Turk J Gastroenterol 2014; 25: 233-47 What is gastritis? What is gastropathy? How is it classified? STOMACH Serra Kayaçetin, Servet Güreşçi Review Department of Pathology, Ankara Numune Education and Training Hospital, Ankara, Turkey ABSTRACT Stomach endoscopic biopsies are made to determine the diagnosis of the illness, its stage, and follow-up after the treatment. It is very significant to collaborate with the clinician while evaluating endoscopic biopsies. Besides the clinical and laboratory information of the patient, the endoscopic appearance of the lesion should be known. The clinician and pathologist should use the same language and the same terminology. Although new classifications have been made to prevent the confusion of terminologies in neoplastic processes recently, most centers around the world have reported non-invasive neoplasias without giving any certain diagnosis by just commenting on it. The clinician should understand what the pathologist wants to say; pathologists should know the approach of the clinician (repetition of the biopsy, endoscopic resection, surgery). There is Helicobacter pylori (HP) in most of the stomach pathologies as the etiologic agent. No matter if the factor is HP or other etiologic agents, the tissue gives similar responses. That is why clinical-endoscopic indications should be taken into consideration, as well as histological indications, and the reports of the endoscopy should be seen. A good clinicopathologic correlation increases the accuracy of the diagnosis. Keywords: Gastritis, gastropathy, classification Gastritis is an infectious or auto-immunological inflam- images of gastritis based on different etiologies, and mation. Gastropathy can be described as a pathology there may be more than one etiologic agent in a gas- that displays epithelial injury and regeneration, and it is tritis chart. secondary to endogenous or exogenous irritants. Gastritis was categorized as chronic and acute in 1947 In practice, “gastritis” may be accompanied by mucosal for the first time. Then, chronic gastritis was categorized injury, while “gastropathy” may show, even if minimal, into two subgroups: namely, superficial and atrophic. an inflammatory reaction. After Marshall and Warren demonstrated in 1983 that a CLASSIFICATION bacteria called Campylobacter pylori caused gastritis, a There is no universal categorization of gastritis and tendency of an etiology-oriented denotation began. For gastropathy, but they can be categorized according this purpose, a group of gastropathologists prepared a to their duration of development (according to the in- classification in 1990 in Sydney for the first time to clas- flammation type) and acute/chronic etiology. sify and rank gastritis. Within this period, the importance of the findings of gastritis, atrophy, and metaplasia in GASTRITIS Correa’s chart in 1992 was realized, and these findings Gastritis is an inflammatory condition of gastric mu- were included in the first classification. However, due to cosa that displays changes related to etiology and the differences between observers in the rating of especially host response. It was identified in the 1800s as a re- chronic gastritis and atrophy over time, the Sydney clas- sult of autopsies. There may be similar morphological sification was reviewed, and a visual analog scale was Address for Correspondence: Serra Kayaçetin, Department of Pathology, Ankara Numune Education and Training Hospital, Ankara, Turkey E-mail: [email protected] Received: 10.6.2014 Accepted: 18.6.2014 © Copyright 2014 by The Turkish Society of Gastroenterology • Available online at www.turkjgastroenterol.org • DOI: 10.5152/tjg.2014.7906 233 Kayaçetin and Güreşçi. What is gastritis? What is gastropathy? How is it classified? Turk J Gastroenterol 2014; 25: 233-47 prepared by preserving the basic principles. Despite all these Etiology efforts, inconsistencies, especially in the rating of atrophy, drew • Medication, uremia, ischemia, shock, corrosive agent, attention. Thus, the team that made the first Sydney classifica- radiation, sepsis, trauma, acute alcohol, severe burns, tion put forward a metaplastic/nonmetaplastic atrophy rating alkaline reflux, surgery in 2002 (1-7). Physiology The morphological changes that are observed in a gastritis • Decrease in mucus secretion chart can be summarized as follows: • Decrease in mucosal blood flow 1. Epithelial degeneration • DNA, PG synthesis Review 2. Foveolar hyperplasia • Decrease in mucosal barrier 3. Mucosal hyperemia and edema 4. Neutrophilic infiltration Endoscopy 5. Eosinophilic infiltration • Stress, fundus-corpus; NSAID, antrum 6. Mononuclear inflammatory cell infiltration • Multiple round-shaped severe erosions with a diameter 7. Lymphoid follicles of several millimeters. 8. Atrophy • Mucosal edema, hyperemic 9. Intestinal metaplasia 10. Endocrine cell hyperplasia ACUTE GASTRITIS (Acute erosive/hemorrhagic gastritis- 11. Parietal cell alterations tress-induced gastritis) This is a transient type of gastritis that has an acute beginning, APPROACH TO GASTRIC BIOPSY and it causes gastrointestinal pain and hemorrhage. It can de- Acute velop in a hemorrhagic or nonhemorrhagic, ulcero-erosive or • Edema, congestion, hemorrhage nonerosive manner, and it develops as a result of the stress that • Acute inflammation (neutrophil, eosinophil) the mucosa is exposed to. • Erosion, ulcer 1. Physiological stress Chronic Severe burns, trauma, SSS injury, etc. • Chronic inflammation (lymphocyte, plasma cell) • Lymphoid aggregate, follicle 2. Toxic stress, medication, especially NSAII • Atrophy Corrosive substances, alcohol, bile reflux, etc. • Metaplasia (intestinal, pyloric, pancreatic) Specific (Lymphocytic, Eosinophilic, Granulomatous) 3. Hemodynamic stress Hypovolemia and shock, ischemia, hypotension Reparative, Reactive • Regenerative activity Morphological findings • Foveolar hypertrophy Sharply circumscribed, superficial erosions that are generally • Granulation tissue smaller than 2 mm. These erosions are typically multiple, and they have a tendency to occur in proximal. Ulcerations are SYSTEMATIC ANALYSIS OF BIOPSY smaller than 1 cm, and the base is grayish green, sanguineous, • Localization- corpus, fundus, or antrum and slightly swollen. • Distribution of gastritis (pangastritis) • Gastritis-gastropathy differentiation ACUTE GASTRITIS CHANGES RELATED TO BIOPSY Microscopy • Edema • Hemorrhage and edema in superficial lamina propria • Vascular dilatation • Mucosal necrosis, neutrophil infiltration (low) • Hemorrhage in focal lamina propria • Regenerative epithelium, syncytial glandular structure • Flattening in surface epithelia (there is no epithelial de- • Erosive surface epithelium generation or acute inflammation) Differential diagnosis ACUTE GASTRITIS • HP Chronic active gastritis Lymphoplasmacytic inflammation Classification Neutrophilic cryptitis Hemorrhagic, nonhemorrhagic, erosive, nonerosive, diffuse, • Dysplasia and intense (Figure 1). Nuclear stratification 234 Turk J Gastroenterol 2014; 25: 233-47 Kayaçetin and Güreşçi. What is gastritis? What is gastropathy? How is it classified? Lamina propria expanded with inflammation Lamina propria with little or no inflammation Acute Gastritis - Erosion, edema, hemorrhage - Caustic injury, Alcohol - Shock, hypotension Diffuse Focal Granuloma(s) - latrogenic: Iron, etc... - Radiation Reactive Gastropathy - Foveolar hyperplasia w/ Review Autoimmune gastritis Focally Enhancing Gastritis Granulomatous Gastritis - "Corkscrew appearance" - NSAID, other drugs - Corpus predominant - Admixed lymphohistiocytic and - Crohn disease - Lymphoplasmacytic infiltrate neutrophilic infiltrate - Bile reflux - Sarcoidosis - (Alcohol) - Parietal cell destruction - IBD, autism, bone marrow - Others: Parasite, Foreign - ECL cell hyperplasia transplant body, Mycobacteria, etc - Unknown (25%) GAVE Lymphocytic gastritis - Rule out other causes even if - Antrum predominant vascular - Increased IELs H. pylori positive ectasia - H. pylori +/- - Intravascular thrombi - History of celiac sprue +/- - Myofibroblastic proliferation - Others: Crohn, HIV, etc... PHG Eosinophilic gastritis - Corpus predominant - Increased intra-epithelial or vascular ectasia lamina propria eosinophils - Edema, congestion - History of allergy, connective - Mural thickening tissue disease, parasites etc. - History of cirrhosis/portal HT Collagenous gastritis GVHD - Subepithelial collagen band - Increased apoptosis - Increased IEL's +/- - Similar changes secondary to - History of sprue, collagenous cytoreductive regimens colitis - Difficult diagnosis within 3 weeks of transplantation Figure 1. Schematic approach to the diagnosis of non-Helicobacter pylori gastritis Hyperchromasia • Mucus depletion Increased mitosis, regenerated epithelium amphophilic • Mitosis cytoplasm, regular nuclear contour • Chemical gastropathy Mucosal changes Mucosal elongation Variable Smooth muscle hyperplasia Slight congestion, edema Regenerated change Superficial erosion • Biopsy trauma: clinical history, endoscopic findings Massive necrosis Deep ulcers NSAI usage Inflammation degree depends on the severity of the injury Mucosal erosion, petechial telangiectasia, acute hemorrhagic During recovery gastritis, erosion, loss in glands Regenerative changes Foveolar hyperplasia ACUTE EROSIVE GASTRITIS “Acute hemorrhagic gastritis” related to NSAI and alcohol During acute phase Slight or no inflammation • Vascular congestion • Edema and hemorrhage in lamina propria CHRONIC GASTRITIS • Superficial necrosis • HP-related