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Gastritis
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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]:
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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].
Socioeconomic and environmental hygiene are the essential factors in the transmission of H.
pylori infection worldwide. These factors include family-bound hygiene, household density,
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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
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Histopathology
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].
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
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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].
Evaluation
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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).
• 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.
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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).
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