Best Practice & Research Clinical Gastroenterology 28 (2014) 1031e1042

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Best Practice & Research Clinical

Gastroenterology

Chronic gastritis e An update

Mariya Varbanova, MD, Fellow/Resident at the Department of
Gastroenterology, Hepatology and Infectious Diseases a,
€ger, Fellow/Resident at the Institute of
Katrin Frauenschla
Pathology b,
Peter Malfertheiner, MD, Professor, Director of the Department
of Gastroenterology, Hepatology and Infectious Diseases a, *
a
Department of Gastroenterology, Hepatology and Infectious Diseases, Otto-von-Guericke University
of Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany
b
Institute of Pathology, Otto-von-Guericke University of Magdeburg, Leipziger Str. 44,
39120 Magdeburg, Germany

a b s t r a c t

Keywords: Helicobacter pylori is the main aetiologic factor for chronic gastritis
Gastritis worldwide. The degree of inflammation and the evolution of this
Helicobacter pylori form of chronic gastritis can vary largely depending on bacterial
Autoimmune gastritis
virulence factors, host susceptibility factors and environmental
Pernicious anaemia
conditions. Autoimmune gastritis is another cause of chronic
inflammation in the stomach, which can occur in all age groups.
This disease presents typically with vitamin B12 deficiency and
pernicious anaemia. The presence of anti-parietal cell antibodies is
highly specific for the diagnosis. The role of H. pylori as a trigger for
autoimmune gastritis remains uncertain.
Other rare conditions for chronic gastritis are chronic inflamma-
tory conditions such as Crohn's disease or on the background of
lymphocytic or collagenous gastroenteropathies.
© 2014 Published by Elsevier Ltd.

Introduction

Helicobacter pylori (H. pylori) infection is the most common cause of chronic inflammation of the
stomach worldwide. The bacterium discovered by Warren and Marshall in 1982 colonizes around half

* Corresponding author. Tel.: þ49 391 6713100.

E-mail address: peter.malfertheiner@med.ovgu.de (P. Malfertheiner).

http://dx.doi.org/10.1016/j.bpg.2014.10.005
1521-6918/© 2014 Published by Elsevier Ltd.
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of the world population. All H. pylori infected individuals develop chronic gastritis; the degree of
mucosal inflammation results from the interplay of bacterial virulence factors, host susceptibility genes
and environmental factors. Corpuspredominant gastritis, severe gastric atrophy and intestinal meta-
plasia confine a risk for the development of gastric cancer as shown in large prospective cohorts [1e3].
Autoimmune gastritis (AIG) is another cause of chronic inflammation of the stomach. The term AIG
refers to a variety of definitions such as atrophic body gastritis, pernicious anaemia and Morbus
Biermer. The clinical presentation can be variable, most typically with vitamin B12 deficiency and
manifest pernicious anaemia (PA), but iron deficiency may also be a consequence. At the time of
diagnosis, the oxyntic mucosa is usually transformed and shows severe glandular atrophy.
The traditional concept of AIG needs to be revisited because of the role of H. pylori infection in the
development of AIG through mimicry of the proton pump of parietal cells (Hþ/Kþ-ATPase). The risk for
type 1 gastric neuroendocrine neoplasm, as well as the co-occurrence with various autoimmune
diseases is reviewed in this article.
Besides H. pylori gastritis and AIG, several other chronic inflammatory conditions of the gastric
mucosa are discussed. They include collagenous gastritis, lymphocytic gastritis, M. Menetrier and M.
Crohn and are rare forms.

H pylori gastritis

Epidemiology

The excusive permanent reservoir of H. pylori is the human stomach. Local prevalence of H. pylori
varies greatly from 8% (North America) to 90% (Siberia) depending on geographic region and socio-
economic conditions [4]. A selection of H. pylori prevalence in the adult population from different
continents is shown in Table 1. The bacterium is found in feces and the oral cavity of infected in-
dividuals [5] but exclusively colonizes and persists in the gastric mucosa. Since the wide-spread use of
antibiotic treatment and the improvement of hygiene in industrialized countries, prevalence of H.
pylori infection of children and young individuals gradually decreases [6], and lies below 10% in chil-
dren in western populations [7,8].

Pathogenesis

Bacterial factors
H. pylori is an obligate pathogen in the human stomach. The bacterium possesses various virulence
factors which facilitate survival, cell adhesion, cell damage and evasion from immune response. Table 2
shows a list of the best known virulence factors and their functions, excellently reviewed recently by
Posselt et al. [9]. The pathogenicity island cytotoxin-associated gene a (cagA) in particular is expressed
by a large number of strains and is considered a potent inductor of inflammation [10]. The cagA gene
exhibits strong variations in different geographic locations correlated with incidence of gastric cancer
[11,12]. Attention was drawn on variations in the conserved sequence of the cagA gene Glu-Pro-Ile-Tyr-
Ala (EPIYA) motifs. Particularly the number of C tyrosine phosphorylations seems to play a decisive role
in virulence as reviewed in another chapter of this edition. Two or more EPIYA C motifs point to an

Table 1
Reports of H. pylori prevalence in the largest studies in adults from different continents published between 2010 and 2011 using
tests for active infection. Modified from Goh et al [6].

Continent Country N Test Prevalence

Asia Korea 10,102 RUT 51%

Africa Morocco 755 Histology 69%
South America Chile 5664 RUT 78%
North America USA 78,985 Histology 8%
Europe Albania, 101 Albanian Histology 54%
Greece 101 Greek 34%
 M. Varbanova et al. / Best Practice & Research Clinical Gastroenterology 28 (2014) 1031e1042 1033

Table 2
Selected H. pylori virulence factors and their basic functions.

Virulence factor Description Function Association with disease

OipA Outer inflammatory protein A Adhesion, inflammation Gastritis

BabA/B Blood-group-antigen-binding Adhesion Gastric cancer
adhesion
SabA Sialic acid binding adhesion Adhesion Gastritis
Ure A/B Urease, functional enzyme Colonization, disruption Gastritis
of tight junctions
LPS Lipopolysaccharides, membrane Evasion, inflammation Gastritis
component
CagA Cytotoxin-associated gene A protein Disruption of tight junctions, Gastritis
translocation of proteins Ucer disease
inflammation Gastric cancer
VacA Vacuole-inducing toxin Cell damage (vacuolization), Ulcer disease
apoptosis Gastric cancer

increased risk for the development of atrophic gastritis and gastric carcinoma with calculated odds
ratio (OR) of 12 and 51, respectively [13].

Host factors
Host susceptibility factors such as polymorphisms in genes coding for toll like receptors or specific
cytokines have also been reported to influence the progression of chronic gastritis to preneoplastic
conditions and gastric cancer [14]. For example, it has been shown that the concurrence of infection
with cagA and vacA s1m1 positive strains in subjects with IL-1b-511*T polymorphism increases the risk
of chronic gastritis to progress to GC 25-fold [15]. Testing for specific factors is however not recom-
mended in clinical practice, as none can sufficiently predict the clinical outcome of infection [16].
Infiltration of the gastric mucosa with neutrophil granulocytes is a histopathological hallmark for
infection. This reaction is an essential part of the immune response against H. pylori triggered by high
interleukin 8 (IL-8) levels produced by gastric epithelial cells after contact with the bacterium [17]. IL-8
attracts neutrophils, which release oxyradicals (oxidative burst) leading to cell damage while being
tolerated by H. pylori equipped with enzymes to block oxidative stress (catalase, hydrogenase). On the
other hand, lymphocyte infiltration is also typically observed, in some cases accompanied by the
formation of lymphoid follicles. It represents the cellular response mediated foremost by a Th1- and
Th17-response with secretion of proinflammatory cytokines such as IFN-g and IL-17 [18]. New insights
into the capacity of H. pylori to overcome the life-long immune response of the host were gained by the
discovery of pronounced infiltration of mucosa with immunosuppressive regulatory T cells (Treg) [19].
Neutrophil and lymphocyte infiltration represent the activity and chronicity of H. pylori induced
gastritis. Grading of these parameters of inflammation is performed standardized by a visual scale
proposed in the Updated Sydney system [20].

Diagnosis and treatment

Invasive and non-invasive tests for H. pylori infection are available for clinical practice. Several
invasive methods can be used to determine the presence of H. pylori: histological staining (Fig. 1), culture,
rapid urease test and molecular detection via PCR, all of which require gastric biopsies obtained during
upper endoscopy. High consumption of resources and avoidance of endoscopy give way to non-invasive
test modalities for the first diagnostic steps such as urea breath test (13C e UBT), stool faecal antigen test
and serology. One essential problem is co-medication with proton pump inhibitors (PPI), which leads to
false negative results in the invasive and non-invasive tests for active infection due to suppression of H.
pylori density and urease during PPI therapy [21,22]. Serological detection of antibodies against H. pylori
can be utilized in such cases; however it does not allow the discrimination between active or past
infection.
Current recommendations for the clinical management and treatment of H. pylori infection have
been stated in the IV Maastricht/ Florence Consensus report [16]. First line treatment is usually a
1034 M. Varbanova et al. / Best Practice & Research Clinical Gastroenterology 28 (2014) 1031e1042

Clarithromycin/ PPI based regimen combined with amoxicillin or metronidazole, except in areas with
high clarithromycin resistance. Here a quadruple bismuth containing therapy would be the first choice,
alternatively non bismuth quadruple therapy. After two eradication failures it is recommended to
obtain a culture of H. pylori and test for antibiotic resistance.

Practice points

 H. pylori is the main etiologic factor for chronic gastritis worldwide

 Currently there is no biomarker (either host- or bacteria related) which can reliably predict the
outcome of the infection
 H. pylori gastritis therefore whenever detected requires eradication therapy

Research agenda

 Assessment of genetics and mechanisms of virulence and host factors which determine risk
of gastric cancer
 Monitoring antibiotic resistance in order to select effective eradication therapies

Autoimmune gastritis

Epidemiology

Due to the frequent asymptomatic nature of disease, the prevalence of AIG in the general population
is probably underestimated. A recent epidemiological study in Germany including 9,684 subjects aged
50e74 years revealed the presence of anti-parietal cell antibodies (PCA) in approximately 20%, along
with a strong association with gastric atrophy as determined by low pepsinogen I levels [23]. In another
epidemiological study on the general population on the Canary Islands, PCA were found in 8% and in
10% of the women [24].

Fig. 1. A Helicobacter pylori gastritis (Warthin-Starry-stain) with a dense inflammatory infiltrate of neutrophiles, lymphocytes and
plasma cells in the upper Lamina propria. Furthermore, there is a moderate foveolar hyperplasia, identified by the elongated and
contorted foveolae (white arrow heads). B Long lasting Helicobacter pylori gastritis with a lymphoid follicle (black arrow heads). C A
close-up view of the comma-shaped Helicobacter pylori bacteria (white arrows) on the surface of the foveolar epithelium.
 M. Varbanova et al. / Best Practice & Research Clinical Gastroenterology 28 (2014) 1031e1042 1035

A large number of elderly patients with undiagnosed pernicious anaemia (PA) has been reported in
a prospective study from the United States (n ¼ 729, age >60 years) [25]. Vitamin B12 deficiency and
positive intrinsic factor antibodies were found in 1.9% of the study population and in 4% of the women.
An Israeli study suggested a possibly high number of undiagnosed AIG in young patients as well.
Notably, 30% of a cohort of asymptomatic PA patients were aged below 40 years [26]. Another
important epidemiological aspect is the frequent association of autoimmune gastritis with other
autoimmune disorders: the prevalence of AIG in type 1 diabetes mellitus and autoimmune thyroid
disease is five- to ten- fold higher than in the general population [27,28].

Pathogenesis

Anti-parietal cell antibodies (PCA) and antibodies against intrinsic factor (IFA) were discovered back
in the early 1960ies. Almost 30 years later, the Hþ/Kþ-ATPase was identified as the causal antigen [29],
which triggers the autoimmune response and the progress of the disease by consecutive destruction of
parietal cells and functional loss of the oxyntic gastric mucosa [30].
It is assumed that during epithelial turnover some amount of the Hþ/Kþ-ATPase protein (the main
functional component of parietal cells) is accessible for dendritic cells in the gastric mucosa. When
presented as an antigen to naïve T cells, a pathogenic clone of CD4þ antigen specific T cells can arise
in predisposed individuals [31]. It infiltrates the gastric mucosa providing the stimulus for the
eventually observed Th1 driven immune response. By the involvement of B cells on the mucosal level,
autoantibody production is initiated and maintained, a process dependent on antigen presentation.
The exact mechanisms exerting parietal cell death are not clear. A possible death by Fas ligand
induced apoptosis has been suggested based on the observation that gastric epithelial cells express
Fas ligand in experimental autoimmune gastritis possibly interacting with Fas ligand on infiltrating T
cells [32]. A similar process of tissue loss has been described in other autoimmune diseases [33]. The
reduced acid production invokes reactive and ineffective excess of gastrin levels used as a diagnostic
criterion of AIG. As an acidic milieu is needed to extract iron from proteins, iron deficiency anaemia
caused by hypochlorhydria can be an early sign of disease in 20e37% of AIG patients [34,35].
Another target of the autoimmune response is the intrinsic factor, an essential protein for vitamin
B12 (cobalamin) uptake. Vitamin B12 deficiency dominates the clinical picture in PA patients, a
condition which probably requires decades from the onset of AIG to develop.

The role of H. pylori

The classic concept of three types of gastritis (A for autoimmune, B for bacterial and C for chemical)
discriminates an infectious from an autoimmune principle cause of inflammation. In a prospective
controlled case control trial from 1991 H. pylori infection was reported as a rare finding in the group of
patients with pernicious anaemia [36]. However, this concept is challenged by a growing body of
literature supporting the idea of H. pylori as an infectious trigger of autoinflammation.
Diagnosis of H. pylori by histology or other tests for active infection in severe atrophy can be difficult.
However, according to more recent reports, H. pylori can be detected on histology in up to 30% of
patients with pernicious anaemia and about a half of them by serology [37]. An even larger proportion
of H. pylori seropositive patients (75%) was observed in a cohort of 150 AIG cases [38]. Interestingly, the
H. pylori negative patients were 10 years older than the H. pylori positive group and 75% of them had
pernicious anaemia vs. 12% in the H. pylori positive group. This trend of H. pylori ‘loss’ with age was
demonstrated even more clearly in a prospective study from Israel using UBT. High prevalence of active
H. pylori infection (88% positive) was found in very young patients with AIG (age <20 years), which
decreased to 13% in the elderly [26]. A recent study focused on patients with atrophic corpus gastritis
classified as H. pylori negative by histology and serology. By use of immunoblotting antibodies against
cagA and/or vacA were revealed in almost all patients [39], suggesting an impact of H. pylori even if not
detectable at present.
These findings support the hypothesis that acute infection leading to massive epithelial cell
damage (rather than normal mucosal turnover) may cause the exposure of the Hþ/Kþ-ATPase to
antigen presenting cells, which will provoke an autoimmune response in susceptible individuals.
Furthermore, bacterial peptides seem to have sequences in common with the proton pump of the
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parietal cells, which have been described as molecular mimicry. CD4þ T cells reactive to both H. pylori
lipoproteins and human Hþ/Kþ-ATPase were isolated from gastric biopsies of infected patients with
AIG. These T cell clones reacted to different epitopes (mainly on the alpha subunit of the proton
pump) than the clones, which reacted to the proton pump alone [40]. Currently, data are not suffi-
cient in order to establish a causative link between autoinflammation of the gastric mucosa and H.
pylori as an infectious agent; further research is needed to confirm these new aspects of patho-
physiology of AIG.

Risk of progression
Chronic inflammation in autoimmune gastritis generally progresses to atrophy of the oxyntic
mucosa. In a large series of 562 patients with AIG 90% exhibited atrophy in the body of the stomach
and 80% had severe loss of glandular tissue, partially replaced by metaplastic glands in half of these
patients [41]. Enterochromaffine-like (ECL) cell hyperplasia represents another typical finding in AIG,
which can occur in a linear form (41%) or micronodular form (25%). ECL-cell hyperplasia becomes
more frequent with the increasing grade of atrophy, but it harbours a low potential for neoplastic
transformation i.e. the development of type 1 neuroendocrine gastric tumours (NET), formerly called
carcinoids [42]. The severity of ECL-cell hyperplasia and the presence of ECL-cell dysplasia were
identified as risk factors for the development of gastric NET [43]. However, concomitant occurrence of
ECL-cell hyperplasia and early gastric cancer was observed in only 1% of 482 resected specimen of
early gastric cancer [44].
On the other hand, the capacity of autoimmune inflammation to induce gastric cancer (adeno-
carcinogenesis) has been shown clearly in an experimental model, where all mice expressing a T cell
clone against Hþ/Kþ-ATPase developed dysplasia and intraepithelial neoplasia at the age of 12 months
[45]. In humans, a recent population-based study on 4.5 million US males reported a relative risk (RR)
of 3.2 for the development of gastric cancer from PA, suggesting an impact of PA for gastric carcino-
genesis [46]. Previous studies from Denmark [47] and Sweden [48,49], described slightly lower RR of
2.4 and 2.9, respectively.

Diagnosis

Despite the considerable progress in the understanding of pathogenesis and the triggers of chronic
inflammation in AIG and PA, there is no official consensus on the diagnostic criteria and definitions.
In autoimmune gastritis diagnosis is based on atrophic gastritis of the gastric corpus/fundus on
histology and the presence of PCA [50]. AIG can be considered a precursor condition of PA and subjects
don't need to present with symptoms; literature data on association of AIG with PCA is scarce. In a
cohort of 109 patients with AIG 83% were positive for PCA [51] . In another cohort of 150 patients with
atrophic corpus gastritis 75% had PCA, which correlated positively with the grade of atrophy [38]. The
positive predictive value of PCA for the development of AIG was 25% in a follow up period of 5 years in
patients with autoimmune thyroid disease [28].
Pernicious anaemia can be defined as a condition of macrocytic anaemia associated with low
cobalamin levels and atrophic corpus/ fundus gastritis associated with PCA or IFA [37,52]. PA and
vitamin B12 deficiency can manifest with various symptoms (weakness, palpitations, paraesthesia, and
neuropsychiatric abnormalities) and even a critical condition [53,54]. The haematopoietic deficit
presenting as megaloblastic anaemia or pancytopenia along with varying neurological symptoms is
also known as Morbus Biermer (a synonymous term for PA). In pernicious anaemia PCA and IFA were
found in 55e90% and 39e70% of patients respectively [55e57]. Longitudinal data suggest a decrease of
PCA and an increase of IFA levels over a time (median follow up 70 months) [57]. Recently, the com-
bined use of tests for these antibodies using the ELISA method yielded a sensitivity of 73% and 100%
specificity for the diagnosis of PA (defined by vitamin B12 deficiency and macrocytic anaemia) in
patients with atrophic corpus gastritis [58].
Histology alone cannot provide a definitive diagnosis of autoimmune gastritis, although some
findings may be highly suggestive such as a corpus predominant pattern of chronic inflammation as
well as severe atrophic or metaplastic changes of the oxyntic mucosa [20] (Fig. 2). However, the latter
can also appear in late stages of H. pylori infection. Antral atrophy does not exclude AIG as it was
 M. Varbanova et al. / Best Practice & Research Clinical Gastroenterology 28 (2014) 1031e1042 1037

Fig. 2. A Biopsy from the corpus mucosa showing the typical findings in a long standing autoimmune gastritis. There is a complete
loss of the gastric glands, corresponding to severe intestinal metaplasia with goblet cells (*) and paneth cells (**) at the bottom of the
gastrtic glands. The Lamina propria shows a diffuse infiltrate of lymphocytes and plsma cells. On the left side, below the gastric pits,
a small area of pyloric metaplasia (arrow) with adjecent small nests of an ECL-cell hyperplasia (encircled). B A magnified image of an
area of interest from 3A. C Staining for chromogranin, which colours neuroendocrine cells in a patient with atrophic autoimmune
gastritis. Separate nodules as well as an increased number of neuroendocrine cells are visualised in the bottom of the gastric pits. D
Antrum biopsy from a patient with autoimmune gastritis. There is mild atrophy, detectable by less dense arrangement of the gastric
glands.
1038 M. Varbanova et al. / Best Practice & Research Clinical Gastroenterology 28 (2014) 1031e1042

Fig. 3. Recommended panel of diagnostic tools for the assessment of autoimmune gastritis.

present in 26% with PA along with fundal atrophy, intestinal metaplasia and lymphoid follicles in 100%,
43% and 50% respectively [59]. Another common finding is the ECL-cell hyperplasia in the atrophic
glands. The accurate pathological diagnosis requires at least 4 non-targeted biopsies from antrum and
corpus [42,60] transferred to the pathology unit in two separate and labelled containers. A thorough
endoscopic examination can be recommended at initial diagnosis with sampling of conspicuous
lesions and, where available, augmented with high resolution magnification [60]. Fig. 3 shows a
comprehensive approach for the exact definition and diagnosis of AIG.

Treatment

Management of PA comprises substitution of deficient iron and vitamin B12 as well as endoscopic
surveillance for cancer risk (gastric cancer and NET). Treatment of PA by administration of liver diet was
rewarded with the Nobel Prize in 1934 and is presented in detail in the historical review of Okuda [61].
PA was a disease with lethal outcome until the discovery of effective treatment by the parenteral
substitution of 1000 mg vitamin B12 [62]. A Cochrane analysis of two randomized controlled trials
comparing oral vs. intramuscular substitution concluded that oral administration of 1000e2000 mg
vitamin B12 can achieve an improvement of anaemia and neuropathological symptoms [63]. Oral
administration of vitamin B12 is the preferred route in patients with compromised coagulation or
requiring anticoagulation treatment. Iron and folate levels need monitoring and other causes of
macrocytic anaemia (i.e. myelodysplastic syndrome) or vitamin B12 deficiency must be excluded [37].
Endoscopic surveillance is a central issue in AIG and PA. Current recommendations are rather
related to the extent of atrophy and the presence of preneoplastic lesions than to the degree of chronic
inflammation in AIG. The European Guidelines for the Management of Preneoplastic Conditions and
Lesions in the stomach (MAPS) [64] propose a follow up period of three years for subjects with
extensive gastric atrophy. Scandinavian studies on patients with PA suggest endoscopic follow up
ranging from two to five years [65e67]. It is debated if AIG patients presenting at an early stage with
mild atrophy (20% according to retrospective data [41]) should be followed. H. pylori should be erad-
icated if present according to the Maastricht IV guidelines [16] as patients with corpus predominant
gastritis are at high risk for the development of gastric cancer.
The management of NET arising from AIG remains uncertain. Endoscopic resection has been
recently shown to ensure disease free survival in all patients with small gastric NET for a follow up
period of up to 14 years [68]. The European Neuroendocrine Tumour Society (ENETS) guidelines
suggest a follow up period of 6e12 months as recurrence rates of 60% after endoscopic resection are
high [69].
 M. Varbanova et al. / Best Practice & Research Clinical Gastroenterology 28 (2014) 1031e1042 1039

Practice points

 Autoimmune gastritis can occur in all age groups including young patients and AIG should
be tested for in patients with other autoimmune diseases
 Anti-parietal cell antibodies and intrinsic factor antibodies are sensitive for autoimmune
gastritis

Research points

 A consensus is needed for the optimal diagnostic approach and criteria in AIG
 Progression of autoimmune gastritis to pernicious anaemia needs to be further explored (in
longitudinal studies)
 The role of H. pylori as a trigger for AIG is uncertain

Other entities of chronic gastritis

The differential diagnosis of non-infectious and non-autoimmune chronic gastritis comprises rare
entities such as lymphocytic gastritis, collagenous gastritis and involvement of the upper gastroin-
testinal tract by Crohn's disease. Literature data consists mostly of case reports.

Rare entities of gastritis

Lymphocytic gastritis is defined as 25 lymphocytes per 100 epithelial cells with reported preva-
lence of less than 1% of endoscopic biopsies. A single center study on the aetiology of 103 cases with
lymphocytic gastritis reported strong association with H. pylori infection (29%) and celiac disease (38%)
[70]. However, a prospective controlled study of gastric mucosal findings in celiac disease patients
identified lymphocytic gastritis only in 3% of 104 patients [71]. Still, it appears reasonable to seek for
etiologies in patients presenting this rare finding on histology.
Collagenous gastritis is an extremely rare disease of unknown aetiology and only 330 cases have
been reported so far [72]. The condition is defined by the presence of a thick subepithelial collagen
layer other than the physiological type IV collagen in the gastrointestinal tract leading to chronic
inflammation of the gastric mucosa. Adult patients present with watery diarrhoea, an association with
collagenous colitis has been shown [73]. In children (mostly girls), the disease manifested with
anaemia (71%), abdominal pain (41%) and typically nodular gastritis on endoscopy [74]. Therapeutic
attempts using systemic or topic corticosteroids were only partially effective, spontaneous resolution
was also described in some cases.
One recent study observed a high association of eosinophilic gastritis with eosinophilic oesopha-
gitis in children [75]. The disease was highly associated with atopy and responded to dietary restriction
of known oral antigens (milk, soy, wheat) in 80% of the cases.

Crohn's gastritis

Crohn's disease can involve virtually all organs of the gastrointestinal tract including the stomach. In
a recent study on the topography of upper GI Crohn's disease lesions, the stomach was affected in 73%
of the cases, while noncaseating granulomas were detected in one third of the patients [76]. Upper GI
tract involvement was described in 13% of a large cohort of 1000 Crohn's disease patients associated
with age <20 years at time of diagnosis and penetrating disease behaviour [77]. In a study on 314
Crohn's disease patients, upper GI tract involvement practically did not occur without disease
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manifestation in the lower GI tract [78]. However, patients with proximal lesions (oral cavity, stomach
and duodenum) were of younger age (mean 19.2 years) and had a more severe course of disease
including early surgery with loss of more small bowel than the patients with distal disease. Chronic
inflammatory changes of gastric mucosa specific for Crohn's disease always indicate more extensive
pattern of disease.

Conclusion

Infection with H. pylori represents the main etiologic factor for the development of chronic
inflammation of the gastric mucosa. Successful eradication therapy heals chronic nonatrophic gastritis
and prevents from complications. Autoimmune gastritis is a distinct form of chronic gastritis, however
in some cases it might be triggered by an infectious agent (i.e. H. pylori). Strict diagnostic criteria and
definition of this ‘silent’ disease (and related disorders such as pernicious anaemia) are still missing and
consensual algorithms are essential in order to estimate its prevalence and risk of progression. Ulti-
matively this will allow to provide recommendations for the clinical management of autoimmune
gastritis. Rare entities of chronic gastritis may appear in the context of an associated gastroenteropathy
such as coeliac disease and Crohn's disease.

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email=edson_guzman@hotmail.com, c=PE
Fecha: 2014.12.18 21:19:46 -05'00'

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