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Most gastric tumours are malignant: nearly all are adenocarcinomas; the rest are lymphomas or rarely, carcinoid tumours or sarcoma. True adenomatous gastric polyps are rare; most gastric polypoid lesions are small benign hyperplastic nodules.
Tumours of small bowel are rare. Of the malignant tumours, lymphomas and gastrointestinal stromal tumours (GIST) are much more common than adenocarcinomas. Peutz–Jeghers syndrome is a rare inherited disorder characterised by multiple benign polyps in the small bowel and perioral pigmentation plus increased risk of breast, colorectal and other cancers. Patients are fairly commonly encountered at student examinations (see Ch. 27 , p. 378).
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 later; 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%.
Gastric cancer is the fifth most common cancer in the world, causing 14% of cancers, and is the fifth most frequent cause of cancer deaths at 11% (2012 figures: see http://www.cancerresearchuk.org/sites/default/files/cs_report_world.pdf ). The disease is rare before the age of 50 years and increases in frequency thereafter. Males have two to three times the risk of females, and the disease is more common in lower socioeconomic groups. Korea has overtaken Japan in having the highest annual incidence—a crude rate of 62 per 100,000 per year in men and 25 in women (2015). In the United Kingdom, equivalent rates are 13.6 for men and 7.2 for women (2015). 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 because of 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 46 in 2012.
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 socioeconomic groups, suggests that environmental factors are important in its genesis. There is probably no universal aetiological factor but rather a combination of cofactors 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.
Multifocal atrophic gastritis (type B) is a condition that precedes intestinal-type gastric cancer. It probably represents one step of a sequence running from superficial gastritis, via atrophic gastritis to intestinal and colonic metaplasia, dysplasia and eventually to cancer. Multifocal atrophic gastritis is the result of chronic inflammation . Risk factors for type B gastritis include Helicobacter pylori infection and certain items of diet. The diffuse corporeal type of gastritis (type A) of pernicious anaemia is a much weaker aetiological factor for cancer. Patients with this have a three- to sixfold increase in risk, but the absolute risk remains low.
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. 346).
Dietary factors shown to increase the incidence of gastric cancer include excess intake of salt and nitroso compounds and a low intake of ascorbic acid. In this respect, diets high in dried and salted fish and salt-cured and smoke-cured meats appear to be a particular risk. Lettuce grown in temperate climates appears to offer some protective effect.
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 tumours just below the gastrooesophageal junction.
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 T 3 ), 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 .
Often asymptomatic until a late stage
Nonspecific epigastric pain and dyspepsia
Iron deficiency anaemia
Nausea and vomiting
Anorexia and early satiety
Feeling of abdominal fullness or discomfort
Marked weight loss (cachexia)—late stage
Epigastric mass (late stage)
Left supraclavicular mass (metastasis in Virchow node)
Obstructive jaundice (metastases in the porta hepatis)
Pelvic mass (metastases to ovaries)
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