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| Issue 8 2000 |  |
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Prof. Robert Eckstein Head, Anatomical Pathology Contact: tel +61 2 9926 7085 e-mail: beckstei@med.usyd.edu.au |
| "Gastritis"
is a somewhat nebulous term, having different implications for the layman,
treating clinician, endoscopist and histopathologist. At endoscopy, erythema
and oedema reflect changes in vascular function, frequently difficult to
appreciate in a biopsy. Conversely, in biopsies inflammatory cell infiltration
is most easily recognised, and this may not be reflected as grossly visible
changes. Thus symptoms, endoscopic appearances and histological appearances
complement each other and should all be taken into account in the assessment
of gastritis.
Recent years have seen the discovery of Helicobacter pylori gastritis, increasing appreciation of the role of irritants such as NSAIDS, and the delineation of some unusual forms of gastritis. There has been increasing appreciation of the role of some forms of chronic gastritis in the development of peptic ulceration and neoplasia. |
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Figure 1a. H. pylori induced gastritis showing the characteristic inflammatory cell infiltrate. (Click on image for high resolution version) |
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Helicobacter pylori-induced gastritis H. pylori infection induces an active chronic gastritis with infiltration of the gastric mucosa by both neutrophils (known as active gastritis or "activity") and mononuclear inflammatory cells (chronic inflammation). The antrum is worse affected than the body-fundus region of the stomach, although this can change under the influence of proton-pump inhibitors. The organisms cause damage as a result of their adhesion to the mucosal epithelial cells, and the degree of damage is in part related to the strain of organism. In some individuals with on-going infection, glands are destroyed (atrophy) and there is replacement of gastric cells by intestinal cells (intestinal metaplasia). This is regarded as a prerequisite, via dysplastic change, for the development of neoplasia. After successful treatment, a mild chronic gastritis usually persists, but continuing "activity" generally indicates persistence of the organism. Rarely, another Helicobacter, H. heilmanii (formerly Gastrospirillum hominis) transmitted from animals, can be responsible for a similar pattern of gastritis. |
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Figure 1b. H. pyloriorganisms are seen closely adherent to foveolar cell surfaces. (Click on image for high resolution version) |
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| Figure 2. Chemical gastropathy showing marked foveolar epithelial regeneration and minimal inflammatory cell infiltration. (Click on image for high resolution version) |
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Autoimmune chronic atrophic gastritis
In this condition, in which pernicious anaemia may develop, and which is associated with autoantibodies to parietal cells and intrinsic factor, inflammation is directed against the acid (and intrinsic factor) - producing parietal cells of the gastric body-fundus. As might be expected, therefore, inflammatory cell infiltration is more severe in the body than the antrum. Loss of normal body-type glands, antro-pyloric metaplasia and intestinal metaplasia can result in conversion of the body mucosa to one resembling atrophic antrum. For this reason the origin of the biopsy, whether from antrum or body, should be indicated by the endoscopist to the pathologist. |
Multifocal atrophic gastritisGastric glandular atrophy with intestinal metaplasia, with variable chronic inflammation, and predominantly involving the antrum, is a common finding in countries with high incidences of gastric cancer. This is presumably related to present or past Helicobacter pylori infection, in association with dietary influences, such as lack of fresh vegetables and excessive salt. |
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Chemical gastropathies ("reactive gastritis")Non steroidal antiinflammatory drugs (NSAIDS), bile reflux and other less well defined insults damage the gastric mucosa, causing degenerative and regenerative epithelial and stromal changes. An important feature is the dearth of accompanying inflammatory cell infiltration. The term gastropathy is used to emphasise the last feature. |
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Unusual forms of gastritis Infections other than H. pylori are uncommon in biopsies, and seen mainly in the immunosuppressed. The organisms of cytomegalovirus infection, cryptosporidiosis, MAIC and candidiasis may be visualized. Iatrogenic gastritis includes graft versus host disease, which shows a characteristic loss of epithelial cells through apoptosis. |
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| Type | Aetiological Factors |
| Acute (haemorrhagic, erosive) | NSAIDs, shock syndrome, infections |
| Chronic Non-atrophic | H. pylori |
| Atrophic autoimmune Atrophic non-autoimmune |
Autommunity H. pylori / dietary |
| Chemical | NSAIDs, bile reflux |
| Iatrogenic | Radiation, chemotherapy |
| Infective | Bacteria, fungi, virus, parasites |
| Lymphocytic | Coeliac, H. pylori, Menetrier's |
| Granulomatous | Crohn's, infection, etc |
| Eosinophilic | Dietary allergy |
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Lymphocytic gastritis
is defined by the presence of numerous T-lymphocytes within
the foveolar epithelium. It causes enlarged gastric folds, nodules and
erosions mainly in the gastric body-fundus. Its cause is usually not known.
It is occasionally associated with severe protein loss and Menetrier's
disease. A proportion of patients have coeliac disease.
Granulomatous gastritis may be idiopathic, due to Crohn's disease, sarcoid, infections or other systemic granulomatous disease. More often involvement of the stomach in Crohn's disease is seen as aphthoid lesions without granulomas. Vascular gastropathies includes gastric antral vascular ectasia (GAVE, or watermelon stomach). In this condition, anaemia is accompanied by haemorrhagic antral mucosa at endoscopy. Ectatic capillaries containing thrombi are seen in biopsies. The gastric body often shows autoimmune-type gastritis. In patients with portal hypertension, biopsies of gastric body mucosa may show dilated capillaries, but in practice this is often difficult to assess. Eosinophilic gastritis defined by numerous mucosal eosinophils, represents a manifestation of food or other allergy which is often systemic. |
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Development of Neoplasia Any form of chronic gastritis in which intestinal metaplasia develops probably predisposes to neoplasia (see Figure 3). The role of Biopsy For assessment of gastritis separately labelled biopsies of adequate size should be taken as follows:
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Figure 3.
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| NEWS FROM PaLMS |
| The importance
of good communications with our customers can not be underestimated, that
is why PaLMS has appointed a number of Account Managers. Jane Flynn is
our Senior Account Manager and has been in this role for almost two years.
Her key customers are North Shore Private Hospital (NSPH), Greenwich Hospital
and Royal Rehabilitation Centre Sydney. Most recently Rita Castles & Ric
Main have taken on Account Management roles. Rita will be looking after
Royal North Shore Hospital (RSNH) and surrounding areas including North
Shore Medical Centre as well as referring laboratories. Ric will be providing
support for the doctors in the Hornsby & Ryde areas. You can contact any
of our Account Managers via the Customer Support Unit on 8425 3065 or
the PaLMS Service Centre on 9926 6066.
PaLMS Collection facilities continue to be upgraded in order to increase accessibility and convenience for our patients. At the Ryde campus the Collection Rooms have been relocated into larger premises, which include a quiet waiting room. The most recent upgrade has been at the Hornsby campus where the Collection Rooms have moved to Palmerston Road, adjacent to the front entrance of the hospital. Plans are underway to upgrade the Collection Room at the Manly campus. There are also Collection Rooms at our Mona Vale and St Leonards campuses. In addition to Collection Rooms, PaLMS provides a Home Collection Service for housebound patients. You can contact the PaLMS Collection Rooms via the PaLMS Service Centre on 9926 6066 or phone them direct. NSPH (Home Collections) - 8425 3066 We are keen to work with you to ensure that you and your patients receive quality pathology, together with a service tailored to meet your needs. Please contact me if there is any aspect of our service you feel could be improved.
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Publication by PaLMS Staff
Member Dr Barbara Young has coauthored the recently published 4th Edition of Wheater's Functional Histology with Prof JW Heath of the University of Newcastle. Barbara is a Senior Staff Specialist in Anatomical Pathology and a member of the PaLMS Education Team. She is currently working on a multiple choice question book in histology and is about to commence the 4th Edition of Wheater's Basic Histopathology. In addition to writing medical textbooks, her interests are renal, gynaecological and urological pathology. |
