HISTOPATHOLOGICAL STUDY OF CHRONIC GASTRITIS Thesis submitted in partial fulfillment of M.Sc. Degree in Pathology By Somaia AbduLatif Mahmoud Soliman M.B.B.Ch Faculty of Medicine, Cairo University Supervised by Prof. Dr. Dalal Anwar Elwi Professor of pathology Faculty of Medicine Cairo University Ass. Prof. Dr. Mostafa Mohamed Salem Assistant Professor of pathology Faculty of medicine Cairo University Dr. Ahmed Abd- El Monem Soliman Lecturer of Pathology Faculty of Medicine Cairo University Faculty of Medicine Cairo University 2012
20
Embed
HISTOPATHOLOGICAL STUDY OF CHRONIC GASTRITIS · HISTOPATHOLOGICAL STUDY OF CHRONIC GASTRITIS Thesis submitted in partial fulfillment of M.Sc. Degree in Pathology By Somaia AbduLatif
This document is posted to help you gain knowledge. Please leave a comment to let me know what you think about it! Share it to your friends and learn new things together.
Transcript
HISTOPATHOLOGICAL STUDY OF CHRONIC GASTRITIS
Thesis submitted in partial fulfillment ofM.Sc. Degree in Pathology
By
Somaia AbduLatif Mahmoud Soliman M.B.B.Ch
Faculty of Medicine, Cairo University
Supervised by
Prof. Dr. Dalal Anwar ElwiProfessor of pathology
Faculty of MedicineCairo University
Ass. Prof. Dr. Mostafa Mohamed Salem
Assistant Professor of pathologyFaculty of medicine
Cairo University
Dr. Ahmed Abd- El Monem SolimanLecturer of PathologyFaculty of Medicine
Cairo University
Faculty of Medicine Cairo University
2012
الرحمن الرحیمهللابسم
أخرجك ھاتكم ـوهللا م من بطون أممع ـعل لك ـشیئا وج ال تعلمون م الس
.واألبصار واألفئدة لعلكم تشكرون
العظیم هللاصدق
)٧٨:النحل(
Acknowledgement
First and foremost "Thanks to God", the most merciful and kind.
I am honored to have Prof. Dr. Dalal Anwar Elwi, Professor of Pathology, Faculty of Medicine, Cairo University, as a supervisor of this work. I am deeply grateful and most appreciative to her great efforts, kind guidance and valuable advice that encouraged and helped me to finish this work.
My profound gratitude goes to Prof. Dr. MostafaMohammed Samy Salem assistant Professor of Pathology, Faculty of Medicine, Cairo University for his close supervision and precious remarks throughout the course of this study.
Special thanks are owed to Dr. Ahmed Abd-Elmonem Soliman, lecturer of Pathology, Faculty of medicine, Cairo University, who saved no time and effort in helping me, his constant support, continuous encouragement and constructive comments allowed me to accomplish this work.
Finally, I would like to thank my family for their patience, love, motivation and support throughout this work.
Somia AbduLatif
Contents
Introduction & Aim of the work 1Review of literature:
Structure of the stomach 5 Classification 9 Chronic gastritis associated with Helicobacter pylori infection 13 Autoimmune gastritis 26 Reactive gastropathy 32 Radiation gastritis 35 Lymphocytic gastritis 36 Granulomtous gastritis 38 Esinophilic gastritis 43 Other causes of infectious gastritis 46 Vascular gastropathy 51 Collagenous gastritis 54 Ureamic gastropathy 56 Graft Versus Host Disease 57
Introduction & aim of the workـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
-1-
Introduction
The incidence and natural history of chronic gastritis has been
greatly clarified by the systematic use of endoscopic gastric biopsy (Wyatt et
al., 2001).
Chronic gastritis is a histopathologic entity characterized by chronic
inflammation of the stomach mucosa. Gastritis can be classified based on the
underlying etiologic agent (e.g, Helicobacter pylori, bile reflux, nonsteroidal
anti-inflammatory drugs [NSAIDs], autoimmunity, allergic response) and the
histopathologic pattern, which may suggest the etiologic agent and clinical
course (e.g, H. pylori –associated multifocal atrophic gastritis) (Merck, 2007.
Retrieved 2009).
Although minimal inflammation is observed in some gastropathies, such
as those associated with NSAID intake, these entities are frequently included in
the differential diagnosis of chronic gastritis. Chemical or reactive gastritis is
caused by injury of the gastric mucosa by reflux of bile and pancreatic
secretions into the stomach, but it can also be caused by exogenous substances,
including NSAIDs, acetylsalicylic acid, chemotherapeutic agents, and alcohol.
These chemicals cause epithelial damage, erosions, and ulcers that are followed
by regenerative hyperplasia detectable as foveolar hyperplasia, and damage to
capillaries, with mucosal edema, hemorrhage, and increased smooth muscle in
the lamina propria. Inflammation in these lesions caused by chemicals is
minimal or lacking; therefore, the term gastropathy or chemical gastropathy is
more appropriate to describe these lesions than is the term chemical or
reactive gastritis as proposed by the updated Sydney classification of gastritis
(Gao et al., 2009).
Introduction & aim of the workـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
-2-
No single classification of gastritis provides an entirely satisfactory
description of all types of gastritis. However, an etiologic classification provides
a direct target toward which therapy can be directed (Sepulveda et al., 2008).
Infectious gastritis: Chronic gastritis caused by H. pylori infection.
This is the most common cause of chronic gastritis. The most important advance
in the field of chronic gastritis & other gastric diseases (peptic ulcer, carcinoma
& malignant lymphoma) has been the awareness of the crucial role played by
H.pylori (Wu et al., 2001). Infection by Helicobacter heilmannii, granulomatous
gastritis associated with gastric infections in mycobacteriosis, syphilis,
histoplasmosis, mucormycosis, South American blastomycosis, anisakiasis, or
anisakidosis. Chronic gastritis associated with parasitic infections such as
Chronic granulomatous disease of childhood, eosinophilic granuloma, allergic
granulomatosis and vasculitis, plasma cell granulomas, rheumatoid nodules,
tumoral amyloidosis and granulomas associated with gastric carcinoma, gastric
lymphoma, Langerhans cell histiocytosis (Maeng et al., 2004). Eosinophilic
gastritis, radiation injury to the stomach, GVHD, ischemic gastritis, gastritis
secondary to drug therapy (Quentin et al., 2006). Lymphocytic gastritis,
including gastritis associated with celiac disease (also called collagenous
gastritis) (Leung et al., 2009).
Introduction & aim of the workـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
-3-
Cases of histologically documented chronic gastritis are diagnosed as
chronic gastritis of undetermined etiology or gastritis of undetermined type
when none of the findings reflect any of the described patterns of gastritis and a
specific cause cannot be identified (Galiatsatos et al., 2009).
Introduction & aim of the workـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
-4-
AIM OF THE WORK
Histopathological revision of all available archival material of chronic
gastritis in the last 2 years (2009-2010), collected from the pathology
department, Faculty of medicine, Cairo University Hospital, then statistical
evaluation and correlation between age, clinical data, endoscopy or any relevant
data available in the request sheets and the histopathological findings.
Assessment of histopathological types, their incidence, & complications
in order to have better treatment chances.
Review of literatureـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
-5-
Structure of the stomach
*Anatomy:
Anatomically, the stomach is divided into four regions:
Cardia: It is a narrow portion immediately distal to gastro-esophageal junction.
Fundus: It is gastric portion that extends above the level of gastro-esophageal
junction.
Body (corpus): It is the part that extends proximal to incisura angularis (angle
along the lesser curvature).
Antrum: It is the part that extends distal to incisura angularis.
(Owen, 1986)
* Histology:
I- The Mucosa:
The normal gastric mucosa consists of epithelium, delicate stroma of connective
tissue (lamina propria) and muscularis mucosa.
The epithelium:
It has as distinct glandular compartments, superficial zone, neck zone and
deep zone.
The superficial glandular zone: Composed of straight, narrow, tubular pits
(foveolae) lined by surface mucous cells and neck mucous cells. They remain the
same through out the stomach.
Review of literatureـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
-6-
The surface mucous cells: tall columnar with basal nuclei and clear luminal
cytoplasm due to accumulation of large mucin vacuoles towards the luminal
surface.
The neck mucous cells: smaller because they are compressed and distorted
by adjacent cells. They have basal nucleus and finely granular cytoplasm due to
presence of small mucin vacuoles smaller than those in the surface mucous cells
distributed throughout the cytoplasm.
The deep zone: is composed of glands which their bases lies close to or in
the muscularis mucosa and their upper ends open into the bases of the superficial
zone pits. It has variable composition throughout the different gastric histological
patterns.
The neck zone or the isthmus: it lies between superficial and deep zone. It
is lined by immature stem cells mixed with some neck mucous cells. The stem cells
proliferate and migrate upward after differentiation to replace the mucous cells of
the superficial zone and downward to replace the various cell types in the deep
zone glands (Stevens and Lowe, 1997).
There are three main histological patterns which delineate the main areas of
the stomach: the cardia, the fundus or the pylorus (Lewin et al., 1992).
The cardiac mucosa: The superficial and deep zones are of about equal
thickness. The deep zone is composed of tubular and branched glands; some of
them are complex and coiled. They are lined by mucous cells, few acid producing
cells and scattered endocrine cells. The cardiac glands are quite similar to pyloric
glands but more coiled and dilated (Helander et al., 1986).
Review of literatureـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
-7-
The body (fundic) glands: The superficial zone accounts 25% or less of the
mucosal thickness. The deep zone is composed of tightly packed long straight
tubular glands, 5-15mm long, and end blindly at the muscularis mucosa. They are
lined by acid producing cells (parietal or oxyntic cells), enzyme producing cells
(chief or peptic or zymogen cells), neck mucous cells and scattered endocrine cells
(Owen, 1997).
The pyloric (antral) glands: The superficial zone occupies slightly more
than 50% of the mucosal thickness and the crypts are often branched. The deep
zone is composed of tortuous or branched glands. They are lined by mucous cells,
scattered acid producing cells and numerous endocrine cells. The acid producing
cells become more numerous close to the pyloric spincter (Helander et al., 1986).
The lamina propria:
It is fibroreticular connective tissue that is situated between the surface
epithelium and muscularis mucosa, forming the stroma in between the glands. It
contains fine capillary plexus, nonmyelinated nerves, some fibroblasts, occasional
smooth muscle cells passing from the muscularis mucosa and rare plasma cells
(Owen, 1997).
The muscularis mucosa:
It consists of poorly defined layer of smooth muscle fibers (Owen, 1997).
II- The Submucosa:
Consists of loose connective tissue that supports the large blood vessels, lymphatics
and the Miessner’s plexus of nerves. It also contains small collection of fat cells
and some esinophils (Lawson, 1988).
Review of literatureـــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
-8-
III- The Muscularis Propria:
The muscular wall of the stomach differes from the standard digestive
pattern by the presence of third layer of oblique muscle fibers (inner oblique) which
is absent in the pyloric region (Owen, 1986).
IV- The Serosa:
It consists of thin layer of connective tissue covered by a layer of flat
mesothelial cells (Owen, 1986).
Figure (1): Diagram of 4 anatomical & 3 histological areas of the stomach.
Review of literatureــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــــ
-9-
Classification of chronic gastritis
Chronic gastritis represents the non-specific histopathological sequelae to
diffuse long-standing and multifactorial injury to the gastric mucosa. In a long-
standing condition, histological appearances change with time and similar
histological appearances may result from differing etiologies, Whitehead et al.,
advocate classification of chronic gastritis according to mucosal type, the grade
of gastritis, whether it is superficial or atrophic, and the type of associated
metaplasia (Whitehead et al., 1972).
Strickland, & Mackay, 1973 identified type A and type B chronic
gastritis based on topography. Type A refers to chronic atrophic gastritis
involving the corpus and often associated with parietal cell autoantibodies and
minimal antral involvement. Type B gastritis involves the distal stomach
predominantly with only patchy involvement of the corpus. This is not
associated with parietal cell autoantibodies and is considerably more prevalent
than type A.
This classification has been widely adopted and continues to be used. The
discovery of H. pylori and its association with chronic gastritis has cast new
light on the condition, Wyatt, & Dixon, 1988 proposed a classification based on
histological features and pathogenesis. This consisted of type A (autoimmune),
type B (bacterial), and reflux or chemical gastritis.
The most widely used classification of chronic gastritis is the Sydney
system which was devised by an international Working Party of experts and
attempts to draw many previous classifications together (Price. 1991).
This system combines etiology, topography and morphology. The system
relies on at least two mucosal biopsies from both the antrum and the corpus, in