Tumours of the stomach and small intestine

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Tumours of the stomach and small intestine

Carcinoma of stomach

Pathology of gastric carcinoma

Gastric carcinomas are almost exclusively adenocarcinomas. Two distinct histopathological groups are recognised, each with its own epidemiological associations. The intestinal type has histological features similar to intestinal epithelium. Cells grow in clumps and there is marked inflammatory infiltrate. The second variety is the diffuse type. Here the cells are singular, often arranged in single file and surrounded by a marked stromal reaction. Tumour cells have large intracellular mucin droplets which displace the nucleus to the cell periphery, giving the characteristic signet ring appearance (Fig. 23.1). Intestinal-type carcinomas have a better prognosis than mucin-producing signet ring carcinomas.

Gastric carcinomas develop in three morphological forms described below; the intestinal type largely produces fungating tumours and malignant ulcers, and the diffuse type causes infiltrating carcinomas:

• Fungating tumours—these polypoid lesions may grow to a huge size

• Malignant ulcers—these probably result from necrosis in broad-based solid tumours. Malignant ulcers are often larger than peptic ulcers (except for giant benign ulcers of the elderly) with a heaped-up indurated (hardened) margin

• Infiltrating carcinomas—this form spreads widely beneath the mucosa, and diffusely and extensively invades the muscle wall. This causes thickening and rigidity and the entire stomach contracts to a very small capacity. This is known as linitis plastica and its appearance likened to a ‘leather bottle’. Linitis plastica affects a slightly younger age group than intestinal-type cancer and has a very poor prognosis. Diagnosis may be delayed because endoscopic changes are often subtle and standard biopsies of mucosa may not show malignancy

Early gastric cancer’ is defined as cancer limited to the mucosa and submucosa. This is found most often as a result of endoscopic screening or whilst investigating possible peptic ulcer. Results of surgery in this group are excellent, with a surgical cure rate of about 90%.

Epidemiology of gastric carcinoma

Gastric cancer is the fourth most common cancer in the world, causing 8% of cancers, but is the second most frequent cause of cancer deaths at 10%; its mortality is surpassed only by that of lung cancer (2008 figures). The disease is rare before the age of 50 and increases in frequency thereafter. Males have two to three times the risk of females, and the disease is more common in lower socio-economic groups. Korea has overtaken Japan in having the highest annual incidence—a crude rate of 70 per 100 000 per year in men and 27 in women (2002). In the UK, equivalent rates are 12.6 for men and 5.2 for women. The offspring of Japanese immigrants to America carry no greater risk than other Americans, evidence that environmental rather than racial factors are central in the aetiology. In much of the Western world, the incidence and death rates of gastric cancer have steadily decreased over recent years, and this is almost entirely due to a decline in the intestinal type. In Japan, the age standardised incidence for men has fallen from 80 per 100 000 per annum in 1975 to 50 in 2005.

The epidemiology gives enticing clues as to the causes of the disease. There are marked regional variations in incidence, largely explained by disparities in the rate of intestinal-type carcinomas. This, and the fact that this type is more prevalent in lower socio-economic groups, suggests that environmental factors are important in its genesis. There is probably no universal aetiological factor but rather a combination of co-factors that bring about malignant change. Japan, with its very high incidence of this disease, continues to play a leading role in research into early detection and management.

Aetiology of gastric carcinoma and premalignant conditions

Helicobacter pylori infection

H. pylori is known to initiate peptic ulceration, and chronic H. pylori infection has become a prime suspect for initiating intestinal-type gastric cancer. The organism can colonise gastric mucosa over long periods and cause chronic gastritis which may progress to type B multifocal atrophic gastritis. In one biopsy study of gastric cancers, H. pylori was found in 90% of intestinal-type cancers, whilst only 30% of the diffuse type were infected. The carcinogenic mechanism of H. pylori may involve alterations to the gastric acid–pepsin environment, with increased cell turnover and possibly enhanced mucosal susceptibility to ingested carcinogens. H. pylori eradication does not reverse gastric atrophy but does improve the enzymic and hormonal secretory capacity of the stomach. H. pylori also appears likely to be involved in gastric lymphoma of the mucosa-associated lymphoid tissue (MALT) type (see p. 322).

Clinical features of gastric carcinoma

Symptoms are often minimal until late in the course of the disease so that 70% of patients present with advanced local and/or metastatic disease. Lesions at the inlet or outlet of the stomach cause obstructive symptoms earlier than those elsewhere where the diameter allows for substantial growth before encroachment. Vomiting occurs if the gastric outlet becomes obstructed, typically by tumours of the antrum, and dysphagia occurs with gastro-oesophageal tumours.

In advanced disease, up to half the patients are asymptomatic and the rest have pain, nausea, vomiting, anorexia or a feeling of fullness after small meals (early satiety). Sometimes these symptoms are there months before the patient presents. Anaemia from chronic occult blood loss is common and one-third have positive stool tests for occult blood. One-third have cachexia (severe weight loss and wasting). This usually indicates metastatic disease and may be the only manifestation of cancer at the time. Of the 70% who present with advanced local disease (stage T3), more than half have extensive abdominal nodal spread and half have distant metastases. The presenting features of gastric carcinoma are summarised in Box 23.1.

Spread of gastric cancer

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