H.pylori gastritis pathophysiology: Difference between revisions

Jump to navigation Jump to search
VisualWikitext
 
(32 intermediate revisions by the same user not shown)
Line 4: Line 4:


==Overview==
==Overview==
 
The ''[[H. pylori]]'' induced [[gastritis]] includes the following stages. They are [[acute gastritis]], active chronic gastritis, [[atrophy]] and [[metaplasia|intestinal metaplasia]].


==Pathophysiology==
==Pathophysiology==
The H.pylori induced gastritis includes the following stages: They are
*The ''[[H. pylori]]'' induced [[gastritis]] includes the following stages: They are
*The acute gastritis
:*The [[acute gastritis]]
*Active chronic gastritis
:*Active chronic gastritis
*Atrophy
:*[[Atrophy]]
*Intestinal metaplasia
:*[[Metaplasia|Intestinal metaplasia]]
*The ''[[H. pylori]]'' induced [[gastritis]] is classified based on location into:
:*Antral predominant gastritis
:*Corpus predominant gastritis


=='''The acute gastritis'''==
=='''The acute gastritis'''==
 
*In the majority of patients, the initial acute phase of [[gastritis]] is [[subclinical infection|subclinical]] and is of short duration (about 7 to 10 days).  
*In majority of patients, the initial acute phase of gastritis is subclinical (does not often give rise to clinical symptoms) and is of short duration (about 7 to 10 days).  
*The organisms are spontaneously cleared in a small minority of people, especially in childhood.
*The organisms are spontaneously cleared in a small minority of people, especially in childhood.
*In the majority of cases, the infection is not eliminated and there will be gradual accumulation of chronic inflammatory cells over the next 3 or 4 weeks.<ref name="pmid1752479">{{cite journal| author=Sobala GM, Crabtree JE, Dixon MF, Schorah CJ, Taylor JD, Rathbone BJ et al.| title=Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations. | journal=Gut | year= 1991 | volume= 32 | issue= 11 | pages= 1415-8 | pmid=1752479 | doi= | pmc=1379180 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1752479  }} </ref>
*In the majority of cases, the infection is not eliminated and there will be gradual accumulation of chronic inflammatory cells over the next 3 or 4 weeks.<ref name="pmid1752479">{{cite journal| author=Sobala GM, Crabtree JE, Dixon MF, Schorah CJ, Taylor JD, Rathbone BJ et al.| title=Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations. | journal=Gut | year= 1991 | volume= 32 | issue= 11 | pages= 1415-8 | pmid=1752479 | doi= | pmc=1379180 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1752479  }} </ref>


<small>'''pathogenesis'''</small>
==='''pathogenesis'''===
*Following transmission, H.pylori penetrates the mucous layer of stomach and multiplies close to the surface epithelial cells.
*Following transmission, ''[[H. pylori]]'' penetrates the [[gastric mucosa]] and multiplies close to the surface [[epithelial cells]].
*Following adhesion to epithelial cells, the bacteria releases lipopolysaccharides (endotoxin) and chemotactic mediators which penetrate the surface epithelial cells.<ref name="pmid9861460">{{cite journal| author=Slomiany BL, Piotrowski J, Slomiany A| title=Induction of caspase-3 and nitric oxide synthase-2 during gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide. | journal=Biochem Mol Biol Int | year= 1998 | volume= 46 | issue= 5 | pages= 1063-70 | pmid=9861460 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9861460  }} </ref>Crabtree, J. E. "Gastric mucosal inflammatory responses to Helicobacter pylori." Alimentary pharmacology & therapeutics 10.Sup1 (1996): 29-37.
*Following adhesion to [[epithelial cells]], the [[bacteria]] releases [[lipopolysaccharides]] ([[endotoxin]]) and [[chemotaxis|chemotactic mediators]] which penetrate the surface epithelial cells.<ref name="pmid9861460">{{cite journal| author=Slomiany BL, Piotrowski J, Slomiany A| title=Induction of caspase-3 and nitric oxide synthase-2 during gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide. | journal=Biochem Mol Biol Int | year= 1998 | volume= 46 | issue= 5 | pages= 1063-70 | pmid=9861460 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9861460  }} </ref><ref name="pmid8730257">{{cite journal| author=Crabtree JE| title=Gastric mucosal inflammatory responses to Helicobacter pylori. | journal=Aliment Pharmacol Ther | year= 1996 | volume= 10 Suppl 1 | issue=  | pages= 29-37 | pmid=8730257 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8730257  }} </ref>
*These bacterial factors attract the polymorphonuclear leukocytes to the site of infection and also caused mast cell degranulation, which releases acute inflammatory mediators. Mast cell degranulation leads to:
*These bacterial factors attract the [[polymorphonuclear leukocytes]] to the site of [[infection]] and also caused [[degranulation|mast cell degranulation]], which releases acute inflammatory mediators. [[Degranulation|Mast cell degranulation]] leads to:
:*Increased vascular permeability
:*Increased [[vascular permeability]]
:*Increased polymorph emigration
:*Increased [[polymorphonuclear leukocytes]] [[emigration]]
:*Increased expression of leukocyte adhesion molecules
:*Increased expression of [[cell adhesion molecules|leukocyte adhesion molecules]]
:*The platelet activating factors (PAF) released from mast cells causes microthrombosis in mucosal capillaries resulting in hypoxic injury to the epithelium  
:*The [[platelet activating factor|platelet activating factors (PAF)]] released from [[mast cells]] causes [[thrombosis|microthrombosis]] in [[capillary|mucosal capillaries]] resulting in [[hypoxia|hypoxic injury]] to the [[epithelium]]
*The macrophages release IL-1 and tumor necrosis factor alpha (TNF-α) which stimulates gastric epithelium to produce IL-8.
*The [[macrophages]] release [[IL-1]] and [[tumor necrosis factor alpha|tumor necrosis factor alpha (TNF-α)]] which stimulates gastric epithelium to produce [[IL-8]].
*The acute phase is associated with profound hypochlorhydria and a decreased ascorbic acid secretion into the gastric juice.<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949  }} </ref>
*The acute phase is associated with profound [[hypochlorhydria]] and a decreased [[ascorbic acid]] secretion into the [[gastric juice]].<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949  }} </ref>
*The acid output reaches pre-infection levels after several weeks but the ascorbic acid remains lower than normal for the duration of chronic gastritis, indicating that it is due to persisting inflammation rather than hypochlorhydria.<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949  }} </ref>
*The acid output reaches pre-infection levels after several weeks but the [[ascorbic acid]] remains lower than normal for the duration of [[chronic]] [[gastritis]], indicating that it is due to persisting [[inflammation]] rather than [[hypochlorhydria]].<ref name="pmid8174949">{{cite journal| author=Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF et al.| title=Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations. | journal=Gut | year= 1993 | volume= 34 | issue= 8 | pages= 1038-41 | pmid=8174949 | doi= | pmc=1374349 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8174949  }} </ref>


<small>'''Histology'''</small>
===='''Microscopic pathology'''====
*Surface epithelial degeneration
*Surface epithelial [[degeneration]]
*Increased cell exfoliation
*Increased cell [[exfoliation]]
*Increased neutrophil polymorphonuclear leucocytes in the superficial lamina propria
*Increased [[neutrophil]] polymorphonuclear [[leucocytes]] in the superficial [[lamina propria]]


=='''Active chronic gastritis'''==
=='''Active chronic gastritis'''==
In majority of cases, the h.pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis.
In the majority of cases, the ''[[H. pylori]] infection persists leading to accumulation of large number [[chronic]] [[inflammatory cells]] leading to active chronic gastritis.


<small>'''Pathogenesis'''</small>
==='''Pathogenesis'''===
*The major diagnostic feature of chronic gastritis is an influx of lymphocytes and plasma cells (normally the antral mucosa is devoid of plasma cells and lymphocytes). Hence the presence of these cells is indicative of gastritis.<ref name="pmid8505036">{{cite journal| author=Genta RM, Hamner HW, Graham DY| title=Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy. | journal=Hum Pathol | year= 1993 | volume= 24 | issue= 6 | pages= 577-83 | pmid=8505036 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8505036  }} </ref>
*The major diagnostic feature of chronic gastritis is an influx of [[lymphocytes]] and [[plasma cells]] (normally the antral mucosa is devoid of [[plasma cells]] and [[lymphocytes]]). Hence the presence of these cells is indicative of [[gastritis]].<ref name="pmid8505036">{{cite journal| author=Genta RM, Hamner HW, Graham DY| title=Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy. | journal=Hum Pathol | year= 1993 | volume= 24 | issue= 6 | pages= 577-83 | pmid=8505036 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8505036  }} </ref>
*H.pylori colonizes more in the antrum than the corpus. Hence there is increased inflammatory cell infiltration in the antrum.
*''[[H. pylori]] colonizes more in the [[antrum]] than the corpus. Hence there is increased inflammatory cell infiltration in the antrum.
*The direct acting antigens of H pylori like lipopolysaccharides, urease etc along with interleukins 1 and 6, activate T-helper cells which produce variety of cytokines including IL4, IL5 and IL6.
*The direct acting [[antigens]] of ''[[H. pylori]]'' like [[lipopolysaccharides]], [[urease]] etc along with [[interleukins|interleukins 1 and 6]], activate [[T-helper cells]] which produce the variety of [[cytokines]] including [[IL4]], [[IL5]], and [[IL6]].
*These interluekins differentiate into plasma cells releasing cytokines and anti-H.pylori infection like IgM-opsonizing and complement-fixing antibodies.  
*These [[interleukins]] differentiate into [[plasma cells]] releasing [[cytokines]] and anti-H.pylori infection like [[opsonization|IgM-opsonizing]] and complement-fixing antibodies.  
*The main role of the mucosa immune response is taht the IgA prevents bacterial adhesion and IgG causes opsonisation and complement activation.
*The main role of the [[mucosa]] in the immune response is that the [[IgA]] prevents bacterial adhesion and [[IgG]] causes [[opsonization]] and [[complement]] activation.
*Due to acidic environment, the antibodies produced quickly lose their adhesive properties and catalase produced by H.pylori protects against polymorphs.
*Due to the acidic environment, the [[antibodies]] produced quickly lose their adhesive properties and [[catalase]] produced by ''[[H. pylori]]'' protects against polymorphs.
*However, this immune response is insufficient to eradicate the organism leading to development of immune response directed towards preventing the damaging effects of the H.pylori.
*However, this immune response is insufficient to eradicate the organism leading to the development of immune response directed towards preventing the damaging effects of the ''[[H. pylori]]''.
*Hence the persistent antigenic stimulation leads to formation of follicles, which is the consistent feature of chronic H.pylori infection.
*Hence the persistent antigenic stimulation leads to the formation of [[lymphoid follicles]], which is the consistent feature of chronic ''[[H. pylori]]'' infection.
*These lymphoid follicles in the gastric mucosa constitutes mucosa-associated lymphoid tissue (MALT) from which gastric mariginal zone (B-cell) lymphoma (MALToma) arises.
*These [[lymphoid follicles]] in the [[gastric mucosa]] constitutes [[MALT|mucosa-associated lymphoid tissue (MALT)]] from which gastric [[marginal zone]] [[B-cell lymphoma|B-cell lymphoma (MALToma)]] arises.
*Also, these polymorphs accumulate around the pit isthmus, which is a proliferative compartment, causing lethal damage to stem cells resulting in glandular atrophy.
Also, these [[polymorphs]] accumulate around the pit isthmus, which is a proliferative compartment, causing lethal damage to [[stem cells]] resulting in glandular atrophy.


<small>'''Histopathogenesis'''</small>
===='''Microscopic pathology'''====
*Variable epithelial degeneration
*Variable epithelial [[degeneration]]
*Neutrophil infiltration in the epithelium and the lamina propria
*[[Neutrophil]] infiltration in the epithelium and the [[lamina propria]]
*Variable H.pylori colonisation
*Variable ''[[H. pylori]]'' colonization
*lymphocytes and plasma cell infiltration
*[[Lymphocytes]] and [[plasma cell]] infiltration
*Lymphoid follicles(typical feature of chronic gastritis)
*[[Lymphoid follicles]] (typical feature of chronic gastritis)
<gallery>
Sydney system of grading of chronic gastritis<ref name="pmid8827022">{{cite journal| author=Dixon MF, Genta RM, Yardley JH, Correa P| title=Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. | journal=Am J Surg Pathol | year= 1996 | volume= 20 | issue= 10 | pages= 1161-81 | pmid=8827022 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8827022  }} </ref>
{| class="wikitable"
!Feature
!Definition
!Grading guidelines
|-
|Chronic inflammation
|Increased [[lymphocytes]] and [[plasma cells]] in [[lamina propria]]
|
* Mild, moderate or severe increase in density
|-
|Activity
|[[Neutrophil|Neutrophilic]] infiltrates of the [[lamina propria]], pits or surface [[epithelium]]
|
* Mild: less than one-third of pits and surface infiltrated
* Moderate: one-third to two-thirds
* Severe: more than two-thirds
|-
|[[Atrophy]]
|Loss of specialized glands from either antrum or corpus
|
* Mild, moderate, or severe loss
|-
|''[[Helicobacter pylori]]''
|''[[H. pylori]]'' density
|
* Mild colonization: scattered organisms covering less than one-third of the surface
* Moderate colonization: intermediate numbers
 
* Severe colonization: large clusters or a continuous layer over two-thirds of surface
|-
|Intestinal [[Metaplasia]]
|Intestinal [[metaplasia]] of the epithelium
|
* Mild: less than one-third of mucosa involved
* Moderate: one-third to two-thirds
* Severe: more than two-thirds
|}


=='''Atrophy'''==
=='''Atrophy'''==
Atrophy of stomach is defined as loss of glandular tissue due to continuous mucosal injury. This leads to thinning of gastric mucosa.
[[Atrophy]] of [[stomach]] is defined as loss of glandular tissue due to continuous mucosal injury. This leads to thinning of [[gastric mucosa]].
*The prevalence and severity of atrophy of stomach increases with age among the patients chronic gastritis due to longer duration of H.pylori infection.
*The [[prevalence]] and severity of [[atrophy]] of [[stomach]] increases with age among the patient's [[chronic]] [[gastritis]] due to longer duration of ''[[H. pylori]]'' infection.
*Due to glandular atrophy, the prevalence of H.pylori positivity decreases. The main reasons are as follows:
*Due to glandular [[atrophy]], the prevalence of ''[[H. pylori]]'' positivity decreases. The main reasons are as follows:
:*Due to intestinal metaplasia that are usually present in atrophic stomachs, the organisms are absent as they usually colonizes only gastric epithelium.
:*Due to intestinal [[metaplasia]] that is usually present in atrophic stomachs, the organisms are absent as they usually colonize only gastric epithelium.
:*As ''[[H. pylori]]'' requires partially acidic environment to thrive, [[hypochlorhydria]] creats hostile environment to ''[[H. pylori]]'' to survive.<ref name="pmid1916500">{{cite journal| author=Neithercut WD, Milne A, Chittajallu RS, el Nujumi AM, McColl KE| title=Detection of Helicobacter pylori infection of the gastric mucosa by measurement of gastric aspirate ammonium and urea concentrations. | journal=Gut | year= 1991 | volume= 32 | issue= 9 | pages= 973-6 | pmid=1916500 | doi= | pmc=1379031 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1916500  }} </ref>
:*The [[metaplasia|metaplastic epithelium]] secretes acidic [[glycoproteins]] which create the most hostile environment for ''[[H. pylori]]''.
*Hence, based on above reasons, failure to demonstrate ''[[H. pylori]]'' does not deny the role of the organism in [[atrophic gastritis]].
 
==='''Pathogenesis'''===
*The continuous mucosal injury due to long-standing ''[[H. pylori]] infection, leads to [[atrophy]] of stomach.
*This continuous pathological process results in [[gastric erosion|erosion]] or [[ulcer|ulceration]] of the mucosa leading to the destruction of the glandular layer and followed by fibrous replacement.
*The destruction of the glandular [[basement membrane]] and the sheath of supporting cells prevents orderly regeneration. This uneven regeneration follows a divergent differentiation pathway producing [[metaplasia|metaplastic glands]] (pseudo-pyloric appearance) which are composed of cells of the 'ulcer-associated cell lineage'(UACL).<ref name="pmid11358897">{{cite journal| author=Pera M, Heppell J, Poulsom R, Teixeira FV, Williams J| title=Ulcer associated cell lineage glands expressing trefoil peptide genes are induced by chronic ulceration in ileal pouch mucosa. | journal=Gut | year= 2001 | volume= 48 | issue= 6 | pages= 792-6 | pmid=11358897 | doi= | pmc=1728308 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11358897  }} </ref>
 
===='''Microscopic pathology'''====
*Reduced number of [[oxyntic cells]]. No intestinal [[metaplasia]]
*The [[mucosa]] is infiltrated with [[neutrophils]]
*''[[H. pylori]]'' is not seen on [[H&E stain]]. [[Immunohistochemical|immunohistochemical stain]] of ''[[H. pylori]]'' detects the organisms.
 
=='''Intestinal metaplasia'''==
*The intestinal metaplasia increase in [[prevalence]] according to duration of ''[[H. pylori]]'' infection.<ref name="pmid1612473">{{cite journal| author=Craanen ME, Blok P, Dekker W, Ferwerda J, Tytgat GN| title=Subtypes of intestinal metaplasia and Helicobacter pylori. | journal=Gut | year= 1992 | volume= 33 | issue= 5 | pages= 597-600 | pmid=1612473 | doi= | pmc=1379284 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1612473  }} </ref>
*The damaged [[epithelium]] by ''[[H. pylori]]'' infection will be further eroded by bile reflux and replaced by intestinal type cells during the regenerative process. This [[metaplasia]] is transient but with repetitive injury it aggravates and become more permanent.<ref name="pmid12477745">{{cite journal| author=Walker MM| title=Is intestinal metaplasia of the stomach reversible? | journal=Gut | year= 2003 | volume= 52 | issue= 1 | pages= 1-4 | pmid=12477745 | doi= | pmc=1773527 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12477745  }} </ref>
*Hence ''[[H. pylori]]'' infection and [[bile reflux]] are independent risk factors for intestinal [[metaplasia]] of [[stomach]].
*Intestinal metaplasia is a protective mechanism as ''[[H. pylori]]'' does not attach to intestinal-type cells and also intestinal cells are more resistant to damaging effects of bile than [[gastric mucosa]].


<Small>'''Pathogenesis'''</small>
====Microscopic pathology====
*The continuous mucosal injury due to long standing H.pylori infection, leads to atrophy of stomach.
*Absence of ''[[H. pylori]]''
*This continuous pathological process results in erosion or ulceration of the mucosa leading to destruction of the glandular layer and followed by fibrous replacement.
*[[Gastric mucosa|Gastric mucosal cells]] replaced by [[epithelium]] resembling intestinal cells
*The destruction of the glandular basement membrane and the sheath of supporting cells prevents orderly regeneration. This uneven regenration follows a divergent differentiation pathway producing metaplastic glands (pseudo-pyloric appearance) which are composed of cells of the 'ulcer-associated cell lineage'(UACL).<ref name="pmid11358897">{{cite journal| author=Pera M, Heppell J, Poulsom R, Teixeira FV, Williams J| title=Ulcer associated cell lineage glands expressing trefoil peptide genes are induced by chronic ulceration in ileal pouch mucosa. | journal=Gut | year= 2001 | volume= 48 | issue= 6 | pages= 792-6 | pmid=11358897 | doi= | pmc=1728308 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11358897  }} </ref>


=='''Updated Sydney classification (Sydney criteria for gastritis)'''==
=='''Updated Sydney classification (Sydney criteria for gastritis)'''==


The updated sydney classification of H.pylori induced classification include:<ref name="pmid8827022">{{cite journal| author=Dixon MF, Genta RM, Yardley JH, Correa P| title=Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. | journal=Am J Surg Pathol | year= 1996 | volume= 20 | issue= 10 | pages= 1161-81 | pmid=8827022 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8827022  }} </ref>
The updated sydney classification of ''[[H. pylori]]'' induced classification include:<ref name="pmid8827022">{{cite journal| author=Dixon MF, Genta RM, Yardley JH, Correa P| title=Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994. | journal=Am J Surg Pathol | year= 1996 | volume= 20 | issue= 10 | pages= 1161-81 | pmid=8827022 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8827022  }} </ref>
{| class="wikitable"
{| class="wikitable"
!Feature
!Feature
Line 85: Line 142:
|Corpus only
|Corpus only
|-
|-
|Atrophy & metaplasia
|[[Atrophy]] & [[metaplasia]]
|Nil
|Nil
|Atrophy present, metaplasia at incisura
|Atrophy present, metaplasia at incisura
|Corpus only
|Corpus only
|}
{| class="wikitable"
!Antral predominant gastritis
!Corpus predominant gastritis
|-
|More predominant in antrum in developed countries
|Less predominant in developed countries
|-
|High acid output
|Low acid output
|-
|Associated with duodenal ulceration
|
|}
|}


==References==
==References==
{{Reflist|2}}
{{Reflist|2}}

Latest revision as of 02:05, 23 January 2017

Helicobacter pylori infection Microchapters

Home

Patient Information

Overview

Historical Perspective

Classification

Pathophysiology

Gastritis
Peptic ulcer disease
Gastric adenocarcinoma
MALT lymphoma

Causes

Differentiating Helicobacter pylori infection from other Diseases

Epidemiology and Demographics

Risk Factors

Screening

Natural History, Complications and Prognosis

Diagnosis

Guideline Recommendation

ACG guidelines
ESPGHAN and NASPGHAN guidelines

History and Symptoms

Physical Examination

Diagnostic tests

Endoscopic tests
Nonendoscopic tests

Electrocardiogram

X Ray

CT

MRI

Ultrasound

Other Diagnostic Studies

Treatment

Medical Therapy

Surgery

Primary Prevention

Secondary Prevention

Cost-Effectiveness of Therapy

Future or Investigational Therapies

Case Studies

Case #1

H.pylori gastritis pathophysiology On the Web

Most recent articles

Most cited articles

Review articles

CME Programs

Powerpoint slides

Images

American Roentgen Ray Society Images of H.pylori gastritis pathophysiology

All Images
X-rays
Echo & Ultrasound
CT Images
MRI

Ongoing Trials at Clinical Trials.gov

US National Guidelines Clearinghouse

NICE Guidance

FDA on H.pylori gastritis pathophysiology

CDC on H.pylori gastritis pathophysiology

H.pylori gastritis pathophysiology in the news

Blogs on H.pylori gastritis pathophysiology

Directions to Hospitals Treating Helicobacter pylori infection

Risk calculators and risk factors for H.pylori gastritis pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]

Overview

The H. pylori induced gastritis includes the following stages. They are acute gastritis, active chronic gastritis, atrophy and intestinal metaplasia.

Pathophysiology

  • Antral predominant gastritis
  • Corpus predominant gastritis

The acute gastritis

  • In the majority of patients, the initial acute phase of gastritis is subclinical and is of short duration (about 7 to 10 days).
  • The organisms are spontaneously cleared in a small minority of people, especially in childhood.
  • In the majority of cases, the infection is not eliminated and there will be gradual accumulation of chronic inflammatory cells over the next 3 or 4 weeks.[1]

pathogenesis

Microscopic pathology

Active chronic gastritis

In the majority of cases, the H. pylori infection persists leading to accumulation of large number chronic inflammatory cells leading to active chronic gastritis.

Pathogenesis

Also, these polymorphs accumulate around the pit isthmus, which is a proliferative compartment, causing lethal damage to stem cells resulting in glandular atrophy.

Microscopic pathology

Sydney system of grading of chronic gastritis[6]

Feature Definition Grading guidelines
Chronic inflammation Increased lymphocytes and plasma cells in lamina propria
  • Mild, moderate or severe increase in density
Activity Neutrophilic infiltrates of the lamina propria, pits or surface epithelium
  • Mild: less than one-third of pits and surface infiltrated
  • Moderate: one-third to two-thirds
  • Severe: more than two-thirds
Atrophy Loss of specialized glands from either antrum or corpus
  • Mild, moderate, or severe loss
Helicobacter pylori H. pylori density
  • Mild colonization: scattered organisms covering less than one-third of the surface
  • Moderate colonization: intermediate numbers
  • Severe colonization: large clusters or a continuous layer over two-thirds of surface
Intestinal Metaplasia Intestinal metaplasia of the epithelium
  • Mild: less than one-third of mucosa involved
  • Moderate: one-third to two-thirds
  • Severe: more than two-thirds

Atrophy

Atrophy of stomach is defined as loss of glandular tissue due to continuous mucosal injury. This leads to thinning of gastric mucosa.

Pathogenesis

  • The continuous mucosal injury due to long-standing H. pylori infection, leads to atrophy of stomach.
  • This continuous pathological process results in erosion or ulceration of the mucosa leading to the destruction of the glandular layer and followed by fibrous replacement.
  • The destruction of the glandular basement membrane and the sheath of supporting cells prevents orderly regeneration. This uneven regeneration follows a divergent differentiation pathway producing metaplastic glands (pseudo-pyloric appearance) which are composed of cells of the 'ulcer-associated cell lineage'(UACL).[8]

Microscopic pathology

Intestinal metaplasia

  • The intestinal metaplasia increase in prevalence according to duration of H. pylori infection.[9]
  • The damaged epithelium by H. pylori infection will be further eroded by bile reflux and replaced by intestinal type cells during the regenerative process. This metaplasia is transient but with repetitive injury it aggravates and become more permanent.[10]
  • Hence H. pylori infection and bile reflux are independent risk factors for intestinal metaplasia of stomach.
  • Intestinal metaplasia is a protective mechanism as H. pylori does not attach to intestinal-type cells and also intestinal cells are more resistant to damaging effects of bile than gastric mucosa.

Microscopic pathology

Updated Sydney classification (Sydney criteria for gastritis)

The updated sydney classification of H. pylori induced classification include:[6]

Feature Non-atrophic

Helicobacter

Atrophic Helicobacter Autoimmune
Inflammation pattern Antral or diffuse Antrum & corpus, mild inflammation Corpus only
Atrophy & metaplasia Nil Atrophy present, metaplasia at incisura Corpus only
Antral predominant gastritis Corpus predominant gastritis
More predominant in antrum in developed countries Less predominant in developed countries
High acid output Low acid output
Associated with duodenal ulceration

References

  1. ↑ Sobala GM, Crabtree JE, Dixon MF, Schorah CJ, Taylor JD, Rathbone BJ; et al. (1991). "Acute Helicobacter pylori infection: clinical features, local and systemic immune response, gastric mucosal histology, and gastric juice ascorbic acid concentrations". Gut. 32 (11): 1415–8. PMC 1379180. PMID 1752479.
  2. ↑ Slomiany BL, Piotrowski J, Slomiany A (1998). "Induction of caspase-3 and nitric oxide synthase-2 during gastric mucosal inflammatory reaction to Helicobacter pylori lipopolysaccharide". Biochem Mol Biol Int. 46 (5): 1063–70. PMID 9861460.
  3. ↑ Crabtree JE (1996). "Gastric mucosal inflammatory responses to Helicobacter pylori". Aliment Pharmacol Ther. 10 Suppl 1: 29–37. PMID 8730257.
  4. ↑ 4.0 4.1 Sobala GM, Schorah CJ, Shires S, Lynch DA, Gallacher B, Dixon MF; et al. (1993). "Effect of eradication of Helicobacter pylori on gastric juice ascorbic acid concentrations". Gut. 34 (8): 1038–41. PMC 1374349. PMID 8174949.
  5. ↑ Genta RM, Hamner HW, Graham DY (1993). "Gastric lymphoid follicles in Helicobacter pylori infection: frequency, distribution, and response to triple therapy". Hum Pathol. 24 (6): 577–83. PMID 8505036.
  6. ↑ 6.0 6.1 Dixon MF, Genta RM, Yardley JH, Correa P (1996). "Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994". Am J Surg Pathol. 20 (10): 1161–81. PMID 8827022.
  7. ↑ Neithercut WD, Milne A, Chittajallu RS, el Nujumi AM, McColl KE (1991). "Detection of Helicobacter pylori infection of the gastric mucosa by measurement of gastric aspirate ammonium and urea concentrations". Gut. 32 (9): 973–6. PMC 1379031. PMID 1916500.
  8. ↑ Pera M, Heppell J, Poulsom R, Teixeira FV, Williams J (2001). "Ulcer associated cell lineage glands expressing trefoil peptide genes are induced by chronic ulceration in ileal pouch mucosa". Gut. 48 (6): 792–6. PMC 1728308. PMID 11358897.
  9. ↑ Craanen ME, Blok P, Dekker W, Ferwerda J, Tytgat GN (1992). "Subtypes of intestinal metaplasia and Helicobacter pylori". Gut. 33 (5): 597–600. PMC 1379284. PMID 1612473.
  10. ↑ Walker MM (2003). "Is intestinal metaplasia of the stomach reversible?". Gut. 52 (1): 1–4. PMC 1773527. PMID 12477745.
Retrieved from "https://www.wikidoc.org/index.php?title=H.pylori_gastritis_pathophysiology&oldid=1285435"