CHRONIC GASTRITIS/GASTRIC EROSIONS

Chapter 5b

CHRONIC GASTRITIS/GASTRIC EROSIONS

1. DEFINITION AND OVERVIEW

Chronic gastritis is a condition defined by a cellular infiltrate of chronic inflammatory cells in the gastric mucosa, attracting Codes ICD 10 AM K29.3, 29.4 and 29.5. A simple classification is:

• chronic atrophic gastritis Type A

• chronic atrophic gastritis Type B And rare forms

• lymphocytic gastritis

• eosinophilic gastritis

• granulomatous gastritis

• Crohn’s disease

• sarcoidosis

Chronic gastritis is a complex and confusing subject. Fortunately, the clinical and epidemiological aspects are fairly clear. The term is used in at least three aspects in medicine:

• clinical : a syndrome characterised by epigastric pain/discomfort, nausea, bleeding

• endoscopic : changes in the texture, colour, contour of the stomach at endoscopy

• histological : a variety of changes in mucosal cell nature and appearance, structure produced and nature of the cellular infiltrate.

Beyond this, it can be classified from multiple aspects:

• clinical

• endoscopic

• at least four histological classifications

44 4 chapter 5b

• aetiological :

• H.pylori

• Immunological

• Others

• topographic

To confuse the issue further:

• there is little or no correlation between the clinical, endoscopic and histological appearances

• changes in the mucosa are often patchy, so that the five standard biopsies from various parts often vary considerably in their appearance

• there are at least four current classifications, none used universally.

In chronic gastritis, the cellular infiltrate consists mainly of lymphocytes and plasma cells. The sequence is generally regarded as:

• Superficial gastritis. Inflammatory changes are limited to the lamina propria; the gastric glands are preserved with possibly a diminution of mucus in the glands.

• Atrophic gastritis. The inflammatory infiltrate extends deeper into the mucosa with progressive distortion and destruction of gastric glands.

• Gastric atrophy. The glandular structures are greatly diminished, as is the cellular infiltrate. The mucosa is thin and at endoscopy the changes are evident with vessels visible through the mucosa. This is one of the few occasions when a confident pathological diagnosis can be made at endoscopy.

• Intestinal metaplasia may be present in patches and predispose to gastric carcinoma.

• Type A gastritis is regarded as having an auto-immune basis and mainly effects the fundus and body of the stomach. It impairs gastric acid secretion and so is associated with hypo or achlorhydria, raised serum gastrin levels and, often, parietal and intrinsic factor antibodies. Its only significance is a small increase in the risk of gastric cancer. It occurs in two situations:

1. In pernicious anaemia. This is associated with parietal cell antibodies in 90% and with intrinsic factor antibodies in 40%.

2. Chronic gastritis (fundal) not associated with pernicious anaemia. In these patients about 60% have parietal cell antibodies but no intrinsic factor antibodies. Such patients may have relatives with pernicious anaemia.

• Type B chronic gastritis is associated with H.pylori colonisation

(1). It begins and predominates in the antrum but may, over a

period of 15 to 20 years extend to involve the whole stomach. In

CHRONIC GASTRITIS/GASTRIC EROSIONS 45 its early stages H.pylori is readily demonstrated but as the atrophy progresses the organism it becomes more difficult to demonstrate (2). There is some evidence that treatment with H

RA or PPI may hasten the onset of gastric atrophy and so theoretically of gastric carcinoma. There is also evidence that H.pylori organisms carrying the CagA genotype are the major culprit in the development of chronic gastritis type B.

2. RISK FACTORS FOR CHRONIC GASTRITIS Although the acquisition of appropriate strains of H.pylori is regarded as the major determinant of type B gastritis, there are suggestions of other causes:

• alcohol abuse

• NSAIDs

• Duodenogastric reflux following gastric surgery

Apart from H.pylori infection, there are some infective causes, most of which are rare and seen mainly in the immunocompromised, as in AIDS

• viral - CMV and Herpes virus

• bacterial

• fungal

There are also granulomatous gastropathies

• Crohn’s disease – quite uncommon

• Sarcoid – rare

References

1. Fontham ETII, Ruiz B, Perez A, Hunter F, Correa P. Determinants of Helicobactor pylori infection and chronic gastritis. Am. J. Gastroenterol. 90,1094-1101 (1995).

2. Kuipers EJ, Appelmelk BJ. Helicobactor pylori and gastritis. Biomed. Pharmacother.

51,105-5 (1997).