Laparoscopic management of hypertrophic hypersecretory gastropathy with protein loss: a case report (original) (raw)

A Rare Etiology of Abnormally Large Gastric Folds: Menetrier’s Disease

Case Reports in Gastrointestinal Medicine, 2019

Menetrier’s disease (MD) is described as hypertrophied giant gastric folds causing hypoproteinemia due to protein losing gastropathy and is associated with higher risk of gastric adenocarcinoma. We present a case of a 58-year-old male who presented to our clinic with Melena and endoscopic work up showed enlarged gastric folds and erythematous mucosa in the antrum and three nonbleeding angioectasias in the duodenum. Mucosa biopsies were negative for H. pylori infection. He underwent polypectomy which showed fundic gland polyps. After 1½ years, EGD was repeated for abnormal computerized tomography of abdomen which showed enlarged gastric folds and biopsy revealed gastric fundic mucosa with foveolar hyperplasia, dilated fundic glands, and chronic gastritis. Stomach biopsy results were consistent with MD. Our patient had progressive disease in one and half years. It is important to follow patient with large gastric folds regular as they can develop MD over time which has increased risk ...

An Unusual Presentation of Ménétrier's Disease

Ménétrier's Disease (MD) is a rare acquired hypertrophic gastropathy characterized by giant hypertrophic rugal folds, hypochlorhydria, and hypoproteinemia. The definitive etiology of MD is controversial, although infection with Helicobacter pylori (H. pylori) has been implicated in adults. It presents as a constellation of symptoms including epigastric pain, fatigue, vomiting, weight loss, anorexia, and edema. None of these signs and symptoms is specific for the disease. The gastrointestinal symptoms and the degree of hypoalbuminemia can be profound, the latter resulting from the leakage of protein from the gastric lining. The disease is more common in males. Herein, we report a case of a young woman presenting with the chief complaint of peripheral edema with minimal gastrointestinal symptoms, which was diagnosed as MD on endoscopic evaluation and histopathological examination of gastric biopsy. A high index of suspicion is needed to correctly diagnose this condition for its optimal management.

Menetrier's disease. A diagnostic and therapeutic challenge

Medicina, 2021

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.

Menetrier’s disease: A rare diagnosis established by ultrasonography and computed tomography

International journal of radiology and diagnostic imaging, 2022

Menetrier's disease is a rare condition of the stomach characterized by giant mucosal folds in the gastric fundus and body, diminished acid secretory capacity, and a protein-losing state with hypoalbuminemia. It is also called protein-losing hypertrophic gastropathy. It was first described by the French pathologist Pierre Menetrier in 1888. Menetrier's disease has also a recognized premalignant potential although the precise risk of progression to gastric cancer is not known. Several studies reported regression of disease after treatment with the monoclonal antibody against the EGFR receptor. But the only satisfactory treatment has historically been and remains the surgical intervention with total or partial gastrectomy. A case report of A 10-year male presented to the emergency room with a history of progressively increasing abdominal pain on and off for 1 month with epigastric region fullness, nausea, and vomiting. Generalized edema was noted on examination. An abdominal ultrasound examination was performed, and the patient was found to have diffuse mucosal thickening of the gastric wall with prominent rugal folds and echogenic mucosal lining with generalized subcutaneous edema and mild ascites. The patient underwent surgery and the diagnosis was confirmed by the histopathological report.

Menetrier’s Disease: a Surgical and Pathological Challenge

SAS Journal of Surgery, 2022

Menetrier’s disease (MD) is a rare hypertrophic gastropathy clinically characterized by digestive signs as epigastric pain, nausea, vomiting and diarrhea, with hypoalbuminemia and anemia, endoscopically by giant rugal folds and histologically by tortuous foveolar hyperplasia with dilated glands and hypertrophic muscularis mucosae. The current study presents a case of MD in 44 year-old-man admitted to the hospital of Hassan II in Fez, Morocco with epigastralgia, vomiting and weight loss. Physical examination fond a pale face and anemia in laboratory studies. A total gastrectomy was performed given the resistance to treatment and the persistence of symptoms, as well as the suspect endoscopic aspect. Macroscopic examination showed hypertrophic and polyploid gastric mucosa resembles cerebral convolutions. Histological examination showed a foveolar hyperplasia, tortuosity and dilatation of the glands. Hypertrophic muscularis mucosae with smooth muscle bundles extending into the lamina pr...

Gastric carcinoids in patients with hypergastrinemia

Journal of the American College of Surgeons, 2004

BACKGROUND: Hypergastrinemia in patients with pernicious anemia is a major regulator contributing to enterochromaffin-cell hyperplasia and, ultimately, to gastric carcinoids. STUDY DESIGN: Between 1990 and 2003, we studied 8 women and 10 men with pernicious anemia and gastric carcinoids; their mean age was 50 years. Serum gastrin levels ranged from 740 to 4,000 pg/mL (mean 1,000 pg/mL). Six patients underwent antrectomy, four total gastrectomy, and eight endoscopic resection or biopsy. During the same period, 22 patients with Zollinger-Ellison tumors and hypergastrinemia (20 men and 2 women, mean age 49 years) had no gastric carcinoids, but 1 of 7 patients with Zollinger-Ellison and multiple endocrine neoplasia (MEN1) tumors had hypergastrinemia and gastric carcinoids. RESULTS: Mean followup for pernicious anemia patients was 6 years after antrectomy and 1 to 10 years after endoscopic resection or biopsy. Tumor regression was observed in one patient after antrectomy and one patient after biopsy. There were no deaths in this group in spite of lymph node metastasis in two patients. The patient with Zollinger-Ellison and MEN1 syndrome has been followed 3 years after diagnosis and 2 years after total gastrectomy. CONCLUSIONS: Gastric carcinoids are indolent tumors occurring with increasing frequency in patients with pernicious anemia. Antrectomy or biopsy and observation are preferred methods of treatment. Total gastrectomy is reserved for patients with extensive tumor involvement of the gastric wall or for emergency bleeding.