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Protein losing enteropathy (PLE), a very rare disease with hypoproteinemia and edema as its characteristics, is caused by various diseases resulting in protein depletion from the gut. The diagnosis is relatively difficult due to its complex pathogeneses. The present paper reported a case whose symptom started with acute diarrhea and hypoproteinemia. Gastrointestinal endoscopies showed digestive ulcers and colon polyp. The treatments contained albumin infusion, Chinese herbal decoction and other symptomatic therapies. The hypoproteinemia become even worse and edema occurred after 4 days' treatment. A larger dose of albumin infusion (40-60 g/d) and modified herbal decoctions were prescribed. A final diagnosis of eosinophilic gastroenteritis (EG) complicated with PLE was confirmed by histopathological examination of a repeated gastroscopy. After three weeks' treatment, the serum albumin level was raised and the edema subsided gradually. In conclusion, herbs may have an effect on PLE patients, but PLE resulting from EG is very complex and easy to misdiagnose, especially in atypical conditions. Further studies are required to find the exact mechanisms.

A 44-year-old female with varioliform gastritis and duodenitis had gastrointestinal protein loss revealed by 111indium chloride scintigraphy. Treatment with omeprazole, a proton pump inhibitor, for 2 months, followed by famotidine, resulted in clinical improvement with resolution of the gastroduodenal lesions and protein loss. Colonization of the stomach with Helicobacter pylori was found before and after the treatment. The results in this patient suggest that omeprazole can be of value for the treatment of varioliform gastritis associated with protein-losing gastroenteropathy. The role of Helicobacter pylori in the pathogenesis of this disease is unclear.

Seven patients with giant hypertrophic gastropathy participated in a gastric intubation perfusion study to investigate the route and mechanism of protein leakage associated with this disease. All patients had gastric tight junctions wider than those in healthy controls. Acute administration of propantheline bromide reduced gastric albumin leakage (-50.7%, p less than 0.05) and concurrently decreased width of tight junctions (p less than 0.05) in all patients. Another antisecretory agent, cimetidine, had no consistent effect on protein leakage or on the width of tight junctions. Pentagastrin and bethanechol chloride increased protein loss but had no effect on the width of tight junctions. These results are consistent with the hypothesis that proteins may take a paracellular route via the tight junctions as they traverse the gastric mucosa and that this may have a cholinergic mechanism.

A patient with chronic erosive gastritis and protein-losing gastropathy is reported. Presentation was with weight loss and abdominal discomfort. There were endoscopic and radiological features of erosive gastritis. Radioactive chromium studies confirmed that the low serum albumin was associated with fecal protein loss. No improvement occurred with bed rest or Caved S but coincided with DeNol therapy.

There is considerable evidence, both in patients with Menetrier's disease and from animal models of protein-losing gastropathy, that antisecretory drugs can acutely decrease or abolish gastric plasma protein shedding. Serial measurements on serum protein components were performed in a patient with Menetrier's disease before, during, and after long term treatment with propantheline bromide. Total serum protein concentration increased significantly during the treatment period from 4.3 +/- 0.50 to 5.9 +/- 0.55 g per dl during treatment, while albumin increased from a pretreatment value of 2.5 +/- 0.12 to 3.4 +/- 0.16 g per dl. The improvement in serum proteins and symptoms continued after therapy was stopped. Intensive anticholinergic drug therapy should be tried in this disease before resorting to gastrectomy.

In five cases of giant hypertrophic gastritis (Menetrier's disease) biopsied gastric mucosa was examined for fibrinolytic activity; in all cases there was marked elevation of the activity due mainly to tissue plasminogen activator. The patients were given antifibrinolytic therapy with oral tranexamic acid (trans-4-aminomethyl cyclohexane carboxylic acid; trans-AMCHA), and four of the patients showed marked improvement of their hypoproteinemia as well as their mucosal disorders. One patient, who showed moderate increase of serum protein level but no reduction of the mucosal disorder, finally received gastrectomy. It was concluded that antifibrinolytic therapy seemed to block the vicious circle of 'membrane disorders', 'increased tissue fibrinolysis', 'increased vascular permeability' and 'hypoproteinemia' in Menetrier's disease.