Ménétrier-like disease in a Pointer with concurrent granulomatous gastritis, helicobacteriosis and leishmaniosis: a case report.

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-like hypertrophic gastritis in two red-capped mangabeys (Cercocebus torquatus).

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.

Canine giant hypertrophic gastritis treated successfully with partial gastrectomy.

A 4 yr old castrated male Jack Russell terrier was presented with a 2 mo history of vomiting, anorexia, and weight loss. Abdominal radiographs and ultrasound supported the diagnosis of gastric outflow obstruction. Celiotomy and gastrotomy revealed a large, narrowly based mass originating from the mucosa of the dorsal gastric body, occupying the lumen of the stomach and protruding through the pylorus into the duodenum. A partial gastrectomy was performed to excise the mass along with a 1 cm margin of grossly normal tissue. Giant hypertrophic gastritis was diagnosed via histopathology of the excised tissue. Giant hypertrophic gastritis is a rarely diagnosed disease of canines, characterized by giant gastric folds, hypoalbuminemia, and mucosal hypertrophy. Long-term treatment success has not been previously reported. In the case described herein, surgical excision of the affected gastric tissue provided complete resolution of clinical signs. Twelve mo following surgery, no recurrence of either vomiting or weight loss had been noted and the dog was clinically normal.

Gastric carcinoma associated with Menetrier's-like disease in a West Highland white terrier.

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.

Ménétrier disease and gastric adenocarcinoma in 3 Cairn terrier littermates.

Ménétrier disease is a rare hypertrophic gastropathy that is characterized by hyperplasia of the mucous cells with concurrent loss of chief and parietal cells within the gastric glands. There are few reports of this disease in dogs, and little is known about the clinical presentation and progression of canine Ménétrier disease. Three Cairn terrier littermates developed hypertrophic gastropathy with histological features of Ménétrier disease. One dog remained clinically asymptomatic for 2 years after diagnosis. The development of this disease in 3 siblings suggests a possible inherited predisposition. All 3 dogs also developed gastric neoplasia, which has been reported in human Ménétrier disease but has not been associated previously with hypertrophic gastropathy in domestic species.

Giant hypertrophic gastritis (Menetrier's-like disease) in an Old English sheepdog.

An 11-year-old, male Old English sheepdog was admitted for weight loss and intermittent vomiting of 1 month's duration. A cranioventral abdominal mass, anemia, hypoproteinemia, and hypoalbuminemia were the prominent abnormal findings. Imaging studies identified a remarkably thickened gastric wall with multilobulated folds protruding into the gastric lumen. Gastrotomy revealed the presence of giant cerebriform rugal folds arising from the fundus and body of the stomach. Pronounced gastric glandular hyperplasia and lack of evidence of cellular atypia were suggestive of giant hypertrophic gastritis. The dog was treated with prednisolone, cimetidine, and hyoscine butylbromide, only to experience a short-term remission.

Cytomegalovirus-associated discrete gastrointestinal masses in macaques infected with the simian immunodeficiency virus.

Cytomegalovirus (CMV)-associated gastrointestinal masses have been reported in human acquired immune deficiency syndrome patients. This is the first report on CMV-associated gastrointestinal masses in simian immunodeficiency virus (SIV)-infected macaques. Two SIV-infected macaques presented at necropsy with multiple nodular or umbilicated masses within the gastrointestinal tract. In one animal, the masses were located throughout the gastrointestinal tract, whereas in the other, the masses were restricted to the proximal small intestine. Grossly, the masses were indistinguishable from those caused by neoplastic conditions such as lymphoma and, histologically, were composed of hyperplastic glandular tissue, dense neutrophilic infiltrates within the lamina propria, and multifocal proprial hemorrhage. Frequent cytomegalic cells with basophilic intranuclear inclusions were found in affected regions. Immunohistochemistry for CMV demonstrated frequent immunopositive cells within affected areas. Furthermore, immunohistochemistry for the proliferation marker Ki-67 demonstrated increased proliferation in hyperplastic glands and crypts. CMV should be considered a cause of discrete mass lesions in the gastrointestinal tract of SIV-infected macaques.

Metastatic gastric adenocarcinoma and diffuse hyperplastic gastritis resembling human Menétrier's disease in a camel (Camelus ferus bactrianus).

A captive 16-year-old male camel (Camelus ferus bactrianus) was euthanized after a prolonged period of inappetence leading to cachexia. At necropsy, there was a 7 cm large, tan, firm, well-demarcated nodule in the tunica muscularis and serosa of the distal region of C3. Histologically, a gastric adenocarcinoma was diagnosed. Numerous metastases were found in the liver and the hepatic lymph nodes, in the wall of the portal vein and the aorta, in the lung, heart, and pleura parietalis. Osseous metaplasia was found within the pleural and aortic metastases. In the mucosa of the glandular region of the C3 compartment a diffuse marked hypertrophy of rugae resembling cerebral convolutions was observed. The lesion was characterized by glandular hyperplasia and stromal inflammation and oedema. These changes closely resembled Menétrier's disease described in humans. To our knowledge, this is the first report of concomitant metastatic gastric adenocarcinoma and gastric hyperplasia in a camel.

Gastric mucosal phospholipids in dogs with familial stomatocytosis-hypertrophic gastritis.

In dogs, hypertrophic gastritis, which resembles Ménétrier's disease in man, has been demonstrated to be part of a hereditary syndrome called familial stomatocytosis-hypertrophic gastritis. In addition to hypertrophic gastritis, affected dogs exhibit abnormal blood phospholipid composition. Phospholipids may play a role in maintaining gastric mucosal integrity, and this may be compromised in gastritis. The question arises whether the differences in blood phospholipids may result from a disorder that might also be revealed in the composition of gastric mucosal phospholipids. We analysed the phospholipid composition of gastric mucosa from four dogs with familial stomatocytosis-hypertrophic gastritis. The general phospholipid composition and the molecular composition of phosphatidylcholine from mucosal tissue in the corpus of the stomach where hypertrophic gastritis was evident were not different from that of the antrum, where the tissue was normal. These results do not corroborate a relation between the gastric mucosal phospholipid composition and hypertrophic gastritis.

Hyperplastic foveolar gastropathy and hyperplastic foveolar gastritis in baboons.

While reviewing gastric specimens from 215 baboons, we found diffuse giant mucosal folds in 2 specimens and multiple giant mucosal nodules in another 3. The increased mucosal thickness in those areas was due to giant hyperplasia of the foveolar epithelium. The former 2 specimens were classified as Menetrier's disease (MD) and the latter 3 as Varioliform Lymphocytic Gastritis (VLG), since they were histologically identical to those gastropathies in humans. Whereas MD had diffuse giant hyperplastic foveoli (without lymphocytic infiltration) and prominent glandular cysts, VLG had nodules due to giant hyperplastic foveoli with intraepithelial lymphocytosis. Since the causes leading to gastric MD and VLG in humans remain unknown, the spontaneous occurrence of these two conditions in the baboon may open new avenues for the investigation of possible etiologic factors in the laboratory.

Normal cations and abnormal membrane lipids in the red blood cells of dogs with familial stomatocytosis-hypertrophic gastritis.

Examination of the red blood cells (RBCs) of eight dogs with familial stomatocytosis-hypertrophic gastritis (FS-HG), a multiorgan disease associated with hemolytic anemia, hereditary stomatocytosis (HSt), and hypertrophic gastritis resembling Ménétrier's disease in man, showed abnormal osmotic fragility, normal mean corpuscular volume, slightly increased cell water, and normal cation content and cation fluxes. Cholesterol was decreased in RBC and increased in plasma. In both RBCs and plasma, total phospholipid (PL) was normal, phosphatidylcholine (PC) decreased, and sphingomyelin increased. The palmitic acid content of PC was increased, and the stearic acid content of PC was decreased. Sodium dodecyl sulfate electrophoresis of RBC membrane proteins was normal. These findings have not been described previously in HSt. They suggest that in FS-HG, abnormal composition of the PL in RBCs secondary to abnormal PL in plasma causes defective membrane function and stomatocytic shape-change. This conclusion was supported by a shortened half-life of 51Cr-labeled RBCs from normal dogs after transfusion in dogs with FS-HG. It was concluded (1) that not all hereditary forms of stomatocytosis are necessarily associated with an intrinsic structural defect of the RBC membrane, but that the change in shape of RBC may also be induced by abnormal composition of the plasma; (2) that stomatocytosis may be caused by loss of membrane surface area rather than by the increased cation uptake such as has been shown in some human kindreds with HSt, (3) that FS-HG is a disorder of lipid metabolism, and by consequence, (4) that abnormal lipid metabolism might be involved in the pathogenesis of Ménétrier's disease.

Chronic cryptosporidiosis in Australian elapid snakes: control of an outbreak in a captive colony.

An outbreak of chronic cryptosporidiosis resulting in hypertrophic gastritis occurred in a captive colony of Australian elapid snakes. Two species of the genus Notechis were involved: Notechis ater (Black Tiger Snake) and Notechis scutatus (Eastern or Mainland Tiger Snake). The infection was eventually fatal in all 9 affected snakes. Typical histopathological findings of the stomach included mucosal thickening with cystic dilatation of gastric glands, moderate oedema and fibrosis of the lamina propria, and a mild to moderate patchy infiltration of inflammatory cells. Procedures implemented to contain the outbreak included the use of a formaldehyde-based disinfectant, prompt removal of faecal matter, uneaten and regurgitated food from enclosures, and examination of faecal specimens for Cryptosporidium oocytes and other pathogens.

[3 cases of hypertrophic gastritis associated with a Ollulanus tricuspis infection in cats]. / Drie gevallen van hypertrofische gastritis, geassocieerd met een Ollulanus tricuspis-infectie bij de kat.

An infection with Ollulanus tricuspis was found in three cats with hypertrophic gastritis. Two cats were put down because of chronic vomiting and emaciation. The third cat died shortly after the appearance of blood in its vomit and faeces.

Familial stomatocytosis--hypertrophic gastritis (FSHG), a newly recognised disease in the dog (Drentse patrijshond).

A newly recognised disease, which we have given the provisional name of familial stomatocytosis-hypertrophic gastritis (FSHG), is described in two families of dogs of the Drentse partrijshond breed. The affected dogs consisted of 3 females and 5 males, 3 to 19 (mean 9.5) months of age at admission. The main clinical problems were diarrhoea, icterus, and ataxia and paresis of the pelvic limbs. Laboratory evaluation revealed abnormal red cell shape (stomatocytosis), increased osmotic fragility, haemolytic anaemia, and increased liver enzymes and serum bilirubin. Gastroscopic and histopathologic examination of the gastric mucosa revealed hypertrophic gastritis resembling Ménétrier's disease in man. Histologic findings in the liver were suggestive of progressive liver disease. Cysts were found in the kidneys of the five oldest patients. Electroneurography in 2 dogs revealed polyneuropathy. In the parents of 2 patients (sister and brother), there were no clinical or laboratory abnormalities. An autosomal recessive hereditary defect of lipid metabolism is suspected.

[Hypertrophic gastropathy similar to Ménétrier's disease in pigs slaughtered in accordance with regulations]. / Contributo allo studio della gastropatia ipertrofica, simile alla sindrome di Ménétrier, in suini regolarmente macellati.

The authors found during a study concerning the gastric pathology in pigs 2828 cases of hypertrophic gastropathy in 8408 regularly slaughtered animals. After a description of the morphologic patterns of the lesions, the authors make some pathogenetic hypothesis and conclude that this lesion is like Ménétrier's disease of man.

Pancreatic polypeptide and insulin-secreting tumor in a dog with duodenal ulcers and hypertrophic gastritis.

A 7-year-old spayed female Cocker Spaniel was hospitalized with a history of chronic vomiting, anorexia, and weight loss. Laboratory abnormalities included leukocytosis, metabolic alkalosis, hypoglycemia, hypoproteinemia, and hyperinsulinemia. Gastroscopy and ultrasonography revealed multiple gastric masses and a possible pancreatic mass, respectively. Examination of tissues obtained at necropsy showed a pancreatic adenocarcinoma with hepatic metastasis, gastric hypertrophy, and multiple duodenal ulcers. Immunocytochemical staining of the neoplasia was positive for pancreatic polypeptide (PP) and insulin and negative for gastrin, calcitonin, adrenocorticotropic hormone (ACTH), serotonin, L-enkephalin, chromagranin, glucagon, and somatostatin. Subsequent serum gastrin and PP assays showed a fasting hypergastrinemia with a normal response of gastrin to provocative testing and extremely increased PP values. The high PP values may have resulted in the vomiting and gastrointestinal ulceration. A PP-secreting tumor has not previously been reported in the dog.