A 6-year-old MN Shetland sheepdog (BCS 4/9) presented with an 18-month history of bilious vomiting, reduced appetite and lethargy. Biochemistry abnormalities included hypoalbuminaemia, azotaemia, an elevated cholesterol and a high UPC (8.3), which was believed to be consistent with protein-losing nephropathy. Ultrasound findings revealed diffuse circumferential thickening of the mucosal layer throughout the fundus and body, becoming asymmetric just before the pyloric antrum. The thickened mucosa had the appearance of giant cerebriform mucosal folds, containing multiple rounded cyst-like structures (Fig 1A). The kidneys had mild/moderate loss of corticomedullary distinction, bilateral pyelectasia of 4 mm and there was a small renal cyst within the left kidney. Gastroscopy revealed thickened rugal folds in the body and fundus that did not flatten with insufflation. Inter-rugal regions had a cerebriform appearance (Fig 1B). Multiple grab biopsies were obtained from the rugal folds and samples were also obtained from ‘normal’ pylorus and angularis. The combined findings of ultrasonographic, endoscopic and histopathological changes lead to a diagnosis of giant hypertrophic gastritis (GHG), a condition which shares many characteristics of Menetrier’s disease in humans. It is a rare condition in dogs and has been associated with Helicobacter infection in people and one dog, which also had concurrent Leishmania infection. However, Helicobacter was deemed unlikely due to the absence of spiral-like organisms or associated inflammation on gastric histopathology. Where underlying Helicobacter infection has not been identified, treatment of GHG in people has been varied and comprised proton pump inhibitors, high-protein diets, partial gastrectomy, monoclonal antibody therapy against transforming growth factor receptor (cetuximab) and octreotide. As many of these treatment options are unavailable in veterinary medicine, treatment with prednisolone (1 mg/kg po Q24h), omeprazole (1 mg/kg po Q12h), maropitant (2 mg/kg po Q24h) and mirtazapine (1.5 mg/kg po Q24h) was initiated. The patient was euthanised 4 weeks later due to progression of azotaemia, which may have been a consequence of persistent proteinuria. Hypoalbuminaemia in GHG is typically attributed to gastric mucosal loss, but in this case the marked elevation in UPC supported glomerular loss. While proteinuria can be identified secondary to underlying pathology, rather than primary renal disease, it is not typically associated with this magnitude of UPC. Proteinuria (UPC 6.04) has been reported in a previous veterinary case with GHC. Therefore, an association between the two conditions cannot be entirely excluded. A renal biopsy was not performed to confirm the underlying cause of the proteinuria, due to the patient’s condition. This case highlights the need to have giant hypertrophic gastritis on the differential list for a diffusely thickened stomach wall. S. Christie: Writing – original draft. B. Gomes: Ultrasound images and interpretation. N. Reed: Endoscopy images and input on clinical management. Video S1. Ultrasound video of stomach: the mucosa is thickened and diffusely echogenic with irregular mucosal lumen interphase similar to giant cerebriform mucosal folds; which contains multiple small (2–3 mm diameter), rounded anechoic cyst-like structures. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Christie et al. (Tue,) studied this question.