Search

Paediatric Menetrier disease (PMD) is a protein-losing gastropathy, presenting with generalized oedema and abdominal symptoms. PMD commonly has an acute course and may be associated with Cytomegalovirus (CMV) infection. The aim of this retrospective study is to assess the epidemiological and clinical data, diagnostic procedures, treatment and outcome of CMV-associated PMD. The medical charts of the patients with PMD and CMV infection diagnosed at our hospital have been reviewed. Then, a systematic literature's review of all the cases of PMD and a selection of those associated with CMV infection have been performed. Three previously healthy boys were admitted for vomiting and oedema. Endoscopy showed hypertrophic gastric folds and CMV infection was diagnosed. Albumin was administered in all cases, with clinical resolution within few weeks. In literature, PMD has been described in 150 children and the association between CMV and PMD was found in 89 cases. Clinical and laboratory data, radiological and histological exams, therapy and outcome were reviewed.Conclusions: Basing on the present experience and on the current knowledge, PMD has a benign course without long-term sequelae. Although PMD is rare in children, we recommend paediatricians to consider CMV-related PMD when facing children with vomiting and diffuse oedema. What is Known: • Paediatricians should consider Menetrier disease (MD) when facing oedematous child complaining of abdominal symptoms with hypoalbuminemia, without proteinuria and liver dysfunction. • Typical ultrasound features (hypertrophic gastric folds) suggest such condition which requires endoscopy and biopsy for definitive diagnosis. What is New: • A familial susceptibility to CMV gastric infection has been recently suggested; thus when suspecting MD, the family history of gastric diseases should be investigated. • Menetrier disease has been found associated with other unusual conditions either benign (such as gastric bezoar) or malign as neoplasms (acute lymphatic leukaemia and adenocarcinoma) even in children.

Background Ménétrier’s disease (MD) is a protein-losing gastropathy characterized by gastric hypertrophy, foveolar hyperplasia and hypoalbuminemia. MD is uncommon in childhood with nonspecific clinical symptoms, and the exact cause of pediatric MD is still unclear. Case presentation Here, we reported a 4 year and 10-month boy presenting with MD from China. The patient was suffered with vomiting, abdominal pain, hypoproteinemia and edema. Laboratory tests showed that the boy was infected with Clostridium difficile (CD). Gastrointestinal endoscopy revealed giant gastric folds, and histological gastric biopsies showed foveolar hyperplasia with glandular atrophy, infiltration of eosinophils in the lamina propria of the patient. Finally, the boy was recovered after supportive therapy with intravenous albumin and CD eradication. Conclusion For the nonspecific clinical symptoms of MD, gastrointestinal endoscopic evaluations with gastric tissue biopsies are required to establish the diagnosis of MD in children with unexplained hypoalbuminemia.

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.Presentamos un caso infrecuente de gastropatía hipertrófica asociada a pérdida de proteínas. Un hombre de 35 años fue hospitalizado por cambios en los hábitos intestinales, dolor abdominal, edema generalizado y anemia sintomática. Los hallazgos de laboratorio pertinentes incluyeron anemia ferropénica (Hb 6.7 g/dl, ferritina 5 ng/ml) e hipoalbuminemia marcada (albúmina 2.5 g/dl). Las muestras de biopsia endoscópica de pliegues gástricos gigantes observados a lo largo de la curvatura mayor gástrica revelaron hiperplasia foveolar y pérdida significativa de células parietales. La ecografía endoscópica mostró engrosamiento parietal gástrico con arquitectura conservada y capas de pared gástrica normales. Se diagnosticó enfermedad de Menetrier y se trató al paciente con cetuximab, un anticuerpo monoclonal que inhibe la unión del ligando del factor de crecimiento transformante alfa (TGFa), evitando la proliferación de células de la mucosa gástrica. Después de doce meses de tratamiento, el paciente refirió mejoría de los síntomas y los niveles de la proteína marcadora de proliferación Ki-67 en biopsia gástrica habían disminuido.

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.

IgG4 related disease is a systemic autoimmune disease, which can affect different organs. The most common digestive manifestation is autoimmune pancreatitis (AIP), followed by involvement of bile ducts and the major papilla. The stomach is only rarely involved. We report a 71 years old diabetic woman consulting for jaundice and weight loss. Abdominal CAT scan, cholangio resonance imaging, endosonography and a serum IgG4 of five times the normal value, lead to the diagnosis of an autoimmune pancreatitis. An upper gastrointestinal endoscopy showed a diffuse thickening of gastric folds. The pathological study confirmed the presence of IgG4 positive plasma cells. The patient was successfully treated with steroids.

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.

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.

Ménétrier’s disease (MD) is a rare gastropathy characterised by giant rugal folds which can present with nausea, vomiting, abdominal pain and protein losing gastropathy. We report a 21-year-old woman with comorbid MD and ulcerative colitis (UC). Management was complicated by limited treatment options for MD, significant symptom burden, worsening nutrition and difficulty determining which disease was the predominant cause of symptoms. Since age 18 the patient experienced recurrent UC flares characterised by diarrhoea, persistent vomiting and corticosteroid dependence. Endoscopic assessment demonstrated concurrent MD and active UC. Octreotide and cetuximab were trialled given persistent hypoalbuminaemia and suspicion for MD associated protein-losing gastropathy. UC management comprised dose-optimised infliximab and methotrexate. Repeat endoscopic assessment demonstrated improvement in UC without corresponding improvement in symptoms or hypoalbuminaemia. Nasojejunal feeding and parenteral nutrition failed to significantly improve nutritional status and accordingly the patient proceeded to radical total gastrectomy. Postoperatively, MD-associated symptoms and hypoalbuminemia resolved completely.

Ménétrier’s disease (MD), which is characterized by hypertrophic gastric folds and foveolar cell hyperplasia, is the most common gastrointestinal (GI) cause of protein-losing enteropathy (PLE). The clinical course of MD in childhood differs from that in adults and has often been reported to be associated with cytomegalovirus (CMV) infection. We present a case of a previously healthy 22-month-old boy presenting with PLE, who was initially suspected to have an eosinophilic GI disorder. However, he was eventually confirmed, by detection of CMV DNA using polymerase chain reaction (PCR) with gastric tissue, to have MD associated with an active CMV infection. We suggest that endoscopic and pathological evaluation is necessary for the differential diagnosis of MD. In addition, CMV DNA detection using PCR analysis of biopsy tissue is recommended to confirm the etiologic agent of MD regardless of the patient’s age or immune status.

A 57-year-old man, on octreotide treatment for metastatic neuroendocrine tumor pancreas, was referred for whole-body Ga-DOTANOC PET/CT scan to evaluate treatment response. PET/CT scan revealed DOTANOC-avid lesion in the head of the pancreas with multiple tracer-avid soft tissue lesions in the liver, bilateral adrenal glands, and periportal lymph nodes. In addition, diffuse intense DOTANOC-avid mural thickening with intraluminal polypoidal mass formation was noted within the stomach causing significant luminal compromise, histopathological examination of which turned out be hypertrophic hypersecretory gastropathy. This case highlights the possibility of overexpression of somatostatin receptors in gastric hypertrophy, which has been little explored in literature.

IgG4 related disease is a systemic autoimmune disease, which can affect different organs. The most common digestive manifestation is autoimmune pancreatitis (AIP), followed by involvement of bile ducts and the major papilla. The stomach is only rarely involved. We report a 71-year-old diabetic woman consulting for jaundice and weight loss. Abdominal CAT scan, cholangio resonance imaging, endosonography and a serum IgG4 of five times the normal value, lead to the diagnosis of an autoimmune pancreatitis. An upper gastrointestinal endoscopy showed a diffuse thickening of gastric folds. The pathological study confirmed the presence of IgG4 positive plasma cells. The patient was successfully treated with steroids.

Background Menetrier's disease (MD) is a rare disease with unknown aetiology, characterized by hypertrophic folds within the fundus and body of the stomach. Aims We investigated mutations of the candidate genes SMAD4, BMPR1A, TGF-α, and PDX1 within a family with MD. Methods A large 4-generation family with MD was identified. This family had 5 cases of MD, 1 case of MD and juvenile polyposis syndrome (JPS) and 3 cases of JPS. Participants provided saliva for DNA extraction and completed a health questionnaire designed to assess conditions that may be found in patients with MD. Following pedigree analysis, we sequenced the coding regions of the SMAD4 and BMPR1A genes and the regulatory regions of the TGF-α and PDX1 genes in affected and non-affected family members. Results No mutations were identified in the sequenced regions of BMPR1A, TGF-α, or PDX1. A dominant 1244_1247delACAG mutation of SMAD4 was identified in each of the subjects with JPS as well as in each of the subjects with MD. Although this mutation segregated with disease, there were also unaffected/undiagnosed carriers. Conclusion The 1244_1247delACAG mutation of SMAD4 is the cause of JPS and the likely cause of MD in a large family initially diagnosed with MD.

Menetrier's disease is a protein-losing gastropathy that is uncommon in childhood. Its symptoms are unspecific, with abdominal pain, vomiting, and edema. Blood tests show hypoproteinemia and hypoalbuminemia, and upper digestive endoscopy reveals giant gastric folds. In children, cytomegalovirus has been identified as a possible cause. Here we describe two sisters presenting with Menetrier's disease, 2 years apart. This diagnosis should be considered in the presence of hypoalbuminemia in children when a nephrotic syndrome is excluded.

Ménétrier's disease is a protein losing gastroenteropathy. Defined as a rare entity with an unknown cause, most of the reported cases have been associated with viral infections. In pediatric patients, it is characterized by an acute onset with a benign and self-limiting course. It is characterized by thickened gastric folds that generally involve the body and the gastric fundus, associated with hypoalbuminemia due to the loss of serum protein through the mucosa. The following are two clinical cases of infant Ménétrier syndrome associated with cytomegalovirus infection.La enfermedad de Ménétrier es una gastroenteropatía perdedora de proteínas. Definida como una entidad rara y de causa desconocida, la mayoría de los casos reportados la han asociado a infecciones virales. En los pacientes pediátricos, presenta un comienzo agudo con un curso benigno y autolimitado. Se caracteriza por tener pliegues gástricos engrosados que, generalmente, involucran el cuerpo y el fundus gástrico, asociados a hipoalbuminemia, debido a la pérdida de proteína sérica a través de la mucosa. A continuación, se exponen dos casos clínicos de síndrome de Ménétrier infantil asociado a infección por citomegalovirus.

Successful pluripotent stem cell differentiation methods have been developed for several endoderm-derived cells, including hepatocytes, β-cells and intestinal cells. However, stomach lineage commitment from pluripotent stem cells has remained a challenge, and only antrum specification has been demonstrated. We established a method for stomach differentiation from embryonic stem cells by inducing mesenchymal Barx1, an essential gene for in vivo stomach specification from gut endoderm. Barx1-inducing culture conditions generated stomach primordium-like spheroids, which differentiated into mature stomach tissue cells in both the corpus and antrum by three-dimensional culture. This embryonic stem cell-derived stomach tissue (e-ST) shared a similar gene expression profile with adult stomach, and secreted pepsinogen as well as gastric acid. Furthermore, TGFA overexpression in e-ST caused hypertrophic mucus and gastric anacidity, which mimicked Ménétrier disease in vitro. Thus, in vitro stomach tissue derived from pluripotent stem cells mimics in vivo development and can be used for stomach disease models.

Menetrier's disease, also known as hypoproteinemic hypertrophic gastropathy, is a rare condition characterized by the presence of gastric hypertrophy with foveolar infiltration that replaces the normal glandular architecture. We present a case of a 65-year-old female patient who had epigastric pain after meals which progressed to oral intolerance and weight loss. Upper endoscopy was performed showing prominent folds in the gastric mucosa and stenosis at the antrum-pylorus. Biopsy was taken and showed foveolar reactive hyperplasia and reactive glandular epithelium changes suggestive of Menetrier's disease. An abdominopelvic CT was performed showing a dilated stomach and gastric wall thickening. The patient was taken into the operation room for a robot-assisted total gastrectomy with esophagus-jejunum anastomosis. The patient's progress was satisfactory and he was discharged on the eighth postoperative day. Robot-assisted laparoscopic gastrectomy is a feasible and safe option that facilitates the performance of complex procedures.

Epidemiological studies have demonstrated a close association between infection with Helicobacter pylori (H.pylori) and the development of gastric carcinoma. Chronic H.pylori infection increases the frequency of mutation in gastric epithelial cells. However, the mechanism by which infection of H.pylori leads to mutation in gastric epithelial cells is unclear. We suspected that components in H.pylori may be related to the mutagenic response associated with DNA alkylation, and could be detected with the Ames test using a more sensitive strain for alkylating agents. Our investigation revealed that an extract of H.pylori was mutagenic in the Ames test with Salmonella typhimurium YG7108, which is deficient in the DNA repair of O(6)-methylguanine. The extract of H.pylori may contain methylating or alkylating agents, which might induce O (6)-alkylguanine in DNA. Mutagenicity of the alkylating agents N-methyl-N-nitrosourea (MNU) and N-methyl-N'-nitro-N-nitrosoguanidine in the Ames test with S.typhimurium TA1535 was enhanced significantly in the presence of the extract of H.pylori. The tested extracts of H.pylori resulted in a significant induction of micronuclei in human-derived lymphoblastoid cells. Heat instability and dialysis resistance of the extracts of H.pylori suggest that the mutagenic component in the extracts of H.pylori is a heat-unstable large molecule or a heat-labile small molecule strongly attached or adsorbed to a large molecule. Proteins in the extracts of H.pylori were subsequently fractionated using ammonium sulphate precipitation. However, all fractions expressed enhancing effects toward MNU mutagenicity. These results suggest the mutagenic component is a small molecule that is absorbed into proteins in the extract of H.pylori, which resist dialysis. Continuous and chronic exposure of gastric epithelial cells to the alkylative mutagenic component from H.pylori chronically infected in the stomach might be a causal factor in the gastric carcinogenesis associated with H.pylori.

Ménétrier disease is a rare condition of an unknown origin, with a wide spectrum of clinical signs and symptoms at presentation. Diagnosis is made through the combination of clinical, analytical, endoscopic and histological data. Surgery is the classical treatment. However, new medical approaches have emerged.

A 5-year-old boy presented with nausea, vomiting, and intermittent abdominal pain. Images showed giant cerebriform enlargement of rugal folds in the fundus and the body, which were suggestive of Menetrier’s disease.

Chronic lymphoplasmacytic gastritis in two red-capped mangabeys (Cercocebus torquatus) at a zoological facility progressed to severe hypertrophic gastropathy similar to Ménétrier's disease that affects humans. Clinical signs included emesis, diarrhea, hunched posture consistent with abdominal pain, anemia, and hypoproteinemia. Large gastric masses were present and in one case created a gastric outflow obstruction. Both cases were positive for simian immunodeficiency virus and Helicobacter spp. were variably isolated, although the association with the hypertrophic gastropathy is unclear. Medical treatment had varying success and included sucralfate, H2 receptor antagonists, proton pump inhibitors, diet manipulations, and antibiotic therapies targeting Helicobacter spp. Surgical resection of a large portion of the stomach resulted in some palliative improvement in one case. Overall, this disease presented many challenges regarding identification, confirmation of diagnosis, and clinical management. Both aggressive medical and surgical treatments were unrewarding for long-term management of hypertrophic gastropathy in this pair of red-capped mangabeys and resulted in a poor prognosis in these cases.

MeNeTRIER＇S disease （MD） is a rare diseasecharacterized by hypertrophy of gastricfolds, and nausea, emesis, abdominal painand peripheral oedema are the mainmanifestations. Hypochlorhydria and hypoalbuminemiaare also common.1 MD is always misdiagnosed due to itsrarity. Especially, the symptoms caused by hypoalbuminemia,for example, pleural effusions or ascites,make the correct diagnosis more difficult.

Menetrier disease is a rare disease characterised by hyperplasia of the gastric epithelium and large gastric folds. We present a case of a 58-year-old woman who was referred with iron deficiency anaemia, with a family history of a sibling who had undergone gastrectomy for presumed gastric malignancy. Endoscopy showed prominent gastric mucosal folds and biopsies showed hyperplastic gastric mucosa, with prominent foveolar hyperplasia suggestive of Menetrier disease. Further information about her brother’s diagnosis was sought, and it was found that his pathology after gastrectomy showed diffuse glandular hyperplasia also in keeping with Menetrier disease. Adult familial Menetrier disease has so far been a rarity in the literature—review elicits five previous cases of this presentation in siblings.

Introduction: Ménétrier disease (MD) is rare that is involved in both the small bowel and entire colon. The main symptoms and the important clinical findings: We describe a case of a 76-year-old male patient whose clinical presentations include intermittent diarrhea, epigastric pain, nausea, vomiting, asitia, and weight loss. An endoscopy was performed showing a large number of irregular forms and different sizes of polypoid lesions in the gastrointestinal tract, which is rare for MD. The main diagnoses, therapeutics interventions, and outcomes: Herein, this case was diagnosed as MD, mainly dependent on endoscopic evaluation, typical clinical symptoms, and histopathological examination of biopsy. As this patient was also infected with Helicobacter pylori, the eradication of H pylori was administered. Meanwhile, a high-protein diet was enjoined, the aforementioned patient's symptoms were alleviated evidently after 1 month. Conclusion: Although the etiology of MD remained undetermined, we showed that eradication of H pylori in this case might contribute to the disease remission. This study enlarged the present understanding of MD.

A seven-year-old West Highland white terrier was presented for chronic vomiting associated with mild regenerative anaemia and hypoalbuminaemia. Further examination showed a giant polypoid cerebriform mass located in the lesser curvature of the stomach. Partial gastrectomy was performed and histology was consistent with hypertrophic gastritis with typical features of Ménétrier's disease. Five years after surgery, the dog was re-examined for recurrence of vomiting episodes. Endoscopy showed ulceration of the lesser curvature of the stomach and histological analysis revealed a poorly differentiated superficial gastric carcinoma surrounded by hypertrophic gastritis. To the authors' knowledge, this is the second time that coexistence of these two types of lesions is reported, suggesting that recurrence of gastritis could be the starting point of the tumoural process.

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. Clinical Pharmacology & Therapeutics (2012); 92 3, 306–320. doi:10.1038/clpt.2012.77

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.

Ménétrier's disease is a rare hyperproliferative protein-losing gastropathy of the gastric foveolar epithelium. Most common symptoms include epigastric pain with fullness and vomiting, and generalized peripheral edema with hypoalbuminemia. Radiologically, the wall of the gastric body and fundus is diffusely thickened, often with antral sparing. Giant rugal edematous folds are seen on gastroscopy, and histology of biopsy material shows diffuse foveolar hyperplasia with cystic dilatation of the glandular portion of the gastric mucosa in the absence of significant inflammatory infiltrate. The recent discovery of transforming growth factor α overexpression opens the way of epidermal growth factor receptor blockade with cetuximab as first-line treatment modality in severe cases of Ménétrier's disease.

This study reports a case of Ménétrier's disease (MD) in an adult who presented with epigastric pain and peripheric edema. We focused in particular on the imaging and diagnostic aspects of the presenting case as well as clinical, histologic, and therapeutic aspects. Computed tomography (CT) enteroclysis is a new imaging technique which combines enteroclysis and spiral multislice CT. To the best of our knowledge this is the first report on a MD in an adult patient diagnosed by CT Enteroclysis.

Summary Hypertrophic gastritis is described in 21 dogs, eleven times mainly in the corpus mucosa, ten times mainly in the antral mucosa. Except for a group of five Drentse Patrijs dogs, no breed predisposition was found. The age varied from 1/2 to 11 years and the mean age of dogs with hypertrophic gastritis of the corpus (HGC) was lower than that of dogs with hypertrophic gastritis of the antrum (HGA). Twelve dogs were females, nine were males. From six dogs gastric biopsies were examined: in eight dogs partial gastric resection was done. Autopsy was carried out on 12 dogs after euthanasia and on two dogs which died spontaneously. Five types of mucosal change were found, featuring the amount of glandular hyperplasia, formation of folds caused by septal extension of the submucosa, amount and localization of cellular infiltration, partial glandular atrophy, fibrosis, cyst formation and pseudopyloric metaplasia, and/or foveolar hyperplasia. Dogs with HGC showed predominantly a glandular hyperplasia, dogs with HGA especially a foveolar hyperplasia. The findings are compared with the corresponding findings in man and some pathogenetic aspects are discussed. Zusammenfassung Hypertrophische Gastritis bei 21 Hunden Bei 21 Hunden wurde eine hypertrophische Gastritis festgestellt, die 11mal hauptsachlich die Schleimhaut des Corpus und 10mal die Schleimhaut der Pars pylorica (Antrum) betraf. Mit Ausnahme einer Gruppe von 5 Drentse Patrijs Hunden bestand keine Rassendisposition. Das Alter der Tiere variierte zwischen 1/2 und 11 Jahren. Das mittlere Alter der Hunde mit einer hypertrophischen Gastritis des Corpus (HGC) lag niedriger als dasjenige der Tiere mit einer hypertrophischen Gastritis des Antrums (HGA). 12 Hunde waren weiblich, 9 mannlich. Von 6 Hunden konnten Magenbiopsieproben untersucht werden und bei 8 Hunden wurde eine partielle Magenresektion durchgefuhrt. Sektionen wurden bei 12 Tieren nach Euthanasie sowie bei 2 spontan gestorbenen Hunden durchgefuhrt. Es liesen sich 5 verschiedene Arten von Schleimhautveranderungen feststellen, wobei folgende Kriterien berucksichtigt wurden: Ausmas der glandularen Hyperplasie, Bildung von Falten durch septenformige Wucherungen der Submukosa, Ausmas und Lokalisation der zellularen Infiltrationen, partielle Drusenatrophie, Fibrosierung, Zystenbildung und pseudopylorische Metaplasien und/oder foveolare Hyperplasie. Hunde mit HGC zeigten hauptsachlich eine glandulare, Hunde mit HGA besonders eine foveolare Hyperplasie. Die Befunde werden mit analogen Beobachtungen beim Menschen verglichen und bezuglich pathogenetischer Aspekte diskutiert. Resume Gastrite hypertrophiante chez 21 chiens Une gastrite hypertrophiante a ete constatee chez 21 chiens qui a concerne 11 fois principalement la muqueuse du Corpus et 10 fois la muqueuse de Pars pylorica (Antrum). On n'a pas constate de disposition de race a l'exception de 5 chiens Drentse Patrijs. L'âge des animaux a varie entre 1/2 a 11 ans. L'âge moyen des chiens avec une gastrite hypertrophiante du corpus (HGC) fut plus bas que celui des animaux avec une gastrite hypertrophiante de l'antrum (HGA). Il y avait 12 chiennes et 9 chiens. Des biopsies stomacales ont ete examinees chez 6 chiens et une ressection partielle de l'estomac a ete faite chez 8 chiens. 12 animaux ont ete autopsies apres euthanasie et 2 chiens apres une mort spontanee. On a pu etablir 5 sortes differentes de lesions de la muqueuse en retenant les criteres suivants: mesure de l'hyperplasie glandulaire, formation de plis par des croissances en forme de separations de la submucuosa, mesure et localisation des infiltrations cellulaires, atrophie partielle des glandes, fibrose, formation de kystes, metaplasie pseudopylorique et/ou hyperplasie en fossettes. Les chiens avec HGC ont presente principalement une hyperplasie glandulaire et ceux avec HGA une hyperplasie en fossettes. Les resultats sont compares avec des observations analogues chez l'etre humain et discutes en fonction des aspects pathogenetiques. Resumen La gastritis hipertrofica en perros En 21 perros se diagnostico una gastritis hipertrofica, la cual afecto 11 veces, sobre todo, a la mucosa del cuerpo y 10 veces a la mucosa de la parte pilorica (antro). Con la excepcion de un grupo de 5 perros Drentse Patrijs (patricios de Drente), no existia predisposicion racial. La edad de los animales variaba entre 1/2 y 11 anos. La edad media de los perros con una gastritis hipertrofica del cuerpo (HGC) era menos que la de los animales con una gastritis hipertrofica del antro (HGA). 12 eran hembras, 9 machos. En 6 perros se pudieron examinar muestras de biopsias gastricas y en 8 perros se llevo a cabo una reseccion parcial del estomago. En 12 animales se efectuaron necropsias tras eutanasia, y tambien en otros 2 que habian muerto de forma espontanea. Se pudieron establecer 5 variedades diferentes de modificaciones en la mucosa, considerandose los criterios siguientes: magnitud de la hiperplasia glandular, formacion de pliegues por proliferaciones septales de la submucosa, grado y localizacion de las infiltraciones celulares, atrofia glandular parcial, fibrosis, formacion de quistes y metaplasias pseudopiloricas y/o hiperplasia foveolar o de la fosita. Los perros con HGC solian mostrar una hiperplasia glandular, mientras que los perros con HGA una hiperplasia foveolar. Los hallazgos obtenidos se comparan con observaciones analogas hechas en el hombre, discutiendose con respecto a los aspectos de su patogenia.

A 75-year-old man presented with steadily increasing upper abdominal pain, worse after meals, over 6 weeks. He also described anorexia, early satiety, intermittent postprandial nausea and bilious vomiting, as well as bilateral ankle edema and an unintentional 10-lb weight loss, despite daily use of lansoprazole and furosemide. He described no heartburn, dysphagia, melena, hematemesis, diarrhea, fevers, night sweats, or other cardiopulmonary or urinary symptoms. His past medical history was notable for mild gastroesophageal reflux, hypertension, depression, and benign prostatic hyperplasia. Current medications included lansoprazole, valsartan, furosemide, and escitalopram. He had a negative family history and did not smoke or drink alcohol. Physical examination was normal except for 2? bilateral pitting edema to the knees. Laboratory studies were notable mainly for an albumin level of 1.5 g/dl. His white blood cell count was 10,800/ mm (54% neutrophils, 22% lymphocytes, 22% eosinophils), hematocrit 42%, and platelets 338,000/mm. Other liver function tests and serum chemistries were normal except for calcium of 6.9 mg/dl. Urinalysis was normal. Chest X-ray was normal, as was his electrocardiogram. IgA and IgG for Helicobacter pylori were positive. Abdominal computed tomography (CT) after intravenous and oral contrast showed significant thickening of the proximal gastric body and fundus with associated engorgement of the perigastric vessels and no mass (Fig. 1). The distal stomach wall was normal. Endoscopy revealed markedly thickened gastric folds with nodularity, erythema, and exudate involving the proximal stomach (Fig. 2a, b), but sparing the antrum and pylorus. The stomach was poorly distensible, and a small hiatal hernia was seen. Multiple superficial cold forceps biopsies revealed no evidence for active H. pylori infection and failed to show eosinophilia, viral inclusions, epithelial malignancy, or lymphoma. Interestingly, there were elongated gastric foveolae, many of which exhibited a corkscrew-like appearance. These hyperplastic foveolae were lined by gastric epithelium without regenerative features or mucin depletion. Atrophy of the parietal cell layer and mild lamina propria chronic inflammation were also noted. The patient was treated empirically for H. pylori with a 14day course of amoxicillin, clarithromycin, and lansoprazole based on the positive H. pylori serologies. After treatment, he continued taking a proton pump inhibitor twice daily but his symptoms did not change. He was also prescribed a brief course of prednisone that improved his peripheral eosinophilia; however, his symptoms continued to worsen. Full-thickness gastric biopsies, obtained using a jumbo forceps during a repeat endoscopy, showed foveolar hyperplasia with tortuous, corkscrew shapes and dilated mucin-filled gastric pits, atrophy of the parietal cell layer, and mild chronic inflammation of the lamina propria (Fig. 3). Some foveolar cells exhibited mucin depletion. There were no H. pylori organisms or cytomegalovirus M. Rothenberg (&) Division of Gastroenterology and Hepatology, Stanford University Medical Center, 300 Pasteur Drive, MC: 5187, Stanford, CA 94305-5187, USA e-mail: rothenbergmike@gmail.com

Ménétrier's Disease is a giant fold gastropathy whose precise etiology has remained enigmatic. However, mucosal changes characteristic of Ménétrier's Disease have been linked to diverse pathologies, both infectious and malignant. Here, we describe a novel association: Ménétrier's mucosa developing on top of underlying Kaposi's Sarcoma. Two male patients, ages 24 and 31, with HIV/AIDS underwent gastric biopsies that demonstrated Kaposi's Sarcoma. When the former patient expired, a more complete postmortem histologic examination of his stomach was undertaken. For each patient, endoscopic findings at the time of biopsy revealed thickened gastric mucosa overlying the Kaposi's changes. Microscopically, this thickened mucosa comprised hyperplastic foveolar cells that extended to the muscularis mucosa, characteristic of Ménétrier's mucosa. In both cases, special stains confirmed this impression. Dissection of the 24 year-old patient's stomach at autopsy demonstrated that the Ménétrier's mucosa was limited to areas where there was underlying Kaposi's Sarcoma, and that this mucosa was not present when the underlying stroma was normal. Our findings indicate, therefore, an association between Ménétrier's mucosal changes and Kaposi's Sarcoma; such an association has not, to our knowledge, been described previously in the literature.