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Linitis plastica is typically due to an infiltrating adenocarcinoma. The term, however, is descriptive rather than diagnostic.
A man of 63 was admitted because of long-term weight loss and worsening symptoms of gastric outlet obstruction. There had been no abdominal pain or change in bowel habit, no haematemesis or melaena. Initial treatment was nasogastric aspiration, intravenous hydration and an intravenous proton pump inhibitor. Endoscopy showed moderate reflux and a poorly distensible stomach with gastric outlet obstruction; the appearances were in keeping with infiltrating adenocarcinoma (linitis plastica) but repeated biopsies showed only inflammatory changes. On CT there was pronounced thickening of the wall of the entire stomach, measuring up to 2 cm, with severe narrowing of the lumen (Figure 1). No gas bubbles were evident in the stomach walls. These findings supported the provisional diagnosis of carcinoma and staging laparoscopy was undertaken. This showed a greatly thickened and rigid stomach with the consistency of rubber. Because there was no evidence of spread beyond the stomach, a total gastrectomy was performed. Postoperative recovery was satisfactory. On histological examination the stomach showed typical changes of diverticular disease, with pouches of mucosa extending through the muscularis propria into adjacent fat (Figure 2). The muscularis propria was hypertrophic and the submucosa showed oedema and fibrosis. In the mucosa there were areas of chronic inflammation with some ulceration; no metaplasia, dysplasia or malignancy was seen.
The typical gastric diverticulum is solitary and does not cause symptoms.1,2 Diverticula are found in 0.03-0.3% of necropsies,3 with three-quarters of them high on the posterior wall of the stomach and the remainder in the prepyloric region.1,2 Multiple gastric diverticulosis is rarer still and is more likely to cause illness.1 Of the previously reported cases only two have been associated with gastric outlet obstruction.4,5 Our patient represents the third such case and had diverticula throughout the entire stomach with relative sparing of the pylorus—in contrast to the patient of Schweiger et al.,5 whose diverticula were almost exclusively prepyloric.
With such a rare condition it is difficult to establish an aetiology. Most prepyloric diverticula are associated with peptic ulcer disease, malignant disease or previous surgery2 but some may be congenital in origin. In addition, traction diverticula may result from extragastric disease such as pancreatitis or cholecystitis.5 With regard to the association with pyloric stenosis, one could hypothesize that the diverticula result from high intragastric pressure. Alternatively, prepyloric diverticula might lead to gastric stasis, pyloric ulceration and stenosis. In both instances local muscular weakness must play an important part since even longstanding pyloric stenosis is seldom associated with diverticulosis; gastric diverticula have lately been reported in a patient with Caroli's disease,6 a deficiency of the fibromuscular matrix of the biliary tree.
In the present case, the true diagnosis became evident only after gastrectomy. A technique that might possibly have led to earlier diagnosis is endoscopic ultrasound-guided fine-needle aspiration biopsy.7