Lagerstedt et al. BMC Veterinary Research (2021) 17:98 https://doi.org/10.1186/s12917-021-02802-3 CASE REPORT Open Access Ménétrier-like disease in a Pointer with concurrent granulomatous gastritis, helicobacteriosis and leishmaniosis: a case report E. Lagerstedt1*, T. Spillmann1, N. Airas2, L. Solano-Gallego3 and S. Kilpinen1 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. (Continued on next page) * Correspondence: emma.lagerstedt@helsinki.fi 1 Department of Equine and Small Animal Medicine, Faculty of Veterinary Medicine, University of Helsinki, P.O. Box 57, FI-00014 Helsinki, Finland Full list of author information is available at the end of the article © The Author(s). 2021 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data. Lagerstedt et al. BMC Veterinary Research (2021) 17:98 Page 2 of 8 (Continued from previous page) 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. Keywords: Ménétrier’s-like disease, Menetrier's disease, Giant hypertrophic gastritis, Helicobacter spp., Leishmania, Foveolar hyperplasia Background before moving to Finland six years before presentation. Ménétrier’s disease (MD) is a rare hypertrophic gastro- On physical examination, the dog´s body condition score pathy in humans, characterized macroscopically by giant was 3/9 and it had mild periodontitis. cerebriform gastric mucosal folds in the corpus and fun- Complete blood count results were within reference dus of the stomach, sparing the antrum and pylorus [1, intervals. Serum biochemical abnormalities included 2]. Histopathologically, hyperplasia of the mucous cells mild hypoproteinaemia, mild hypoalbuminaemia and within the neck and base areas of the fundic glands and hypocobalaminaemia. C-reactive protein was mildly loss of parietal and chief cells are typical [1]. The criteria elevated. Antibody titres against Leishmania infantum for diagnosis of MD in dogs have not yet been estab- antigens (immunofluorescence antibody test, Ludwig lished in detail, which is why the term Ménétrier-like Maximilian University of Munich) were markedly ele- disease (MLD), instead of MD, is preferred in dogs. vated (Table 1). Serum gastrin concentration was 26 ng/l MLD has been reported earlier in only seven dogs repre- (reference interval 10–40 ng/l, Michigan State Univer- senting five different breeds: a Boxer, an Old English sity). To rule out hypoadrenocorticism, basal serum cor- Sheepdog, a West Highland White Terrier, three Cairn tisol concentration was measured and it was 34 nmol/l Terrier littermates and a Jack Russell Terrier [3–7]. In (reference interval 10–100 nmol/l, IDEXX Laboratories) all reported canine cases, hyperplasia of the mucous cells [9]. Serum Dirofilaria immitis antigen and antibodies in the corpus and fundus of the stomach was described, against Borrelia burgdorferi, Anaplasma phagocytophi- and in four cases also the loss of parietal and chief cells lum and Ehrlichia canis were negative (SNAP 4Dx, [6, 7]. The most common clinical signs and findings in IDEXX Laboratories). affected dogs include vomiting, anorexia, weight loss and Faecal examination for endoparasites by flotation, anti- hypoalbuminaemia [3–7]. The aetiology underlying gen testing for Giardia duodenalis (FASTest Giardia) MLD in dogs is unknown, but in humans and mice, one and bacterial culture for Yersinia spp., Salmonella spp., factor in the pathogenesis of MD is suggested to be in- Campylobacter spp., Clostridium difficile and Clostrid- creased signalling of epidermal growth factor receptors ium perfringens were negative. Urinalysis including urine (EGFR) [1]. In humans, MD usually shows chronic pro- protein-creatinine ratio was unremarkable. Abdominal gressive features, but variants with acute onset and spon- ultrasonography revealed a partial mild gastric wall taneous remission have been reported, and have been thickening with slight loss of wall layering, mild thicken- associated with Helicobacter pylori infection in adults ing of the colonic wall with normal wall layering, en- and cytomegalovirus (CMV) infection in children [2, 8]. larged and slightly heterogenic medial iliac lymph nodes, This report describes for the first time the coexistence of prominent mesenteric lymph nodes and hyperechoic MLD with granulomatous gastritis, a severe manifest- sports in both renal cortices. ation of Helicobacter-like organisms and leishmaniosis To exclude food-responsive enteropathy, an elimin- in a Pointer. ation diet was started with a hydrolysed diet in addition to palliative treatment comprising famotidine (Pepcid; Case presentation Janssen-Cilag, 0.7 mg/kg orally q12h), ondansetron A nine-year-old spayed female Pointer weighing 15 kg (Ondansetron Stada; Stada Arzneimittel, 0.3 mg/kg or- was presented with a nine-month history of intermittent ally q8h) and maropitant citrate (Cerenia; Zoetis, vomiting and marked weight loss to the University of 3.2 mg/kg orally q24h). Cobalamin supplementation was Helsinki Veterinary Teaching Hospital, Finland. The dog initiated (Betolvex; Ratiopharm, 0.06 mg/kg orally q24h). was born in Greece and had lived one year in Germany Treatment for leishmaniosis was not started until Lagerstedt et al. BMC Veterinary Research (2021) 17:98 Page 3 of 8 Table 1 Summary of changes in clinical biochemistry parameters and results of additional diagnostic tests Serum parameter (reference interval) FP 1 MAFP 2 MAFP 4 MAFP 7 MAFP 10 MAFP 17 MAFP 24 MAFP 32 MAFP 39 MAFP Albumin 25.7 NT 26.1 31.3 33.4 30.8 34.2 33.3 34.4 33.2 (30–41 g/l) Total proteins (58–77 g/l) 53.0 NT 57.0 62.0 58.0 57.0 63.0 64.0 66.0 70.0 Cobalamin 163 NT 737 1180 NT 176 766 839 904 725 (200–850 pg/ml) C-reactive protein 26.2 45.4 < 10 NT NT NT NT NT NT NT (< 10 mg/l) Leishmania infantum antibodies (< 1:32) 1:512 NT NT NT NT 1:256 NT NT 1:64 1:64 Values beyond the reference interval are bolded FP First presentation, MAFP Months after the first presentation, NT Not tested gastroduodenoscopy was performed and gastric biopsies observed. The organisms seen intralesionally stained examined. positively in both periodic acid Schiff’s (PAS) and Gastroduodenoscopy was performed one month after Grocott’s methenamine silver special stainings. the first presentation since the dog did not improve after A PCR for fungi was performed on a fresh frozen gas- initiating treatment. The gastric mucosa of the corpus, tric mucosal biopsy sample (HUSLAB), and DNA from fundus and proximal antrum was macroscopically ir- Malassezia globosa was found [10]. Leishmania spp. was regular, showing cerebriform mucosal folds (Fig. 1a). examined by immunohistochemistry from a formalin The distal antrum (Fig. 1b) and duodenum were macro- fixed gastric biopsy (Universitat Autònoma de Barce- scopically unremarkable. Histopathological examination lona) and by real-time PCR from a fresh frozen gastric of the duodenum revealed a mild diffuse chronic lym- biopsy (IDEXX Laboratories); both were negative [11]. phoplasmacytic enteritis with a mild multifocal neutro- Fluorescence in situ hybridization (FISH) from a forma- philic component. Gastric mucosal biopsies showed a lin fixed gastric biopsy detected eubacteria, but no sig- moderate multifocal chronic granulomatous gastritis nificant amounts of Escherichia coli, Salmonella spp., with fewer lymphocytes and plasma cells (Fig. 1c) and Helicobacter spp., Cryptococcus spp., Campylobacter occasional intralesional, round to ovoid, 3–6 µm in spp., Leptospira spp. or Streptococcus spp. (Langford diameter single-cell organisms, which were detected Vets Diagnostic Laboratories). both within the cytoplasm of macrophages and extracel- Based on these findings, the dog was treated for heli- lularly. In addition, severe manifestation of Helicobacter- cobacteriosis with amoxicillin (Amovet vet; Orion, like organisms (HLOs) and multifocal mild cystic dilata- 25 mg/kg orally q12h), clarithromycin (Clarithromycin tion of glands at the midlevel of the lamina propria were Ratiopharm; Teva, 8 mg/kg orally q12h) and Fig. 1 First gastroduodenoscopy. a Endoscopic view of gastric corpus and proximal antrum showing cerebriform thickened gastric mucosal folds. b Endoscopic view of distal antrum and pylorus was macroscopically unremarkable. c Histopathology of the gastric mucosal biopsy showing multifocal moderately increased number of macrophages (arrow), lymphocytes and plasma cells. Haematoxylin and eosin staining 20X. Insert: Numerous spiral-shaped Helicobacter-like organisms (arrow) are present in gastric mucosa. Warthin-Starry silver staining, bar 5 µm Lagerstedt et al. BMC Veterinary Research (2021) 17:98 Page 4 of 8 metronidazole (Metronidazol Ratiopharm; Ratiopharm, diffuse chronic eosinophilic gastritis (Fig. 3b). Mild 8 mg/kg orally q12h) for two weeks. The palliative treat- granulomatous inflammation was noted only focally in ment continued with ondansetron and maropitant cit- the corpus area. Single-cell organisms seen previously rate, in addition to esomeprazole (Nexium; AstraZeneca, were no longer detected, but a small number of HLOs 1 mg/kg orally q24h). Oral supplementation of cobala- was seen. The palliative treatment and allopurinol were min was also continued. continued. One month later, the dog still vomited every other Seven months after the first presentation, the dog day. A second gastroduodenoscopy was performed. The showed signs of heat for the first time after being spayed gastric mucosal changes had the same magnitude and seven years earlier in Greece and was diagnosed ultraso- cerebriform appearance as in the first gastroduodeno- nographically with an ovarian remnant on the left side. scopy (Fig. 2a). Histopathological examination revealed a A laparotomy was performed and the ovarian remnant severe diffuse chronic lymphoplasmacytic gastritis with was removed and two full-thickness biopsies were taken fewer macrophages. Some single-cell organisms were from the gastric fundus and antrum. The aerobic and still present, but HLOs were no longer detected (Fig. 2b). anaerobic bacterial culture of the gastric biopsies was The palliative treatment was continued. Based on the negative. Histological examination of the fundic biopsy high antibodies against L. infantum antigens and persist- showed hyperplasia of the mucous cells within the neck ent clinical signs, treatment for leishmaniosis was started and base areas of the fundic glands, multifocal cystic according to LeishVet guidelines [12] with miltefosine enlargement of mucinous glandular structures at the (Milteforan; Virbac, 2 mg/kg orally q24h for 4 weeks) border between the lamina propria and lamina muscu- and allopurinol (Zyloric; Aspen, 10 mg/kg orally q12h). laris mucosae and loss of parietal and chief cells (Fig. 4). One month later, the vomiting had stopped and the Occasional glandular structures were growing between dog had gained weight. Serum total protein and albumin the muscular bundles on the lamina muscularis mu- concentrations increased to the reference intervals, after cosae. The fundic glandular changes were consistent which the oral cobalamin supplementation was discon- with the histopathological findings described in MD. A tinued. A third gastroduodenoscopy was performed. The mild multifocal granulomatous inflammation in the sub- macroscopically changed mucosal area was the same size mucosa remained. There were no specific histopatho- and had the same appearance as during the first two en- logical changes in the antral biopsy. doscopies, but the mucosa was somewhat firmer (Fig. 3a). The dog had gained weight, achieving a normal body Histopathological examination now revealed a moderate condition score (5/9), and with palliative treatment and Fig. 2 Second gastroduodenoscopy. a Endoscopic view of the gastric corpus and proximal antrum showing the same giant cerebriform gastric mucosal folds as in the first endoscopy. b Histopathology of the gastric mucosal biopsy after treatment for Helicobacter-like organisms revealing a severe chronic diffuse lymphoplasmacytic gastritis (lymphocytes short arrow, plasma cells long arrow) with a decreased number of macrophages relative to the first gastric biopsies. Haematoxylin and eosin staining 20X. Insert: No Helicobacter-like organisms were detected. Warthin-Starry silver staining, bar 5 µm Lagerstedt et al. BMC Veterinary Research (2021) 17:98 Page 5 of 8 Fig. 3 Third gastroduodenoscopy. a Endoscopic view of the gastric corpus and proximal antrum showing the same giant cerebriform gastric mucosal folds as in the previous endoscopies. b Histopathology of the gastric mucosal biopsy revealed fundic glands surrounded by eosinophilic granulocytes (arrow), lymphocytes and plasma cells. Haematoxylin and eosin staining 40X. allopurinol it had only vomited approximately twice a granulomatous gastritis, with simultaneous helicobacter- month. The palliative medications continued, but at a iosis and leishmaniosis. The pathogenesis of MLD in lower dose, with esomeprazole 0.7 mg/kg orally q24h, dogs is unknown, but in MD in humans and mice, one maropitant citrate 0.8 mg/kg orally q24h and ondanse- factor is suggested to be increased signalling of EGFR tron 0.3 mg/kg orally q24h. If any of the palliative medi- [1]. Especially in children, MD is strongly associated cations were stopped or titrated down, the dog started with CMV infection, and CMV has been shown to acti- vomiting again daily. vate EGFR signalling [2]. In CMV-associated cases, there Ten months after the first examination, the dog devel- is a spontaneous remission of MD [2]. Especially in oped hypocobalaminaemia again (Table 1), so cobalamin adults, some MD cases have been associated with H. pyl- was started orally at 0.03 mg/kg q24h. Oral cobalamin ori infection and the eradication of H. pylori has resolved supplementation was successful again (Table 1). Serum the endoscopic and histopathological findings [8]. In this albumin concentration remained within the reference dog, a severe manifestation of HLOs was present in the interval. Thirty-nine months after the first presentation, first mucosal biopsies of the stomach, which has not pre- the dog was still on allopurinol, ondansetron and maro- viously been reported in MLD cases in dogs [3–7]. pitant citrate and was vomiting approximately twice a The dog showed chronic upper gastrointestinal signs, month. such as weight loss, anorexia and vomiting in connection with hypoalbuminaemia, which are typical clinical signs Discussion and conclusions for MLD in dogs and MD in humans [1, 3–5, 7]. In this This case report describes the coexistence of two rare case, vomiting slightly decreased when palliative treat- gastropathies in the dog, namely MLD and ment was initiated and later slightly more with Fig. 4 Histopathology of the full-thickness biopsies of the fundus showing histopathological features of MD. a Cystic enlargement of mucinous glandular structures (arrow). Haematoxylin and eosin staining 10X. b Hyperplasia of the mucous cells (arrow head) and loss of parietal cells (short arrow) and chief cells (long arrow). Haematoxylin and eosin staining 40X. Lagerstedt et al. BMC Veterinary Research (2021) 17:98 Page 6 of 8 treatment for Helicobacter spp., but it did not cease. The pancreatic proteases in the duodenum and then free co- Helicobacter spp. treatment also did not result in reso- balamin is bound to intrinsic factor [16]. Intrinsic factor lution of MLD. This could be explained with the chronic is mainly produced in dogs by the exocrine pancreas, features of the dogs’ disease. H. pylori –associated MD but also in the stomach in parietal cells [16, 17]. Parietal in humans going into remission, typically has an acute cells, which produce both haptocorrin and intrinsic fac- onset of symptoms [2]. After treatment for leishmanio- tor, are typically lost in MD [1, 16, 17], which could be sis, the vomiting ceased, the dog gained weight and the one possible factor contributing to the hypocobalami- hypoalbuminaemia resolved. It seems likely that part of naemia in this dog. the clinical signs were caused by leishmaniosis. Six The serum gastrin concentration was measured to months after the miltefosine treatment, the antibody ti- rule out gastrinoma as a differential diagnose for the tres against L. infantum had halved, indicating that the hypertrophic changes in the stomach. The typical leishmaniosis was in remission. The dog always started changes of MLD were not evident in the endoscopic vomiting if any of the palliative treatment medications: gastric mucosal biopsies, but the diagnosis was maropitant citrate, ondansetron or esomeprazole, were achieved from the full-thickness biopsies. In humans, stopped or titrated down. At this point, the vomiting the diagnosis for MD is obtained from endoscopic bi- was probably a sign of MLD. opsies, but large snare biopsies are recommended in In humans, treatments other than H. pylori eradica- macroscopically hypertrophic lesions, instead of stand- tion for MD have also been tried, such as antibiotics, ard forceps biopsies [2]. In the previous canine case steroids, acid suppressants, anticholinergic agents and reports, the diagnosis was made from full-thickness octreotide therapy, but the findings have been incon- biopsies in all cases [3–7]. In one case, the first biop- sistent [2, 13]. In humans, promising results have sies were taken by gastroscopy and they had con- been shown with cetuximab, a human monoclonal tained only the superficial part of the mucosa from antibody that blocks EGFR signalling [1]. A “cani- which the diagnosis of MLD could not be made [3]. nized” anti-EGFR antibody has been investigated only In the case presented here, it is uncertain why the in vitro in canine cancer, however, no canine anti- characteristic changes of MLD were not seen in the EGFR antibody is commercially available. Human first three endoscopic mucosal biopsies because all anti-EGFR antibodies could cause adverse reactions in samples had contained the lamina propria of the gas- dogs such as anaphylaxis [14]. Partial or total gastrec- tric mucosa and the macroscopic appearance of the tomy has been done in cases with severe symptoms, gastric lesion at the endoscopies and the laparotomy and it has been reported to be a successful treatment had remained the same. Based on this, full-thickness also in two canine cases [2, 5, 7, 13]. In this case, the biopsies should probably be the preferred method in affected area was too large to be removed surgically dogs with suspected MLD. Full-thickness biopsies are without affecting the function of the stomach; pallia- also more accurate for the evaluation of possible neo- tive treatment was given since the dog responded to plastic changes. People with MD have a higher risk of it. Thirty-nine months after first presentation, the dog developing gastric neoplasia [1]. Four cases of MLD was clinically well, vomiting approximately twice a in dogs have been reported to progress to gastric car- month, despite the low daily doses of the palliative cinoma [5, 6]. In three littermates, gastric adenocar- treatments. Previously, the longest reported survival cinoma was diagnosed [6]. In two of the dogs, the time in a dog not treated surgically was 27 months diagnosis was set at the same time as the diagnosis of [6]. That dog had a subclinical disease for two years, MLD [6]. In the third dog, the diagnosis was made but was given a gastric protectant, a proton pump in- 27 months after diagnosis of MLD [6]. In one dog, a hibitor and a non-steroidal anti-inflammatory drug for poorly differentiated superficial gastric carcinoma was an unknown period [6]. diagnosed five years after a partial gastrectomy was The dog here was hypocobalaminaemic and was sup- done and MLD was diagnosed [5]. plemented orally with cobalamin [15]. The supplementa- Granulomatous gastritis in dogs is far less common tion led to hypercobalaminaemia and was discontinued, than lymphoplasmacytic or eosinophilic gastritis and has after which the dog developed hypocobalaminaemia been described in rare cases of infections caused by again. In dogs, aetiologies for hypocobalaminaemia are fungi, parasites or bacteria [18]. The cause for the granu- exocrine pancreatic insufficiency, chronic inflammatory lomatous gastritis in this dog was extensively examined, enteropathies and alimentary lymphoma among others yet remained unknown. Granulomatous inflammation in [16]. This dog showed no evidence of these diseases. In the gastrointestinal tract of dogs in endemic areas of the stomach, free cobalamin is bound to haptocorrin, leishmaniosis has been reported in L. infantum infection which in dogs is mostly produced by parietal cells in the [19]. However, L. infantum was not detected in the gas- gastric mucosa [17]. Haptocorrin is digested by tric biopsies by PCR or immunohistochemistry. The Lagerstedt et al. BMC Veterinary Research (2021) 17:98 Page 7 of 8 aerobic and anaerobic bacterial culture of the biopsy was Acknowledgements negative. The PCR examination for fungi revealed a The authors thank Pernilla Syrjä for fruitful cooperation in histopathological examinations and Jere Lindén for help with histopathological figures. small amount of DNA from M. globosa. The PAS- positive intralesional structures in the stomach were Authors’ contributions morphologically compatible with single-cell yeast. EL examined the patient several times and drafted the manuscript. SK and TS performed the gastroduodenoscopies and were major contributors to the Malassezia spp. was not thought to be the cause for the writing of the manuscript. NA conducted the histopathological examinations granulomatous gastritis. The PAS-positive structures of the stomach and wrote the sections about histopathological findings in also disappeared from the biopsies without a treatment the article. LSG analysed and interpreted the patient data regarding the L. infantum immunohistochemistry of the gastric biopsies. All authors read and for Malassezia spp. FISH detected eubacteria within the approved the final manuscript. gastric tissue samples, but not significant numbers of E. coli, Salmonella spp., Helicobacter spp., Cryptococcus Funding No funding was received. spp., Campylobacter spp., Leptospira spp. or Streptococ- cus spp. It is unclear why the severe manifestation of Availability of data and materials HLO was not detected by FISH since in previous studies All data are presented in the main paper and the accompanying figures. Helicobacter spp. have been detected by FISH with high Ethics approval and consent to participate sensitivity [20, 21]. In one study, Helicobacter spp. was Not applicable. detected by FISH in all gastric biopsies, but in a few bi- opsies from the small and large intestine they were not Consent for publication Consent for publication of the clinical details of the case was obtained from detected by FISH, even though Helicobacter spp. PCR the dog’s owner. had been positive [20]. This was thought to be associated with either a difficulty of the probes in penetrating the Competing interests The authors have no competing interests to declare. crypts or too few bacteria in the sample [20]. This could also be the case in our biopsies. Author details 1 The role of Helicobacter spp. in the granulomatous Department of Equine and Small Animal Medicine, Faculty of Veterinary Medicine, University of Helsinki, P.O. Box 57, FI-00014 Helsinki, Finland. gastritis of this dog is unknown. Typically, Helicobacter 2 Department of Veterinary Biosciences, Faculty of Veterinary Medicine, spp. infection in dogs manifests as mild lymphoplasma- University of Helsinki, P.O. Box 57, FI-00014 Helsinki, Finland. 3Departament cytic gastritis, but can also be asymptomatic [22, 23]. In de Medicina i Cirurgia Animals, Facultat de Veterinària, Universitat Autònoma de Barcelona, Bellaterra, 08193 Barcelona, Spain. some human cases, it has been suggested that there might be an association between H. pylori infection and Received: 23 October 2020 Accepted: 16 February 2021 granulomatous gastritis [24, 25]. In this case, the severity of the granulomatous gastritis markedly decreased after References the treatment for Helicobacter spp, which supports a 1. Fiske WH, Tanksley J, Nam KT, Goldenring JR, Slebos RJ, Liebler DC et al possible connection between the two conditions. How- (2009) Efficacy of cetuximab in the treatment of Ménétrier’s disease. 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