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

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 ((131)I)-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 ((14)C)-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 ((125)I)-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.