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Practical Approach to the Pathologic Diagnosis of Gastritis



Gastritis refers to a group of diseases characterized by inflammation of the gastric mucosa. Histologic examination of gastric mucosal biopsies is necessary to establish a diagnosis of gastritis. In clinical practice, the role of the pathologist who evaluates a gastric biopsy for gastritis is to find the cause of gastritis because that will provide direct targets toward which therapeutic measures can be directed. An etiologic classification of gastritis is presented at the end of this section. Comprehensive reviews of gastritis have been published.1,2,3 The goal of this article is to present a practical approach to the diagnosis of the most common types of gastritis encountered in a large practice of gastrointestinal pathology. The reader will be presented several cases representative of typical forms of gastritis; for each case, the reader will be prompted through a series of questions to examine the histologic features of the mucosa, leading to a pattern of answers and to a final diagnosis.

The first question is aimed at determining whether or not there are features of chronic or acute (active) gastritis present. If the biopsy shows chronic gastritis, the following questions should be posed:

1. Are there features of chronic gastritis present? Lymphocytic and plasmacytic inflammatory reaction indicates chronic gastritis.

2. Are there neutrophils neutrophils (ner·ō·trōˑ·filz),
n.pl white blood cells with cytoplasmic granules that consume harmful bacteria, fungi, and other foreign materials.
 in the mucosa? The presence of neutrophils indicate active gastritis.

3. Is there Helicobacter?

4. Is there glandular glandular /glan·du·lar/ (glan´du-ler)
1. pertaining to or of the nature of a gland.

2. glanular.


glan·du·lar
adj.
1.
 atrophy? Is intestinal metaplasia metaplasia /meta·pla·sia/ (met?ah-pla´zhah) the change in the type of adult cells in a tissue to a form abnormal for that tissue.  present?

5. What is the topography of lesions (predominantly in the oxyntic oxyntic /ox·yn·tic/ (ok-sint´ik) secreting acid, as the parietal (oxyntic) cells.

ox·yn·tic
adj.
Forming or secreting acid, as the parietal cells of gastric glands.
 mucosa of the body and fundus fundus /fun·dus/ (fun´dus) pl. fun´di   [L.] the bottom or base of anything; the bottom or base of an organ, or the part of a hollow organ farthest from its mouth. , predominantly in antrum antrum /an·trum/ (an´trum) pl. an´tra, antrums   [L.] a cavity or chamber.an´tral

cardiac antrum
, or involving both locations)?

6. Are there special features (such as granulomas, foveolar hyperplasia, viral inclusions)?

7. What ancillary studies are indicated, and what are the results?

TYPES OF CHRONIC GASTRITIS

Infectious Gastritis

Helicobacter pylori infection is the most common cause of chronic gastritis. Other forms of infectious gastritis include the following: Helicobacter heilmannii-associated gastritis; granulomatous granulomatous /gran·u·lom·a·tous/ (-lom´ah-tus) containing granulomas.
Granulomatous
Resembling a tumor made of granular material.
 gastritis associated with gastric infections in mycobacteriosis, syphilis, histoplasmosis histoplasmosis: see fungal infection. , mucormycosis, South American blastomycosis South American Blastomycosis Definition

South American blastomycosis is a potentially fatal, chronic fungus infection that occurs more often in men.
, anisakiasis or anisakidosis; chronic gastritis associated with parasitic infections; and viral infections, such as cytomegalovirus cytomegalovirus (sī'təmĕg'əlōvī`rəs), member of the herpesvirus family that can cause serious complications in persons with weakened immune systems.  and herpesvirus herpesvirus, any of the family (Herpesviridae) of common DNA-containing viruses, many of which are associated with human disease. See cytomegalovirus; Epstein-Barr virus; herpes simplex; herpes zoster.  infection.

Noninfectious Gastritis

Noninfectious gastritis is associated with autoimmune gastritis; reactive or chemical gastropathy, usually related to chronic bile reflux or nonsteroidal anti-inflammatory drug nonsteroidal anti-inflammatory drug, a drug that suppresses inflammation in a manner similar to steroids, but without the side effects of steroids; commonly referred to by the acronym NSAID (ĕn`sĕd).  (NSAID NSAID: see nonsteroidal anti-inflammatory drug. ) intake; uremic uremic

pertaining to or emanating from uremia.


uremic poisoning
see uremia, visceral gout.

uremic toxins
 gastropathy; noninfectious granulomatous gastritis; lymphocytic gastritis, including gastritis associated with celiac disease; eosinophilic eosinophilic /eo·sin·o·phil·ic/ (-fil´ik)
1. readily stainable with eosin.

2. pertaining to eosinophils.

3. pertaining to or characterized by eosinophilia.
 gastritis; radiation injury to the stomach; graft-versus-host disease; ischemic Ischemic
An inadequate supply of blood to a part of the body, caused by partial or total blockage of an artery.

Mentioned in: Antiangiogenic Therapy, Subarachnoid Hemorrhage, Ventricular Fibrillation


ischemic
 gastritis; and gastritis secondary to chemotherapy.

Many cases of gastritis are of undetermined cause and present as chronic, inactive gastritis with various degrees of severity.3

TYPES OF ACUTE GASTRITIS

Many of the forms of chronic gastritis may present with an acute form, with progression to chronic gastritis because of persisting injury or sequelae sequelae Clinical medicine The consequences of a particular condition or therapeutic intervention . This is the case of gastritis associated with long-term intake of aspirin and other NSAIDs and bile reflux into the stomach; excessive alcohol consumption; heavy smoking; cancer chemotherapeutic drugs and radiation; acids and alkali in suicide attempts; uremia uremia (yrē`mēə), condition resulting from advanced stages of kidney failure in which urea and other nitrogen-containing wastes are found in the blood. ; severe stress (trauma, burns, surgery); ischemia and shock; systemic infections; mechanical trauma, such as intubation intubation /in·tu·ba·tion/ (in?too-ba´shun) the insertion of a tube into a body canal or hollow organ, as into the trachea.

endotracheal intubation
 associated mucosal lesions; and viral infections.

Case 1

A 60-year-old man underwent esophagogastroduodenoscopy. A biopsy of gastric antrum was submitted to pathology to rule out H pylori. The histologic findings are shown in Figure 1, A through C.

Findings. Examination of the biopsy material available gives the following answers:

1. Are there features of chronic gastritis? Yes. The gastric antral mucosa shows expansion of the lamina propria by chronic inflammatory cells, consisting of plasma cells and small lymphocytes, predominantly located toward the luminal aspect of the mucosa, a pattern that is suggestive of H pylori infection.

2. Are there neutrophils in the mucosa? Yes. Therefore, this represents active gastritis. This is a mild form of active gastritis.

3. Is there Helicobacter? Yes. Hematoxylin-eosin (H&E) examination reveals diagnostic H pylori bacterial forms in the surface mucus layer in close proximity to the apical apical /ap·i·cal/ (ap´i-k'l) pertaining to an apex.

a·pi·cal
adj.
1. Relating to the apex of a pyramidal or pointed structure.

2.
 aspect of surface epithelial cells.

4. Is there glandular atrophy? The biopsy sample available is not adequate for evaluation of atrophic gastritis; multiple biopsies, including samples of gastric body, are necessary for adequate evaluation of glandular atrophy. Is there intestinal metaplasia? Yes.

5. What is the topography of lesions? The chronic gastritis in this case involves, at minimum, the gastric antrum; it is advisable to obtain biopsy samples of both gastric antrum and body for a better evaluation of gastritis, as recommended by the updated Sydney guidelines4 for classification of gastritis.

6. Are additional special features present? No.

7. Are special stains recommended? No.

Diagnosis. Gastric antral mucosa with H pylori-associated chronic gastritis, mildly active, and focal intestinal metaplasia.

HPYLORI-ASSOCIATED CHRONIC GASTRITIS

The Helicobacter species consist of gram-negative rods that infect the gastric mucosa. Helicobacter pylori bacteria are 3.5 µm long and are generally comma-shaped or have slightly spiral forms. Helicobacter heilmannii, a rare agent of chronic gastritis, is a 5- to 9-µm-long bacterium, with a characteristic tightly corkscrew-shaped, spiral form.5 Helicobacter pylori infection usually is acquired during childhood, persisting as chronic gastritis if the organism is not eradicated. During progression of gastritis over the years, the gastric mucosa undergoes a sequence of changes that may lead to glandular atrophy, intestinal metaplasia, increased risk of gastric dysplasia and carcinoma,6-9 and mucosa-associated lymphoid tissue lymphoma mucosa-associated lymphoid tissue lymphoma See MALT lyphoma. ,10,11 reported as extranodal, marginal zone, B-cell lymphoma in the World Health Organization classification.12

Helicobacter pylori infection is associated with the histologic pattern of active and chronic gastritis, reflecting the presence of neutrophils and mononuclear mononuclear /mono·nu·cle·ar/ (-noo´kle-er)
1. having but one nucleus.

2. a cell having a single nucleus, especially a monocyte of the blood or tissues.


mon·o·nu·cle·ar
adj.
 cells (lymphocytes and plasma cells) in the mucosa, respectively. The term active gastritis is preferred to acute gastritis because H pylori gastritis is a long-standing chronic infection with ongoing activity. Lymphoid lymphoid /lym·phoid/ (lim´foid) resembling or pertaining to lymph or tissue of the lymphoid system.

lym·phoid
adj.
Of or relating to lymph or the lymphatic tissue where lymphocytes are formed.
 aggregates and lymphoid follicles follicles,
n the masses that are embedded in a meshwork of reticular fibers within the lobules of the thyroid gland. See also thyroid gland.
 may be observed expanding the lamina propria, and rare lymphocytes may enter the epithelium. Helicobacter pylori organisms are found within the gastric mucus layer that overlays the apical side of gastric surface cells, and lower numbers are found in the lower portions of the gastric foveolae. Helicobacter pylori may be found within the deeper areas of the mucosa in association with glandular cells in patients on acid blockers, such as the commonly used proton pump inhibitors Proton Pump Inhibitors Definition

The proton pump inhibitors are a group of drugs that reduce the secretion of gastric (stomach) acid. They act by binding with the enzyme H+, K(+)-ATPase, hydrogen/potassium adenosine triphosphatase
.13

Helicobacter pylori-associated gastritis can display different levels of severity. The severity of H pylori gastritis activity may be indicated in a pathology report as mild (rare neutrophils seen), moderate (obvious neutrophils within the glandular and foveolar epithelium), or severe (numerous neutrophils with glandular microabscesses and mucosal erosion or frank ulceration).4,14

Helicobacter pylori-associated chronic gastritis can manifest as a pangastritis involving the area from the pylorus pylorus /py·lo·rus/ (pi-lor´us) the distal aperture of the stomach, opening into the duodenum; variously used to mean pyloric part of the stomach, and pyloric antrum, canal, opening, or sphincter.  to the gastric body and cardia cardia /car·dia/ (kahr´de-ah)
1. the cardiac opening.

2. the cardiac part of the stomach, surrounding the esophagogastric junction and distinguished by the presence of cardiac glands.
, or it may predominantly involve the antrum. Patients with gastric ulcers generally have antral-predominant gastritis, whereas pangastritis, or at least multifocal multifocal /mul·ti·fo·cal/ (mul?te-fo´k'l) arising from or pertaining to many foci.

mul·ti·fo·cal
adj.
Relating to or arising from many foci.
 gastritis, is more common in patients with gastric carcinoma. The latter generally have significant intestinal metaplasia and gastric oxyntic glandular atrophy coexisting in the background stomach. It is important to make a pathologic diagnosis of atrophic gastritis because gastric atrophy is associated with increased risk of gastric cancer.15,16 Patients with chronic atrophic gastritis may have up to a 16-fold increased risk of developing gastric carcinoma, compared with the general population. 15,17

When large numbers of H pylori are present in the mucosa, the identification of typical organisms is generally possible on H&E stains. However, there are cases of chronic, active gastritis with features suggestive of H pylori gastritis in which the organisms are not detected. Several special stains have been extensively used to help identify H pylori organisms in the gastric mucosa, including modified-Giemsa, Genta, thiazine thi·a·zine or thi·a·zin
n.
Any of a class of organic chemical compounds containing a ring composed of one sulfur atom, one nitrogen atom, and four carbon atoms, used in making dyes.
 stains, and immunohistochemistry against Helicobacter antigens. The selection of the special stain used is largely dependent on preferences related to individual practices. Although, overall, no major differences in sensitivity and specificity have been reported, studies have recommended immunohistochemical stains in a subset of cases.18,19 In our practice, we prefer to use immunohistochemical stains for detection of H pylori if organisms are not found on H&E stains in the following cases: (1) if moderate to severe chronic gastritis or any grade of active gastritis is present but no Helicobacter organisms are identified on H&E; (2) when extensive intestinal metaplasia is present because H pylori density is reduced in areas of intestinal metaplasia; and (3) during follow-up biopsies after antibiotic treatment for H pylori.

Helicobacter heilmannii may cause similar pathology, and the treatment is similar to H pylori.5

Case 2

A 45-year-old man is seen to rule out H pylori. He presents with a history of Crohn disease. The histologic findings are shown in Figure 2.

Findings. Examination of the biopsy material results in the following pattern of answers:

1. Are there features of chronic gastritis? Yes. The gastric antral mucosa shows expansion of the lamina propria by chronic inflammatory cells, consisting of admixed plasma cells and small lymphocytes, throughout the thickness of the mucosa.

2. Are there neutrophils in the mucosa? Yes, with an occasional glandular abscess abscess, localized inflamation associated with tissue necrosis. Abscesses are characterized by inflamation, which is due to the accumulation of pus in the local tissues, and often painful swelling. ; therefore, there is active gastritis. Of note, the active gastritis has a patchy distribution.

3. Is there Helicobacter? No. Examination with H&E stain does not reveal such bacterial forms. Immunohistochemical stain is performed.

4. Is there atrophy? The biopsy sample available is not adequate for evaluation of atrophic gastritis because the biopsy material is only from the gastric antrum; multiple gastric body biopsies are necessary for adequate evaluation of glandular atrophy. There is no intestinal metaplasia.

5. What is the topography of lesions? The chronic gastritis involves, at minimum, the gastric antrum.

6. Are additional special features seen? No. Although in a case of Crohn disease gastritis, epithelioid epithelioid /ep·i·the·li·oid/ (-the´le-oid) resembling epithelium.

ep·i·the·li·oid
adj.
Of or resembling epithelium.



epithelioid

resembling epithelium.
 granulomas may be present; in this case, no granulomas were seen.

7. Are special stains recommended? Yes. Helicobacter pylori immunohistochemical stain, which is helpful in cases where Crohn disease is suspected because the absence of H pylori organisms in chronic active gastritis is consistent with Crohn disease. The H pylori immunohistochemical stain in this case is negative.

Diagnosis.- Gastric antral mucosa with chronic active gastritis, moderately active, patchy. No H pylori organisms are identified by H&E or immunohistochemistry. Note: These features are consistent with Crohn disease-associated gastritis.

CROHN DISEASE-ASSOCIATED GASTRITIS

The hallmark histopathologic features of Crohn disease-associated gastritis are the presence of patchy, acute inflammation with possible gastric pit or glandular abscesses, commonly with a background with lymphoid aggregates. Recent studies20 reported the presentation of gastritis in patients with Crohn disease as a focally enhanced gastritis, characterized by small collections of lymphocytes and histiocytes surrounding a small group of gastric foveolae or glands, often with infiltrates of neutrophils. In severe cases, there may be diffuse inflammation in the lamina propria, with variable glandular loss, fissures, ulcers, transmural transmural /trans·mu·ral/ (trans-mu´ral) through the wall of an organ; extending through or affecting the entire thickness of the wall of an organ or cavity.

trans·mu·ral
adj.
 inflammation, and fibrosis. Noncaseating epithelioid granulomas may be present in about one third of cases of Crohn disease gastritis but are often not seen, at least in part, because of limited tissue sampling.

When granulomas are identified, the differential diagnosis includes other forms of granulomatous gastritis. There are infectious and noninfectious causes of granulomatous gastritis. Noninfectious diseases represent the usual cause of gastric granulomas and include Crohn disease, sarcoidosis Sarcoidosis Definition

Sarcoidosis is a disease which can affect many organs within the body. It causes the development of granulomas. Granulomas are masses resembling little tumors. They are made up of clumps of cells from the immune system.
, and isolated granulomatous gastritis. Sarcoidlike granulomas may be observed in cocaine users, and foreign material is occasionally observed in the granulomas. Sarcoidosis of the stomach is usually associated with granulomas in other organs, especially the lungs, hilar hi·lar
adj.
Of or relating to a hilum.
 nodes, or salivary glands. A diagnosis of idiopathic, isolated, granulomatous gastritis is rendered when known entities associated with granulomas are excluded.

Case 3

A 60-year-old man presents with a nodularity of the gastric body to rule out H pylori. Esophagogastroduodenoscopy with biopsy of the nodular nodular

marked with, or resembling, nodules.


nodular dermatofibrosis
see dermatofibrosis.

nodular episcleritis
see nodular fasciitis (below).

nodular fasciitis
a firm painless nodular swelling, 0.
 areas was performed. The histologic findings are shown in Figure 3, A and B.

Findings.- Examination of the biopsy material results in the following pattern of answers:

1. Are there features of chronic gastritis? Yes.

2. Are there neutrophils in the mucosa? Yes. There are neutrophils in the mucosa, representing active gastritis.

3. Is there Helicobacter? No. Examination with H&E stain does not reveal H pylori bacterial forms. Immunohistochemical is performed.

4. Is there atrophy? Yes. There is a reduced number of oxyntic glands in the biopsy. There is no intestinal metaplasia.

5. What is the topography of lesions? The chronic gastritis involves, at minimum, the gastric body.

6. Are additional special features seen? No.

7. Are special stains recommended? Yes. Helicobacter pylori immunohistochemical stain, which is positive.

Diagnosis. Gastric oxyntic mucosa with H pylori-associated chronic active gastritis and glandular atrophy, moderate. No intestinal metaplasia is identified. Helicobacter organisms are identified by immunohistochemistry.

ATROPHIC GASTRITIS

Several publications, including those reporting the Sydney system and the updated Houston classification of gastritis, have proposed criteria for the evaluation of atrophic gastritis. Interobserver variability is significant, especially in the evaluation of antral atrophy.4,21 Recent advances that appear to decrease the interobserver variation in the assessment of gastric atrophy have been reported.14 Atrophy is more accurately assessed after resolution of severe inflammation of the mucosa; therefore, if there is H pylori gastritis, the infection should be eradicated before atrophy is difinitively evaluated. When marked inflammation is present, a diagnosis of indefinite for atrophy may be offered, especially if there is no intestinal metaplasia.

The recommended definition of atrophy is the loss of appropriate glands, and atrophy can be scored according to the degree of severity as mild, moderate, or severe.22 In this definition, intestinal metaplasia represents a form of atrophy described as metaplastic metaplastic

characteristic of metaplasia.
 atrophy (or gastric glandular atrophy with intestinal metaplasia).

Gastric atrophy is usually associated with intestinal metaplasia. However, in limited endoscopic biopsies, intestinal metaplasia might not be sampled, whereas the mucosa shows definitive atrophy. Usually gastric atrophy and intestinal metaplasia occur on a background of chronic gastritis, hence the term atrophic gastritis.

Sampling of the mucosa for evaluation of atrophy and gastritis is generally adequate by using the 5 biopsies recommended by the Sydney system, including 2 biopsies from the antrum, 2 from the corpus or body, and 1 from the incisura incisura /in·ci·su·ra/ (in-si-su´rah) pl. incisu´rae   [L.] notch.  angularis.4,21 It is essential for the pathologist to have a means of determining the specific site in the stomach where a biopsy is sampled from because specific topography of atrophy characterizes the different types of atrophic gastritis. In atrophic gastritis associated with H pylori, glandular atrophy and intestinal metaplasia involve both the gastric antrum and body, whereas in autoimmune atrophic gastritis, the disease is essentially restricted to the gastric body. Ideally, the precise location is indicated by the endoscopist endoscopist A health professional who performs endoscopic procedures. See Nurse endoscopist. , and the biopsies from different sites are submitted in separate containers. However, using special stains can help the pathologist determine the location of the biopsy fragments received. This approach is exemplified in case 5.

Gastric atrophy and intestinal metaplasia are associated with increased gastric cancer risk, but unlike the intestinal metaplasia of Barrett syndrome, no specific recommendations for surveillance have been established in the United States, although published data in other populations have suggested a benefit.23 In that study,23 patients with extensive atrophic gastritis and intestinal metaplasia had an 11% risk of gastric malignancy.

Case 4

Esophagogastroduodenoscopy of a 60-year-old man shows gastritis. The pathologist needs to rule out H pylori and gastric atrophy. The gastric site of the biopsy is not specified. Figure 4, A through C, represents the histologic findings.

Findings. Examination of the biopsy material results in the following pattern of answers:

1. Are there features of chronic gastritis? Yes.

2. Are there neutrophils in the mucosa? Yes. There are neutrophils in the mucosa; therefore, there is a component of active gastritis.

3. Is there Helicobacter? No. Examination with H&E stains do not reveal H pylori bacterial forms. Immunohistochemical stain is performed.

4. Is there atrophy? If the biopsy is from gastric oxyntic mucosa then there is atrophy, however, if the specimen is from the antrum, it may represent chronic gastritis without atrophy. There is no intestinal metaplasia.

5. Are special stains recommended? Yes. Immunohistochemical stains for synaptophysin and gastrin are performed. Immunohistochemical stains for synaptophysin (Figure 4, B), show a linear pattern of synaptophysin-positive cells, whereas the gastrin stain is negative. Because gastrin is negative, the biopsy is not from the gastric antrum (G cells are characteristically located in the antrum and pylorus), and therefore, it can be established that the biopsy is of oxyntic mucosa with reduced oxyntic glandular profiles, establishing a diagnosis of atrophy. The linear arrays of synaptophysin-positive cells represent enterochromaffin-like cell hyperplasia. Enterochromaffinlike cell hyperplasia occurs in response to hypergastrinemia that results from hypochlorhydria associated with gastric oxyntic cell atrophy.

6. Are additional special features seen? No.

7. Is immunohistochemical stain for H pylori positive? No.

Diagnosis.- Gastric oxyntic mucosa with chronic active gastritis and glandular atrophy, severe. No intestinal metaplasia is identified. No Helicobacter organisms are identified. Note: These features are most suggestive of autoimmune gastritis.

AUTOIMMUNE ATROPHIC GASTRITIS

This form of gastritis (reviewed in Sepulveda et al1 and Capella et al24) is caused by antiparietal cell and anti-intrinsic factor antibodies and presents as a chronic gastritis with oxyntic cell injury, and glandular atrophy essentially restricted to the oxyntic mucosa of the gastric body and fundus. The histologic changes vary in different phases of the disease. During the early phase, there is multifocal infiltration of the lamina propria by mononuclear cells and eosinophils Eosinophils
A leukocyte with coarse, round granules present.

Mentioned in: Histiocytosis X

eosinophils
 and focal T-cell lymphocyte infiltration of oxyntic glands with glandular destruction. Focal mucous neck cell hyperplasia (pseudopyloric metaplasia), and hypertrophic Hypertrophic
Enlarged.

Mentioned in: Heart Failure


hypertrophic

characterized by a state of hypertrophy.


hypertrophic pulmonary osteoarthropathy
see hypertrophic osteopathy.
 changes of parietal cells are also observed. During the florid florid /flor·id/ (flor´id)
1. in full bloom; occurring in fully developed form.

2. having a bright red color.


flor·id
adj.
Of a bright red or ruddy color.
 phase, there is increased lymphocytic inflammation, oxyntic gland atrophy, and focal intestinal metaplasia. The end stage is characterized by diffuse involvement of the gastric body and fundus by chronic atrophic gastritis associated with multifocal intestinal metaplasia. In contrast to the gastric body, the antrum is spared. Recently, a distinct form of autoimmune gastritis, characterized by atrophic pangastritis, was reported in a small group of patients with systemic autoimmune disorders.25

Autoimmune gastritis is a relatively rare disease but represents the most frequent cause of pernicious anemia in temperate climates. The risk of gastric adenocarcinoma adenocarcinoma: see neoplasm.  was reported to be at least 2.9 times higher in patients with pernicious anemia than in the general population, and there is also an increased risk of gastric carcinoid carcinoid /car·ci·noid/ (kahr´si-noid) a yellow circumscribed tumor arising from enterochromaffin cells, usually in the gastrointestinal tract; the term is sometimes used to refer specifically to the gastrointestinal tumor  tumors.

Case 5

A 47-year-old woman presents with a history of celiac disease. Esophagogastroduodenoscopy was performed, with biopsy of gastric antrum. The pathologist needs to rule out H pylori. Figure 5, A and B, illustrates the histologic findings.

Findings. Examination of the biopsy material results in the following pattern of answers:

1. Are there features of chronic gastritis? Yes. There are large numbers of intraepithelial lymphocytes.

2. Are there neutrophils in the mucosa? No.

3. Is there Helicobacter? No. Examination with H&E stain does not reveal H pylori bacterial forms. Immunohistochemical is performed.

4. Is there atrophy? No. There is no glandular atrophy and no intestinal metaplasia.

5. What is the topography of lesions? The chronic gastritis involves, at minimum, the gastric antrum.

6. Are additional special features seen? Yes. The specific features in this biopsy include a characteristic intraepithelial lymphocytosis lymphocytosis /lym·pho·cy·to·sis/ (-si-to´sis) an excess of normal lymphocytes in the blood or an effusion.

lym·pho·cy·to·sis
n.
. Immunohistochemical stain for CD3 is positive, highlighting a population of T lymphocytes in the mucosa and, typically, many intraepithelial lymphocytes.

7. Are special stains recommended? Yes. Immunohistochemical stain for H pylori, which is negative.

Diagnosis. Chronic gastritis with increased intraepithelial T lymphocytes. No Helicobacter organisms are identified. Note: These features are consistent with lymphocytic gastritis-associated with celiac disease.

LYMPHOCYTIC GASTRITIS

Lymphocytic gastritis is a type of chronic gastritis characterized by marked infiltration of the gastric surface and foveolar epithelium by T lymphocytes and by chronic inflammation in the lamina propria. A diagnosis can be rendered when 30 or more lymphocytes per 100 consecutive epithelial cells are observed, and the counts are recommended in biopsies from the gastric corpus. The endoscopic en·do·scope  
n.
An instrument for examining visually the interior of a bodily canal or a hollow organ such as the colon, bladder, or stomach.



en
 pattern is, in some cases, described as varioliform gastritis. The cause of lymphocytic gastritis is usually unknown, but some cases are seen in patients with glutensensitive enteropathy/celiac disease and in Me?ne?trier Trier (trēr), Latin Augusta Treverorum, city (1994 pop. 99,183), Rhineland-Palatinate, SW Germany, a port on the Moselle (Ger. Mosel) River, near the Luxembourg border.  disease. Smaller numbers of intraepithelial lymphocytes can also be seen in H pylori gastritis, but the diagnosis of lymphocytic gastritis should be reserved for cases with marked intraepithelial lymphocytosis in the absence of active H pylori gastritis. Lymphocytic gastritis can be observed in children but is usually detected in late adulthood, with average age of diagnosis of 50 years.

Case 6

A 75-year-old woman presents after esophagogastroduodenoscopy. Gastric antrum shows gastritis; the pathologist is asked to rule out H pylori. The histologic findings are shown in Figure 6.

Findings. Examination of the biopsy material results in the following pattern of answers:

1. Are there features of chronic gastritis? There is minimal chronic gastritis.

2. Are there neutrophils in the mucosa? No.

3. Is there Helicobacter? No. Examination of H&E stains does not reveal H pylori bacterial forms.

4. Is there atrophy? No. There is no atrophy or intestinal metaplasia.

5. What is the topography of lesions? The chronic gastritis involves, at minimum, the gastric antrum.

6. Are additional special features seen? Yes. There are diagnostic special features, including foveolar hyperplasia with a corkscrew corkscrew

a deformity in which the affected part is spiraled like a corkscrew.


corkscrew claw
a probably heritable defect of the lateral claw, usually of the front feet, of cattle causing serious lameness.
 appearance of the foveolae. The foveolar epithelium shows reactive cytologic features, including reduced cytoplasmic cytoplasmic

pertaining to or included in cytoplasm.


cytoplasmic inclusions
include secretory inclusions (enzymes, acids, proteins, mucosubstances), nutritive inclusions (glycogen, lipids), pigment granules (melanin, lipofuscin,
 mucin mucin: see glycoprotein. . The lamina propria shows congestion The condition of a network when there is not enough bandwidth to support the current traffic load.

congestion - When the offered load of a data communication path exceeds the capacity.
 and smooth muscle hyperplasia, with prominent muscularization of the most superficial mucosa.

7. Are special stains recommended? No ancillary tests are performed.

Diagnosis.- Gastric antral mucosa with features consistent with reactive gastropathy. No H pylori organisms are identified.

CHRONIC, REACTIVE (CHEMICAL) GASTROPATHY

Chronic reactive gastropathy (also know as chemical gastropathy) is very common in current clinical practice. The mucosal changes are usually more prominent in the prepyloric region, but they may extend to involve the oxyntic mucosa. The usual underlying causes include chronic bile reflux and long-term NSAID intake. The histopathologic features include mucosal edema edema (ĭdē`mə), abnormal accumulation of fluid in the body tissues or in the body cavities causing swelling or distention of the affected parts. , congestion, fibromuscular hyperplasia in the lamina propria, and foveolar hyperplasia with a corkscrew appearance in the most severe forms. The foveolar epithelium characteristically shows reactive nuclear features and reduction of mucin. The epithelial changes occur with little background chronic inflammation. However, if there is erosion of the mucosa, superficial neutrophils may be present. Erosive e·ro·sive
adj.
Causing erosion.
 gastritis (Figure 7, A) can present clinically as acute gastritis, often associated with NSAID intake.

The features associated with bile reflux are typically found in patients with partial gastrectomy gastrectomy

Surgical removal of all or part of the stomach to treat peptic ulcers. It eliminates the cells that secrete acid and halts the production of gastrin, the hormone that stimulates them. Once a common operation, it is now a last resort.
, in whom, the lesions develop near the surgical stoma stoma
 or stomate

Any of the microscopic openings or pores in the epidermis of leaves and young stems. They are generally more numerous on the undersides of leaves.
. However, alterations induced by bile reflux also affect the intact stomach. A recent study26 reported altered mucin expression in reactive gastropathy, including aberrant expression of MUC MUC Mount Union College (Ohio)
MUC Multi User Chat
MUC Message Understanding Conference
MUC Montreal Urban Community
MUC Malaspina University College (Canada) 
5Ac in pyloric glands. Evaluation of mucin-expression patterns can be useful to support a diagnosis of reactive gastropathy; however, additional studies are warranted to validate this potential application of mucin immunohistochemistry.

Case 7

A 45-year-old woman presents with a history of bone marrow transplant bone marrow transplant: see bone marrow. . Esophagogastroduodenoscopy shows gastric erosion. The histologic findings are represented in Figure 7, B.

Findings. Examination of the biopsy material results in the following pattern of answers:

1. Are there features of chronic gastritis? Yes. The sample of gastric mucosa reveals mucosal erosion with granulation tissue and associated chronic and acute inflammation.

2. Are there neutrophils in the mucosa? Yes. There are superficial neutrophils in the mucosa, but they are limited to the area of mucosal erosion.

3. Is there Helicobacter? No. Examination with H&E stain does not reveal such bacterial forms.

4. Is there atrophy? No. There is no atrophy or intestinal metaplasia.

5. What is the topography of lesions? Away from the areas of erosion, there is no evidence of gastritis; therefore, the location of the biopsy is not contributory in this case.

6. Are additional special features seen? Yes. There are special features including enlarged cells, arousing suspicion of cytomegalovirus inclusions in the granulation tissue.

7. Are special stains recommended? Yes. Immunohistochemical stain for cytomegalovirus reveals rare but characteristic viral inclusions (not shown).

Diagnosis.- Gastric antral mucosa with erosion and cytomegalovirus inclusions, consistent with cytomegalovirusassociated gastritis.

CYTOMEGALOVIRUS GASTRITIS

Cytomegalovirus infection of the stomach is observed in patients with underlying immunosuppression immunosuppression

Suppression of immunity with drugs, usually to prevent rejection of an organ transplant. Its aim is to allow the recipient to accept the organ permanently with no unpleasant side effects.
. Histologically, intranuclear in·tra·nu·cle·ar  
adj.
Situated or occurring within the nucleus of an atom or cell.
 eosinophilic inclusions and smaller intracytoplasmic intracytoplasmic /in·tra·cy·to·plas·mic/ (-si?to-plaz´mik) within the cytoplasm of a cell.  inclusions in enlarged cells are characteristic. A patchy, mild inflammatory infiltrate is observed in the lamina propria. Viral inclusions are present in endothelial endothelial /en·do·the·li·al/ (-the´le-al) pertaining to or made up of endothelium.
Endothelial
A layer of cells that lines the inside of certain body cavities, for example, blood vessels.
 or mesenchymal cells in the lamina propria and may be seen in gastric epithelial cells. Severe activity may result in mucosal ulceration.

COMMENT

Most types of gastritis can be diagnosed with H&E stains. To reach a determination of etiology and a specific diagnostic entity, a limited list of questions can be used to evaluate the histopathology his·to·pa·thol·o·gy
n.
The science concerned with the cytologic and histologic structure of abnormal or diseased tissue.


Histopathology
The study of diseased tissues at a minute (microscopic) level.
 of gastric biopsies, which can lead to a pattern of answers that corresponds to a specific diagnosis of the most common types of gastritis. Although not ideal, the diagnosis of gastritis can be reached from limited biopsy material, even when the location of the biopsy is not indicated. If the biopsy site is not known, immunohistochemical stains for synaptophysin and gastrin can help determine the biopsy location, permitting a specific diagnosis of atrophic gastritis type. Helicobacter pylori immunohistochemical stains can be particularly useful when moderate to severe chronic gastritis or any active gastritis is present but no Helicobacter organisms are identified on H&E stains, when extensive intestinal metaplasia is present, and to evaluate follow-up biopsies after antibiotic treatment for H pylori.

At the end of the day, there are a number of cases with a diagnosis of chronic inactive gastritis, generally mild, for which a specific etiology cannot be determined by histopathologic examination alone. This may be accounted for by limited tissue sampling, nonspecific nonspecific /non·spe·cif·ic/ (non?spi-sif´ik)
1. not due to any single known cause.

2. not directed against a particular agent, but rather having a general effect.


nonspecific

1.
 focal, mild, chronic inactive gastritis associated with various systemic disorders, or as yet uncharacterized forms of gastritis.

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Author:Antonia R Sepulveda and Madhavi Patil
Publication:Archives of Pathology & Laboratory Medicine
Date:Oct 1, 2008
Words:4210
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