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We present a case report describing the diagnosis and management of a patient who presents with a rare diagnosis of Menetrier’s disease. This condition poses a diagnostic challenge to clinicians due to its nonspecific clinical presentation and is oftentimes misdiagnosed for more common gastric disorders. Menetrier’s disease is characterized by gastric mucosal hypertrophy and subsequent protein loss, resulting in gastric symptoms and widespread edema. While the etiology remains unclear, notable associations have been observed with Helicobacter pylori infection and overexpression of transforming growth factor alpha. The management often involves supportive measures with medical and surgical interventions for refractory cases and when necessary. This report includes a comprehensive review of the literature on the clinical presentation, diagnostic approach, and management of this rare disease. By documenting such cases in the medical literature, we aim to enhance the clinician’s ability to recognize and manage this disorder, thereby preventing the development of more severe manifestations such as diabetes mellitus. Menetrier’s disease is a rare disorder that should be suspected in patients with upper gastrointestinal complaints and hypertrophied gastric mucosa. With a rather broad differential diagnosis consisting of Zollinger-Ellison syndrome, hypertrophic lymphocytic gastritis, hypertrophic hypersecretory gastropathy, gastric adenocarcinoma, gastric polyps, infections such as histoplasmosis and tuberculosis, autoimmune-like inflammatory conditions such as sarcoidosis, and more commonly, gastrointestinal disease, it is often overlooked in the diagnostic workup. Therefore, it is crucial for clinicians to conduct a thorough evaluation and maintain a high clinical suspicion when there is concurrent H.pylori infection and/or imaging findings suggestive of hypertrophied gastric mucosa to avoid missing this disease.

We present a case report describing the diagnosis and management of a patient who presents with a rare diagnosis of Menetrier’s disease. This condition poses a diagnostic challenge to clinicians due to its nonspecific clinical presentation and is oftentimes misdiagnosed for more common gastric disorders. Menetrier’s disease is characterized by gastric mucosal hypertrophy and subsequent protein loss, resulting in gastric symptoms and widespread edema. While the etiology remains unclear, notable associations have been observed with Helicobacter pylori infection and overexpression of transforming growth factor alpha. The management often involves supportive measures with medical and surgical interventions for refractory cases and when necessary. This report includes a comprehensive review of the literature on the clinical presentation, diagnostic approach, and management of this rare disease. By documenting such cases in the medical literature, we aim to enhance the clinician’s ability to recognize and manage this disorder, thereby preventing the development of more severe manifestations such as diabetes mellitus. Menetrier’s disease is a rare disorder that should be suspected in patients with upper gastrointestinal complaints and hypertrophied gastric mucosa. With a rather broad differential diagnosis consisting of Zollinger-Ellison syndrome, hypertrophic lymphocytic gastritis, hypertrophic hypersecretory gastropathy, gastric adenocarcinoma, gastric polyps, infections such as histoplasmosis and tuberculosis, autoimmune-like inflammatory conditions such as sarcoidosis, and more commonly, gastrointestinal disease, it is often overlooked in the diagnostic workup. Therefore, it is crucial for clinicians to conduct a thorough evaluation and maintain a high clinical suspicion when there is concurrent H.pylori infection and/or imaging findings suggestive of hypertrophied gastric mucosa to avoid missing this disease. [ABSTRACT FROM AUTHOR]

Menetrier's Disease is a rare and mysterious stomach disorder characterised by giant gastric folds, excessive mucus production, and protein loss. This comprehensive research article examines Menetrier's Disease, focusing on its clinical features, diagnosis, and available treatment options. The article aims to provide a complete understanding of Menetrier's Disease, fill the knowledge gap, and encourage improved clinical management. Description of the State of Knowledge Menetrier's Disease is a rare condition, and its cause is still unknown, though it may be linked to previous viral and bacterial infections and increased expression of transforming growth factor-alpha (TGF-a). Diagnosis can be established by endoscopic examination and histological analysis of material from a full-thickness mucosal biopsy. Treatment options are limited and concentrated on symptom relief, while the outcome of the therapy may vary. Summary Menetrier's Disease presents significant difficulties in both diagnosis and treatment. This review outlines the clinical features, classification, diagnostic approaches, available treatment options, and prognosis for healthcare professionals and researchers seeking to understand this disease better. Better understanding of Menetrier's Disease is crucial to improve patient care and explore new, potential therapeutic avenues. [ABSTRACT FROM AUTHOR]

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Introduction Menetrier's Disease is a rare and mysterious stomach disorder characterised by giant gastric folds, excessive mucus production, and protein loss. This comprehensive research article examines Menetrier's Disease, focusing on its clinical features, diagnosis, and available treatment options. The article aims to provide a complete understanding of Menetrier's Disease, fill the knowledge gap, and encourage improved clinical management. Description of the State of Knowledge Menetrier's Disease is a rare condition, and its cause is still unknown, though it may be linked to previous viral and bacterial infections and increased expression of transforming growth factor-alpha (TGF-α). Diagnosis can be established by endoscopic examination and histological analysis of material from a full-thickness mucosal biopsy. Treatment options are limited and concentrated on symptom relief, while the outcome of the therapy may vary. Summary Menetrier's Disease presents significant difficulties in both diagnosis and treatment. This review outlines the clinical features, classification, diagnostic approaches, available treatment options, and prognosis for healthcare professionals and researchers seeking to understand this disease better. Better understanding of Menetrier's Disease is crucial to improve patient care and explore new, potential therapeutic avenues.

The generalized edematous syndrome or anasarca is present secondary to an imbalance in the body's water, electrolyte and osmolar homeostasis. In adults, the state of anasarca is more frequent secondary to heart failure; in pediatrics, generalized edema is associated with more frequency due to low protein intake, low protein synthesis or due to protein loss of gastrointestinal or renal origin. The decrease in plasma oncotic pressure generates generalized fluid leakage into interstitial compartments and produces edema. There are multiple pathologies and mechanisms for the production of generalized edema; knowledge of the pathophysiology of its development allows a clinical, laboratory and office analysis that guides the diagnosis. Cytomegalovirus infection is a rare cause of generalized edema; recognizing this entity and reaching an appropriate differential diagnosis is the objective of this review. [ABSTRACT FROM AUTHOR]

To advance the diagnostic accuracy of juvenile polyposis syndrome, an important yet often difficult diagnosis, we describe in detail a new and medically significant presentation. This hereditary and high-risk GI cancer syndrome is often associated with hereditary hemorrhagic telangiectasia, as in this 47-year-old female patient with a SMAD4 germline pathogenic mutation. Total gastrectomy revealed giant gastric folds with inflamed foveolar hyperplasia consuming most of the gastric cardia and body but sparing the antrum. Together, this gross and histologic pathology mimics Ménétrier’s disease, an exceedingly rare and acquired protein-losing hypertrophic gastropathy. Classical gastric juvenile polyposis almost always and principally involves the antrum with multiple distinctive inflammatory polyps rather than the newly illustrated giant gastric folds of this case. No reports of giant gastric folds in juvenile polyposis have appeared in the literature. The distinction between juvenile polyposis and Ménétrier’s disease is essential due to their disparate clinical outcomes and management. The differential considerations for giant gastric folds and inflamed gastric foveolar hyperplasia are fully reviewed. On the basis of this report, the differential for giant gastric folds must now expand to include juvenile polyposis syndrome. Genetic testing for pathogenic germline mutations of the 2 known causative genes of this syndrome, namely SMAD4 and BMPR1A, are readily available and should become part of the evaluation of giant gastric folds, particularly in view of the neoplastic and hereditary aspects of juvenile polyposis syndrome.

Menetrier's Disease is a hypertrophied gastropathy rarely encountered in pediatric population presenting with protein loss. It has acute and self-limiting disease course in children. In our patient the disease had long duration of progression lasting over 3 years. Eight year old boy had presented with failure to thrive and hypoproteinemia. Endoscopically he found to have thickened gastric folds from which biopsy was taken. Histopathological examination showed typical microscopic features of Menetrier's disease with squamous metaplasia. The squamous metaplasia seen associated with Menetrier's disease has not been noticed before in a child. Clinical suspicion along with endoscopic biopsy and histopathological study is essential in diagnosis.

Abstract 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.

Abstract 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.

Menetrier's Disease is a hypertrophied gastropathy rarely encountered in pediatric population presenting with protein loss. It has acute and self-limiting disease course in children. In our patient the disease had long duration of progression lasting over 3 years. Eight year old boy had presented with failure to thrive and hypoproteinemia. Endoscopically he found to have thickened gastric folds from which biopsy was taken. Histopathological examination showed typical microscopic features of Menetrier's disease with squamous metaplasia. The squamous metaplasia seen associated with Menetrier's disease has not been noticed before in a child. Clinical suspicion along with endoscopic biopsy and histopathological study is essential in diagnosis. [ABSTRACT FROM AUTHOR]

To advance the diagnostic accuracy of juvenile polyposis syndrome, an important yet often difficult diagnosis, we describe in detail a new and medically significant presentation. This hereditary and high-risk GI cancer syndrome is often associated with hereditary hemorrhagic telangiectasia, as in this 47-year-old female patient with a SMAD4 germline pathogenic mutation. Total gastrectomy revealed giant gastric folds with inflamed foveolar hyperplasia consuming most of the gastric cardia and body but sparing the antrum. Together, this gross and histologic pathology mimics Ménétrier's disease, an exceedingly rare and acquired protein-losing hypertrophic gastropathy. Classical gastric juvenile polyposis almost always and principally involves the antrum with multiple distinctive inflammatory polyps rather than the newly illustrated giant gastric folds of this case. No reports of giant gastric folds in juvenile polyposis have appeared in the literature. The distinction between juvenile polyposis and Ménétrier's disease is essential due to their disparate clinical outcomes and management. The differential considerations for giant gastric folds and inflamed gastric foveolar hyperplasia are fully reviewed. On the basis of this report, the differential for giant gastric folds must now expand to include juvenile polyposis syndrome. Genetic testing for pathogenic germline mutations of the 2 known causative genes of this syndrome, namely SMAD4 and BMPR1A, are readily available and should become part of the evaluation of giant gastric folds, particularly in view of the neoplastic and hereditary aspects of juvenile polyposis syndrome. [ABSTRACT FROM AUTHOR]

Copyright of Medicina (Buenos Aires) is the property of Medicina (Buenos Aires) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

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. [ABSTRACT FROM AUTHOR]

Introduction: Primary peritonitis (PP) and Ménétrier's Disease (MD) are both rare conditions among pediatric population. Although about 150 MD cases have been described in the scientific literature to date, its onset with a PP is an unusual condition.Case Presentation: We present a case of an 11-year-old boy who was admitted to our unit because of abdominal pain and distension. Complementary tests showed ascites, bilateral pleural effusion, leukocytosis, increased acute phase reactants and hypoproteinemia with hypoalbuminemia. Laparoscopy ruled out appendicitis or visceral perforations and exposed purulent peritoneal fluid, compatible with PP. Biochemical stool analysis showed increased clearance of alpha-1-antitrypsin, which was consistent with a protein-losing enteropathy. Gastroscopy findings were compatible with MD. The clinical course was favorable and he had no recurrence after 12 months of follow-up.Conclusion: PP can be the first clinical manifestation of pediatric MD. Knowledge of MD and its generally benign nature in children is important in order to avoid excessive testing and unnecessary treatment.

Thickened gastric folds (TGF) are not an uncommon finding on radiological imaging or endoscopy. It is an enigmatic condition requiring a systematic approach with correlation between clinical, laboratory, radiological, endoscopic, and histological parameters to reach a final diagnosis. It has a varied number of differential diagnosis and reaching the final diagnosis is often challenging even to an astute clinician. Findings on endoscopy are similar and biopsy results often equivocal. Differentiating between benign and malignant conditions is challenging. Routine pinch biopsy usually does not sample deep enough to get an adequate tissue sample, and other methods of biopsy may be required. Newer modalities, such as endoscopic ultrasound (EUS) and EUS‑guided sampling, are helpful in differentiating benign from malignant causes. At times, exploratory laparotomy and full‑thickness biopsy may be required for final diagnosis. In this review, we discuss the various differentials of TGF, with special emphasis on how to approach a case of TGF.

Résumé: Les gros plis muqueux gastriques peuvent correspondre à des lésions histologiques très variées, allant de maladies inflammatoires banales à des entités rares correspondant réellement à une augmentation du nombre des cellules épithéliales muqueuses, et même à des maladies tumorales malignes. L'augmentation de la visibilité des plis, généralement secondaire à un accroissement de leur taille, peut être due à un épaississement de la muqueuse et/ou de la sous-muqueuse. Les gastropathies hypertrophiques sont définies par une épaisseur de la muqueuse supérieure à 2 mm et une modification du rapport des cryptes et des glandes. La maladie de Ménétrier est très peu fréquente et son diagnostic est souvent évoqué en endoscopie mais très rarement confirmé histologiquement. La lésion histologique la plus importante est une hyperplasie majeure des cryptes gastriques par rapport aux glandes. Classiquement, les lésions atteignent tout le fundus mais respectent l'antre. La lésion la plus significative, l'hyperplasie des cryptes, peut s'observer dans de nombreux autres contextes et il est recommandé, pour établir le diagnostic, de disposer de biopsies de grande taille et profondes, intéressant toute l'épaisseur de la muqueuse et si possible la musculaire muqueuse. Le traitement de la maladie de Ménétrier repose sur l'utilisation des analogues de la somatostatine et, en cas d'échec, le cétuximab. Le traitement chirurgical est un traitement de recours ou en cas de suspicion de cancer gastrique. La gastrite lymphocytaire hypertrophique est une entité de définition microscopique histologique associée le plus fréquemment à l'infection à Helicobacter pylori ou à la maladie cœliaque. Les gastropathies à gros plis hypertrophiques constituent un groupe hétérogène dû à une infiltration du chorion muqueux par des cellules inflammatoires ou tumorales, ou éventuellement par des dépôts extra-cellulaires. Les gros plis peuvent être liés à des polypes hyperplasiques, à la polypose proximale gastrique et à des polyposes hamartomateuses. Large gastric mucosal folds may correspond to very varied histological lesions, ranging from common inflammatory lesions, to rare entities actually corresponding to an increase in the number of mucous epithelial cells, and even to malignant infiltration. The increased visibility of the folds, usually secondary to an increase in their size, may be due to thickening of the mucosa and/or submucosa. Hypertrophic gastropathies are defined by a thickness of the mucosa greater than 2 mm and a change in the ratio of crypts and glands. Ménétrier's disease is very rare and its diagnosis is often evoked by endoscopy, but very rarely confirmed histologically. The most important histological lesion is a major hyperplasia of the gastric crypts compared to the glands. Classically, the lesions affect the entire fundus but respect the antrum. The most significant lesion, foveolar cells hyperplasia, can be observed in many other contexts and it is recommended for the diagnosis to have large and deep biopsies, involving the entire thickness of the mucosa and if possible muscularis mucosae. The treatment of Ménétrier's disease is based on the use of somatostatin analogues and, if this is not successful, cetuximab. Surgical treatment is a of last intention treatment or if gastric cancer is suspected. Hypertrophic lymphocytic gastritis is a microscopically defined entity which is most commonly associated with Helicobacter pylori infection or celiac disease. The gastropathies with large hypertrophic folds constitute a heterogeneous group due to an infiltration of the submucosae by inflammatory or malignant cells, or possibly by extra-cellular material. Large folds may be related to hyperplastic polyps, gastric proximal polyposis, and hamartomatous polyposis. [ABSTRACT FROM AUTHOR]

• The etiology of Menetrier's disease is still unclear and no definite diagnostic criteria exist. • Our patient presented with a lower extremity DVT as initial sign of Menetrier's disease. • Overexpression of transforming growth factor-α (TGF- α) seems to play a significant role in the pathogenesis of the disease and erbitux is one of the main therapeutic options. Menetrier's disease is a rare hyperproliferative protein-losing gastropathy of the gastric foveolar epithelium. It is characterized by giant hypertrophic folds, excess mucus secretion, decreased acid secretion and hypoproteinemia due to selective loss of serum proteins across the gastric mucosa. The discovery of transforming growth factor-α overexpression opened the way of epidermal growth factor receptor blockade with cetuximab as first-line treatment modality for Menetrier's disease. We present the case of a 46-year-old female patient with Menetrier's disease. The diagnosis was based on clinical, endoscopic and histological criteria. Two years before the diagnosis of the disease the patient had an episode of deep vein thrombosis and pulmonary embolism. Real time PCR revealed mutation of the gene responsible for coagulation factor II. The patient received anticoagulation therapy and after a period of 6 months a severe anemia due to a gastrointestinal bleeding was presented. The appropriate investigation revealed the presence of Menetrier's disease. The patient was referred to the surgical clinic with persistence of symptoms such as excessive weight loss, anemia and weakness, even after multiple medical treatment, including the monoclonal antibody against the EGFR receptor. A total gastrectomy was performed and the postoperative course was uneventful. One year follow up showed remarkable improvement of her health status. A combination of clinical, laboratory, endoscopic and histopathologic findings is necessary for the diagnosis of this rare disease. Gastrectomy is the treatment of choice for those patients with intractable symptoms and signs refractory to medical therapy. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

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.

Ménétrier'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 Ménétrier's disease, 2 years apart. This diagnosis should be considered in the presence of hypoalbuminemia in children when a nephrotic syndrome is excluded. [ABSTRACT FROM AUTHOR]

A rare case of successful surgical treatment of giant MALT-lymphoma with Menetrier’s disease complicated by gastric obstruction has been presented.

Ménétrier’s disease is a rare protein-losing hypertrophic gastropathy. Histologically, it can be mistaken for other disorders showing hypertrophic gastropathy. The pathogenesis of Ménétrier’s disease is not fully understood; however, it appears that the epidermal growth factor receptor (EGFR) ligand, transforming growth factor alpha, contributes to the pathogenesis of this disorder. In this review, we will discuss disease entities that can mimic Ménétrier’s disease and the role of EGFR signaling in Ménétrier’s disease.

Introduction: Menetrier´s disease is rare in pediatrics. With no established etiology has been associated with viral and bacterial infections most of them able to generate an inflammatory process and protein-loosing with clinical abdominal pain, nausea, vomiting and edema, spontaneous resolution after 4-6 weeks without sequelae. The main objective is to describe a menetrier´s disease case in a male child in pediatric. Clinical case: a three years old male child without perinatal history, with clinical profile of five days with vomiting, abundant diarrhea, not dysentery, and fever, in the last two days with bipalpebral edema. After the cropology test the patient presented Giardia lamblia cysts, treated with metronidazole. The child is remitted to Hospital Infantil Napoleón Franco Pareja in Cartagena-Colombia, because of evidence of edema bipalpebral. In the emergency room male child presented good general condition with acute illness, stable vital signs, blood count with mild leukocytosis, blood smear with toxic granulations in neutrophils, partial urine without proteinuria, serum albumin 1.26 g../ dl. normal transaminases, normal serum electrolytes, normal lipid profile, ultrasound with distended bowel moderate, upper endoscopy with hypertrophy folds mucosa and gastric body, hyperemia and friability without erosions. The biopsy showed chronic active gastropathy with marked foveal hyperplasia compatible with Menetrier disease. During his hospitalization was administered albumin 1 g / kg for four days with resolution of edema and serum protein, the patient was discharged with normal albumin and subsequent controls and then he continued asymptomatic with complete resolution of the clinical disease. Conclusion: Menetrier´s disease in children is self-limiting with duration from 4 to 6 weeks; it can present abdominal pain, vomiting, nausea and edema. With the clinical and endoscopic findings of gastric folds hypertrophy can be presumed diagnosis. It is confirmed by histopathological report; the natural course of this disease is benign, with complete resolution of symptoms. Rev.cienc.biomed. 2015; 6(2):354-359 KEYWORDS Menetrier’s disease; Hypoalbuminemia; Edema; Cytomegalovirus.

This review article aims to provide a comprehensive overview of recent epidemiology, pathogenesis, risk factors, and premalignant conditions of gastric cancer. Worldwide, gastric cancer is one of the most common and most fatal cancers. The incidence and mortality remain high in regions such as East Asia and Eastern Europe. Although there is a lower incidence in the United States, it remains a deadly disease. Age, gender, and race are non-modifiable demographic risk factors for developing gastric cancer. There have been several dietary and lifestyle risk factors such as salt preserved foods, N-nitroso compounds containing foods, tobacco smoke, alcohol use, and obesity that have been shown to contribute to the development of gastric cancer. Infections have additionally been shown to have a clear role in the pathogenesis of gastric cancer as Helicobacter pylori eradication has shown a significant reduction in the incidence of gastric cancer as well as other pathogens such as Epstein-Barr virus. There are certain premalignant lesions that increase the risk of developing gastric cancer. These include atrophic gastritis, and intestinal metaplasia amongst others., Competing Interests: Conflicts of interest: The authors declared no potential conflicts of interest with respect to the research, authorship, and publication of this article., (© 2023 Greater Baltimore Medical Center.)

Thickened gastric folds (TGF) are not an uncommon finding on radiological imaging or endoscopy. It is an enigmatic condition requiring a systematic approach with correlation between clinical, laboratory, radiological, endoscopic, and histological parameters to reach a final diagnosis. It has a varied number of differential diagnosis and reaching the final diagnosis is often challenging even to an astute clinician. Findings on endoscopy are similar and biopsy results often equivocal. Differentiating between benign and malignant conditions is challenging. Routine pinch biopsy usually does not sample deep enough to get an adequate tissue sample, and other methods of biopsy may be required. Newer modalities, such as endoscopic ultrasound (EUS) and EUS-guided sampling, are helpful in differentiating benign from malignant causes. At times, exploratory laparotomy and full-thickness biopsy may be required for final diagnosis. In this review, we discuss the various differentials of TGF, with special emphasis on how to approach a case of TGF. [ABSTRACT FROM AUTHOR]

Ménétrier's disease is a rare form of acquired gastropathy characterized by giant rugal folds in the stomach and protein-losing gastropathy. Children with Ménétrier's disease tend to follow a benign self-limited course with symptoms typically completely resolving within 2 to 10 weeks in contrast to the chronic course in adults. A 9-year-old girl presented with a history of gradually worsening abdominal distension, increasing body weight, and abdominal pain for 2 weeks. Physical examination on admission indicated periorbital swelling, pitting edema in both the legs, and abdominal distension with mild diffuse tenderness and shifting dullness. Laboratory tests on admission showed hypoalbuminemia, hypoproteinemia, and peripheral eosinophilia. The test result for anticytomegalovirus immunoglobulin M was negative. Increased fecal alpha 1 anti-trypsin excretion was observed. Radiological findings showed massive ascites and pleural effusion in both the lungs. On gastroscopy, large gastric folds, erythema, erosion, and exudation were noted in the body and fundus of the stomach. Microscopic findings showed infiltration of eosinophils and neutrophils in the gastric mucosa. Her symptoms improved with conservative treatment from day 7 of hospitalization and resolved completely.

The article presents a case study of a 26-year-old man with Ménétrier's Disease who is infected with Cytomegalovirus and Helicobacter Pylori bacteria. It mentions that the disease is always misdiagnosed due to its rarity. It informs that the patient was admitted due to complaints of early satiety, mild abdominal distention and peripheral oedema. It states that mild epigastric tenderness without rebound or abdominal rigidity was noted in an examination along with bilateral lower limb oedema.

Ménétrier's disease (MD) is a rare disease characterized by markedly hypertrophied gastric mucosal folds typically associated with hypoalbuminemia and anemia. However, the natural history of MD in adults remains unclear and is rarely reported in the literature. The current study presents a case of MD with a 9-year follow-up. A 56-year-old man was diagnosed with MD in 2005. The patient was followed up and underwent surveillance endoscopy once or twice each year. In the present case, the anemia and hypoproteinemia were eliminated following red blood cell transfusion and intravenous iron therapies. The symptoms were relieved after 4 years. Treatment with octreotide had little effect on the gastric mucosa, while antimicrobial combination therapy provided no benefit in the present H. pylori-negative case of MD. In addition, despite abnormalities of the gastric mucosa in the patient persisting after 9 years of follow-up with no evidence of malignancy, malignant transformation in MD should not be overlooked, and regular monitoring of the gastric mucosa via endoscopy is necessary. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]