21. Columnar Epithelial Dysplasia In Barrett’s Mucosa - Definition And Grading
The term dysplasia is ordinarily applied to in situ changes in Barrett’s mucosa that the observer feels appear neoplastic. Comparable cytologic and other abnormalities are also seen in invasive neoplasia. The term is not simply a synonym for “atypia”.
The criteria for dysplasia in Barrett’s mucosa, which are fundamentally no different from those used for colonic and gastric epithelial dysplasia, can include nuclear enlargement, irregularity, and hyperchromatism, loss of nuclear polarity, nuclear stratification, and back-to-back glands (cribriforming) (1-4). Presence of dysplastic changes in surface as well as glandular epithelium is an important feature since it helps distinguish true dysplasia from “reactive atypia” (non-neoplastic nuclear abnormalities that often accompany heightened cell turnover in response to injury or inflammation). Presence or absence of surface dysplasia can also be useful for distinguishing between definite dysplasia and indefinite changes (4).
A diagnosis of intramucosal carcinoma requires evidence that the dysplastic epithelium has penetrated through the basement membrane and thereby entered the lamina propria. At that stage the carcinoma is believed to still be confined to the mucosa and has not invaded through the muscularis mucosa into the submucosa. Presence or absence, however, of extramucosal (“Invasive”, or “Infiltrative”) carcinoma often cannot be fully determined because biopsy samples are usually too shallow.
Clinicians need to realize that reaching a decision about presence of dysplasia, even between experienced pathologists, is often difficult and that differences of opinion are common (3,4). Observer variation is especially frequent for specimens in the indefinite and low grade categories (3,4). From a practical standpoint observer variation is best dealt with by encouraging opinions from multiple pathologists. Specimen sampling is another extremely important limitation in detection and assessment of dysplasia. Both clinicians and pathologists should remain constantly aware of these operational uncertainties and the value of multiple biopsies at multiple sites.
A large proportion of patients with high grade dysplasia in Barrett’s esophagus are later found to have invasive (i.e., cancerous) disease on esophageal resection (1,5) (see slide 22). For this reason high grade dysplasia in Barrett’s esophagus is usually considered especially ominous and an indication for surgical or other definitive treatment. Specific examples of dysplasia are covered in other slides.
1) Hamilton SR, Smith RRL. The relationship between columnar epithelial dysplasia and invasive adenocarcinoma arising in Barrett’s esophagus. Am J Clin Pathol 1987;87:
2) Haggitt RC. Barrett’s esophagus, dysplasia, and adenocarcinoma. Hum Pathol ;25(10):
3) Reid BJ, Haggitt RC, Rubin CE, Roth G, Surawicz CM, Van Belle G, Lewin K, Weinstein WM, Antonioli DA, Goldman H, MacDonald W, Owen D. Observer variation in the diagnosis of dysplasia in Barrett’s esophagus. Hum Pathol. 1988;19:
4) Montgomery E, Bronner MP, Goldblum JR, et al. Reproducibility of the diagnosis of dysplasia in Barrett esophagus: a reaffirmation. Hum Pathol 2001;32:368-78
5) Montgomery E, Goldblum JR, Greenson JK, et al. Dysplasia as a predictive marker for invasive carcinoma in Barrett esophagus: a follow-up study based on 138 cases from a diagnostic variability study. Hum Pathol 2001;32:

22. Dysplasia In Biopsies From Barrett’s Esophagus As A Predictive Marker For Progression To Adenocarcinoma
22. Dysplasia In Biopsies From Barrett’s Esophagus As A Predictive Marker For Progression To Adenocarcinoma.
The bar graph shown here summarizes data resulting from a follow-up study of 138 patients whose esophageal biopsies were reviewed during a rigorous, blinded assessment of criteria for dysplasia in Barrett’s esophagus (BE) (1,2). The data shown here are based on results for 99 patients on whom “majority diagnoses” were reached by the grading panel. For purposes of this analysis, progression (the end-point) was defined as demonstration of adenocarcinoma, rather than a higher grade of dysplasia (1). The results favored the following conclusions:
i) The likelihood of cancer appearing in patients with BE who lack dysplasia is low (all in this group (100%) were cancer-free after a median time of 48 mos.), a finding that supports conservative follow-up of such patients.
ii) For patients with “Indefinite” and “Low-grade” dysplasia similar proportions remained cancer-free (86% and 80%). These findings support continued regular surveillance follow-up, but also justifies combining these two categories for surveillance purposes.
iii) On the other hand, patients with “High-grade” dysplasia showed a much lower proportion (40%) who had cancer-free survival. Viewed in another way, adenocarcinomas were detected in 9 of 15 patients in this group at a median of 7 months. Thus the data support the assertion that high grade dysplasia is strongly associated with adenocarcinoma.
iv) Patients with intra- and extramucosal (infiltrating) adenocarcinoma at the outset of their study had, by definition, already reached their end-point.
1) Montgomery E, Goldblum JR, Greenson JK, et al. Dysplasia as a predictive marker for invasive carcinoma in Barrett esophagus: a follow-up study based on 138 cases from a diagnostic variability study. Hum Pathol 2001;32:
2) Montgomery E, Bronner MP, Goldblum JR, et al. Reproducibility of the diagnosis of dysplasia in Barrett esophagus: a reaffirmation. Hum Pathol 2001;32:

23. Non-Dysplastic And Dysplastic Barrett’s Mucosa - Histology
This slide compares non-dysplastic Barrett’s mucosa with mucosa showing low and high grade dysplasia. The non-dysplastic mucosa (far left panel) consists mainly of gastric-type columnar mucous cells with finely dispersed mucus droplets and scattered intervening goblet cells with their distinctive large apical collection of mucus (see slides 19 and 20 for further details). Note the uniform size and basal location of the nuclei. By contrast, the low grade dysplasia (center panel) a villiform configuration, nuclear stratification, and some nuclear size variability. The example of high grade dysplasia (right hand panel) shows exaggerated changes like those seen with low grade dysplasia with a high degree of nuclear pleomorphism and distortion, a reduced number of goblet cells, gland distortion, and almost complete loss of nuclear polarity (nuclei not basally located).

24. Barrett’s Mucosa - Epithelial Changes Indefinite For Dysplasia - Two Examples
Both biopsy specimens presented here show some features strongly suggesting epithelial dysplasia, but both also have features that are inconsistent with that conclusion. The positive features are presence in both specimens of nuclear pleomorphism and hyperchromatism, and irregularly shaped and crowded glandular outlines, especially in specimen A, and with notably atypical looking cells in specimen B. Glands with readily apparent glandular and nuclear abnormalities are indicated (arrows). Features against dysplasia are non-dysplastic looking surface epithelium (uppermost epithelial layer in both specimens), a finding that always reduces the likelihood of definite dysplasia. In addition, in specimen B there is active inflammation, seen as infiltration by neutrophilic polymorphonuclear leukocytes (PMN’s). Presence of active inflammation always introduces the possibility of reactive change that may at least partially account for any epithelial atypia.
Epithelial changes indefinite for dysplasia are often the most difficult for pathologists to reckon with and can be a great cause of differences of pathologic opinion when reviewing biopsies from patients with Barrett’s esophagus. This was brought out well in a controlled study of observer agreement and disagreement about presence or absence of dysplasia in Barrett’s esophagus; in that study the level of agreement was best for high grade dysplasia (1).
1) Reid BJ, Haggitt RC, Rubin CE, Roth G, Surawicz CM, Van Belle G, Lewin K, Weinstein WM, Antonioli DA, Goldman H, MacDonald W, Owen D. Observer variation in the diagnosis of dysplasia in Barrett’s esophagus. Hum Pathol. 1988;19:

25. Infiltrating Adenocarcinoma (ICA) Arising In Dysplastic Barrett’s Mucosa And Invading Smooth Muscle (SM)
25. Infiltrating Adenocarcinoma (ICA) Arising In Dysplastic Barrett’s Mucosa And Invading Smooth Muscle (SM).
An infiltrating adenocarcinoma, which arose in a setting of in situ high grade dysplasia like that shown in slide 23, is depicted at low magnification (panel A). Malignant behavior of the lesion is made evident from the presence of infiltrating carcinoma (ICA) invading into deeper structures such as smooth muscle (SM) under the superficially located primary tumor. As is typical for these tumors, no luminal mass is evident at the primary site. At higher magnification (panel B) penetration of the carcinomatous glands (ICA) between and into the deeply located bundles of smooth muscle (SM) are seen in greater detail.

26. Candidal Esophagitis: Endoscopic And Histologic Views
On endoscopic examination (panel A) candidiasis is characterized by multiple whitish raised plaques on the esophageal mucosa. These may be small and isolated or extensive and confluent. The plaques have been likened to cottage cheese in the esophagus. When the plaques are removed an erythematous base remains. The white plaques seen endoscopically consist of a mixture of sloughed epithelium, fibrinoinflammatory exudate, and candidal organisms. The diagnostic feature histologically is demonstration of candidal yeasts and pseudohyphae. The pseudohyphae (PSH) characteristically invade the upper layers of the esophageal squamous epithelium, as seen here in a periodic acid-Schiff (PAS) stained specimen (panel B).
Candidiasis is the most frequently recognized infection of the esophagus and is especially common in patients with compromised immune systems, e.g., in AIDS, leukemia, lymphoma, and in patients receiving chemotherapy or immuno-suppressive treatment. In the general hospital population candidal esophagitis is infrequent (about 0.1%). The finding of oropharyngeal candidiasis and esophageal symptoms is highly predictive of esophageal candidiasis. Endoscopy with biopsy is the most sensitive way to diagnose esophageal candidiasis and to identify mixed infections of the esophagus, e.g., herpesvirus and Candida.
1) Kodsi BE, Wickremesinghe C, Kosinin PJ. Candida Esophagitis: A prospective study of 27 cases. Gastroenterology 1976;71:715.
2) Sutton FM, Graham DY, Goodgame RW. Infectious esophagitis. Gastrointestinal Clinics of N. America 1994;4:713.

27. Herpes Simplex Esophagitis: Gross Appearance
Herpetic lesions in autopsy specimens. The early lesions (left hand panel) occur as discrete, punched-out ulcers, usually with a slightly raised, yellowish, granular margins. The late (more advanced) cases some ulcers are confluence, but the ulcers remain well demarcated and have flat margins. In severe cases there can be almost complete loss of the mucosa over the segment of esophagus. Note that the ulceration stops abruptly at the gastroesophageal junction (bottom). (Case material kindly provided by Dr. Gerald Nash, Dept. of Pathology, Baystate Medical Center, Springfield, MA 01199)
1) Nash G, Ross JS. Herpetic esophagitis. A common cause of esophageal ulceration. Human Pathology 1974;5: ; 1974.

28. Herpetic Esophagitis With Ulcers - Endoscopy and Histology
An endoscopic view of herpetic esophagitis in an immunosuppressed patient (left hand panel) shows typical punched out ULCERS surrounded by yellowish, raised margins. The herpesvirus infected squamous epithelial cells are seen at low and high magnifications in biopsies taken from the edge of an ulcer (“lo mag” and “hi mag”, right hand panels) (1,2). At high magnification acidophilic nuclear inclusions are demonstrated in both mono- and multi-nucleated epithelial cells.
One hundred percent of adults have serologic evidence of Herpes simplex virus and viable virus may be found in 2%. Although herpes esophagitis may occur in immunologically normal individuals, most clinically recognized cases are identified in immunodeficiency states (e.g., AIDS, malignancy, immunosuppressive treatment, radiotherapy, and debilitating illness) (3). Herpes accounts for up to 1/3 of post-transplant infectious esophagitis.
In one large study of AIDS patients 65% of those with esophageal symptoms had an identifiable infectious cause (Candida 50%, CMV 25%, HSV 10%, and with 25% having multiple infectious agents)(4).
Findings pointing to infectious esophagitis may be seen on barium swallow x-rays or at endoscopy, but definitive diagnosis of herpes esophagitis is provided by finding the characteristic intranuclear inclusions in epithelial cells by cytologic examination or histologically in biopsies taken from the margins of ulcers, or by culture of HSV from biopsies or cytologic brushings.
Endoscopically, multiple or single ulcers may be found as well as pre-ulcerative lesions. One of these findings is sufficiently specific to establish the diagnosis.
1) Hamilton SR. Esophagitis. In: Ming SC, Goldman H (eds.) Pathology of the gastrointestinal tract. Baltimore, Williams and Wilkins, 1998, Chap 20, 2nd Edition. Pgs
2) McKay JS, Day DW. Herpes simplex oesophagitis. Histopathology 1983;7:409.
3) McBane RD, Gross JB, Jr. Herpes esophagitis: clinical syndrome, endoscopic appearance, and diagnosis in 23 patients. Gastrointest Endosc 1991;37:600-3.
4) Bonacini M, Young T, Laine L. The causes of esophageal symptoms in human immunodeficiency virus infection. A prospective study of 110 patients. Arch Intern Med 1991;151:

29. Pill-induced Esophagitis Occurs Above Sites Where Transit Is Normally Delayed
Pill-induced esophagitis is a form of caustic injury to the esophagus. When solids (pills) are taken without sufficient liquid, and especially in the reclining position, their passage past the aortic indentation in the upper esophagus or through the LES is delayed. If the delay is long enough for the medication to dissolve, and the medication is caustic, mucosal injury may occur. Pill-induced esophagitis has been reported with more than 70 different medications. Because the esophagitis is localized and the inflammatory response may be intense, pill-induced esophagitis may be mistaken for cancer by the endoscopist. Iron medication induces a form of upper GI injury that can be identified histopathologically as brown crystalline iron material (5).
1) Kikendall JW. Pill-induced esophageal injury. Gastroenterol Clin North Am 1991;20:835.
2) Channer KS, Virjee JP. The effect of size and shape of tablets on their esophageal transit. J Clin Pharmacol 1986;26:141.
3) Delpre G., Kadish U, Stahl B. Induction of esophageal injuries by doxycycline and other pills: a frequent but preventable occurrence. Dig Dis Sri 1989;34:797.
4) Castell DO. “Pill esophagitis” - the case of alendronate. N Engl J Med 1996;335:
5) Abraham SC, Yardley JH, Wu T-T. Erosive injury to the upper gastrointestinal tract in patients receiving iron medication. Am J Surg Pathol 1999;23:

30. Linear Erosion And Esophagitis Secondary To Mechanical Injury
An autopsy specimen consisting of lower esophagus and proximal stomach from a patient who underwent prolonged nasogastric intubation is shown. A linear, hemorrhagic erosion extends across the gastro-esophageal (G-E) junction. Such linear erosions are commonly noted in patients who have been intubated, especially if they are also receiving mechanical ventilation (1). The injury results from a combination of mechanical injury from tube insertion and respiratory movement of the esophagus combined with reflux of gastric and any associated duodenal contents around the tube.
1) Wilmer A, Tack J, Frans E, Dits H, Vanderscheuren S, Gevers A, Bobbaers H. Duodenogastroesophageal reflux and esophageal mucosal injury in mechanically ventilated patients. Gastroenterology 1999;116:

31. Esophagus, Stomach, And Duodenum: Normal Anatomic Outlines And Relationships
This external view gives the major regions and relationships for the upper GI tract. The different colors of the various anatomic regions are also indicative of a different mucosal type and function (see slides 1, 3, 32-34, 108, and 109 for further details of each type).
The short cardiac region of the stomach (in bright red) consists of a narrow zone lined by mucus secreting columnar epithelial mucosa that interface with the esophagus (see slide 1). The cardia is important in regard to diagnostic and pathogenetic aspects of gastroesophageal reflux and Barrett’s esophagus. At the same time, some studies have called into question whether the gastric cardia is a distinct, consistently demonstrable normal anatomic structure and postulates that it is instead an acquired structure which develops in response to acid reflux (1,2). Other investigators have concluded that the cardia is a normal anatomic structure, based on autopsy studies on pediatric cases, including neonates (3).
The body and fundus are lined with the acid-secreting oxyntic mucosa (see slide 33). The gastric antrum is lined by a mucus-secreting epithelium (slide 32) and is functionally important for its role in regulating acid secretion via its included population of neuroendocrine cells.
In the area where the antral and oxyntic mucosae meet, the transitional zone, both mucosal types are commingled. This zone of oxynto-antral mucosa varies in location and extent (see slide 76), but it is approximately demarcated by an indentation on the lesser curve, the incisura angularis (a useful landmark for the endoscopist). Similar commingling of mucosal types is also found where the cardiac and oxyntic mucosae meet.
The term pylorus originally referred to the entire distal third of the stomach, which in turn had two sections, the pyloric antrum and the pyloric sphincter. However, the designation pylorus is now most commonly used to refer only to the sphincter region.
1) Chandrasoma PT, Der R, Ma Y, et al. Histology of the gastroesophageal junction: An autopsy study. Am J Surg Pathol 2000;24:
2) Chandrasoma PT, Lokuhetty DM, Demeester TR, Bremner CG, Peters JH, Oberg S, Groshen S. Definition of histopathologic changes in gastroesophageal reflux disease. Am J Surg Pathol 2000;24:
3) Kilgore SP, Ormsby AH, Gramlich TL, et al. The gastric cardia: fact or fiction? Am J Gastroenterol 2000;95:921-4.

32. Normal Antral Mucosa Showing Gastric Lumen (LUM), Foveolae (FOV), And Antral Glands (AG)
Shown here are histologic sections of normal antral mucosa stained with hematoxylin and eosin (H&E) and by the periodic acid-Schiff (PAS) method for neutral mucopolysaccharides. Note that the gastric foveolae or “pits” (FOV) open out into the lumen (LUM), and that both the foveolar and luminal surfaces are lined by comparable mucus secreting columnar epithelium; these features are common to the entire stomach. In the antral mucosa, however, characteristic glands, the antral glands (AG), are noted in the deeper part of the mucosa, where they are visualized as multiple cross-sections because of their coiled configuration. Secretions from the antral glands, which are seen in the glandular epithelium to be PAS positive, and hence a neutral mucosubstance, reach the gastric lumen via a short region of specialized epithelial cells responsible for epithelial proliferation (the “gland neck”) and thence into the foveolae. There are also functionally important endocrine cells (e.g., gastrin and somatostatin secreting) among the antral glands. Those cells are not separately distinguishable here, but are demonstrated elsewhere by immunostaining (see slide 34).
1) Antonioli DA, Madara JL. Functional anatomy of the gastrointestinal tract. In: Ming SC, Goldman H (eds.) Pathology of the gastrointestinal tract. Baltimore, Williams and Wilkins, 1998, Chap 2, 2nd Edition. Pgs

33. Normal Oxyntic Mucosa Showing Foveolae (FOV), Parietal Cells (PC), And Chief Cells (CC)
The oxyntic mucosa (a term derived from Greek oxynein - to make acid ) is the acid-secreting mucosa of the stomach. The acid secreting cell is the parietal cell (PC) (synonym: oxyntic cell). These cells are concentrated in the upper halves of the oxyntic glands. The basal portions of the glands are mainly occupied by pepsinogen-secreting chief cells (CC) (synonym: zymogenic cells). The straight, uncoiled oxyntic glands are connected to the gastric foveolae (FOV). As in the antrum, the foveolae are lined by a PAS-positive neutral mucopolysaccharide-secreting columnar cells that also extend onto the luminal surface. Additional mucus-secreting cells are found in the region where the oxyntic glands and foveolae connect (the “mucus neck”) and are sparsely scattered among the glandular epithelium mucus neck cells). See also slide 34 for immunostaining demonstration of endocrine cells in oxyntic mucosa.
1) Antonioli DA, Madara JL. Functional anatomy of the gastrointestinal tract. In: Ming SC, Goldman H (eds.) Pathology of the gastrointestinal tract. Baltimore, Williams and Wilkins, 1998, Chap 2, 2nd Edition. Pgs

34. Major Endocrine Cell Types Of The Stomach And Their Products-Immunostain Demonstrations
In this slide each endocrine cell type in the stomach was made evident by exposing a gastric tissue section to an antibody against that endocrine compound. The antibodies were prepared in a non-human species (e.g., rabbit). The rabbit anti-endocrine substance was then localized in the section with an anti-rabbit antibody prepared in still another species (e.g., mouse). That antibody reagent was also conjugated to a compound that could be made visible by reacting it with an appropriate color-producing compound (the “stain”). Exact cellular localization of these physiologically and chemically distinctive endocrine substances was thereby obtained by this “immunostaining” technique.
The hormones are contained in separate cell types that have different designations as follows:
- Gastrin: found in antral G cells
- Somatostatin : found in antral D cells
- Histamine: found in ECL cells of gastric body
The functions and pathophysiological significance of each cell type and its hormone is covered in subsequent slides.
1) Solcia E, et al. In: Ming SC, Goldman H (eds.) Pathology of the gastrointestinal tract. Baltimore, Williams and Wilkins, 1998, Chap 2, 2nd Edition, Pgs

35. Gastropathy And Gastritis - Definitions
It is useful to distinguish between disorders with inflammation and varying degrees of associated epithelial damage and regeneration (gastritis); and those with only damage and repair (gastropathy). In addition, most classifications distinguish acute effects short term disease from chronic, long term disease. The terms acute and chronic are also used as histopathologic descriptors with active (=acute) inflammation denoting neutrophilic inflammatory infiltration while chronic inflammation refers to mononuclear inflammatory cell infiltration, chiefly lymphocytes, plasma cells and macrophages.
Unfortunately, although gastritis is inflammation of the stomach, the term is often used inappropriately to include conditions with only cell injury and regeneration without inflammation. This distinction is not just a semantic issue since gastritis has different pathogenetic and therapeutic implications from gastropathy.
Considerable confusion has been caused by the imprecise or inappropriate use of the term gastritis. Physicians, as well as patients, often use the term when the appropriate term is dyspepsia or indigestion. Endoscopists often report presence of “gastritis” as a synonym for erythema or friability of the mucosa, even though there is a very poor correlation between these findings and the presence of histologically demonstrated mucosal inflammation (see slide 36). Radiologists often use the term gastritis to indicate mucosal irregularities seen on contrast studies without confirmation that mucosa is actually inflamed.

36. Poor Correlation Between Endoscopic And Pathologic Diagnosis Of Gastritis
The bar graphs depict data from a study done to determine the significance of the endoscopic classification of gastritis proposed in the “Sydney System” (1). Gastric endoscopic and biopsy studies were performed and assessed prospectively on 167 patients (2). The results show that the number of patients judged to have histologic changes of gastritis in patients who also showed endoscopic “gastritis” was not statistically different from the number with histologic gastritis among patients with “normal” endoscopy (2). The authors concluded that “These findings confirm the inappropriateness of an endoscopic diagnosis of gastritis and it is suggested such a term should be reserved for the histological findings.” A similar conclusion had been reached earlier by others (1,3).
1) Tytgat GNJ, The Sydney System: Endoscopic division. Endoscopic appearances in gastritis/duodenitis. Europ. J Gastroent. Hepatol. 6: ,1991.
2) Khakoo SI, Lobo AJ, Shepherd NA, Wilkinson SP. Histological assessment of the Sydney classification of endoscopic gastritis. Gut 1994;35:1172.
3) Elta GH, Appelman HD, Behler EM, Wilson JAP, Nostrant TJ. A study of the correlation between endoscopic and histological diagnoses in gastroduodenitis. Am J Gastroenterol 1987;82:

37. Classification Of Gastropathy And Gastritis
The goal of the system for classifying gastritis and gastropathy used in this unit is to provide a practical framework for patient diagnosis and management. The classification given here has close kinship with most aspects of the Sydney System in both its original (1) and updated (2) versions, and the distinction between gastritis and gastropathy advocated by Carpenter and Talley (3).
Complicating any classification scheme is the fact that a patient can have more than one type of gastritis or gastropathy. Furthermore, for many patients, the available evidence does not permit specific categorization. Gastritis in those patients should be considered indeterminate.
1) Price AB. The Sydney system: Histological division. J Gastroenterol and Hepatol 1991;6:209.
2) Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis: The updated Sydney System. Am J Surg Pathol 1996;20:1161.
3) Carpenter HA, Talley NJ. Gastroscopy is incomplete without biopsy: Clinical relevance of distinguishing gastroscopy from gastritis. Gastroenterology 1995;108:917.

38. Understanding Of Gastritis & Gastropathy Has Been Hampered By The Multitude Of Terms Used
A system for classifying gastritis and gastropathy should provide a logical framework for their diagnosis and treatment and for understanding their pathogenesis. In the past, a multitude of terms have been used to designate various inflammatory and “reactive” changes in biopsies and other pathologic specimens. Most of these designations were based originally on histologic features and on postulated disease mechanisms proposed by many different observers. As a consequence, a variety of terms have evolved for describing the same or similar entities, many of which are summarized alongside the terminology used in this unit and summarized in this slide.
Gastritis, which means “inflammation of the stomach”, is precise for such conditions as Helicobacter pylori gastritis, the commonest type of gastritis in most populations. Before H. pylori was recognized as a cause of gastritis, however, multiple terms were used to describe the entity, the most prevalent being “chronic superficial gastritis”. The term “gastritis” has also often been used inappropriately to describe entities in which there is little or no inflammation, e.g., “erosive gastritis”, “chemical gastritis”, “bile gastritis”, “reflux gastritis”. We and others (2,3) favor the term gastropathy as the best designation for these entities. Chemical gastropathy is the most commonly encountered condition in this group.
While “atrophic gastritis" is a widely used term, histologic atrophy is a feature that is variable and often difficult to verify in routine clinical practice. Therefore, we prefer the term metaplastic atrophic gastritis (MAG) (1), which focuses on the more easily recognized feature, metaplasia. Taking note of metaplasia also emphasizes the fact that a process has been set in motion which heightens likelihood of developing neoplasia. The two varieties of MAG are autoimmune (AMAG) and environmental (EMAG), conditions for which a variety of terms have been used (summarized in Slide 38).
1) Yardley JH, Hendrix TR. Gastritis, gastropathy, duodenitis and associated ulcerative lesions. In: Yamada T. Textbook of Gastroenterology, Chapter 66, Philadelphia, Lippincott, Williams and Wilkins, 1999:1464.
2) Dixon MF, Genta RM, Yardley JH, Correa P. Classification and grading of gastritis: the updated Sydney system. Am J Surg Pathol 1996;20:1161.
3) Carpenter HA, Talley NJ. Gastroscopy is incomplete without biopsy: clinical relevance of distinguishing gastropathy from gastritis.

39. Acute Gastropathy And Gastritis - Classification
Gastropathies and gastritides can be acute in both the clinical and morphologic sense, although acute (neutrophilic) inflammation tends to be minimal in ‘acute gastropathies’. Only a limited number of these conditions are associated with detectable endoscopic and/or histopathological findings, and the commonest of these is probably acute hemorrhagic and erosive gastropathy (slides 40-45).

40. Acute Hemorrhagic And Erosive Gastropathy - Principal Features
Acute hemorrhagic and erosive gastropathy usually comes to clinical attention in the evaluation of patients with upper GI bleeding of recent onset, or in its milder forms in the endoscopic examination of patients with nonspecific upper GI symptoms.
Endoscopic findings typically include multiple mucosal hemorrhages, usually punctate, but at times extensive and/or associated with superficial erosions.
Examination of biopsies and resected specimens from those patients reveal surface epithelial damage, intramucosal hemorrhages, edema with little or no inflammatory response, and erosions, usually with evidence of epithelial renewal.
1) Yardley JH, Hendrix TR. Gastritis, gastropathy, duodenitis and associated ulcerative lesions. In Yamada T. Textbook of Gastroenterology, Chapter 66, Philadelphia, Lippincott, Williams and Wilkins, 1999:1469.
2) Sloan JM. Acute haemorrhagic gastritis and acute infectious gastritis caused by physical agents and corrosives, uraemic gastritis. In, Whitehead, Gastrointestinal and Oesophageal Pathology. Edinburgh: Churchill Livingstone, 1989:385.