • Mucosal changes are mild and nonspecific • Ulcerative colitis, Crohn disease, infectious colitis, diversion • Mural changes are related more to underlying diverticulosis colitis, NSAID-associated colitis coli rather than SCAD Diverticular Disease-Associated Colitis Diverticular Disease-Associated Colitis (Left) The mucosa surrounding the openings of diverticula ſt into the colonic lumen is erythematous and granular, consistent with diverticular disease-associated colitis (DDAC) ﬊. (Right) It is not uncommon to find some inflammation or erosions ﬊ around the luminal opening of a colonic diverticulum ſt. To be diagnostic of DDAC, inflammation must involve the mucosa in the interdiverticular region ﬉. Chronic Active Colitis Basal Lymphoplasmacytosis (Left) A chronic colitis pattern of inflammatory infiltrate is seen in both the ulcerative colitis-like and Crohn disease- like variant of DDAC. The mucosal changes are indistinguishable from true inflammatory bowel disease (IBD). (Right) A band of lymphoplasmacytic infiltrate ﬊ is present beneath the base of the crypts ﬇ in the mucosa.
    [Show full text]
  • Gastritis and Gastropathy: More Than Meets The
    10053 Omez advert pRR 5/29/12 6:04 PM Page 1 Gastritis and gastropathy: More than meets the eye This paper discusses the different types of gastritides and gastropathies, focusing on their wide range of aetiologies. W Nel, MB ChB, M Med (Anat Path) Anatomical pathologist, Ampath Pathology Laboratories, Pretoria Willie Nel did his undergraduate training at the University of the Free State and postgraduate training at the University of Pretoria. He joined the private practice of doctors Du Buisson and partners (Ampath) after two years as a consultant at the Institute of Pathology in Pretoria. Amongst his special interests are motorcycling and cattle breeding. Correspondence to: W Nel ([email protected]) Gastrointestinal symptoms such as conjunction with bicarbonate-secreting Acute gastritis in Helicobacter pylori dyspepsia, heartburn, epigastric pain, nausea surface epithelial cells and local prosta- infection and vomiting are extremely common and glandin production, as a protective barrier The initial phase of Helicobacter infection have been experienced by the majority against autodigestion and noxious agents. causes an acute inflammatory reaction of people at some stage in their lifetime. The gastric mucosa also has the ability to and degenerative changes in the surface These complaints are often as a result of proliferate and replace damaged epithe- epithelial cells of the gastric mucosa. pathology in the upper gastrointestinal tract. lium very rapidly. Symptoms may include epigastric pain, a Correlation between the clinical presentation bloated feeling and nausea; these most often (symptoms, signs and endoscopic findings) In 1990 the Sydney system was developed as resolve within a week. After approximately and pathology, including the degree and a guideline for the classification and grading two weeks the reaction evolves into an precise localisation of the disease process, of gastritis by a group of international active chronic gastritis.
    [Show full text]
  • Factors Associated with Gastro-Duodenal Ulcer in Compensated Type 2 Diabetic Patients: a Romanian Single-Center Study
    Clinical research Factors associated with gastro-duodenal ulcer in compensated type 2 diabetic patients: a Romanian single-center study Anca Negovan1, Claudia Banescu2, Monica Pantea1, Bataga Simona1, Simona Mocan3, Mihaela Iancu4 1Department of Clinical Science-Internal Medicine, “George Emil Palade” University Corresponding author: of Medicine, Pharmacy, Science, and Technology of Târgu Mureș, Mureș, Romania Assoc. Prof. Anca Negovan 2Genetics Laboratory, Center for Advanced Medical and Pharmaceutical Research, MD, PhD “George Emil Palade” University of Medicine, Pharmacy, Science and Technology Department of Clinical of Târgu Mureș, Târgu Mureș, Romania Science-Internal Medicine 3Pathology Department, Emergency County Hospital Targu Mures, Mureș “George Emil Palade” 4Department of Medical Informatics and Biostatistics, “Iuliu Haţieganu” University University of Medicine, of Medicine and Pharmacy, Cluj-Napoca, Romania Pharmacy, Science, and Technology Submitted: 25 February 2018 Gheorghe Marinescu Accepted: 10 July 2018 nr. 38, 540139 Tirgu Mures, Romania Arch Med Sci E-mail: DOI: https://doi.org/10.5114/aoms/93098 [email protected] Copyright © 2020 Termedia & Banach Abstract Introduction: Helicobacter pylori infection is accepted as the leading cause of chronic gastritis, ulcer disease and gastric cancer, with an important im- pact on health care burden, especially in countries with a high prevalence of infection. The aim of the study was to investigate the influence of H. pylori infection, medication, associated medical conditions or social habits on en- doscopic ulcer occurrence in the compensated type 2 diabetic population. Material and methods: Two hundred and sixty type 2 diabetic patients in- vestigated on endoscopy (57 patients with peptic ulcer and 203 controls) with a complete set of biopsies, demographic and medical data were enrolled.
    [Show full text]
  • Multinucleated Stromal Giant Cells in the Gastroesophageal Junctional and Gastric Mucosa: a Retrospective Study Taha Sachak, Wendy L
    Sachak et al. Diagnostic Pathology (2019) 14:83 https://doi.org/10.1186/s13000-019-0860-y RESEARCH Open Access Multinucleated stromal giant cells in the gastroesophageal junctional and gastric mucosa: a retrospective study Taha Sachak, Wendy L. Frankel, Christina A. Arnold and Wei Chen* Abstract Background: Atypical multinucleated stromal giant cells (MSGCs) are occasionally encountered in the esophagogastric mucosa. This study aims to investigate the origin and clinical association of MSGCs in the upper gastrointestinal tract. Methods: Three hundred sixty-one contiguous biopsies and 1 resection specimen from the stomach and gastroesophageal junction (GEJ) were identified from archives for morphologic and immunohistochemical studies. Results: MSGCs were identified in 22 cases (6%: 7 gastric, 15 GEJ). Patients’ average age was 53 years. There was no sex predilection. 77% cases had only 1 or 2 MSGCs per 10 high power fields. MSGCs were located in the lamina propria of the gastric or GEJ mucosa, with an accentuation in the subepithelial zone. The median number of nuclei in a MSGC was 5 (ranging from 3 to 16). The nuclei were touching/overlapping, often arranged into “wreath”, “caterpillar”,or“morula” configurations. MSGCs expressed smooth muscle actin, desmin, while negative for cytokeratin AE1/3, CD68, S100, chromogranin, and CD117. The most common clinical history was epigastric pain, gastroesophageal reflux, and Barrett esophagus. The most common associated pathologic diagnoses included reactive (chemical) gastropathy (71% gastric biopsies) and gastroesophageal reflux (73% GEJ specimens). Conclusions: MSGCs in the esophagogastric mucosa show smooth muscle/myofibroblast differentiation by immunohistochemistry and likely represent a reactive/reparative stromal reaction associated with gastroesophageal reflux and reactive (chemical) gastropathy.
    [Show full text]
  • What Is Gastritis? What Is Gastropathy? How Is It Classified?
    Turk J Gastroenterol 2014; 25: 233-47 What is gastritis? What is gastropathy? How is it classified? STOMACH Serra Kayaçetin, Servet Güreşçi Review Department of Pathology, Ankara Numune Education and Training Hospital, Ankara, Turkey ABSTRACT Stomach endoscopic biopsies are made to determine the diagnosis of the illness, its stage, and follow-up after the treatment. It is very significant to collaborate with the clinician while evaluating endoscopic biopsies. Besides the clinical and laboratory information of the patient, the endoscopic appearance of the lesion should be known. The clinician and pathologist should use the same language and the same terminology. Although new classifications have been made to prevent the confusion of terminologies in neoplastic processes recently, most centers around the world have reported non-invasive neoplasias without giving any certain diagnosis by just commenting on it. The clinician should understand what the pathologist wants to say; pathologists should know the approach of the clinician (repetition of the biopsy, endoscopic resection, surgery). There is Helicobacter pylori (HP) in most of the stomach pathologies as the etiologic agent. No matter if the factor is HP or other etiologic agents, the tissue gives similar responses. That is why clinical-endoscopic indications should be taken into consideration, as well as histological indications, and the reports of the endoscopy should be seen. A good clinicopathologic correlation increases the accuracy of the diagnosis. Keywords: Gastritis, gastropathy, classification Gastritis is an infectious or auto-immunological inflam- images of gastritis based on different etiologies, and mation. Gastropathy can be described as a pathology there may be more than one etiologic agent in a gas- that displays epithelial injury and regeneration, and it is tritis chart.
    [Show full text]
  • Gastritis and Carditis David A
    Gastritis and Carditis David A. Owen, M.B. University of British Columbia, Vancouver, British Columbia, Canada ations. Carditis is a controversial topic: currently Dyspepsia is a common clinical problem. Its causes opinions are divided as to whether it is the result of include peptic ulcer disease, gastroesophageal re- gastroesophageal reflux or a proximal extension of flux, and functional (nonulcer) dyspepsia. A detailed H. pylori infection from the remainder of the clinical description of pain does not reliably differ- stomach. entiate the cause. Approximately 80% of gastrosco- pies are performed for the investigation of dyspep- KEY WORDS: Atrophic gastritis, Carditis, Gastric sia. “Gastritis” is diagnosed endoscopically in 59% cardia, Gastric Crohn’s disease, Gastritis, Helicobac- of all stomachs, although in only 3% are the changes ter, Lymphocytic gastritis, Pernicious anemia, Pro- severe. Pathologic examination of unselected gas- ton pump inhibitors, Reactive gastropathy. tric biopsy specimens reveals that abnormalities are Mod Pathol 2003;16(4):325–341 present in 62–73%, but there is only a weak corre- lation between endoscopic and histologic findings. Most gastroscopies are performed for the investiga- For these reasons, it is recommended that endo- tion of dyspepsia (1–7). This is a common clinical scopic examination should always be accompanied problem but is rarely life-threatening. The causes of by biopsy. Ideally, biopsies should be taken in a dyspepsia include peptic ulcer disease (30%), gas- systematic fashion to include sampling of antrum troesophageal reflux (29%), and nonulcer (func- and corpus. Recent evidence suggests that gastric tional) dyspepsia (40%). The cause of functional infection by Helicobacter pylori initially presents as dyspepsia is unclear at the present time, although a superficial gastritis.
    [Show full text]
  • The Gastrointestinal Tract 17 Jerrold R
    To protect the rights of the author(s) and publisher we inform you that this PDF is an uncorrected proof for internal business use only by the author(s), editor(s), reviewer(s), Elsevier and typesetter Toppan Best-set. It is not allowed to publish this proof online or in print. This proof copy is the copyright property of the publisher and is confidential until formal publication. p0520 See TARGETED THERAPY available online at www.studentconsult.com C H A P T E R c00017 The Gastrointestinal Tract 17 Jerrold R. Turner CHAPTER CONTENTS u0170 u0010 CONGENITAL Hypertrophic Gastropathies 768 Pseudomembranous Colitis 791 u0340 u0175 ABNORMALITIES 750 Ménétrier Disease 768 Whipple Disease 791 u0345 u0180 u0015 Atresia, Fistulae, and Duplications 750 Zollinger-Ellison Syndrome 769 Viral Gastroenteritis 792 u0350 u0185 u0020 Diaphragmatic Hernia, Omphalocele, Gastric Polyps and Tumors 769 Parasitic Enterocolitis 794 u0355 u0190 and Gastroschisis 750 Inflammatory and Hyperplastic Polyps 770 Irritable Bowel Syndrome 796 u0360 u0195 u0025 Ectopia 750 Fundic Gland Polyps 770 Inflammatory Bowel Disease 796 u0365 u0200 u0030 Meckel Diverticulum 751 Gastric Adenoma 770 Crohn Disease 798 u0370 u0205 u0035 Pyloric Stenosis 751 Gastric Adenocarcinoma 771 Ulcerative Colitis 800 u0375 u0210 u0040 Hirschsprung Disease 751 Lymphoma 773 Indeterminate Colitis 800 u0380 u0215 Carcinoid Tumor 773 Colitis-Associated Neoplasia 801 u0385 u0220 u0045 ESOPHAGUS 753 Gastrointestinal Stromal Tumor 775 Diversion Colitis 802 u0395 u0050 Esophageal Obstruction 753 Microscopic
    [Show full text]
  • • This Study Confirms the Inverse Relationship Between Eoe and H
    Esophageal Eosinophilia and Gastric Mucosal Pathology: Is There a Link? Cristian I. Robiou, MD1, Evan Dellon, MD2, Robert M. Genta, MD1,3 1Miraca Life Sciences Research Institute, Irving, TX, United States. 2Center for Esophageal Diseases and Swallowing, UNC School of Medicine, Chapel Hill, NC, United States. 3Dallas Veteran Affairs Medical Center and University of Texas Southwestern Medical Center, Dallas, TX, United States. Background Methods Results Study Highlights We have previously reported, and others have confirmed, an inverse relationship We used the Miraca Life Sciences database to extract histopathologic, There were 212,982 unique patients with both esophageal and gastric biopsies. • This study confirms the inverse relationship between EoE andH. between eosinophilic esophagitis and Helicobacter pylori gastritis. demographic, and clinical information from all patients with esophageal and 204,525 had <15 eos/HPF in the esophageal epithelium (median age 57 years, pylori and its sequelae. Other conditions affecting the stomach can include reactive gastropathy, gastric biopsies obtained between 1.2008 and 6.2012; those with upper GI cancer range 3 months - 104; 42.0% M), or esophageal surgery were excluded. Surprisingly, conditions that are clearly unrelated (RG) or autoimmune atrophic gastritis, chronic inactive gastritis, and intestinal metaplasia. 8,457 had ≥15 eos/HPF (median age 45 years, range 1 - 96; 62.2 % male). • However, the relationship between esophageal eosinophilia and these other Patients were arranged in 5 strata according to the numbers of eosinophils per uncertainly linked to H. pylori (AIG) were also less likely in patients Thus, patients with ≥15 eos/HPF were younger (p<.0001) and more likely to be causes of gastric pathology has not been explored.
    [Show full text]