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Gastritis and Gastropathy 

Gastritis and Gastropathy
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Gastritis and Gastropathy
Author(s):

Stephanie L. Hansel

DOI:
10.1093/med/9780199373338.003.0006
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date: 23 February 2020

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Inflammation of the stomach can manifest itself as gastritis or gastropathy. Gastritis is a histologic diagnosis referring to inflammatory processes of the stomach. Gastritis may or may not have identifiable endoscopic findings or clinical symptoms. In comparison, gastropathy refers to epithelial damage with little or no inflammation.

There are several classifications of gastritis and gastropathy. Most of them distinguish between acute and chronic disease and the predominant inflammatory infiltrate seen in biopsy specimens. The etiology of the gastritis or gastropathy is also an important factor in the classification, as is the topography or specific areas of involvement in the stomach. The Sydney System (Table 5.1) often is used to classify chronic gastritis. It requires a total of 6 biopsies, 2 biopsy specimens each from the antrum, the body, and the incisura (Figure 5.1). In some cases, duodenal biopsies may assist in the overall diagnosis of a disease, for example, celiac disease in patients with lymphocytic gastritis, Crohn disease in patients with granulomatous gastritis, and eosinophilic gastroenteritis in patients with eosinophilic infiltration of the antrum.

Table 5.1. Sydney System for Classification of Chronic Gastritis

Type of Gastritis

Etiologic Factors

Gastritis Synonyms

Nonatrophic

Helicobacter pylori

  • Superficial

  • Diffuse antral gastritis

  • Chronic antral gastritis

  • Interstitial follicular

  • Type B

Atrophic-autoimmune

  • Autoimmunity

  • H pylori

  • Type A

  • Diffuse corporeal

  • Pernicious anemia

Atrophic-multifocal

H pylori

  • Type B

  • Environmental

  • Metaplastic

  • Atrophic pangastritis

  • Progressive intestinalizing pangastritis

Chemical/radiation

  • Bile

  • Nonsteroidal antiinflammatory drugs

  • Alcohol or other agents (possibly)

  • Radiation

  • Reactive

  • Reflux

  • Radiation

Lymphocytic

  • Idiopathic

  • Autoimmune

  • Gluten

  • H pylori

  • Varioliform

  • Celiac-associated

Granulomatous

  • Crohn disease

  • Sarcoidosis

  • Wegener granulomatosis

  • Infectious

Isolated granulomatous

Eosinophilic

  • Food sensitivities

  • Allergies

  • Idiopathic

Allergic

Infectious gastritides

  • Bacteria

  • Viruses

  • Fungi

  • Parasites

  • Phlegmonous

  • Cytomegalovirus

  • Anisakiasis

Figure 5.1. Gastric Biopsy Protocol to Diagnose Gastritis. Biopsy specimens (circles) should be obtained from the greater and lesser curvatures of the body and the antrum and from the incisura (dotted line).

Figure 5.1.
Gastric Biopsy Protocol to Diagnose Gastritis. Biopsy specimens (circles) should be obtained from the greater and lesser curvatures of the body and the antrum and from the incisura (dotted line).

Gastritis

Acute Gastritis

By definition, acute gastritis is an acute inflammatory process that involves the stomach with a predominantly neutrophilic infiltration. It may or may not have features of intramucosal hemorrhage, superficial mucosal sloughing, or erosion. Most often, acute gastritis is related to aspirin or nonsteroidal antiinflammatory drugs (NSAIDs), excess alcohol intake, uremic toxins, heavy tobacco use, cancer chemotherapeutic drugs, ischemia, or infection.

Acute gastritis due to Helicobacter pylori (HP) infection is rarely identified. Abdominal pain, nausea, or vomiting may develop. Endoscopic findings such as erythema or erosion are absent or nonspecific. Biopsy specimens show mucosal neutrophilic infiltration in the antrum, with or without desquamation and erosions. In the great majority of persons acutely infected with HP, an active chronic gastritis develops.

Aspirin and NSAIDs can produce an acute injury to the gastric mucosa. With gastritis, endoscopic findings range from minimally visible changes to erythema, petechial hemorrhages, or erosions. Histologically, there can be evidence of superficial lamina propria hemorrhage, mucosal sloughing, neutrophilic infiltration, and mucosal necrosis. The changes are limited to the mucosa and do not extend into the muscularis mucosa. Clinical symptoms such as abdominal pain, nausea, vomiting, or gastrointestinal tract bleeding may or may not be present as well. Similar findings occur after the ingestion of large amounts of alcohol and other toxic substances and after ischemia (Figure 5.2). All these insults impair mucosal barrier function by affecting prostaglandin synthesis (NSAIDs) or mucosal blood flow (alcohol or ischemia) or by direct injury to the surface mucosal cells (NSAIDs, other drugs, or infection). Treatment of acute gastritis includes management of the underlying condition, withdrawal of any offending drug or toxin, and acid-suppression therapy with a proton pump inhibitor.

Figure 5.2. Acute Hemorrhagic Gastritis.

Figure 5.2.
Acute Hemorrhagic Gastritis.

(From Emory TS, Carpenter HA, Gostout CJ, Sobin LH. Atlas of gastrointestinal endoscopy & endoscopic biopsies. Washington, DC: Armed Forces Institute of Pathology, American Registry of Pathology; c2000. p. 101.)

Chronic Gastritis

Chronic gastritis is classified in the Sydney System as nonatrophic, atrophic, or special forms. Mucosal injury occurs in all forms of chronic gastritis. The atrophic forms of chronic gastritis can be autoimmune or multifocal, and, subsequently, metaplasia, dysplasia, and carcinoma may develop.

Nonatrophic Chronic Gastritis

Nonatrophic chronic gastritis is typical in HP-infected persons with acute gastritis who do not clear the infection (Figure 5.3). Endoscopically, gastric mucosal erythema, erosions, granularity, and nodularity may be seen. It usually is most evident in the antrum. Histologically, there is marked lymphoplasmacytic and neutrophilic infiltrate. Lymphoid aggregates or germinal centers may be seen. Gastric atrophy, metaplasia, and dysplasia are not seen. However, this type of active chronic gastritis due to HP infection does increase the risk of duodenal ulcer disease.

Figure 5.3. Active (Nonatrophic) Chronic Gastritis of the Antrum of the Stomach. Stain is hematoxylin-eosin.

Figure 5.3.
Active (Nonatrophic) Chronic Gastritis of the Antrum of the Stomach. Stain is hematoxylin-eosin.

(From Emory TS, Carpenter HA, Gostout CJ, Sobin LH. Atlas of gastrointestinal endoscopy & endoscopic biopsies. Washington, DC: Armed Forces Institute of Pathology, American Registry of Pathology; c2000. p. 90.)

Atrophic Chronic Gastritis

Multifocal Atrophic Gastritis.

Multifocal atrophic gastritis may develop in persons infected with HP. This type of active chronic gastritis includes the loss of glands and metaplastic change principally involving the body and antrum of the stomach (Figure 5.4). Inflammation consists of both acute and chronic inflammatory cells. There is an increased risk of gastric ulcer disease and gastric adenocarcinoma with this type of gastritis.

Figure 5.4. Multifocal Atrophic Gastritis.

Figure 5.4.
Multifocal Atrophic Gastritis.

(From Emory TS, Carpenter HA, Gostout CJ, Sobin LH. Atlas of gastrointestinal endoscopy & endoscopic biopsies. Washington, DC: Armed Forces Institute of Pathology, American Registry of Pathology; c2000. p. 93.)

Autoimmune Atrophic Gastritis.

Patients with autoimmune atrophic gastritis can present with abdominal discomfort or pain, weight loss, and pernicious anemia. This type of gastritis is an autosomal dominant condition and is responsible for less than 5% of all cases of chronic gastritis (Figure 5.5). It involves the body and fundus of the stomach, sparing the antrum. Endoscopically, there is a loss of gastric folds and prominence of the submucosal vasculature. Laboratory findings include autoantibodies to parietal cells and intrinsic factor, elevated serum gastrin level, and low vitamin B12 level. Hypochlorhydria, achlorhydria, iron deficiency, or pernicious anemia may develop in some but not all patients. Histologically, the abnormal findings are limited to the body and fundic mucosa. Typically, there is a loss of oxyntic glands (chief and parietal cells) and a prominent lamina propria lymphocytic and plasma cell infiltration directed at the fundic glands. Patients do have a small risk of gastric carcinoids (<10%) and gastric carcinoma (<3%). Patients or their relatives may have other autoimmune disorders, including Hashimoto thyroiditis, Graves disease, Addison disease, diabetes mellitus, and vitiligo. There is also an association with HLA-B8 and HLA-DR3.

Figure 5.5. Chronic Autoimmune Atrophic Gastritis. A, Gross appearance. B, Section through the body of the stomach (hematoxylin-eosin stain).
Figure 5.5. Chronic Autoimmune Atrophic Gastritis. A, Gross appearance. B, Section through the body of the stomach (hematoxylin-eosin stain).

Figure 5.5.
Chronic Autoimmune Atrophic Gastritis. A, Gross appearance. B, Section through the body of the stomach (hematoxylin-eosin stain).

(From Emory TS, Carpenter HA, Gostout CJ, Sobin LH. Atlas of gastrointestinal endoscopy & endoscopic biopsies. Washington, DC: Armed Forces Institute of Pathology, American Registry of Pathology; c2000. p. 94.)

Special Forms of Gastritis

Infectious Gastritis.

Bacterial gastritis is most often caused by HP (see Chapter 4, “Peptic Ulcer Disease”). However, other species of bacteria may be found in the stomach after antrectomy or in association with achlorhydria. Organisms such as Streptococcus, Staphylococcus, Lactobacillus, Bacteroides, Klebsiella, and Escherichia coli have all been cultured from gastric juice but rarely are of clinical significance. These organisms likely represent oral flora that has been swallowed. In circumstances of ischemia or immunosuppression, these organisms may produce marked morbidity.

Mycobacterium tuberculosis is an important cause of bacterial gastritis in developing countries. Patients present with weight loss, anorexia, night sweats, and fevers and can have symptoms of gastric outlet obstruction. Biopsies from ulcerated or nodular areas with stains for acid-fast bacilli and tuberculosis cultures are necessary for diagnosis. Secondary or tertiary syphilis can also involve the stomach, especially the antrum.

Phlegmonous gastritis is a rare, life-threatening condition associated with full-thickness purulent necrosis of the gastric wall. Multiple bacteria are responsible, and it usually occurs in immunocompromised patients, including alcoholics and patients with diabetes mellitus. Invasive procedures may trigger the onset, with fever, chills, abdominal pain, and hypotension being common. If gas-forming organisms are involved, emphysematous changes may be apparent on imaging studies. The mortality rate is high, and surgery may be required to remove the necrotic portion of the stomach.

Cytomegalovirus (CMV) infection is the most commonly recognized viral infection of the stomach (Figure 5.6). This infection may or may not have endoscopic findings that include edema, erythema, erosions, or ulcers. Patients with CMV infection of the stomach may or may not have symptoms, such as fever, abdominal pain, nausea, vomiting, or bleeding, and they usually are immunosuppressed. Biopsy specimens from macroscopically involved and apparently normal areas may show typical cytomegalic cells and inclusions. When ulceration is present, biopsy specimens from the center of the ulcer are more likely to be diagnostic than specimens from the edge because of vascular endothelial involvement of this virus. In cases in which the diagnosis is in doubt, immunohistochemistry enhances the diagnostic yield.

Figure 5.6. Cytomegalovirus (CMV) Infection of the Stomach. A, Gross appearance of CMV ulcers. B, CMV gastropathy (hematoxylin-eosin stain).
Figure 5.6. Cytomegalovirus (CMV) Infection of the Stomach. A, Gross appearance of CMV ulcers. B, CMV gastropathy (hematoxylin-eosin stain).

Figure 5.6.
Cytomegalovirus (CMV) Infection of the Stomach. A, Gross appearance of CMV ulcers. B, CMV gastropathy (hematoxylin-eosin stain).

(From Emory TS, Carpenter HA, Gostout CJ, Sobin LH. Atlas of gastrointestinal endoscopy & endoscopic biopsies. Washington, DC: Armed Forces Institute of Pathology, American Registry of Pathology; c2000. p. 123.)

Fungal and parasitic infections of the stomach are uncommon. In immunosuppressed patients, gastric infections may be caused by Histoplasma, Candida, Aspergillus, Cryptococcus, Torulopsis, or mucormycosis. Ingestion of raw fish can result in anisakiasis. Cryptosporidium and Strongyloides infections do not commonly involve the stomach, especially in immunosuppressed patients.

Noninfectious Granulomatous Gastritis.

In the absence of infection, granulomatous gastritis (Figure 5.7) occurs most commonly with Crohn disease (52%). The differential diagnosis includes isolated granulomatous gastritis (25%), foreign body granuloma (10%; eg, suture, food), tumor-associated granuloma, sarcoidosis, infection (HP, tuberculosis, histoplasmosis, syphilis), and vasculitis-associated granulomas. Most often, an antral inflammatory infiltration is found. Many patients with granulomatous gastritis are asymptomatic. In a few patients, particularly those with Crohn disease or sarcoidosis, symptoms of gastric outlet obstruction due to ulceration and scarring of the antrum and pylorus can develop. Nonspecific treatment, such as acid-reduction therapy, or therapy directed toward the underlying disorder usually is indicated.

Figure 5.7. Granulomatous Gastritis. A, Gross appearance. B, Histologic appearance of granuloma (hematoxylin-eosin stain).
Figure 5.7. Granulomatous Gastritis. A, Gross appearance. B, Histologic appearance of granuloma (hematoxylin-eosin stain).

Figure 5.7.
Granulomatous Gastritis. A, Gross appearance. B, Histologic appearance of granuloma (hematoxylin-eosin stain).

(From Emory TS, Carpenter HA, Gostout CJ, Sobin LH. Atlas of gastrointestinal endoscopy & endoscopic biopsies. Washington, DC: Armed Forces Institute of Pathology, American Registry of Pathology; c2000. p. 98, 99.)

Lymphocytic Gastritis.

Lymphocytic gastritis is uncommon and often is asymptomatic. If symptoms do occur, dyspepsia and diarrhea are the most common. On endoscopy, mucosal nodules, erosions, and enlarged gastric folds may be seen. Histologically, there is active chronic pangastritis with epithelial infiltration by mature lymphocytes, usually T lymphocytes (Figure 5.8). The lamina propria is expanded by the lymphocytes and plasma cells. Most often, when found in patients with celiac disease, lymphocytic gastritis is antral predominant. However, when lymphocytic gastritis occurs in patients with HP infection, it tends to be gastric body predominant and often has polymorphonuclear cells. Staining for HP should be performed in every case of lymphocytic gastritis. Patients with microscopic colitis or Ménétrier disease may also have lymphocytic gastritis. Therapy is directed toward the underlying condition.

Figure 5.8. Lymphocytic Gastritis. Intraepithelial lymphocytes can be seen without any destruction of surrounding epithelial cells (hematoxylin-eosin stain).

Figure 5.8.
Lymphocytic Gastritis. Intraepithelial lymphocytes can be seen without any destruction of surrounding epithelial cells (hematoxylin-eosin stain).

(From Owen DA. Gastritis and carditis. Mod Pathol. 2003 Apr;16[4]‌:325-41. Used with permission.)

Eosinophilic Gastritis.

A wide variety of disorders are associated with eosinophilic infiltration of the stomach, including parasitic infestation, hypereosinophilic syndrome, gastric Crohn disease, gastric carcinoma, lymphoma, connective tissue disorder, peptic ulcer disease, mast cell disease, and Churg-Strauss vasculitis. Eosinophilic gastroenteritis, also called allergic gastroenteritis, is a rare inflammatory condition. Patients generally have a history of allergy, asthma, food intolerance, eczema, drug sensitivities, or peripheral eosinophilia and increased serum levels of immunoglobulin E. On endoscopy, the gastric mucosa ranges from normal to erosions and erythema. In the most common mucosa-predominant form, biopsy specimens typically show patchy but dense eosinophilic infiltration (Figure 5.9). The antrum is typically involved. Less commonly, full-thickness or open biopsy may be necessary for diagnosis if only the muscle or serosa layers are affected. Corticosteroids are used for treatment.

Figure 5.9. Eosinophilic Gastritis. Note the marked eosinophilic infiltration. A, High-power view. B, Low-power view.
Figure 5.9. Eosinophilic Gastritis. Note the marked eosinophilic infiltration. A, High-power view. B, Low-power view.

Figure 5.9.
Eosinophilic Gastritis. Note the marked eosinophilic infiltration. A, High-power view. B, Low-power view.

(From Emory TS, Carpenter HA, Gostout CJ, Sobin LH. Atlas of gastrointestinal endoscopy & endoscopic biopsies. Washington, DC: Armed Forces Institute of Pathology, American Registry of Pathology; c2000. p. 97.)

Gastropathy

Chemical Gastropathy

Long-term exposure to substances that can damage the gastric mucosa can result in chronic gastropathy. Other common names for this condition include reactive gastritis, reactive gastropathy, and bile reflux gastritis or gastropathy. The etiology includes aspirin or NSAIDs, bile reflux, and alcohol. Endoscopic findings include edema, erythema, erosions, and visible bile in the stomach. The antrum is most commonly involved, and biopsy specimens show foveolar hyperplasia, loss of mucin, proliferation of lamina propria smooth muscle, and vascular congestion in the lamina propria. Bile reflux gastropathy usually follows surgical intervention, such as gastroenterostomy, vagotomy, or pyloroplasty, but can occur in persons with gastric emptying disorders or in stomachs that have not had a surgical procedure. Symptoms such as epigastric discomfort, nausea, and vomiting do not correlate well with endoscopic or histologic findings. Treatment of chemical gastropathy includes discontinuing use of the offending agent if possible and using acid-reducing medication and ursodiol if bile acid is the most likely cause. Cholestyramine, sucralfate, and aluminum-containing antacids have been prescribed for bile acid gastropathy but have mostly been unsuccessful. Ursodiol has been shown to decrease symptoms without improving histologic findings. A surgical Roux-en-Y revision to divert bile from the stomach in patients with previous gastroenterostomy and symptomatic bile reflux gastropathy has been found to reduce symptoms in 50% to 90% of these patients.

Vascular Gastropathies

Vascular gastropathies are defined as abnormalities of the gastric vasculature affecting mucosal blood vessels, with little or no inflammation. Typical examples include congestive gastropathy from congestive heart failure, portal hypertensive gastropathy, and gastric vascular ectasia (ie, watermelon stomach).

In patients with portal hypertension, dilatation and sclerosis of small mucosal and submucosal venules and capillaries can produce an endoscopically recognizable mucosal mosaic pattern, usually most prominent in the fundus and body of the stomach (Figure 5.10). Nodularity and punctate erythema also may be seen. Clinically, patients may have iron deficiency anemia or melena. Treatment involves attempts to lower portal pressure; endoscopic therapy is not effective (see Chapter 26, “Vascular Diseases of the Liver”).

Figure 5.10. Portal Hypertensive Gastropathy. A and B, Gross specimens showing the mosaic mucosal pattern. C, Histologic section showing dilated, tortuous blood vessels (hematoxylin-eosin stain).
Figure 5.10. Portal Hypertensive Gastropathy. A and B, Gross specimens showing the mosaic mucosal pattern. C, Histologic section showing dilated, tortuous blood vessels (hematoxylin-eosin stain).
Figure 5.10. Portal Hypertensive Gastropathy. A and B, Gross specimens showing the mosaic mucosal pattern. C, Histologic section showing dilated, tortuous blood vessels (hematoxylin-eosin stain).

Figure 5.10.
Portal Hypertensive Gastropathy. A and B, Gross specimens showing the mosaic mucosal pattern. C, Histologic section showing dilated, tortuous blood vessels (hematoxylin-eosin stain).

(From Emory TS, Carpenter HA, Gostout CJ, Sobin LH. Atlas of gastrointestinal endoscopy & endoscopic biopsies. Washington, DC: Armed Forces Institute of Pathology, American Registry of Pathology; c2000. p. 116.)

Patients with gastric vascular ectasia develop dilated mucosal capillaries with fibrin thrombi and fibromuscular hyperplasia of the lamina propria with minimal or no inflammation. Endoscopic findings typically include linear or nodular erythematous streaks without a mosaic pattern, usually involving the antrum but sometimes extending into the gastric body (Figure 5.11). Gastric vascular ectasia tends to occur in patients who have an array of underlying conditions, including pernicious anemia, collagen vascular disease, cirrhosis, renal failure, bone marrow transplant, and antral mucosal trauma (as in pyloric prolapse). Similar to patients with portal hypertensive gastropathy, patients may have iron deficiency anemia or melena. Endoscopic therapy with argon plasma coagulation can diminish blood loss in patients with anemia (see Chapter 11, “Nonvariceal Gastrointestinal Tract Bleeding”). Of note, liver transplant can benefit patients with gastric vascular ectasia who have cirrhosis, but transjugular intrahepatic portosystemic shunts are not helpful (see Chapter 26, “Vascular Diseases of the Liver”).

Figure 5.11. Watermelon Stomach (Antrum). A, Gross specimen. B, Histologic section showing thick-walled, ectatic vessels (hematoxylin-eosin stain).
Figure 5.11. Watermelon Stomach (Antrum). A, Gross specimen. B, Histologic section showing thick-walled, ectatic vessels (hematoxylin-eosin stain).

Figure 5.11.
Watermelon Stomach (Antrum). A, Gross specimen. B, Histologic section showing thick-walled, ectatic vessels (hematoxylin-eosin stain).

(From Emory TS, Carpenter HA, Gostout CJ, Sobin LH. Atlas of gastrointestinal endoscopy & endoscopic biopsies. Washington, DC: Armed Forces Institute of Pathology, American Registry of Pathology; c2000. p. 118.)

Hypertrophic Gastropathy

Hypertrophic gastropathy refers to a group of conditions with giant enlargement of the rugal folds. This group includes some cases of chronic gastritis from HP infection or lymphocytic gastritis, Zollinger-Ellison syndrome, infiltrative disorders (sarcoidosis and malignancy), and Ménétrier disease. Patients with Ménétrier disease often have such symptoms as epigastric pain, nausea, vomiting, diarrhea, edema, and weight loss. Many patients have evidence of a protein-losing enteropathy manifested by low serum level of albumin and increased stool clearance of alpha1-antitrypsin. Endoscopically, giant gastric rugal folds and a cobblestone pattern are present but may spare the antrum. A full-thickness gastric biopsy specimen or endoscopic snare biopsy specimen from an enlarged fold usually is necessary to make the diagnosis. Histologic examination shows extreme surface mucous cell hyperplasia with deeper glandular atrophy. Often, gastric hypochlorhydria or achlorhydria is present together with excessive secretion of mucus. Increased levels of transforming growth factor-α‎ may be responsible for the histologic changes. Improvement in symptoms after the subcutaneous administration of octreotide has been inconsistent. In addition to gastric resection, treatment with investigational agents to counteract the effects of transforming growth factor-α‎ has been successful. It is unclear whether patients with Ménétrier disease have an increased risk of gastric adenocarcinoma.

Suggested Reading

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El-Zimaity H. Gastritis and gastric atrophy. Curr Opin Gastroenterol. 2008 Nov;24(6):682-6.Find this resource:

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Park JY, Lam-Himlin D, Vemulapalli R. Review of autoimmune metaplastic atrophic gastritis. Gastrointest Endosc. 2013 Feb;77(2):284-92. Epub 2012 Nov 27.Find this resource:

Ripoll C, Garcia-Tsao G. The management of portal hypertensive gastropathy and gastric antral vascular ectasia. Dig Liver Dis. 2011 May;43(5):345-51. Epub 2010 Nov 20.Find this resource:

Rugge M, Fassan M, Pizzi M, Zorzetto V, Maddalo G, Realdon S, et al. Autoimmune gastritis: histology phenotype and OLGA staging. Aliment Pharmacol Ther. 2012 Jun;35(12):1460-6. Epub 2012 Apr 22.Find this resource:

Notes:

Abbreviations: CMV, cytomegalovirus; HP, Helicobacter pylori; NSAID, nonsteroidal antiinflammatory drug