This is a 55-year-old male patient with a history of chronic inmateur smoking and who underwent surgery at age 40.
Two months before consultation, she presented with diffuse abdominal pain associated with vomiting predominantly evening, postprandial mediate and low weight of 15 kg in this period.
Upper gastrointestinal endoscopy showed diffuse prominent gastric folds, sessile soleous lesions with central ulceration of red background and duodenal ulcer lesions, with positive urease test.
Biopsies reported as chronic nonspecific gastritis and duodenitis were performed.
The laboratory study showed: GOT 50 IU/L, GPT 56 IU/L, GGT 85 IU/L, FA 81 IU/L, hematocrit 55%, prothrombin time 100%, albumin 229 gDH 1.2 g.
Abdominal ultrasound showed hepatic steatosis.
Eradication treatment for Helicobacter pylori was indicated for 14 days, persistence of vomiting, intolerance to oral feeding, so it was decided to hospitalize for nutritional management and performing gastric macrobiopsies.
Upon admission to the Gastroenterology Department of our hospital, a patient with stable hemodynamic instability, mesomorph, without edema, or authenticity stood out.
There were no signs of absence of skin, mucous membranes or phantoms.
Laboratory tests confirmed total proteins 3.5 g/dL, albumin 1.9 g/dL, negative proteinuria and complete blood count without alterations.
Building and subsequent laboratory tests
Abdominal-pelvis computed axial tomography (CAT) showed prominent gastric folds, CT enteroclysis reported absence of radiological lesions in the small intestine.
Upper digestive endoscopy showed diffusely thick gastric folds, some erosions, negative urease test.
Biopsies were reported as gastric mucosa with diffuse foveolar hyperplasia associated with glandular dilatations and mucinous cells.
Focal superficial epithelial erosion with accumulation of polymorphonuclear leukocytes, lamina propria with low inflammatory infiltrate predominantly lymphoplasmacytic, with some eosinophils.
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A study was completed with endosonography resulting in gastric thickening secondary to stenosis of the deep mucosa and cystic areas.
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Due to the extension of the lesion, the risk of transformation and the non-availability of cetuximab, surgical treatment was decided.
Evaluation was requested by the nutrition team, observing pre-malignant albumin, vitamin B12 and erythrocyte folate levels within normal ranges.
Vomiting was controlled with gastrectomy waveform, achieving adequate oral intake, supported with parenteral nutrition for 7 days with which increased albumin to 2.3 gr/dl. At 14 days of admission a favorable event was made
Macroscopic analysis of the surgical specimen showed a thickened gastric wall homogeneously, mucosa with diffusely thickened, congestive folds, some with superficial erosion centimeter of duodenal axis 1 cm diameter.
Histology confirmed the findings described in endoscopic biopsies, with diffuse gastric involvement, and in the duodenum in the described area of polypoid lesion focal fundic metaplasia with foveolar cystic hyperplasia and mucinous cystic dilatation glandular cells were observed.
Diffuse gastric Ménétrier's disease with focal duodenal compromise was concluded.
