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Gastritis

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Gastritis
Samy A Azer
Professor of Medical Education and Gastroenterology Consultant, King Saud University
College of Medicine, Riyadh 11461, Saudi Arabia.

Introduction
Gastritis is defined on the basis of histological features of the gastric mucosa. It is not
erythema observed during gastroscopy, and there are no specific clinical presentations or
symptoms that define gastritis. The current classification of gastritis is based on time course
(acute versus chronic), histological features, anatomic distribution and underlying
pathological mechanisms. If not treated the picture may evolve into chronic gastritis.
Worldwide Helicobacter pylori (H. pylori) is the most common cause of gastritis. However,
60-70% of H. pylori-negative subjects with functional dyspepsia or nonerosive
gastroesophageal reflux were found to have gastritis. H. pylori-negative gastritis is
considered when an individual fulfil all four of these criteria (i) A negative triple staining of
gastric mucosal biopsies (hematoxylin and eosin, the Alcian blue stain and a modified silver
stain), (ii) A negative H pylori culture, (iii) A negative IgG H. pylori serology, and (iv) No
self-reported history of H. pylori treatment. In these patients, the cause of gastritis may be
related to tobacco smoking, consumption of alcohol, and or the use of non-steroidal anti-
inflammatory drugs or steroids. Other causes of gastritis include (1) Autoimmune gastritis
associated with serum anti-parietal and anti-intrinsic factor antibodies and characterized by a
chronic atrophic gastritis limited to the corpus and fundus of the stomach and causing marked
diffuse atrophy of parietal and chief cells, (2) Gastritis caused by organisms other than H.
pylori such as Mycobacterium avium-intracellulare, herpes simplex and cytomegalovirus,
and, (3) Gastritis caused by acid reflux. Rare causes of gastritis include collagenous gastritis,
sarcoidosis, eosinophilic gastritis, and lymphocytic gastritis. Therefore, clinical presentation,
laboratory investigations, gastroscopy and histological and microbial examination of tissue
biopsies are important for the diagnosis of gastritis and its cause. Treatment of H. pylori-
associated gastritis results in the rapid disappearance of polymorphonuclear infiltration and a
reduction of chronic inflammatory infiltrate with the gradual normalization of the mucosa.
Mucosal atrophy and metaplastic changes may resolve shortly, but it is not necessarily the
outcome of treatment of H. pylori in all treated patients. Other types of gastritis should be
treated according to their causes.

Etiology
Gastritis can be acute or chronic. The causes of gastritis can be summarized as follows [1-5]:

1. H. pylori-associated gastritis: This is the most common cause of gastritis worldwide.

2. H. pylori-negative gastritis: The patients should fulfill all four of these criteria (i) A
negative triple staining of gastric mucosal biopsies (hematoxylin and eosin, the Alcian blue
stain and a modified silver stain), (ii) A negative H pylori culture, (iii) A negative IgG H.
pylori serology, and (iv) No self-reported history of H. pylori treatment. In these patients, the
cause of gastritis may be related to tobacco smoking, consumption of alcohol, and or the use
of non-steroidal anti-inflammatory drugs or steroids.
3. Autoimmune gastritis: This is a chronic inflammatory disease characterized by chronic
atrophic gastritis and associated with raised serum anti-parietal and anti-intrinsic factor
antibodies. The loss of parietal cells results in a reduction of gastric acid secretion, which is
required for the absorption of inorganic iron. Therefore, iron deficiency is commonly found

1
in patients with autoimmune gastritis. Iron deficiency in these patients usually precedes
vitamin B12 deficiency. The disease is commonly found in young women.
4. Gastritis caused by organisms other than H. pylori such as Mycobacterium avium-
intracellulare, Enterococcal infection, herpes simplex and cytomegalovirus. Parasitic gastritis
may be caused by Cryptosporidium, Strongyloides stercoralis, or anisakiasis infection.
5. Gastritis caused by bile acid reflux.
6. Radiation gastritis.
7. Crohn’s disease associated gastritis: This is an uncommon cause of gastritis.
8. Collagenous gastritis: This is a rare cause of gastritis. The disease is characterized by
marked subepithelial collagen deposition accompanying with mucosal inflammatory
infiltrate. The exact etiology and pathogenesis of collagenous gastritis are still unclear.
9. Eosinophilic gastritis: This is another rare cause of gastritis. The disease could be part of
the eosinophilic gastrointestinal disorders which is characterized by the absence of known
causes of eosinophilia (not secondary to an infection, systematic inflammatory disease, or
any other causes to explain the eosinophilia).
10. Sarcoidosis-associated gastritis: Sarcoidosis is a multisystemic disorder characterized
by the presence of non-caseating granulomas. Although sarcoidosis can affect any body
organ, the gastrointestinal tract, including the stomach, is rarely affected.
11. Lymphocytic gastritis: This is a rare cause of gastritis. The etiology of lymphocytic
gastritis has not yet been established but an association with H. pylori infection or celiac
disease has been suggested.
12. Ischemic gastritis: This is a rare cause of gastritis and associated with high mortality.
13. Vasculitis-associated gastritis: This is another rare cause of gastritis. Diseases causing
systemic vasculitis can cause granulomatous infiltration of the stomach. For example,
granulomatosis with polyangiitis formerly called Wegner’s granulomatosis.
14. Ménétrier disease: This disease is characterized by- (i) The presence of large gastric
mucosal folds in the body and fundus of the stomach, (ii) Histologically, massive foveolar
hyperplasia of surface and glandular mucous cells, (iii) Protein-losing gastropathy,
hypoalbuminemia, and oedema in 20-100% of patients, and (iv) reduced gastric acid
secretion because of loss of parietal cells [6].

Epidemiology
In the western population, there is evidence of declining incidence of infectious gastritis
caused by H. pylori with an increasing prevalence of autoimmune gastritis [7]. Autoimmune
gastritis is more common in women and older people. The prevalence is estimated to be
approximately 2% to 5%. However, the available data do not provide solid information about
the incidence and prevalence of autoimmune gastritis [8].

Chronic gastritis is still a relatively common disease in developing countries. The prevalence
of H. pylori infection in children in the western population is approximately 10% [9].

In developing countries, the prevalence of H. pylori varies depending on geographical region,

and socioeconomic conditions. It is approximately 69% in Africa, 78% in South America,
and 51% in Asia. The prevalence of H. pylori infection of children in developing countries is
higher than 50% [10].

Socioeconomic and environmental hygiene are the essential factors in the transmission of H.
pylori infection worldwide. These factors include family-bound hygiene, household density,

2
and cooking habits. The pediatric origin of H. pylori infection is currently considered the
primary determinant of H. pylori-associated gastritis in a community [11].

Pathophysiology

• H.pylori-associated gastritis is transmitted via oral-fecal route.

• H. pylori possess a number of virulence factors which facilitate cell adhesion (e.g.,
BabA/B, sabA, OipA), cell damage and disruption of tight junctions (e.g., Ure A/B), and
evasion from the immune response (e.g., LPS). In particular, the cytotoxin-associated gene a
(CagA) is considered a potent inducer of inflammation and correlate with gastric cancer
development [12].
• Another factor influencing H. pylori pathogenic effects is host factors. The host
susceptible factors such as polymorphism in genes coding for tall receptors or specific
cytokines. The infection with H. pylori triggers IL-8 which attracts neutrophils which release
oxyradicals leading to cell damages. Lymphocyte infiltration is also noted in H. pylori
infection.
• Chronic gastritis is mostly caused by H. pylori infection and appears either as non-
atrophic or atrophic form. These two forms are phenotypes of gastritis at different stages of
the same life-long disease [13].
• The progression from acute to chronic gastritis begins in childhood as a simple chronic
superficial mononuclear inflammation of gastric mucosa which progress in years or decades
to atrophic gastritis characterized by loss of normal mucosal glands in the antrum, or corpus
and fundus or both.
• Factors that determine progression to atrophic gastritis and sequelae such as peptic ulcer
and gastric cancer are not clearly understood and cannot be predicted. However, Epstein-Barr
virus (EBV) and human cytomegalovirus (HCMV) have been identified in gastric tumours
and DNA from H. pylori, EBV, and HCMV was determined by PCR in biopsies from
patients with gastric cancer complicating chronic gastritis [14]. The involvement of EBV and
H. pylori in the development of gastric cancer in patients with chronic gastritis has been
confirmed by other authors, they also found no role for human papillomavirus (HPV) in
gastric tumorigenesis [15].
• Nonsteroidal anti-inflammatory drugs cause gastritis through inhibition of prostaglandin
synthesis. Prostaglandins are responsible for the maintenance of protective mechanisms of
gastric mucosa from injuries caused by hydrochloric acid.
• The pathogenesis of autoimmune gastritis is currently based on two theories. According to
the first theory, an immune response against superimposed H. pylori antigen is triggered,
antigen cross-reacting with antigens within the proton-pump protein or the intrinsic factor,
leading to a cascade of cellular changes and causing damages to the parietal cells and
stopping hydrochloric acid secretion and thus these cells gradually become atrophic and not
functioning. The second theory, assume that the autoimmune disorder develops irrespective
of H. pylori infection, and it is directed against the proteins of the proton-pump. As per both
theories, the autoimmune gastritis is the result of a complex interaction between genetic
susceptibility and environmental factors resulting in immunological dysregulation involving
sensitized T lymphocytes and autoantibodies directed against parietal cells and the intrinsic
factor [16].

3
Histopathology

Histologically, gastritis is defined by the presence of at least grade 2 neutrophils or

mononuclear cells in at least one gastric biopsy site or grade 1 neutrophils or mononuclear
cells in at least two sites [17]. A sampling of five gastric biopsy specimens: antrum greater
and lesser curvature, incisura, and corpus greater and lesser curvature. Specimens need to be
put into separate vials and grouped for each site of the lesion. The aim is to maximize the
opportunity to identify H. pylori and hence not to miss the diagnosis.

H. pylori infection first appearance of gastritis tend to be antral. The inflammation,

composing mainly of mononuclear inflammatory cells and plasma cells are superficial and
mostly in the upper layers of the mucosa of the corpus (body of the stomach).

The chronic inflammation of gastric mucosa is associated with neutrophilic inflammation; the
effects are dependent on the cytotoxicity of the H. pylori strain. The most cytotoxic strains
will result in the development of atrophic gastritis. The loss of mucosal glands in atrophic
gastritis is replaced with new immature glandular and epithelial cells resembling glands of
intestinal tissues.

In early phases of autoimmune gastritis, lymphocytic and plasma cell infiltration of oxyntic
mucosa is present with accentuation in deeper glandular portion. Hyperplasia of endocrine
cells in gastric mucosa is an early feature in autoimmune gastritis. Oxyntic glands may be
destroyed and parietal cells show pseudohypertrophy as the disease progress. In advanced
disease, marked atrophy of the oxyntic glands together with diffuse lymphoblastic infiltration
of the lamina propria are present. Intestinal metaplasia can be found in end-stage disease
[18].

History and Physical

There are no typical clinical manifestations of gastritis. Sudden onset of epigastric pain,
nausea, and vomiting have been described to accompany acute gastritis. If not treated the
picture may evolve to chronic gastritis.

History of smoking, consumption of alcohol and intake of non-steroidal anti-inflammatory

drugs or steroids, allergies, radiotherapy or gall bladder disorders should be explored.

The most common initial findings for autoimmune gastritis are (1) hematological disorders
such as anemia (iron-deficiency anemia) detected on routine check-up, (2) positive
histological examination of gastritis, (3) clinical suspect based on the presence of other
autoimmune disorders, neurological symptoms (related to vitamin B12 deficiency) or positive
family history [19].

Iron-deficiency anemia (based on blood film showing microscopic hypochromic changes and
iron studies) is commonly seen in the early stages of autoimmune gastritis. Mainly because of
achlorhydria causing impairment of iron absorption in the duodenum and early jejunum [20].
Iron-deficiency anemia could also be seen in other types of chronic gastritis.

Autoimmune gastritis is associated with other autoimmune disorders mainly thyroid disease
including Hashimoto’s thyroiditis and type 1 diabetes mellitus. The association between
chronic atrophic autoimmune gastritis and autoimmune thyroid disease was described in the

4
early 60s and is described as “thyrogastric syndrome”. Other autoimmune diseases that have
been described with autoimmune gastritis include Addison’s disease. Chronic spontaneous
urticaria, myasthenia gravis, vitiligo, and perioral cutaneous autoimmune disorders especially
erosive oral lichen planus [18].

A history of treatment for inflammatory bowel disease, vasculitic disorders or eosinophilic

gastrointestinal disorders may be explored if no cause of gastritis was found.

Evaluation

• Diagnosis of colitis is based on histopathological examination of gastric biopsy tissues.

While medical history and laboratory tests are helpful, endoscopy and biopsy is the gold
standard in making the diagnosis of gastritis, identifying its distribution, severity and cause.
• The tests used for the diagnosis of H. pylori-associated gastritis can be classified into two
main groups: (1) Invasive methods (requiring gastroscopy and biopsies): These include
histological staining (hematoxylin and eosin, the Alcian blue stain and a modified silver
stain) and culture, rapid urease test, and molecular detection-PCR DNA. (2) Non-invasive
methods (not requiring gastroscopy and biopsies): These include urease breath test (13C-
UBT), fecal antigen test and serology. However, co-medications with proton-pump inhibitors
lead to false negative results in both invasive and non-invasive tests [21]. Also, patients
treated with proton-pump inhibitors usually have negative histological staining for H. pylori.
Staining of gastric mucosal biopsies by immunohistochemistry is recommended to detect H.
pylori.
• The diagnosis of gastritis is based on histological examination. Non-invasive tests are of
no value in the diagnosis of H-pylori-associated gastritis.
• Serological tests for detection of antibodies against H. pylori cannot differentiate between
active and past infection.
• The diagnosis of autoimmune gastritis is based on laboratory and histological
examination. These tests include: (1) atrophic gastritis of gastric corpus (body) and fundus of
the stomach, (2) autoantibodies against the intrinsic factor and the parietal cells, (3) raised
serum gastrin levels, (4) serum pepsinogen 1 level and (5) pepsinogen 1/pepsinogen 2 ratios
[22][23].
• Compared to intrinsic factor antibodies, the most sensitive serum biomarker in
autoimmune gastritis is parietal cell antibodies.
• The risk of gastric cancer in autoimmune gastritis is determined by (1) low levels of
pepsinogen 1, (2) low pepsinogen 1/pepsinogen 2 ratios, (3) high fasting serum gastrin, (4)
atrophic gastritis of the corpus and fundus. In these patients, the risk of cancer is high
irrespective of whether they have or do not have on-going H. pylori infection.
• Pernicious anemia is defined as a condition of macrocytic anemia associated with low
cobalamin levels and atrophic corpus-fundus gastritis associated with parietal cell antibodies
or intrinsic factor autoantibodies.
• Other tests that may be indicated in autoimmune gastritis are gastrin-17, IgG and anti-H.
pylori antibodies, cytokines (such as IL-8) and ghrelin (a growth-hormone-releasing peptide
that is produced mainly by the gastric funding mucosa) [24].
• Gastroscopy and histological diagnosis are needed for all other causes of gastritis- helping
in defining the diagnosis, assessing the extent and severity of the disease and any
complications.

5
Treatment/ Management
• Treatment regimes differ from antibiotics (in H. pylori gastritis) to vitamin
supplementation (in autoimmune metaplastic atrophic gastritis), to immunomodulatory
therapy (in autoimmune enteropathy), to dietary modifications (in eosinophilic gastritis).

• H. pylori-associated gastritis: A triple-therapy comprising Clarithromycin/proton-pump

inhibitor/amoxicillin for 14-21 days is considered the first line of treatment. Clarithromycin is
preferred over metronidazole/proton-pump inhibitor/amoxicillin because the recurrence rates
when clarithromycin is used are far less compared to a triple-therapy using metronidazole.
However, in areas where clarithromycin resistance is known, metronidazole should be used.
Quadruple bismuth containing therapy would be of benefit, particularly if metronidazole is
used [25].

• After two eradication failures, H. pylori culture and tests for antibiotic resistance should
be considered.

• Autoimmune gastritis: Substitution of deficient iron and vitamin B12 (parenteral 1000 µg
or oral 1000-2000 µg). Monitor Iron and folate levels, and eradicate any co-infection with H.
pylori. Endoscopic surveillance for cancer risk and gastric neuroendocrine tumours (NET) is
required [26][27].

• Other forms of treatment in gastritis include cessation of alcohol, smoking, and anti-
inflammatory drugs, avoiding spicy food, managing stress, immunomodulatory therapy in
autoimmune enteropathy, and dietary modification in eosinophilic gastritis.

Differential Diagnosis
• Infectious gastritis
• Non-infectious gastritis.
• Peptic ulcer disease.
• Gastric cancer.
• Cholecystitis
• Zollinger-Ellison syndrome.
• Dyspepsia/gallstone disease.
• Pancreatitis.
• Autoimmune gastritis.
• Myocardial ischemia
• Gastric involvement in the setting of inflammatory bowel disease, particularly Crohn’s
disease.
• Ménétrier disease.
• Lymphoma.
• Celiac disease
• Multiple endocrine neoplasias.

6
Complications

• Peptic ulcer.
• Chronic atrophic gastritis (loss of appropriate glands, resulting mainly from long-standing
H. pylori infection).
• Gastric metaplasia/dysplasia.
• Gastric cancer (adenocarcinoma).
• Iron-deficiency anemia (chronic gastritis and early stages of gastric autoimmunity).
• Vitamin B12 deficiency (autoimmune gastritis)
• Gastric bleeding.
• Achlorhydria (autoimmune gastritis, chronic gastritis).
• Gastric perforation.
• Mucosa-Associated Lymphoid Tissue (MALT) lymphoma. NET (previously referred as
gastric carcinoid; complicates autoimmune gastritis). Autoimmune gastritis predisposes to the
development of both gastric adenocarcinoma and gastric type 1 neuroendocrine tumours
(NET). The development of NET in these patients is related to mucosal atrophy, and
hyperplasia of immature mucus neck cells. The enhanced differentiation of immature
precursor neck cells into histamine-producing enterochromaffin-like (ECL) cells secondary to
hypergastrinemia.
• Vitamin C, vitamin D, folic acid, zinc, magnesium, and calcium deficiency (atrophic
autoimmune gastritis).

Pearls and Other Issues

Diagnosis of gastritis is based on the histological features of gastric biopsies. While history
and laboratory tests are helpful, gastric mucosal biopsies are the gold standard in making the
diagnosis, identifying its distribution, severity and etiologic cause.

Enhancing Healthcare Team Outcomes

Infection with H. pylori represents the common cause of chronic gastritis. The majority of
patients may present to the general practitioner or the emergency department because of
complications. Successful eradication therapy should heal chronic non-atrophic gastritis and
prevent patients from complications. The public and patients should be educated about the
transition of infection via the fecal-oral route, the importance of hand washing habits, and
hygiene practices to prevent infection with H. pylori. However, it is not known how to help
people maintain hand washing habits and hygiene practices in the long term. Because the
presentation of gastritis is not well defined in terms of the clinical picture, and diagnosis is
only based on histological examination of gastric mucosa, healthcare workers including
doctors, nurses, and pharmacists need to be aware of the diagnosis, sequelae and
complications. Patients with autoimmune gastritis need regular surveillance for early
detection of cancer risk of gastric neuroendocrine tumour and gastric carcinoma. The risk of
gastric cancer is high in patients not treated for H. pylori eradication.

7
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