Gastrointestinal Pathology
There have been many advances in the field of gastrointestinal pa thology which are of considerable clinical significance during the 13 years since the last publication of a volume of Current Topics in Pathology devoted to this subject. Many have arisen
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DIXON
2 2.1 2.2 2.3 2.4 2.5 2.6
Type B Chronic Gastritis Morphological Observations Human and Animal Infection Immunological Studies . Biochemical Mechanisms Treatment Studies Conclusion
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3 3.1 3.2 3.3
Type A Chronic Gastritis Campylobaeter Status Pathogenesis ECL Cells and Polyps
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4 4.1 4.2 4.3 4.4
Lymphocytic Gastritis Relationship to Varioliform Gastritis Prevalence Campylobaeter Status Aetiology
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5 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 5.9 5.10
Reflux Gastritis Foveolar Hyperplasia Paucity of Inflammatory Cells Hyperaemia Pathogenesis Specificity Campylobaeter Status Reflux in the Intact Stomach Reflux and Ulceration Hyperplasia Versus Dysplasia Gastric Antral Vascular Ectasia
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Pathogenetic and Diagnostic Classification of Gastritis
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7 7.1 7.2 7.3 7.4
Duodenitis Duodenitis and Duodenal Ulcer . Histopathological Aspects Gastric Metaplasia and C. pylori Conclusions
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Introduction
References
G. T. Williams (ed.), Gastrointestinal Pathology © Springer-Verlag Berlin Heidelberg 1990
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M.DIXON
1 Introduction Although for many years a simple classification of 'non-specific' gastritis into acute, chronic superficial and chronic atrophic categories has sufficed in routine histopathological practice, the clinical significance of the latter diagnoses is uncertain. While acute gastritis has well established and consistent clinical associations (a recent history of drug ingestion or alcohol excess leading to haemorrhagic erosions), the clinical features of chronic gastritis are much more nebulous. The finding of chronic gastritis in 'healthy volunteers' (KREUNING et al. 1978) and in random population surveys (VILLAKO et al. 1976) has led some to conclude that the condition is a normal aging process of no clinical consequence. While this is a minority view, even those who believe it to be a pathological process have difficulty in recognising at what point the density of the inflammatory cell infiltration becomes 'abnormal', and the relationship between this inflammatory process, symptomatology and associated pathology. There have been several attempts to refine the histological classification of chronic gastritis, the best known being that of WHITEHEAD et al. (1972), who advocated a system based on the type of mucosa, subdivision into superficial and atrophic forms, the 'activity' (presence of polymorph infiltration), and the presence and type of metaplasia. Thus according to their scheme a biopsy might be reported as showing 'antral active chronic superficial gastritis without metaplasia' or 'body inactive chronic atrophic gastritis with intestinal metaplasia'. These authors also endorsed the additional category of 'gastric mucosal atrophy' for biopsies showing marked glandular atrophy, widespread metaplasia and negligible inflammmatory cell infiltration. However, others, such as CHELl and GIACOSA (1983), prefer to consider this picture as simply the severe end of the spectrum found in chronic atrophic gastriti
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