Gastritis is an inflammatory status of the stomachic mucous membrane. Gastritis can be classified based on the underlying etiology i.e. Helicobacter pylori, non steroidal anti-inflammatory drugs, autoimmunity, gall reflux, allergic response and the histopathologic form ( Srivastava and Lauwers, 2007 ) .

Warren & A ; Marshall in 1984 discovered that H. pylori are the most frequent causative agent of gastritis. H. pylori gastritis is a primary infection of the tummy and is the most common cause of chronic gastritis ( Suzana et al. , 2009 ) . H. pylori are Gram-negative rods that have the ability to colonise and infect the stomachic mucous membrane. The bacterium survive within the mucose bed that covers the stomachic surface epithelial tissue and the upper parts of the stomachic foveolae. This being colonizes the stomachic mucous membrane in a assortment of ways: it is present free in mucous secretion every bit good as surface adhesion, intercellularly and sometimes intracellularly. Once the being has passed through the mucose bed, and has become established at the luminal surface of the tummy, an intense inflammatory response of the implicit in tissue develops.

It is estimated that half of the universe ‘s population is infected with H. pylori ( BauerA andA Meyer, 2011 ) . Infection withA H. pyloriA occurs worldwide, but the prevalence varies greatly among states and among population groups within the same state ( Suerbaum and Michetti, 2002 ) . World over at least 50 % of all people are infected, but an exact finding is non available, largely because exact informations are non available from developing states ( Salih, 2009 ) .A H. pylori infection is extremely prevailing in Asia and in developing states, and multifocal atrophic gastritis and stomachic glandular cancer are more prevailing in these countries ( Tanih et al. , 2009 ) . In the USA about 30-40 % of grownups are infected with H. pylori ( Everhart et al, 2000 ) . The prevalence of infection in minority groups and immigrants from developing states is much higher ( Mukherjee, 2012 ) . Poor hygiene and crowded conditions may ease transmittal of infection among the household members. The infection is related with poorness, limited instruction and abode in rural countries ( Turner, 2010 ) . In a big cross-sectional study of grownups in the United Kingdom, male gender, increasing age, shorter tallness, baccy usage, and lower socioeconomic position are all associated with positive H. pylori serology and the overall prevalence has been found to be 26 % ( Jackson et al. , 2009 ) .

In the underdeveloped states like Pakistan, India, Bangladesh and Thailand, infection with H. pylori is more frequent among general population and is acquired at an early age ( Singh and Ghoshal, 2006 ) . Harmonizing to a survey carried out in Pakistan 84 per centum patients with gastritis and 100 per centum with duodenal ulcer had H. pylori infection ( Shah et al. , 2008 ) . In Pakistan, H. pylori infection rate additions with promotion of age and lowering of socioeconomic position ( Qureshi et al. , 1999 ) . A survey in Pakistan revealed an early colonization/infection of babies with H. pylori and a prevalence of 67 % at 9 months of age in a peri-urban community in Karachi ( Nizami et al. , 2005 ) . In another survey done at Karachi the overall prevalence of H. pylori is 87.03 % and in chronic gastritis it is 66.66 % ( Asif et al. , 2011 ) .

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H. pylori infection is non merely linked to chronic gastritis but

besides to incomplete and seldom complete enteric metaplasia ( Khan et al. , 2003 ) , peptic ulcer, glandular cancer ( Schneller et al. , 2006 ) and stomachic lymphoma originating from mucous membrane associated lymphoid tissue ( MALT ) ( Kumar et al. , 2006 ) . H. pylori in its first colonisation cause an acute superficial gastritis including neutrophilic infiltration between surface and foveolar epithelial cells and within stomachic cavities. The surface epithelial tissue shows degenerative alterations with loss of mucin and increased exfoliation and the lamina propria is dropsical ( Suzana et al. , 2009 ) . Histological alterations of chronic gastritis include lymph cells, plasma cells infiltration and other inflammatory cells in lamina propria ( Alireza et al. , 2008 ) . Neutrophilic infiltration is seen in active instances of disease. Lymphoid sum with originative Centre can besides be observed. Chronic H. pylori gastritis exhibits more outstanding gastritis in the antrum than in the principal ( Dixon et al. , 1996 ) .

In disease of longer continuance, stomachic wasting and enteric metaplasia are observed ( Guarner et al. , 2001 ) . Harmonizing to the informations in the West, wasting and enteric metaplasia are premalignant conditions seen in patients with H. pylori associated chronic gastritis ( Micu et al. , 2010 ) . With enlargement of enteric metaplasia, the figure of H. pylori beings that are noticeable in the tummy decreases because H. pylori are excluded from countries of metaplastic epithelial tissue ( Mukherjee et al. , 2010 ) . The prevalence of wasting in Dutch patients is 42 % and in Chinese patients is 52 % . The prevelance of enteric metaplasia in China is 26 % and in Denmark is 32 % ( Chen et al. , 2001 ) . In the United Arab Republic ( high incidence of stomachic malignant neoplastic disease ) , the prevalence of wasting is 26 % , and enteric metaplasia is 11 % ( Zaitoun, 1994 ) . Significant betterments in gastricA atrophyA and enteric metaplasia after H. pylori obliteration may diminish the hazard of stomachic malignant neoplastic disease ( Khodama et al. , 2012 ) . Intestinal type stomachic malignant neoplastic disease may be the terminal phase in a patterned advance from simple gastritis to gastric wasting, metaplasia, dysplasia and carcinoma. The important measure is in these events is the development of wasting ( Wong et al. , 2004 ) . The remotion ofA H. pyloriA before the development of wasting appears to forestall carcinogenesis ( Wong et al. , 2004 ) . Therefore, the chief function of H. pyloriA in enteric type gastric malignant neoplastic disease appears to be the initiation of wasting, connoting that research should concentrate on this procedure. The H. pylori showing of population and intervention has the potency of dramatically cut downing planetary stomachic malignant neoplastic disease mortality ( Moayyedi and Hunt, 2004 ) . Furthermore, the bacterial denseness has been correlated with stomachic redness ( Gallo et al. , 2003 ) . A survey carried out at Civil Hospital, Karachi shows frequence of H. pyloriA in biopsy proven gastritis and its association with lymphoid follicle formation ( Siddiqui et al. , 2011 ) .

The Sydney System is a fresh categorization and scaling of gastritis that was devised by a group of experts at the 9th World Congress of Gastroenterology in Sydney, Australia in 1990. Experts emphasized the importance of uniting topographical, morphological and aetiologic information for the diagnostic rating of gastritis. In 1994 in Houston, Texas, experts devised the new Updated Sydney System ( Dixon et al. , 1996 ; Grieken et al. , 2001 ) . The duplicability of rating H. pylori related gastritis is high utilizing the Updated Sydney System. Therefore, a system which could prolong good duplicability in describing these observations is really of import ( Amoueian et al. , 2008 ) . The Updated Sydney System has a graduated table of 0-3 for hiting the characteristics of chronic gastritis ( Dixon et al. , 1996 ) . In order to better appraisal of minor grades of change, a elaborate histopathological categorization can be used, which besides provides numerical informations for statistical analysis. We did non happen any local literature back uping the important association of H. pylori burden or denseness with badness of wasting, enteric metaplasia, activity or grade of chronic inflammatory infiltrate. In order to turn to this issue the present survey was designed.


The purposes and aim of this survey in patients of chronic gastritis were to: ( a ) Determine the denseness of H. pylori.

( B ) Determine the grade of inflammatory activity, chronic inflammatory infiltrate, wasting and enteric metaplasia semi quantitatively.

( degree Celsius ) Explore the association of denseness of H. pylori with grade of:

Neutrophilic activity

Chronic inflammatory infiltrate


Intestinal metaplasia

Chapter 2



2.1.1 Gross Anatomy ( Snell, 2012 ) .

The tummy is situated in the upper portion of the venters, widening from beneath the left costal border part into the epigastric and umbilical parts. Much of the tummy lies under screen of the lower ribs. It is approximately J-shaped and has two gaps, the cardiac and pyloric openings ; two curvatures, the greater and lesser curvatures ; and two surfaces, an anterior and a posterior surface. The tummy is divided into the undermentioned parts:

Fundus is dome-shaped and undertakings upward and to the left of the cardiac opening. It is normally full of gas. Body extends from the degree of the cardiac opening to the degree of the incisure angularis, a changeless notch in the lower portion of the lesser curvature. Pyloric antrum extends from the incisure angularis to the pylorus. Pylorus is the most cannular portion of the tummy. The thick muscular wall is called the pyloric sphincter, and the pit of the pylorus is the pyloric canal.

The tummy has two curvatures, the lesser and the greater curvature. The cardiac opening is where the gorge enters the tummy. The pyloric opening is formed by the pyloric canal, which is about 1 in. ( 2.5 centimeter ) long.

Blood Supply

The arterias are derived from the subdivisions of the celiac arteria. The left stomachic arteria arises from the celiac arteria. It supplies the lower tierce of the gorge and the upper right portion of the tummy. The right gastric arteria arises from the hepatic arteria. It supplies the lower right portion of the tummy. The short gastric arterias arise from the splenetic arteria at the hilus of the lien and base on balls frontward in the gastrosplenic omentum ( ligament ) to provide the fundus. The left gastroepiploic arteria arises from the splenetic arteria at the hilus of the lien and passes frontward in the gastrosplenic omentum ( ligament ) to provide the tummy along the upper portion of the greater curvature. The right gastroepiploic arteria arises from the gastroduodenal subdivision of the hepatic arteria. It supplies the tummy along the lower portion of the greater curvature.

2.1.2 Histology ( Ross and Pawlina, 2011 )

The wall of the tummy is composed of four beds i.e. mucous membrane, submucosa, muscularis propria and serous membrane. The mucous membrane is thrown into outstanding creases and consists of stomachic secretory organs that extend from the degree of muscularis mucous membrane to open into stomach lms via stomachic cavities or foveoli. The submucosa is loose and distensible and contains larger blood vass. The muscularis propria is composed of inner oblique, in-between handbill and outer longitudinal beds. The serosal surface covers the peritoneal surface.

The different types of cells present in stomachic mucous membrane are: Surface mucous cells which line the luminal surface of the tummy and stomachic secretory organs. Neck mucose cells are present in the cervix and base of secretory organs. Parietal or oxyntic cells are distributed throughout the length of the secretory organ, but legion in the in-between part. These areA big, rounded cells with eosinophilic cytol and centrally located karyon which produce stomachic acid. Chief, peptic or zymogenic cells are clustered at the base of the secretory organ and are identified by basally located karyon and strongly basophilic farinaceous cytol. These are the pepsin releasing cells. Stem cells are found chiefly in the cervix of the stomachic secretory organs. These uniform cells divide continuously to replace all other cell types. Neuroendocrine cells are portion of diffuse neuroendocrine system and are present at the base of secretory organs.

The stomachic mucous membrane consists of surface epithelial tissue, stomachic cavities and stomachic secretory organs. The stomachic secretory organs extend from the muscular mucous membrane to widen into the tummy lms via stomachic cavities. The foveolar cells run alonging the surface and stomachic cavities are indistinguishable throughout the tummy. The stomachic secretory organs vary in different parts of tummy. Gastric pits occupy about 25 % of the mucous membrane. Pits lie parallel to one another. These are separated by the lamina propria. There is more lamina propria dividing the cavities than between the secretory organs. In normal stomachic biopsy grade ofA cavity and glandular separation should be the same through out the biopsy.

Cardia is the little country of preponderantly mucus releasing secretory organs environing the entryway of the gorge. Glands are less coiled than in the antral secretory organs. The cavities are shorter than the antropyloric cavities. The fundus or organic structure consists of heterosexual, cannular secretory organs. Strands of muscularis mucosae extend between the secretory organs from the base. The secretory organs secrete stomachic juices every bit good as protective mucous secretion so parietal and main cells are legion in fundic secretory organs. Pylorus or antrum, the secretory organs here are branched and unfastened into deep guerrilla shaped cavities. The secretory organs are composed of mucous secretion releasing cells. Mucus secreted by pyloric secretory organs lubricates and protects entryway to the duodenum. Scattered ‘G ‘ cells ( endocrinal cells ) , secrete gastrin.


The motor maps of the tummy are threefold:

( 1 ) Storage of big measures of nutrient until the nutrient can be processed in the tummy, duodenum, and lower enteric piece of land.

( 2 ) Mix of this nutrient with stomachic secernments until it forms a semii¬‚uid mixture called chyme

( 3 ) Slow voidance of the chyme from the tummy into the little bowel at a rate suited for proper digestion and soaking up by the little bowel ( Hall, 2011 ) .


H. pyloriA are Gram-negative bacteriums that infect the tummy. It is the cause of stomachic redness which is strongly linked to the development of gastric or duodenal ulcers. H. pylori survive in the extremely acidic pH of the tummy by releasing high sums of urease enzyme which serves as its protective covering. It is besides a extremely variable bacteria ; even in a individual septic patient, all the bacteriums are non indistinguishable due to its independent versions to the altering conditions in the tummy ( Castillo, 2010 ) .

2.3.1 History

During the 1970s, there was a sudden addition in the incidence of peptic ulcer disease and gastritis. In the twelvemonth 1979, due to his involvement in the new stomachic biopsies, Warren who was a life scientist, noticed little curved bacteriums turning on the surface of 50 % of the stomachic biopsies taken. These stomachic biopsies were taken from the antrum of the tummy of the patients. He besides noted marks of redness in the country where the bacteriums were seen.

Over the following 2 old ages, he fastidiously gathered legion illustrations of stomachic biopsies with the bacteriums and showed that it normally occurs with chronic gastritis. In 1981, Warren met Marshall who was a clinician to speak about the freshly found curved bacteriums from the stomachic biopsies. Together, the two

found that the bacteriums nowadays in about all patients with gastritis, duodenal ulcer or stomachic ulcer. The Nobel award in physiology or medical specialty of 2005 was awarded to Marshall and Warren for their find of bacteria H. pylori and its function in the development of gastritis and peptic ulcer disease in worlds ( Castillo, 2010 ) .

2.3.2 Structure

H.A pylori are motile, with a rapid cork-screw-like or slower wave-like gesture due to flagellar activity. Strains of most species have packages of multiple sheathed scourge with a polar or bipolar distribution. Other species have merely a individual polar or bipolar scourge ( Solnick and Vandamme, 2001 ) .

H. pylori are non spore forming gm negative bacteriums. The cellular morphology may be curved, coiling, or fusiform, typically 0.2 to 1.2 I?m in diameter and 1.5 to 10.0 I?m long. The coiling wavelength may change with the age, the growing conditions, and the species individuality of the cells. In old civilizations or those exposed to air, cells may go coccoid.


The disease most frequently presents as most preponderantly antral gastritis with high acid production, although the degrees of gastrin are low. In some patients the gastritis progresses to affect the organic structure or fundus. This pangastritis is associated with multifocal mucosal wasting, reduced acerb secernment, enteric metaplasia, and increased hazard of stomachic glandular cancer.

H. pylori beings have adapted to the ecologic niche provided by stomachic mucous secretion. Although H. pylori may occupy the gastric mucous membrane, this is non apparent histologically and the part of invasion to disease is non known. Four characteristics are linked to H. pylori virulency. These are as follows:

Flagella, which allow the bacteriums to be motile in syrupy mucous secretion.

Urease, which generates ammonia from endogenous urea and thereby elevates local stomachic pH.

Adhesins, which enhance their bacterial attachment to come up foveolar cells.

Toxins, such as cytotoxin-associated cistron A ( Cag A ) .that may be involved in ulcer or malignant neoplastic disease development by ill defined mechanisms ( Turner, 2010 ) .

2.4.1 Interaction between host and H. pylori

The chronic antral gastritis may come on to pangastritis, ensuing in multifocal atrophic gastritis. The interaction between host and H. pylori seems to play an of import function. Particular polymorphisms in the cistron encoding pro inflammatory cytokine interleukin-1B ( IL-1B ) and tumor mortification factor ( TNF ) influence the result in H. pylori infection. Badness of the disease may be influenced by familial fluctuation among H. pylori. For illustration, the CagA cistron, a marker of pathogenicity is present in 90 % of H. pylori isolates found in populations with elevated stomachic malignant neoplastic disease hazard ( Turner, 2010 ) .

2.4.2 Forms of H. pylori gastritis

In the bulk of septic persons, H. pylori gastritis is to some grade more marked in the antrum than in the principal. When there is a significant difference between the two compartments, such that there is minimum redness in the principal and marked engagement of the antrum, the gastritis is designated “ antral predominant. ” This form is found in patients with duodenal and prepyloric ulceration ( Dixon, 2001 ) .

If the H. pylori colonise the antrum of the tummy, the inflammatory response of the G cells in the site is to release more gastrin. The addition in gastrin will so trip the parietal cells in the principal of the tummy to bring forth more stomachic acids. Increase in acids amendss the duodenum and ulcerations may happen. On the other manus, if the H. pylori colonise the principal of the tummy where the acid releasing cells called parietal cells are located, there will be a pronounced lessening in acerb production and secernment which will finally do wasting of the tummy run alonging which may take to stomachic ulcers ( Castillo, 2010 ) .


2.5.1 Activity

The initial, acute stage of infection is subclinical in the great bulk of topics. Following consumption, organisms penetrate through the viscid mucose bed and multiply in close propinquity to the surface epithelial cells. The epithelial tissue responds to infection by mucin depletion, cellular exfoliation, and compensatory regenerative alterations. Neutrophils infiltrate into foveolar and surface epithelial tissue, and lamina propria hydrops is conspicuous. Collections of neutrophils in the foveolae or secretory organs ( pit abscesses ) and adherent neutrophilic exudation on the surface may besides be present. The acute stage is short lived. In a little minority of people, and peculiarly in childhood, the beings may be spontaneously cleared, the polymorph infiltrate resolutenesss, and visual aspects return to normal. In the bulk, nevertheless, the host immune response fails to extinguish the infection and over the following 3 or 4 hebdomads at that place is a gradual accretion of chronic inflammatory cells that come to rule the histological image. As a effect, the diagnosing of an acute neutrophilic gastritis gives manner to that of an active chronic gastritis ( Sobala et al. , 1991 ) .

2.5.2 Chronic inflammatory infiltrate

Diffuse chronic H. pylori gastritis preponderantly affects the pyloric mucous membrane. Although the inflammatory alterations are pantie in the principal, beings may be found throughout the surface mucous secretion. The mucous membrane shows a heavy inflammatory infiltrate, in which plasma cells are outstanding. In the principal any redness nowadays is confined to superficial zone. In the antral mucous membrane, the infiltrate is preponderantly superficial, but can affect the whole thickness and may divide the secretory organs without doing wasting. Lymphoid follicles with originative centres are normally seen in deeper parts of mucous membrane. This determination is pathognomonic for presence of H. pylori. The surface and foveolar epithelial tissue is infiltrated by neutrophils, which may be so outstanding that cavity abscesses are formed. This neutrophil infiltration is called active gastritis and is seen preponderantly in those countries where H. pylori are most abundant ( Owen, 2010 ) .

2.5.3 Atrophy

Atrophy in the tummy is conventionally defined as loss of glandular tissue from repeated or go oning mucosal hurt and is a common denominator in all pathological procedures doing progressive mucosal harm, including longstandingA H. pylori infection Thus, loss of secretory organs may follow eroding or ulceration of the mucous membrane, with devastation of the glandular bed, or as a consequence of a drawn-out inflammatory procedure in which single secretory organs undergo devastation. When such loss occurs, it is followed by hempen replacing. However, wasting can besides be thought of as merely “ a loss of specialised or functional cells. ” Under this broader definition it is possible to include state of affairss in which there is loss or replacing of parietal and head cells without glandular devastation ( Dixon, 2001 ) .

The prevalence ofA H. pylori positiveness declines with increasing glandular wasting. There are two chief grounds for the loss of beings. First, A H. pyloriA merely colonizes stomachic epithelial tissue ; therefore, the beings are absent from countries of complete enteric metaplasia. Second, the being merely thrives within the narrow pH scope provided by a partly acidic environment and the hypochlorhydric tummy is unfriendly toA H. pyloriA ( Clyne et al. , 1995 ) . Therefore, the failure to demonstrateA H. pyloriA in the atrophic tummy does non deny a function for infection in the causing of the implicit in gastritis.

2.5.4 Intestinal metaplasia

Metaplasia is defined as “ a potentially reversible alteration in which a to the full differentiated cell type is replaced by another differentiated cell type, and normally represents a alteration to cells better able to defy an inauspicious environment ” . Thus, enteric metaplasia represents a alteration from a stomachic epithelial phenotype to a small- or large-intestinal phenotype. Metaplasia is ever associated with some unnatural stimulation of growing, for illustration, during regeneration following mucosal hurt ( Mukawa et al. , 1987 ; Oohara et al. , 1983 ) .

Intestinal metaplasia is a common determination in chronic gastritis of all causes. A Its extent normally, but non constantly, parallels the development of wasting. Intestinal metaplasia is found more often inA H. pylori positive than negative instances ( Dixon, 2001 ) .

2.5.5 Lymphoid follicles

The normal stomachic mucous membrane contains really few lymph cells in the lamina propria. Lymphoid follicles and sums are characteristic of H. pylori associated gastritis ( Chen et al. , 2002 ) . H. pylori infection causes an immunological response, taking to chronic gastritis with formation of lymphoid follicles within the tummy. These lymphoid follicles resemble nodal tissues found throughout the organic structure and are composed of reactive T cells and activated plasma cells and B cells ( Ahmad et al. , 2003 ) .

Chapter 3


3.1 Setting

This survey was conducted in the Department of Pathology, Army Medical College, National University of Sciences and Technology and Military Hospital Rawalpindi, Pakistan.


December 2011 to November 2012


In this survey 100 biopsies of chronic gastritis patients were included.

3.4 Sampling Technique

Non chance convenience trying technique was used.


Inclusion standards:

Gastric antral biopsies of chronic gastritis patients of all ages and both sexes were included in the survey.

3.5.2 Exclusion standards:

Gastric biopsies of patients who were having or had received H. pylori obliteration intervention were non included in the survey.


A cross-sectional correlational survey


Permission of the ethical commission was taken. Biopsies of 100 dyspeptic patients holding H. pylori gastritis were enrolled prospectively into the survey. The specimens were largely received from the Gastroenterology unit of Military Hospital, Rawalpindi. The patients were both serving/ retired military forces every bit good as civilians populating in Rawalpindi and its suburbs. Patients of all ages and both sexes holding undergone stomachic biopsy were included in the survey. Specimens were taken as a whole in 10 % formal saline and were received in the Pathology Laboratory, Army Medical College, Rawalpindi. Sample of each patient were given a research lab figure and record was maintained.

3.7.1 Collection of clinical informations

The relevant clinical information and demographic information was obtained from the research lab petition signifier. Clinical information was collected prospectively from all survey participants in instances where it was non mentioned on petition signifier. Data included the undermentioned information: consequences of endoscopic probes, age, sex, symptoms, attendant medicine ( in peculiar consumption of proton pump inhibitors ( PPI ) , antibiotics or Bi salts, not steroidal anti inflammatory drugs ) . History sing relevant old and attendant diseases including abdominal surgery was taken. All the information was entered in patient ‘s proforma ( Annexure I ) .

3.8 TISSUE Processing

3.8.1 Specimens Processing

The tissue was taken as whole on filter paper and enclosed in decently labeled plastic cassettes with pierced walls and was placed in LEICA TP 1020 ( Germany ) automatic tissue processor. The undermentioned processing agenda was followed. Dehydration

Dehydration was done in go uping series of intoxicant

80 % intoxicant 1 hr

95 % intoxicant 1 hr

Absolute intoxicant – I 1 hr

Absolute intoxicant – II 1 hr Clearing

Two alterations of xylol were used.

Xylene – I 2 hours

Xylene -II 2 hours Impregnation

Paraffin with runing point 56-58 degree Celsius was used for this intent.

First alteration 2 hours

Second alteration 2 hours Embedding

Paraffin implanting Centre ( LEICA EG 1160- Germany ) was usage for this intent. Filtered paraffin with runing point 56-58 degree Celsius was used for implanting. Blocks were made utilizing fictile cassettes. Each cassette was filled with liquefied paraffin wax and tissue was placed in the centre of the cassette. The cassette was so allowed to chill on the cold home base of the paraffin implanting Centre.

3.8.2 Segmenting

Paraffin blocks were placed in block holder of rotary microtome, LEICA RM 22.5 ( Germany ) , and 3-4 um thick subdivisions were made. Sections were floated in warm H2O bath at 45 degree Celsiuss and were taken individually on 2 different slides, which were albumin coated. Slides were farther dipped horizontally in 70 % intoxicant bath to take any folds. The slides were kept in a aslant place for about half an hr to run out surplus of H2O. The subdivision was so dried on hot oven at 60c for about 15-30 proceedingss.

3.8.3 Staining

Following discoloration was used in LEICA autostainer ( Germany ) Forty.

Haematoxylin and Eosin ( H & A ; E ) discoloration for everyday histology ( Appendix II ) .

Giemsa discoloration was used for presentation of H. pylori ( Appendix III ) .


The stomachic biopsies were scored semi quantitatively harmonizing to Updated Sydney System ( Dixon et al. , 1996 ) . The Updated Sydney System has a graduated table of 0-3 for hiting the characteristics of chronic gastritis. In order to better appraisal of minor grades of change, a elaborate histopathological categorization was used, which besides provided numerical informations for statistical analysis ( Chen et al. , 1999 ) . The undermentioned histopathological parametric quantities were examined on each slide: denseness of H. pylori, inflammatory activity, chronic redness, wasting and enteric metaplasia. Each class ( mild, moderate, and severe ) was divided into two subcategories, ensuing in a mark on a graduated table of 0-6 ( none, 0 ; mild, 1-2 ; moderate, 3-4 ; terrible, 5-6 ) . Harmonizing to this categorization, the histopathological parametric quantities were graded as follows:

3.9.1 Density of H. pylori colonisation:

The denseness of H. pylori was graded as follows:

0: none

1: H. pylori found merely in one topographic point after a careful hunt

2: merely a few H. pylori found

3: scattered H. pylori found in separate focal point

4: legion H. pylori in separate focal point

5: about complete stomachic surface covered by bed of H. pylori

6: uninterrupted stomachic surface covered by a thick bed of H. pylori

3.9.2 Degree of inflammatory activity:

The grade of inflammatory activity was graded harmonizing to the denseness of neutrophils in the stomachic mucous membrane:

0: none

1: merely one crypt involved per biopsy

2: two crypts involved per biopsy

3: many crypts ( up to 25 % ) involved per biopsy

4: 25-50 % of crypts involved per biopsy

5: more than 50 % crypts involved per biopsy

6: all crypts involved

3.9.3 Degree of chronic inflammatory infiltrate:

The grade of chronic inflammatory infiltrate was graded as follows:

1: scattered chronic inflammatory cells & lt ; 10 cells / high power field

2: scattered chronic inflammatory cells & gt ; 10 cells /high power field

3: some countries with dense chronic inflammatory cells

4: diffuse infiltration with dense chronic inflammatory cells

5: about the whole mucous membrane contains heavy infiltrate which separates stomachic secretory organs

6: full mucous membrane contains a dense chronic inflammatory cell infiltrate

3.9.4 Degree of wasting:

Atrophy was graded as follows:

0: none

1: focal point where a few stomachic secretory organs are lost or replaced by enteric type of epithelial tissue

2: little countries in which stomachic secretory organs are lost or replaced by enteric type of epithelial tissue

3: up to 25 % stomachic glands lost or replaced by enteric type of epithelial tissue

4: 25-50 % of stomachic secretory organs lost or replaced by enteric type of epithelial tissue

5: more than 50 % of stomachic secretory organs lost or replaced by enteric type of epithelial tissue

6: merely a few little countries of stomachic secretory organs staying

3.9.5 Degree of enteric metaplasia:

The grade of enteric metaplasia was graded harmonizing to the extent of glandular tissue replaced by enteric type of epithelial tissue:

0: none

1: merely one focal point ( one crypt ) replaced by enteric epithelial tissue

2: one focal country ( 1-4 crypts ) replaced by enteric epithelial tissue

3: two separate focal points

4: multiple focal point in the biopsy

5: & gt ; 50 % epithelial tissue replaced by enteric epithelial tissue

6: merely a little country of stomachic epithelial tissue is non replaced by enteric metaplasia

Non quantitative variables

Non quantitative histopathological characteristics like lymphoid sums, ulcer gangrene, superficial epithelial harm and atomic reactive alterations were non graded, but merely assessed in instance of their presence or absence. Dysplasia was besides assessed as an of import factor in the histological sequence taking to stomachic malignant neoplastic disease.


All information was collected through specifically designed proforma ( Appendix I ) . Findingss were entered and analyzed through SPSS version 17. Quantitative variables were represented utilizing frequence and per centums. Spearman ‘s rank correlativity trial was used for ciphering relationship between H. pylori denseness and other variables. The experimental findings were considered statistically important if p value was less than 0.05 ( P & lt ; 0.05 ) .

3.10.1 Spearman ‘s Rank Order Correlation utilizing SPSS

The Spearman ‘s rank-order correlativity is the nonparametric version of theA Pearson product-moment correlativity. Spearman ‘s correlativity coefficient measures the strength and way of association between two ranked variables measured on an ordinal graduated table. It is denoted by the symbolA rsA ( or the Greek letterhttps: //, marked rho ) and measures the inclination of Y to increase or diminish as Ten additions. The trial is used for either ordinal variables or for interval informations that has failed the premises necessary for carry oning the Pearson ‘s product-moment correlativity.


3.10.2 Interpretation of Spearman ‘s Rank Order Correlation CoefficientA rsA

Spearman ‘s Rank Order Correlation Coefficient rsA

Strength of Association




0.1 to 0.5

-0.1 to -0.5


0.5 to 0.75

-0.5 to -0.75


0.75 to 1.0

-0.75 to -1.0


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