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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.

The authors describe a 31 years old male, admitted for hematemesis, epigastric pain and lower limb edema. Laboratorial data showed haemoglobin 18.4g/dl, total proteins 2.8g/dl, albumin 1.6g/dl and hipogammaglobulinaemia. 24h urinary proteins were normal. HIV and CMV serology were negative. Upper GI endoscopy revealed markedly enlarged gastric folds covered by abundant exudative fluid. Endoscopic ultrasound showed ascites, pleural effusion and gastric wall thickening with mucosa expansion and intact submucosa. In gastric biopsies foveolar hyperplastic and regenerative mucosa were observed being suggestive of Ménétrier´s disease. Helicobacter pylori was not detected. Albumin replacement and diuretics corrected anasarca and long-acting octreotide was instituted. Nine months later, the patient was asymptomatic, serum proteins were normal (albumin 4.6g/dl and total proteins 6.5g/dl), signs of endoscopic improvement were observed with marked reduction in gastric folds and mucosal inflammation and no ultrastructural changes were detected in gastric specimens sent for electron microscopy. Ménétrier´s Disease (MD) is a rare form of hypertrophic gastropathy characterized by massive enlargement of gastric folds causing marked protein exudation. The increase in tight junction diameter is the most consistent ultraestrutural change. Octreotide is a somatostatin analogue that acts by modulating TGFαEGFR pathway, which has been associated with the pathogenic mechanisms. As well as other cases reported in literature, this case report highlights the potential of long-acting octreotide for MD treatment avoiding more expensive therapies like cetuximab and gastrectomy., (© Acta Gastro-Enterologica Belgica.)

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.)