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StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2019 Jan-.

Gastritis
Authors

Samy A. Azer1; Hossein Akhondi2.

Affiliations
1 King Saud University, King Khalid UH
2 University of Nevada

Last Update: June 24, 2019.

Introduction
Definition of gastritis has its basis in histological features of the gastric mucosa. It is not erythema observed during gastroscopy, and there are no specific clinical presentations or symptoms defining
it. The current classification of gastritis centers on time course (acute versus chronic), histological features, anatomic distribution, and underlying pathological mechanisms. Acute gastritis will
evolve to chronic, if not treated. Helicobacter pylori (H. pylori) is the most common cause of gastritis worldwide. However, 60 to 70% of H. pylori-negative subjects with functional dyspepsia or
non-erosive gastroesophageal reflux were also found to have gastritis. H. pylori-negative gastritis is a consideration when an individual fulfill all four of these criteria (i) A negative triple staining of
gastric mucosal biopsies (hematoxylin and eosin, 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 relate to tobacco smoking, consumption of alcohol, and/or the use of non-steroidal anti-inflammatory drugs (NSAIDs) or
steroids.

Other causes of gastritis include:

1. Autoimmune gastritis associated with serum anti-parietal and anti-intrinsic factor antibodies; characterized by chronic atrophic gastritis limited to the corpus and fundus of the stomach that is
causing marked diffuse atrophy of parietal and chief cells.

2. Gastritis causes include organisms other than H. pylori such as Mycobacterium avium intracellulare, Herpes simplex, and Cytomegalovirus.

3. Gastritis caused by acid reflux. Rare causes of gastritis include collagenous gastritis, sarcoidosis, eosinophilic gastritis, and lymphocytic gastritis.

Clinical presentation, laboratory investigations, gastroscopy, as well as the histological and microbiological examination of tissue biopsies are essential for the diagnosis of gastritis and its causes.
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 based on their causative etiology.

Etiology
Gastritis can be acute or chronic. The causes of gastritis can be summarized as follows [1][2][3][4][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 relate to tobacco smoking, consumption of alcohol, and/or the use of NSAIDs 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 necessary for the absorption of inorganic iron. Therefore, iron deficiency is commonly a finding in patients with
autoimmune gastritis. Iron deficiency in these patients usually precedes vitamin B12 deficiency. The disease is common in young women.

4. Gastritis may be the result of infection by organisms other than H. pylori such as Mycobacterium avium-intracellulare, enterococcal infection, Herpes simplex, and cytomegalovirus. Parasitic
gastritis may result from cryptosporidium, Strongyloides stercoralis, or anisakiasis infection.

5. Gastritis may result from bile acid reflux.

6. Radiation gastritis.

7. Crohn disease-associated gastritis: This is an uncommon cause of gastritis.

8. Collagenous gastritis: This is a rare cause of gastritis. The disease characteristically presents with 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 remains unestablished, but an association with H. pylori infection or celiac disease has been
suggested.

12. Ischemic gastritis: This is rare and associated with high mortality.

13. Vasculitis-associated gastritis: Diseases causing systemic vasculitis can cause granulomatous infiltration of the stomach. An example is Granulomatosis with polyangiitis, formerly known as
Wegner granulomatosis.

14. Ménétrier disease: This disease is characterized by- (i) Presence of large gastric mucosal folds in the body and fundus of the stomach, (ii) Massive foveolar hyperplasia of surface and
glandular mucous cells, (iii) Protein-losing gastropathy, hypoalbuminemia, and edema in 20 to 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, available data do not have high reliability.[7][8]

Chronic gastritis remains a relatively common disease in developing countries. The prevalence of H. pylori infection in children in the western population is approximately 10% but about 50% in
developing countries.[9][10] In developing countries, the overall 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.

Socioeconomic and environmental hygiene are the essential factors in the transmission of H. pylori infection worldwide. These factors include family-bound hygiene, household density, 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 transmission is via the fecal-oral route. H. pylori possess several 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 present in H. pylori infection.

Chronic gastritis mostly results from 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, corpus, fundus or all.

Factors that determine progression to atrophic gastritis and sequelae such as a peptic ulcer or gastric cancer are not clearly understood and unpredictable. However, Epstein-Barr virus (EBV) and
human cytomegalovirus (HCMV) have been identified in gastric tumors and DNA from H. pylori, EBV, and PCR determined the presence of HCMV in biopsies from patients with gastric cancer
complicating chronic gastritis.[14] Some researchers have confirmed the involvement of EBV and H. pylori in the development of gastric cancer in patients with chronic gastritis. They found no
role for human papillomavirus (HPV) in gastric tumorigenesis.[15]

NSAIDs 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 focuses on two theories. According to the first theory, an immune response against superimposed H. pylori antigen gets 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 assumes that the autoimmune disorder develops irrespective of H. pylori infection, and it directs itself 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]

Histopathology
Histologically, gastritis definitively demonstrates 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] Sampling comes from five gastric biopsy specimens from the following locations: antrum greater and lesser curvature, incisura, and corpus greater and lesser curvature.
Specimens must 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 lost mucosal glands in atrophic gastritis become 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 undergo destruction, 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 are present 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. Many people are asymptomatic or
develop minimal dyspeptic symptoms. If not treated the picture may evolve to chronic gastritis. History of smoking, consumption of alcohol, intake of NSAIDs or steroids, allergies, radiotherapy or
gall bladder disorders should all be considerations. A history of treatment for inflammatory bowel disease, vasculitic disorders, or eosinophilic gastrointestinal disorders might require exploration if
no cause of gastritis is apparent.

The most common initial findings for chronic and autoimmune gastritis are (1) hematological disorders such as anemia (iron-deficiency) detected on routine check-up, (2) positive histological
examination of gastric biopsies, (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 as well as iron studies) commonly presents in the early stages of autoimmune gastritis. Achlorhydria
causing impairment of iron absorption in the duodenum and early jejunum is the main cause.[20] Iron-deficiency anemia could also occur in other types of chronic gastritis.

Autoimmune gastritis is associated with other autoimmune disorders (mainly thyroid diseases) including Hashimoto thyroiditis but also with Addison disease, chronic spontaneous urticaria,
myasthenia gravis, Diabetes type 1, vitiligo, and perioral cutaneous autoimmune disorders especially erosive oral lichen planus.[18] The association between chronic atrophic autoimmune gastritis
and autoimmune thyroid disease earned the name in the early 60s of “thyrogastric syndrome.”

Evaluation

The diagnosis of gastritis has its basis in 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, identifying its distribution, severity, and cause.

The tests used for the diagnosis of H. pylori-associated gastritis fall 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), cultures, 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, simultaneous treatment with proton-pump inhibitors leads 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.

Serological tests for detection of antibodies against H. pylori cannot differentiate between active and past infection.

The diagnosis of autoimmune gastritis centers on laboratory and histological examination. These 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 to pepsinogen 2 ratios.[22][23]

The most sensitive serum biomarker in autoimmune gastritis is parietal cell antibodies (as compared to intrinsic factor antibodies).

The determination of the risk of gastric cancer in autoimmune gastritis is 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 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 necessary for 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 fundus mucosa).[24]

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

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

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

Other forms of treatment in gastritis include cessation of alcohol, smoking, anti-inflammatory drugs, spicy food, as well as 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 with inflammatory bowel disease, particularly Crohn disease

Menetrier disease

Lymphoma

Celiac disease

Multiple endocrine neoplasias

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

Neuroendocrine tumors (NET) (previously referred to as gastric carcinoid; complicates autoimmune gastritis)

Autoimmune gastritis predisposes to the development of both gastric adenocarcinoma and gastric type 1 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 is the process

Vitamin C, vitamin D, folic acid, zinc, magnesium, and calcium deficiency (atrophic autoimmune gastritis)

Pearls and Other Issues

Diagnosis of gastritis depends 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 receive information 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 the general population
maintain hand washing habits and hygiene practices in the long run. The presentation and symptoms of gastritis are not well defined in terms of the clinical picture. Therefore the definite diagnosis
is only based on histological examination of gastric mucosa, and since that is an invasive procedure, many times the diagnosis is estimated and suspected but not confirmed. Healthcare workers,
including doctors, nurses, and pharmacists, need to be aware of this fact when suspecting the disease and be aware of the diagnosis, sequelae, and complications. Patients with autoimmune gastritis
need regular surveillance for early detection of cancer since the risk of gastric neuroendocrine tumor and gastric carcinoma increases. The risk of gastric cancer is also high in patients whose H.
pylori does not get eradicated.

Gastritis diagnosis and treatment require an interprofessional team approach, including physicians, specialists, specialty-trained nurses, and pharmacists, all collaborating across disciplines to
achieve optimal patient results. [Level V]

Questions
To access free multiple choice questions on this topic, click here.

References
1. Watari J, Chen N, Amenta PS, Fukui H, Oshima T, Tomita T, Miwa H, Lim KJ, Das KM. Helicobacter pylori associated chronic gastritis, clinical syndromes, precancerous lesions, and
pathogenesis of gastric cancer development. World J. Gastroenterol. 2014 May 14;20(18):5461-73. [PMC free article: PMC4017061] [PubMed: 24833876]
2. Kulnigg-Dabsch S. Autoimmune gastritis. Wien Med Wochenschr. 2016 Oct;166(13-14):424-430. [PMC free article: PMC5065578] [PubMed: 27671008]
3. Sugano K, Tack J, Kuipers EJ, Graham DY, El-Omar EM, Miura S, Haruma K, Asaka M, Uemura N, Malfertheiner P., faculty members of Kyoto Global Consensus Conference. Kyoto global
consensus report on Helicobacter pylori gastritis. Gut. 2015 Sep;64(9):1353-67. [PMC free article: PMC4552923] [PubMed: 26187502]
4. Kamimura K, Kobayashi M, Sato Y, Aoyagi Y, Terai S. Collagenous gastritis: Review. World J Gastrointest Endosc. 2015 Mar 16;7(3):265-73. [PMC free article: PMC4360446] [PubMed:
25789098]
5. Nayak VH, Engin NY, Burns JJ, Ameta P. Hypereosinophilic Syndrome With Eosinophilic Gastritis. Glob Pediatr Health. 2017;4:2333794X17705239. [PMC free article: PMC5406201]
[PubMed: 28491930]
6. Lambrecht NW. Ménétrier's disease of the stomach: a clinical challenge. Curr Gastroenterol Rep. 2011 Dec;13(6):513-7. [PubMed: 21931998]
7. Coati I, Fassan M, Farinati F, Graham DY, Genta RM, Rugge M. Autoimmune gastritis: Pathologist's viewpoint. World J. Gastroenterol. 2015 Nov 14;21(42):12179-89. [PMC free article:
PMC4641135] [PubMed: 26576102]
8. Carmel R. Prevalence of undiagnosed pernicious anemia in the elderly. Arch. Intern. Med. 1996 May 27;156(10):1097-100. [PubMed: 8638997]
9. Mana F, Vandebosch S, Miendje Deyi V, Haentjens P, Urbain D. Prevalence of and risk factors for H. pylori infection in healthy children and young adults in Belgium anno 2010/2011. Acta
Gastroenterol. Belg. 2013 Dec;76(4):381-5. [PubMed: 24592540]
10. Goh KL, Chan WK, Shiota S, Yamaoka Y. Epidemiology of Helicobacter pylori infection and public health implications. Helicobacter. 2011 Sep;16 Suppl 1:1-9. [PMC free article:
PMC3719046] [PubMed: 21896079]
11. Sipponen P, Maaroos HI. Chronic gastritis. Scand. J. Gastroenterol. 2015 Jun;50(6):657-67. [PMC free article: PMC4673514] [PubMed: 25901896]
12. Azuma T, Yamakawa A, Yamazaki S, Fukuta K, Ohtani M, Ito Y, Dojo M, Yamazaki Y, Kuriyama M. Correlation between variation of the 3' region of the cagA gene in Helicobacter pylori and
disease outcome in Japan. J. Infect. Dis. 2002 Dec 01;186(11):1621-30. [PubMed: 12447739]
13. Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis. The updated Sydney System. International Workshop on the Histopathology of Gastritis, Houston 1994.
Am. J. Surg. Pathol. 1996 Oct;20(10):1161-81. [PubMed: 8827022]
14. Del Moral-Hernández O, Castañón-Sánchez CA, Reyes-Navarrete S, Martínez-Carrillo DN, Betancourt-Linares R, Jiménez-Wences H, de la Peña S, Román-Román A, Hernández-Sotelo D,
Fernández-Tilapa G. Multiple infections by EBV, HCMV and Helicobacter pylori are highly frequent in patients with chronic gastritis and gastric cancer from Southwest Mexico: An
observational study. Medicine (Baltimore). 2019 Jan;98(3):e14124. [PMC free article: PMC6370051] [PubMed: 30653141]
15. de Souza CRT, Almeida MCA, Khayat AS, da Silva EL, Soares PC, Chaves LC, Burbano RMR. Association between Helicobacter pylori, Epstein-Barr virus, human papillomavirus and
gastric adenocarcinomas. World J. Gastroenterol. 2018 Nov 21;24(43):4928-4938. [PMC free article: PMC6250917] [PubMed: 30487702]
16. Rugge M, Genta RM. Staging and grading of chronic gastritis. Hum. Pathol. 2005 Mar;36(3):228-33. [PubMed: 15791566]
17. Varbanova M, Frauenschläger K, Malfertheiner P. Chronic gastritis - an update. Best Pract Res Clin Gastroenterol. 2014 Dec;28(6):1031-42. [PubMed: 25439069]
18. Rodriguez-Castro KI, Franceschi M, Miraglia C, Russo M, Nouvenne A, Leandro G, Meschi T, De' Angelis GL, Di Mario F. Autoimmune diseases in autoimmune atrophic gastritis. Acta
Biomed. 2018 Dec 17;89(8-S):100-103. [PMC free article: PMC6502205] [PubMed: 30561426]
19. Neumann WL, Coss E, Rugge M, Genta RM. Autoimmune atrophic gastritis--pathogenesis, pathology and management. Nat Rev Gastroenterol Hepatol. 2013 Sep;10(9):529-41. [PubMed:
23774773]
20. Hershko C, Ianculovich M, Souroujon M. A hematologist's view of unexplained iron deficiency anemia in males: impact of Helicobacter pylori eradication. Blood Cells Mol. Dis. 2007 Jan-
Feb;38(1):45-53. [PubMed: 17067833]
21. Ricci C, Holton J, Vaira D. Diagnosis of Helicobacter pylori: invasive and non-invasive tests. Best Pract Res Clin Gastroenterol. 2007;21(2):299-313. [PubMed: 17382278]
22. Venerito M, Varbanova M, Röhl FW, Reinhold D, Frauenschläger K, Jechorek D, Weigt J, Link A, Malfertheiner P. Oxyntic gastric atrophy in Helicobacter pylori gastritis is distinct from
autoimmune gastritis. J. Clin. Pathol. 2016 Aug;69(8):677-85. [PubMed: 26729016]
23. Alonso N, Granada ML, Soldevila B, Salinas I, Joaquin C, Reverter JL, Juncà J, Martínez Cáceres EM, Sanmartí A. Serum autoimmune gastritis markers, pepsinogen I and parietal cell
antibodies, in patients with type 1 diabetes mellitus: a 5-year prospective study. J. Endocrinol. Invest. 2011 May;34(5):340-4. [PubMed: 20530988]
24. di Mario F, Cavallaro LG. Non-invasive tests in gastric diseases. Dig Liver Dis. 2008 Jul;40(7):523-30. [PubMed: 18439884]
25. Yang JC, Lu CW, Lin CJ. Treatment of Helicobacter pylori infection: current status and future concepts. World J. Gastroenterol. 2014 May 14;20(18):5283-93. [PMC free article:
PMC4017043] [PubMed: 24833858]
26. Chen WC, Warner RRP, Harpaz N, Zhu H, Roayaie S, Kim MK. Gastric Neuroendocrine Tumor and Duodenal Gastrinoma With Chronic Autoimmune Atrophic Gastritis. Pancreas. 2019
Jan;48(1):131-134. [PubMed: 30531243]
27. Haruma K, Kamada T, Manabe N, Suehiro M, Kawamoto H, Shiotani A. Old and New Gut Hormone, Gastrin and Acid Suppressive Therapy. Digestion. 2018;97(4):340-344. [PubMed:
29587283]

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