A study of six patients with hypertrophy of the gastric mucosa with particular reference to albumin metabolism

Abstract

SUMMARY Six patients with hypertrophy of the gastric mucosa (Menetrier's disease) have been studied. An incorrect diagnosis was initially made in four patients. The correct diagnosis was suggested by the appearances either of barium meal radiographs of the stomach or at gastroscopy. Estimates of both basal and maximal gastric acid secretion were within normal limits. A definitive histological diagnosis requires an adequate full-thickness biopsy of the wall of the stomach; a peroral gastric mucosal biopsy is of no value in this context. There was no evidence of premalignant change in the histological material available but five of the patients were shown to have concomitant superficial gastritis. Subtotal gastrectomy in four of the patients was followed by a striking amelioration of abdominal pain, which was only temporary in one patient.Albumin metabolism was studied in five of the patients, four of whom had concomitant superficial gastritis. None of the patients had hypoalbuminaemia. However, the fractional catabolic rate of albumin measured with ('3II)-albumin was shown in four of these patients to be increased, while the absolute catabolic rate was similar to that in control subjects. Similar results were obtained for albumin synthesis in three of the patients using the ('4C)-carbonate method. In two of the patients subtotal gastrectomy was associated with a marked reduction of the fractional catabolic rate of albumin and in one, using (125I)-fibrinogen,with a relatively less marked reduction in the fractional catabolic rate of fibrinogen. These results indicate that abnormal albumin metabolism can be demonstrated in patients with this syndrome in spite of normal plasma albumin concentrations. The detection of the abnormal albumin metabolism can be of diagnostic value in patients with this gastric lesion. The abnormalities of albumin metabolism found are consistent with excessive loss of albumin into the stomach and the presence of superficial gastritis could have contributed to protein loss. Menetrier (1888) described a syndrome characterized by marked oedema and ascites associated with grossly enlarged gastric mucosal folds. Since then there have been numerous reports of patients with similar lesions of the gastric mucosa, some of whom have also exhibited evidence of fluid retention. The concentrations of the plasma proteins, in particular albumin, when measured have tended to be low in these patients, especially when fluid retention was present (

Haematemesis in Ménétrier's disease

“…A lack of the trophic effect of gastrin has been suggested (Scott et al, 1975), but serum gastrin in patient 1 was high and was within the range that might be expected for patients with gastritis with antral sparing, which may occur in Menetrier's disease (Jones et al, 1972) and hypochlorhydria (Korman, Strickland and Hansky, 1971). The authors are not aware of other reports on gastrin levels in Menetrier's disease and consider that this finding merits further study.…”

“…The characteristic mucosal histology (Jones et al, 1972) was present in full-thickness sections of the operative specimens and in addition patient 1 was shown to have the hypochlorhydric mucus-rich gastric juice which is typical of the disease (Scott et al, 1975). In patient 3 only superficial biopsies were obtained which may be insufficient for a firm diagnosis (Jones et al, 1972) but the clinical and investigational findings make this diagnosis likely.…”

“…Bleeding probably occurs as a result of superficial gastritis (Jones et al, 1972) and although it may cease spontaneously, emergency surgery may be necessary in the face of continued life-threatening haemorrhage. That one of these patients died underlines the potential severity of the complication.…”

Protein-Losing Enteropathies

“…Indeed, this initial study predicted in larger groups of patients with Ménétrier's disease that hypoalbuminemia can be found in about 70% of patients and that in those cases in which this abnormality is investigated in metabolic studies with radioiodinated albumin, the low serum albumin can be shown to be due to an increased fractional albumin catabolic rate (Jones et al, 1972). In addition, it was demonstrated with 51 Cr-albumin studies that excess loss of protein into the GI tract can be noted in 85% of patients.…”

The diagnosis of Ménétrier’s disease

“…The condition was first described by Menetrier in 1888 and since then some 200 cases have been reported in the literature. These reports have concerned the pathology (Butz, 1960), the protein turnover (Jarnum and Jensen, 1972;Jones et al, 1972), the gastric protein loss (Citrin, Sterling and Halstead, 1957) and case reports of the various types of presentation, notably acute gastrointestinal (GI) bleeding (Williams, 1956), chronic GI bleeding (Singh, Cumaraswamy and Corrin, 1979), and oedema (Chokas, Connor and Innis, 1959). Diarrhoea has occasionally been reported.…”