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Ménétrier's disease (MD) is a rare disease of the stomach, characterised by hypertrophic gastric folds leading to protein loss. The association with ulcerative colitis (UC) is rare but has been reported in the literature. We report a case of a 29-year-old male affected by UC with an additional diagnosis of MD 3 years after UC diagnosis. UC was refractory to several treatment lines (thiopurines, infliximab, vedolizumab and ustekinumab), and the patient underwent colectomy. Octreotide was administered for MD normalising blood biochemistry, but it was not effective in inducing endoscopic remission of the stomach. Treatment options in patients with MD and UC are discussed., Competing Interests: Competing interests: None declared., (© BMJ Publishing Group Limited 2021. No commercial re-use. See rights and permissions. Published by BMJ.)

Background: Ménétrier-like disease is a rare hypertrophic canine gastropathy, reported in only seven dogs. Clinical signs are vomiting, anorexia and weight loss. Macroscopically, giant cerebriform gastric mucosal folds are typically seen in the corpus and fundus of the stomach. Histopathologically, fundic mucous cell hyperplasia and loss of parietal and chief cells are typical., Case Presentation: A nine-year-old spayed female Pointer had a history of intermittent vomiting, marked weight loss and hypoalbuminaemia. A gastroduodenoscopy was performed three times within three months with macroscopic changes remaining the same. The gastric mucosa of the corpus, fundus and proximal antrum was markedly irregular, with cerebriform mucosal folds. In the first gastric biopsies, histopathology revealed a moderate granulomatous gastritis, with a severe manifestation of Helicobacter-like organisms. Treatment for Helicobacter spp. decreased the vomiting slightly. The dog was diagnosed with concurrent leishmaniosis; the conventional anti-Leishmania treatment decreased the vomiting moderately, the hypoalbuminaemia resolved and the dog gained weight back to a normal body condition. Granulomatous gastritis was not present in the gastric biopsies after these treatments. The dog increased vomiting when palliative treatment (maropitant citrate, ondansetron and esomeprazole) was discontinued, and thus, full-thickness biopsies of the stomach were taken and Ménétrier-like disease was diagnosed. The affected area was too large to be surgically removed; thus, palliative treatment was reinstated. The dog remained clinically well 39 months after the first clinical presentation., Conclusions: This is the first report of Ménétrier-like disease in a dog with a simultaneous manifestation of granulomatous gastritis, helicobacteriosis and leishmaniosis. The clinical signs decreased after treatment of helicobacteriosis and leishmaniosis, but vomiting remained probably as a sign of Ménétrier-like disease. Treatment options for dogs are surgical removal of the abnormal area or palliative treatment. In humans, promising results for a cure have been shown with cetuximab treatment, a human monoclonal antibody, but no canine antibody is commercially available yet. The dog here was doing well 39 months after first presentation, which is the longest reported survival time for Ménétrier-like disease with only palliative treatment in dogs. Full-thickness biopsies are preferred in macroscopic hypertrophic lesions of the stomach for better assessment of Ménétrier-like disease.

We present a rare case of hypertrophic gastropathy associated with protein loss. A 35-year-old man was hospitalized for bowel habit changes, abdominal pain, generalized edema and symptomatic anemia. Pertinent laboratory findings included iron deficiency anemia (Hb 6.7g/dl, ferritin 5 ng/ml) and marked hypoalbuminemia (albumin 2.5 g/dl). Endoscopic biopsy samples of giant gastric folds observed along the greater gastric curvature revealed foveolar hyperplasia and significant parietal cell loss. Endoscopic ultrasonography showed gastric parietal thickening with preserved architecture and normal gastric wall layers. Menetrier disease was diagnosed and the patient treated with cetuximab, a monoclonal antibody that inhibits ligand binding of transforming growth factor alpha (TGFa), preventing gastric mucosa cell proliferation. After twelve months of treatment, the patient referred symptoms improvement, and gastric biopsy levels of the proliferation marker protein Ki-67 had decreased.

Ménétriere´s disease is a rare disorder of the body and fundus of the stomach, characterized by a massive proliferation of the foveolar cells and subsequent excess mucous secretion. This results in hypoproteinemia due to loss of serum proteins across the gastric mucosa. The cause of Ménétriere´s disease is unknown, and due to the irreversible and premalignant character of the disorder, the patients affected have been subdued to gastrectomy as the only curable treatment. Epidermial growth factor (EGF) has been implicated in the pathogenesis, a finding that makes the disorder receptive to monoclonal antibody treatment against the EGF receptor. In this case report, we present a 41-year-old woman referred to our emergency department due to dizziness, nausea, and vomiting. A thorough medical investigation, combining clinical history, laboratory investigations, an upper endoscopy with full-thickness snare biopsies, and a CT scan confirmed Ménétriere´s disease, and she was successfully treated with the monoclonal antibody cetuximab.

Background: Acquired thrombophilia is a potential sequela of malignancy, chronic inflammation, and conditions characterized by severe protein deficiency (for example, nephrotic syndrome, protein-losing enteropathy). As such, venous thrombosis is often a feature, and occasionally a presenting sign, of systemic disease. Ménétrier's disease is a rare hyperplastic gastropathy that may lead to gastrointestinal protein loss and hypoalbuminemia. To date, reports of venous thrombosis associated with Ménétrier's disease are exceedingly scarce., Case Presentation: We report the case of a 40-year-old white man who presented with unprovoked deep venous thrombosis, pulmonary embolism, and renal vein thrombosis. Upon receiving therapeutic anticoagulation, he developed severe gastrointestinal bleeding, and endoscopic evaluation led to a diagnosis of Ménétrier's disease. A laboratory workup revealed deficiency of protein C, protein S, and antithrombin III, as well as markedly elevated levels of factor VIII. He was determined to have an acquired thrombophilia as a direct result of Ménétrier's disease., Conclusions: This case describes an acquired thrombophilic state in a patient with Ménétrier's disease and profound hypoalbuminemia. Although this association is rarely described, we discuss the probable mechanisms leading to our patient's thrombosis. Specifically, we posit that his gastrointestinal protein loss led to a deficiency of several anticoagulant proteins and a compensatory elevation in factor VIII, as occurs in nephrotic syndrome and inflammatory bowel disease. Of note, this patient's recurrent venous thrombosis was the initial clinical sign of his gastrointestinal pathology.

Ménétrier's disease is a rare hypertrophic gastropathy, causing protein leak. An overexpression of transforming growth factor alpha is involved. In inhibiting the epidermal growth factor receptor, cetuximab and somatostatin analogues are the two most promising treatments, allowing to avoid radical gastrectomy. We report the case of a patient with a sustained clinical remission after treatment with lanreotide, but without complete endoscopic healing. We discuss the available therapeutic options and present a literature review of somatostatin analogues for the treatment of Ménétrier's disease., (Copyright © 2015 Elsevier Masson SAS. All rights reserved.)

Ménétriers disease is a rare mucosal hyperproliferative disorder of the stomach, however, the evidence for long-term care remains limited, especially if a gastrectomy is declined. We present a case of 25-year-old Caucasian woman with a history of end-stage renal failure (ESRF) who experienced worsening symptoms of abdominal pain, haematemesis and abdominal swelling, with her serum albumin dropping to 20 g/L and haemoglobin to 4.9 g/dL. Endoscopy showed markedly hyperplastic gastric folds consistent with Ménétriers disease, confirmed histologically by gland dilation and gastric pit expansion. Intravenous cetuximab was prescribed for 12 months, with clinical, biochemical and endoscopic improvement. However, 5 weeks post cetuximab completion, there was relapse to 50% gastric coverage with Ménétriers. A discussion around gastrectomy was rejected by the patient. This is the first report of relapsing Ménétriers disease in a female patient with ESRF; we suggest that long-term cetuximab should be considered if a gastrectomy is declined., (2014 BMJ Publishing Group Ltd.)

Introduction: Ménétrier disease is a rare disorder characterized by gastric foveolar hyperplasia associated with secondary protein loss. In children, this condition is presented as an edematous syndrome without renal or hepatic impairment and differs from the adult form by the constant presence of edema and spontaneous remission. It has been related to infections in most published cases, especially to Cytomegalovirus (CMV) and Helicobacter pylori (H. pylori)., Objective: To present a pediatric case of Ménétrier disease and endoscopic imaging obtained during the evolution of the patient., Case Report: A five year old preschooler who presented a generalized edema, abdominal pain and malaise. After ruling out renal and hepatic pathologies, an upper endoscopy revealed a severe compromise of the gastric mucosa. Urease test for H. pylori and IgG test for CMV resulted positive. Albumin and H2 receptor antagonists were administered. The evolution was favorable and the patient was discharged after 14 days; 8 month follow-up endoscopy showed no abnormalities., Conclusion: The medical profile and endoscopy are enough evidence to suggest the diagnosis of hypertrophic protein-losing gastropathy. Further studies need to be developed that include a considerable number of patients to assess their association with CMV or H. pylori infections, as these viruses are very common in our population.

Molecular imaging biomarkers of proliferation hold great promise for quantifying response to personalized medicine. One such approach utilizes the positron emission tomography (PET) tracer 3'-deoxy-3'[18F]-fluorothymidine ([18F]FLT), an investigational agent whose uptake reflects thymidine salvage-dependent DNA synthesis. The goal of this study was to evaluate [18F]FLT-PET in the setting of Ménétrier's disease (MD), a rare, premalignant hyperproliferative disorder of the stomach treatable with cetuximab therapy. Over 15 months, a patient with confirmed MD underwent cetuximab therapy and was followed with sequential [18F]FLT-PET. For comparison to MD, an [18F]FLT-PET study was conducted in another patient to quantify uptake in a normal stomach. Prior to cetuximab therapy, stomach tissue in MD was easily visualized with [18F]FLT-PET, with pre-treatment uptake levels exceeding normal stomach uptake by approximately fourfold. Diminished [18F]FLT-PET in MD was observed following the initial and subsequent doses of cetuximab and correlated with clinical resolution of the disease. To our knowledge, this study reports the first clinical use of [18F]FLT-PET to assess proliferation in a premalignant disorder. We illustrate that the extent of MD involvement throughout the stomach could be easily visualized using [18F]FLT-PET, and that response to cetuximab could be followed quantitatively and non-invasively in sequential [18F]FLT-PET studies. Thus, [18F]FLT-PET appears to have potential to monitor response to treatment in this and potentially other hyperproliferative disorders.

Novel treatments for gastrointestinal (GI) diseases are based on molecular targets. Novel pharmacologic and biological agents with greater selectivity and specificity are being developed for a variety of epithelial diseases, including eosinophilic esophagitis (EoE), gastroesophageal reflux disease (GERD), celiac disease, short bowel syndrome (SBS), and inflammatory bowel diseases (IBDs; Crohn's disease and ulcerative colitis). Motility and secretory agents are being developed for gastroparesis, irritable bowel syndrome (IBS), functional constipation, and diarrhea. Here we focus on data from clinical trials involving validated pharmacodynamic or patient response outcomes.

Pediatric Menetrier's disease (MD) is an uncommon, acute, self-limited hypertrophic gastropathy characterized by enlarged gastric folds associated with epithelial hyperplasia and usually accompanied by protein losing gastropathy. Gastric cytomegalovirus infection is found in one third of MD children and its treatment is often associated with remission. Diagnosis often requires full-thickness biopsy due to inability to detect typical histological findings with conventional endoscopic biopsy. We report an uncommon case of non self-limited pediatric MD needing endoscopic mucosal resection for diagnosis which was then successfully treated with octreotide long-acting release (LAR). To the best of our knowledge, this is the first pediatric MD case successfully treated with octreotide LAR. Our experience suggests octreotide LAR as treatment for refractory MD before gastrectomy.

Analysis of cellular signaling networks typically involves targeted measurements of phosphorylated protein intermediates. However, phosphoproteomic analyses usually require affinity enrichment of phosphopeptides and can be complicated by artifactual changes in phosphorylation caused by uncontrolled preanalytical variables, particularly in the analysis of tissue specimens. We asked whether changes in protein expression, which are more stable and easily analyzed, could reflect network stimulation and inhibition. We employed this approach to analyze stimulation and inhibition of the epidermal growth factor receptor (EGFR) by EGF and selective EGFR inhibitors. Shotgun analysis of proteomes from proliferating A431 cells, EGF-stimulated cells, and cells co-treated with the EGFR inhibitors cetuximab or gefitinib identified groups of differentially expressed proteins. Comparisons of these protein groups identified 13 proteins whose EGF-induced expression changes were reversed by both EGFR inhibitors. Targeted multiple reaction monitoring analysis verified differential expression of 12 of these proteins, which comprise a candidate EGFR inhibition signature. We then tested these 12 proteins by multiple reaction monitoring analysis in three other models: 1) a comparison of DiFi (EGFR inhibitor-sensitive) and HCT116 (EGFR-insensitive) cell lines, 2) in formalin-fixed, paraffin-embedded mouse xenograft DiFi and HCT116 tumors, and 3) in tissue biopsies from a patient with the gastric hyperproliferative disorder Ménétrier's disease who was treated with cetuximab. Of the proteins in the candidate signature, a core group, including c-Jun, Jagged-1, and Claudin 4, were decreased by EGFR inhibitors in all three models. Although the goal of these studies was not to validate a clinically useful EGFR inhibition signature, the results confirm the hypothesis that clinically used EGFR inhibitors generate characteristic protein expression changes. This work further outlines a prototypical approach to derive and test protein expression signatures for drug action on signaling networks.

Menetrier's disease is a rare cause of protein-losing gastropathy characterised by hypertrophy of the gastric folds. Three cases are reported. Helicobacter pylori was detected by culture and CLO test in two cases and on follow-up gastroscopy in the other. The first two patients were given eradication therapy and hypertrophic gastropathy resolved whereas in the third the disease remitted prior to the eradication treatment. Typical sonographic features were thickened gastric wall with preservation of the wall stratification. A review of the literature found eight cases of Menetrier's disease associated with H. pylori in children and these cases are briefly reviewed. H. pylori infection should be considered in all children with Menetrier's disease and, if isolated, eradication treatment should be administered.

Ménétrier disease is a rare disorder of unknown etiology. An overexpression of TGF-alpha has been proposed to play a role in the pathophysiology. HIV-1 tat gene product has been shown to stimulate TGF-alpha production leading to a positive feedback autocrine loop. The case of a 41-year-old male with AIDS who presented with weight loss, abdominal pain, ascites, edema, nausea, vomiting, and diarrhea is discussed. A computed tomography (CT) scan of the abdomen showed avid enhancement of the stomach mucosa. Magnetic resonance angiography revealed gastric and small bowel distention with diffuse wall thickening. Biopsies of the stomach showed marked foveolar hyperplasia with active inflammation and gland changes consistent with Ménétrier disease.

Ménétrier's disease is a rare premalignant disorder of the stomach with no proven effective medical therapy. Increased epidermal growth factor receptor signaling has been implicated in the pathogenesis of Ménétrier's disease. We conducted a single-arm clinical trial with cetuximab, a monoclonal antibody that blocks epidermal growth factor receptor signaling, in nine individuals with clinically and histologically documented severe Ménétrier's disease that impaired quality of life to the extent that gastrectomy was being considered. Of the seven patients who completed the 1-month course of treatment, all showed statistically significant improvement both clinically (quality-of-life indices) and biochemically (increased parietal cell mass and gastric acidity). Furthermore, all seven patients who completed the 1-month trial elected to continue treatment, and four subsequently showed near-complete histological remission. Cetuximab should be considered as first-line therapy for Ménétrier's disease.

Scarlet fever is a rare disease in adult patients. We report a patient in whom scarlet fever was associated with hypertrophic gastritis and multiple organ failure. A 62-year-old woman presented with septic shock and multiple organ failure. Bacteriological survey was negative. Abdominal tomodensitometry showed an hypertrophic gastritis. Histological analysis demonstrated a non specific gastritis without any tumoral sign. Cefotaxime and amoxicillin led to improvement and hypertrophic gastritis progressively resolved. A sandpaper rash over the body with finger desquamation, elevation of antistreptolysin O and a recent contact with an infected grandson led to the diagnosis of scarlet fever. Due to antibiotic prescription, scarlet fever is now uncommon. Although classical, ENT or gastroenteritis presentations may be puzzling for the diagnosis of scarlet fever. As 150 years ago, diagnosis of scarlet fever is still a clinical challenge.

An 11-year-old, male Old English sheepdog was admitted for weight loss and intermittent vomiting of 1 month's duration. A cranioventral abdominal mass, anemia, hypoproteinemia, and hypoalbuminemia were the prominent abnormal findings. Imaging studies identified a remarkably thickened gastric wall with multilobulated folds protruding into the gastric lumen. Gastrotomy revealed the presence of giant cerebriform rugal folds arising from the fundus and body of the stomach. Pronounced gastric glandular hyperplasia and lack of evidence of cellular atypia were suggestive of giant hypertrophic gastritis. The dog was treated with prednisolone, cimetidine, and hyoscine butylbromide, only to experience a short-term remission.

Protein-losing gastropathy is an uncommon disease of uncertain etiology, known also as Menetrier's disease. In medical literature only 50 pediatric cases have been described. These childhood forms, in contrast to classic adult Menetrier's disease, have a typical benign and transient course, and require only supportive therapy. The role of Cytomegalovirus (CMV) in the pathogenesis has been demonstrated by gastric biopsy in one third of the cases. Also other infectious, allergic and immunological factors have been hypothesized. We describe a case of hypertrophic gastropathy with important protein-loss, admitted to our Pediatric Department for evaluation because of vomit, weight loss, abdominal pain and hypoalbuminemia. Gastric mucosal biopsy revealed a morphological evidence of CMV infection.

Menetrier's disease is a rare acquired cause of protein losing enteropathy, with premalignant potential. Since its first description in 1888, around 300 cases have been reported. This disease occurs more frequently in males aged 30-50 years. We report here the case of a 31 year- old Sudanese female who presented with generalized edema. Laboratory investigations showed hypoproteinemia and hypoalbuminemia without evidence of renal or liver disease. Upper gastrointestinal endoscopy showed giant gastric folds. The histopathological features of biopsies taken from these folds were consistent with Menetrier's disease. Our patient showed excellent response to treatment with subcutaneous octreotide and this may ameliorate the need for surgery as the definitive treatment of this disease.

Background & Aims: Ménétrier's disease is a rare premalignant hypertrophic gastropathy characterized by large rugal folds, foveolar hyperplasia with glandular atrophy, hypochlorhydria, and hypoalbuminemia. Patients with severe disease often exhibit refractory nausea and vomiting and require gastrectomy. Evidence from both mice and human beings suggests a critical role for epidermal growth factor receptor (EGFR) signaling in the pathogenesis of this disease. We previously reported significant clinical and biochemical improvement of a single patient treated for 1 month with Erbitux, a monoclonal antibody that blocks ligand binding to EGFR., Methods/results: We describe 2 patients who were given longer-term treatment with Erbitux as an alternative to gastrectomy. The first patient presented with nausea, hypoalbuminemia, and peripheral edema that required total parenteral nutrition (TPN) and infusions of albumin. On institution of Erbitux, there was rapid improvement in nausea and vomiting and stabilization of serum albumin with discontinuation of TPN and albumin infusions. Serum albumin remained stable during a 1-year course of Erbitux without supplemental protein. Application before and after Erbitux of the radiopaque dye ruthenium red to biopsies of the gastric oxyntic gland mucosa demonstrated prompt and persistent closure of tight junctions by electron microscopy. The second patient presented with chronic gastric bleeding that required bimonthly blood transfusions. During a 4-month course of Erbitux, his hematocrit stabilized, and transfusion requirements were eliminated., Conclusions: The present report demonstrates the efficacy of prolonged Erbitux therapy in patients with different presentations of severe Ménétrier's disease and also provides insight into the pathophysiology of the protein-losing gastropathy.

Background: Lymphocytic gastritis is a rare condition found in approximately 1% of dyspeptic patients. An association with Helicobacter pylori infection has been described. Hypertrophic lymphocytic gastritis is a rare cause of gastrointestinal protein loss. Here, we describe a patient with hypertrophic lymphocytic gastritis, in whom gastrointestinal protein loss resolved completely following H. pylori eradication., Case Report: A 38-year old obese man without gastrointestinal symptoms showed a markedly decreased serum protein (53 g/l, normal 66-85 g/l), a decreased serum albumin (33 g/l, normal 35-52 g/l) and decreased serum immunoglobulin G and immunoglobulin M levels. A renal cause for protein loss was excluded, liver function was normal. Endoscopy of the upper gastrointestinal tract revealed enlarged rigid gastric folds, and an H. pylori-associated lymphocytic gastritis. 99mTc-labelled albumin scintigraphy showed an increased activity in the upper left abdomen compatible with protein secretion in the stomach, and tracer pooling in the upper small bowel. Push enteroscopy with histology demonstrated a normal upper small bowel. Two months after eradication therapy, cure of H. pylori infection was documented and serum protein (71 g/l) and albumin (41 g/l) had returned to normal, while lymphocytic gastritis was still present. One year after eradication therapy endoscopy of the upper gastrointestinal tract and histology and laboratory values were normal., Conclusion: Protein-losing gastropathy caused by H. pylori-associated hypertrophic lymphocytic gastritis can be cured solely by H. pylori eradication therapy.

Ménétrier's disease is an infrequent clinical entity characterized by thickening of the gastric folds secondary to hyperplasia of the foveolar mucosa cells, frequently associated with loss of enteric proteins and hypoalbuminemia. Its etiology is unknown, although in the last few years it has been related to Helicobacter pylori infection. We present the case of a 38-year-old man with protein-losing gastroenteropathy caused by Ménétrier's disease, in whom eradication of H. pylori infection was followed by symptom improvement and resolution of hypoalbuminemia. In agreement with the criteria of other authors, we investigate the presence of H. pylori infection in all patients with Ménétrier's disease. When positive, the first-line treatment consists of eradication therapy.

Unlabelled: A 2-y-old girl with severe edema, oliguria and hypoalbuminemia caused by protein-losing gastritis was diagnosed with cytomegalovirus-associated Ménétrier's disease. After almost two weeks, during which the patient required repeated albumin transfusions, she was treated with intravenous ganciclovir. Within five days her condition had improved, and no additional albumin replacement was needed. Complete recovery was observed after several weeks., Conclusion: In patients with severe Ménétrier's disease, a course of ganciclovir treatment may be of benefit and should be considered.

Some cases of Ménétrier's disease associated with Helicobacter pylori (HP) have recently been reported in the literature. We report here the case of a 51-year-old man with a diagnosis of Ménétrier's disease who had previously been unsuccessfully treated with H(2) antagonists. A subsequent demonstration of HP infection led us to treat the patient with an eradicating therapy which prompted complete regression of clinical symptoms, resolution of the gastric endoscopic picture, and absence of HP on gastric histology. This result, in accordance with others in the literature, indicates an eventual association of HP infection with Ménétrier's disease and that consequent therapy is mandatory., (Copyright 2001 S. Karger AG, Basel)

We present the case of a 79-year-old female patient with criteria typical for Ménétrier's disease, i.e. enlargement of the gastric folds due to foveolar hyperplasia associated with severe protein-loss along with epigastric pain, nausea, vomiting and weight loss. Gastrin levels were within the normal range, but elevated Helicobacter pylori antibody titers (83 microg/ml) were indicative of a recent infection. Histologic examination of a gastric polyp, which was removed in toto, revealed the presence of early gastric cancer of the mucosal type. After initiation of antibiotic treatment with clarithromycin (3 x 250 mg/day) and metronidazole (2 x 500 mg/day) in combination with lansoprazole (30 mg/day), the patient's condition improved rapidly along with abrogation of protein loss. Under maintenance treatment as indicated above, the patient has been free of symptoms now for a period of more than 2 years. On repetitive endoscopic follow-up, there was no change in gastric mucosa morphology either endoscopically or histologically, and also no evidence of recurrence of a malignant lesion. We conclude that this therapeutic regimen represented an effective alternative to surgical intervention in this patient and should be considered in similar cases.

We report a case of Ménétrier's disease associated with hypoproteinemia who was successfully treated by eradication of Helicobacter pylori infection. A 26-year-old woman had diffuse giant gastric folds with proven protein leakage from the stomach. She received cimetidine, famotidine, and omeprazole for more than 3 months with little benefit. H. pylori infection was detected, and she was treated with clarithromycin (200 mg three times a day), lansoprazole (30 mg/day), and ecabet sodium (1.5 g twice a day) for 2 weeks. After starting the treatment, rapid increase of serum albumin and IgG levels were observed. The treatment resulted in eradication of H. pylori infection, and serum albumin and IgG levels returned to normal. Histologic specimens also showed the improvement of the irregularly elongated gastric pits with inflammatory infiltrates after the treatment. This case report suggests that eradication of H. pylori is recommended therapy for the immediate improvement of Ménétrier's disease associated with hypoproteinemia.

We report a patient with Ménétrier's disease presenting with extensive subcutaneous oedema, ascites and pleural effusion due to hypoalbuminaemia. Gastric secretory studies showed no free basal and stimulated acid secretion. The gastric juice contained significant amounts of albumin (0.2 g/dl) and immunoglobulin G (IgG) (1.11 mg/dl), corresponding to an estimated daily loss of 9.7 g and 45 mg, respectively. Protein-losing gastropathy was initially unsuccessfully treated with famotidine (80 mg/day) for 17 months, but a long-term (25 months) clinical remission was subsequently achieved with omeprazole (20 mg/day). We suggest that excellent clinical remission of Ménétrier's disease and the associated protein-losing gastropathy may be obtained with long-term omeprazole maintenance treatment, possibly due to Helicobacter pylori suppression.

Ménétrier's disease is a rare cause of hypertrophic gastropathy, usually confined to gastric body and fundus, which is characterized by giant rugae, hypoalbuminemia, and foveolar hyperplasia. The etiology of this disease is still unknown. We report a case of a 74-yr-old man who had dyspepsia, hypoalbuminemia, weight loss, and diffuse polypoid, nodular lesions affecting the whole stomach and proximal duodenum on gastroscopy and barium meal study. The histology of gastric and duodenal mucosal lesions fulfilled the diagnosis of Ménétrier's disease, that was not described to involve duodenum in the literature. The disease resolved clinically, endoscopically, and pathologically after therapy with famotidine for 3 months. We speculated that extensive pyloric metaplasia and then foveolar hyperplasia of duodenum in this patient might be a variant of Ménétrier's disease with favorable clinical course.

The case of a patient with Ménétrier's disease in association with inactive ulcerative colitis of 7 years of evolution is presented. Diagnosis was confirmed by exploratory laparotomy and the symptoms of anemia and hypoproteinemia improved following treatment with octreotide. On review of the literature this was found to be the third case of Ménétrier's disease associated with ulcerative colitis described in the world literature. A possible relationship with an increase in alpha TGF is suggested. The diagnostic criteria and the possible etiopathogenic factors of the disease are herein reviewed.

Unlabelled: There is as yet no consensus about the need for treatment of Helicobacter pylori infections, except for H. pylori-associated peptic ulcer. We present a 3-year-old boy with a 3-month history of oedema and hypoproteinaemia associated with hypertrophic gastropathy. Abdominal scintigram using intravenous 99mTc-labelled human serum albumin scintigraphy and direct measurement of protein in gastric juice proved that serum proteins were massively secreted in the stomach. Histological findings of mucosal inflammation were observed and H. pylori was isolated from the gastric mucosa. The protein loss promptly stopped within 2 weeks of the beginning of eradication therapy., Conclusion: Protein-losing hypertrophic gastropathy may be induced by Helicobacter pylori-associated gastritis and should therefore be carefully evaluated by histological and bacteriological examination to provide a basis for eradication of H. pylori.

In an earlier study, we were able to show that giant fold gastritis is probably a special form of Helicobacter pylori-associated gastritis. Proof of this contention, however--namely regression of the giant folds following eradication of the organism--in a large number of patients was not then possible. To rectify this, Helicobacter pylori (HP) eradication treatment with omeprazole and amoxicillin was applied to 47 patients with HP gastritis and giant folds (5 patients with giant folds localized in the anterior or posterior wall, 42 patients with generalised giant folds within the corpus and fundus). The results of treatment were investigated by endoscopy and histology at the earliest 4 weeks after termination of treatment. In 40 of the 47 patients (85.1%), HP eradication treatment was successful. In 7 patients in whom treatment was unsuccessful, follow-up examinations revealed no changes in the endoscopic or histological findings. In 2 out of 3 patients in whom the endoscopic findings were unchanged despite successful HP eradication, biopsy material revealed the cause of the giant folds to be a signet ring cell carcinoma; in the remaining patient the cause of giant fold persistence was unclear. In 36 patients, the endoscopic--findings normalised completely, while in one patient there was obvious regression of the giant folds. We conclude from this study that giant fold gastritis is indeed a special form of HP gastritis, and that eradicating the organism in patients with gastric giant folds may help to distinguish between inflammatory, hyperplastic and tumorous giant folds.

Hypertrophic gastropathy--that is, Ménétrier's disease--was found, in a retrospective analysis, to be associated with Helicobacter pylori in more than 90% of patients. It is proposed that hypertrophic gastropathy represents a special form of H pylori gastritis in these patients. A case is described of a 28 year old woman with Ménétrier's disease associated with proved protein loss from the stomach. Treatment with cimetidine for more than three years had little benefit when colonisation by H pylori was detected. Density of H pylori colonisation and activity of gastritis, which was also present in the first biopsy specimens taken five years ago, were more pronounced in the body than in the antrum, which is in agreement with the characteristics of H pylori gastritis found in other cases with Ménétrier's disease. A 14 day antibacterial treatment course with 750 mg amoxicillin three times a day combined with 40 mg omeprazole three times a day was started in April 1991. This resulted in eradication of H pylori and the return to normal of giant folds and the mucosal histology. Serum protein concentrations returned to normal within six weeks and remained normal at two endoscopies during a two year follow up. This case report suggests that a subgroup of the patients with Ménétrier's disease may be healed by the eradication of H pylori.