Gastritis is a common finding in dogs, with 35% of dogs investigated for chronic vomiting and 26% to 48% of asymptomatic dogs affected. The prevalence in cats has not been determined. The diagnosis of chronic gastritis is based on the histologic examination of gastric biopsies and it is usually subclassified according to histopathological changes and etiology.
Histopathologic Features of Gastritis
Gastritis in dogs and cats is usually classified according to the nature of the predominant cellular infiltrate (eosinophilic, lymphocytic, plasmacytic, granulomatous, lymphoid follicular), the presence of architectural abnormalities (atrophy, hypertrophy, fibrosis, edema, ulceration, metaplasia), and their subjective severity (mild, moderate, severe). A standardized visual grading scheme has been proposed by Happonen et al and has been adapted for pathologists.
The most common form of gastritis in dogs and cats is mild to moderate superficial lymphoplasmacytic gastritis with concomitant lymphoid follicle hyperplasia. Eosinophilic, granulomatous, atrophic, and hyperplastic gastritis are less common.
Despite the high prevalence of gastritis an underlying cause is rarely identified, and in the absence of systemic disease, ulcerogenic or irritant drugs, gastric foreign objects, parasites (Physalloptera and Ollulanus spp. ), and in rare instances fungal infections (Pythium insidiosum, Histoplasma spp. ), it is usually attributed to dietary allergy or intolerance, occult parasitism, or a reaction to bacterial antigens, or unknown pathogens. Treatment is often empirical but can serve to define the cause of gastritis, such as diet responsive, antibiotic responsive, steroid responsive, or parasitic.
Although the basis of the immunologic response in canine and feline gastritis is unknown, recent studies in experimental animals have shed light on the immunologic environment in the gastrointestinal tract and reveal a complex interplay between the gastrointestinal microflora, the epithelium, immune effector cells such as lymphocytes and macrophages, and soluble mediators such as chemokines and cytokines. In health, this system avoids active inflammation by antigen exclusion and the induction of immune tolerance. The development of intestinal inflammation in mice lacking the cytokines IL-10, TGFP, or IL-2 indicates the central importance of cytokines in damping down mucosal inflammation. In many of these murine models gastrointestinal inflammation only develops in the presence of indigenous intestinal microflora, leading to the hypothesis that spontaneous mucosal inflammation may be the result of a loss of tolerance to the indigenous gastrointestinal microflora. The role of these mechanisms in outbred species such as the dog and cat remains to be determined, but clearly loss of tolerance to bacterial of dietary antigens should be considered.
The epithelial cell is also emerging as a “general” in the inflammatory response, with gram-negative or pathogenic bacteria inducing proinflammatory cytokine (e. g., IL-8, ILI-p) secretion from epithelial cells, whereas commensal or bacteria such as S. fecium or Lactobacillus spp. induce the production of the immunomodulatory cytokines TGFB or IL-10.The pro-inflammatory cytokines produced by epithelial cells are modulated by the production of IL-10 from macrophages and potentially by the epithelial cells themselves. In this context, dogs with lymphoplasmacytic gastritis of undetermined etiology showed a correlation between the expression of the immunomodulatory cytokine IL-10 and proinflammatory cytokines (IFN-γ, IL-1β, IL-8). Simultaneous expression of IL-10 and IFN-y mRNA has also been observed in the intestines of beagle dogs (lamina propria cells and the intestinal epithelium) in the face of a Iuminal bacterial flora that was more numerous than that of control dogs. Thus it is tempting to visualize a “homeostatic loop” consisting of proinflammatory stimuli and responses, countered by immunomodulation and repair, with an imbalance in either of these arms manifested as gastritis.
The importance of unknown pathogens in the development of mucosal inflammation is best demonstrated by the gastric bacterium Helicobacter pylori, a gram-negative bacterium, which chronically infects more than half of all people worldwide. Chronic infection of human adults with H. pylori is characterized by the infiltration of polymorphonuclear and mononuclear cells and the up-regulation of pro-inflammatory cytokines and the chemokine IL-8.Mucosal T cells in infected individuals are polarized toward the production of gamma interferon (IFN-γ), rather than IL-4 or IL-5 indicating a strong bias toward a TH-1 type response). This sustained gastric inflammatory and immune response to infection appears to be pivotal for the development of peptic ulcers and gastric cancer in people.
There is also a high prevalence of gastric Helicobacter spp. infection in dogs (67% to 100% of healthy pet dogs, 74% to 90% of vomiting dogs, 100% of laboratory beagles) and cats (40% to 100% of healthy and sick cats). In contrast to people, in whom Helicobacter pylori infection predominates, dogs and cats are colonized by a variety of large spiral organisms (5 to 12 n). In cats from Switzerland, United States, and Germany, Helicobacter heilmannii is the predominant species, with Helicobacter bizzozeronii and Helicobacter felis much less frequent. In dogs from Finland, Switzerland, the United States, and Denmark Helicobacter bizzozeronii and Helicobacter salomonis are most common followed by Helicobacter heilmanni and Helicobacter felis. Helicobacter bilis and Flexispira rappini have also been described. Cats can also be colonized by Helicobacter pylori (2 to 5 p) but infection has been limited to a closed colony of laboratory cats.
Ownership of dogs and cats has been correlated with an increased risk of infection of Helicobacter heilmannii in people. Case reports have also suggested the transmission of Helicobacter spp. from pets to man. Recent studies clearly confirm that dogs and cats harbor H. heilmannii, but the subtypes of H. heilmannii present in dogs and cats (types 2 and 4) are of minor importance (approximately 15% of cases) to humans, who are predominantly colonized by H. heilmannii type 1 (the predominant Helicobacter sp. in pigs).
The effect of eradicating Helicobacter spp. on gastritis and clinical signs, the main form of evidence supporting the pathogenic role of H. pylori in human gastritis, has not been thoroughly investigated to date in dogs and cats. An uncontrolled treatment trial of dogs and cats with gastritis and Helicobacter spp. infection showed that clinical signs in 90% of 63 dogs and cats responded to treatment with a combination of metronidazole, amoxicillin, and famotidine, and that 14 of the 19 animals re-endoscoped had resolution of gastritis and no evidence of Helicobacter spp. in gastric biopsies.
Controlled clinical trials are required to confirm these observations but have been hampered by a much higher apparent recrudescence or re-infection rate than the 1 % to 2% per year observed after treatment of H. pylori-infected people. With such limited information from eradication trials, most current knowledge about the pathogenicity of Helicobacter spp. for dogs and cats comes from the evaluation of animals with and without infections and clinical signs, and a small number of experimental infections.
The large Helicobacter species found in dogs an cats do not attach to the epithelium but colonize the superficial mucus and gastric glands, particularly of the fundus and cardia, and may also be observed intracellularly. Degeneration of gastric glands, with vacuolation, pyknosis, and necrosis of parietal cells is more common in infected than uninfected animals. Inflammation is generally mononuclear in nature and ranges from mild to moderate in severity. Gastric lymphoid hyperplasia is common and can be extensive in dogs and cats infected with Helicobaaer spp. (particularly when full thickness gastric biopsies are evaluated). In addition to this local gastric immune response, a systemic response characterized by increased circulating anti-Helicobacter IgG has been detected in sera from naturally infected dogs and cats. However, the gastritis observed in cats and dogs infected with large HLOs is generally less severe than that observed in Helicobacter pylori infected humans (where neutrophilic aggregates, and moderate to severe gastritis, are commonly encountered), and gastro-intestinal ulcers, gastric neoplasia, or changes in serum gastrin or acid secretion have not been associated with Helicobacter spp. infection in dogs and cats.
These differences between people, dogs, and cats may be attributed to differences in the virulence of the infecting Helicobacter spp., or the host response. Studies that address this issue indicate that Helicobacter pylori evokes a more severe pro-inflammatory cytokine and cellular response in dogs and cats than natural or experimental infection with large Helicobacter spp. The limited mucosal inflammatory response and absence of clinical signs in the vast majority of dogs and cats infected with non-H. pylori Helicobaaer spp., despite significant antigenic stimulation (evidenced by seroconversion and lymphoid follicle hyperplasia) suggest that large gastric Helicobacter spp. are more commensal than pathogenic. With this in mind, it is interesting to speculate that it is the loss of tolerance to gastric Helicobacter spp., rather than the innate pathogenicity of these bacteria, that explains the development of gastritis and clinical signs in some dogs and cats. However, much still remains to be learned about the role of Helicobacter spp. in canine and feline gastritis.
The major clinical sign of chronic gastritis is vomiting of food or bile. Decreased appetite, weight loss, melena, or hematemesis is variably encountered. The concurrent presence of dermatoIogic and gastrointestinal signs raises the likelihood of dietary sensitivity. Access to toxins, medications, foreign bodies, and dietary practices should be thoroughly reviewed. The signalment should not be overlooked as it may increase the probability that chronic gastritis is the cause of vomiting. Hypertrophy of the fundic mucosa is frequendy associated with a severe enteropathy in basenjis and stomatocytosis, hemolytic anemia, icterus, and polyneuropathy in Drentse Patrijshond. Hypertrophy of the pyloric mucosa is observed in small brachycephalic dogs such as Lhasa apso and is associated with gastric outflow obstruction (see Delayed Gastric Emptying and Motility Disorders). Atrophy of the gastric mucosa that may progress to adenocarcinoma has been reported in Lundehunds with protein-losing gastroenteropathy.
Young, large breed, male dogs in the Gulf states of the United States may have granulomatous gastritis caused by Pythium spp. with infection more prevalent in fall, winter, and spring. Physical examination is often unremarkable. Abdominal distension may be related to delayed gastric emptying caused by obstruction or defective propulsion. Abdominal masses, lymphadenopathy, or ocular changes may be encountered in dogs with gastric fungal infections.
A biochemical profile, complete blood count, urinalysis, and T4 (cats) should be performed as a basic screen for metabolic, endocrine, infectious, and other non-GI causes of vomiting, as well as the acid base and electrolyte changes associated with vomiting, outflow obstruction, or acid hypersecretion. Clinicopathologic tests are often normal in patients with chronic gastritis.
Eosinophilia may prompt the consideration of gastritis associated with dietary hypersensitivity, endoparasites, or mast cell tumors. Hyperglobulinemia and hypoalbuninemia may be present in basenjis with gastropathy / enteropathy, or dogs with gastric pythisosis. Panhypoproteinemia is a feature of gastroenteropathy in Lundehunds, moderate to severe generalized inflammatory bowel disease, gastrointestinal lymphoma, and gastrointestinal histoplasmosis. More specific testing, such as an adrenocorticotropic hormone stimulation test, or serology for Pythium isnsidiosum, is performed based on the results of these initial tests. Determination of food specific IgE has not been shown to be useful in the diagnosis of dietary sensitivity in dogs or cats. The utility of noninvasive tests, such as serum pepsinogen and gastric permeability to sucrose, used to diagnose gastritis in people has not been determined in dogs and cats.
Abdominal radiographs are frequently normal in dogs and cats with gastritis but may show gastric distention or delayed gastric emptying (food retained more than 12 hours after a meal). Contrast radiography may reveal ulcers or thickening of the gastric rugae or wall but has largely been supersceded by the combination of ultrasonography to detect mural abnormalities and endoscopy to observe and sample the gastric mucosa.
Endoscopic examination enables the visualization of foreign bodies, erosions, ulceration, hemorrhage, rugal thickening, lymphoid follicle hyperplasia (evident as mucosal pock marks), increased mucus or fluid (dear or bile stained), and increased or decreased mucosal friability. Discrete focal or multifocal mucosal nodules may be observed with Ollulanus spp. infection.
Gastric phycomycosis can be associated with irregular masses in the pyloric outflow tract and may prompt serologic testing by ELISA, Western blotting, and culture of fresh gastric biopsies. Parasites such as Physalloptera spp. may be observed as 1- to 4-cm worms. Large amounts of bile stained fluid is suggestive of duodenogastric reflux-associated gastritis, whereas lots of clear fluid my indicate hypersecretion of gastric acid. Gastric fluid can be aspirated for cytology (Helicobacter spp., parasite ova or larvae) and pH measurement. Impression smears of gastric biopsies are an effective way of looking for Helicobacter spp. (5 to 12 u spirals) and are more sensitive than the biopsy urease test (Helicobacter spp. produce urease). Serum gastrin should be measured in the face of unexplained gastric erosions, ulcers, fluid accumulation, or mucosal hypertrophy.
The endoscopic procedure of dribbling dietary antigens onto the gastric mucosa to ascertain the presence of food allergy has not been useful in dogs or cats: it is highly subjective, detects only immediate hypersensitivity, and does not correlate with the results of dietary elimination trials. The stomach should be biopsied even when it looks grossly normal (usually three biopsies from each region- pylorus, fundus, and cardia). Thickened rugae may require multiple biopsies, and a full-thickness biopsy is often required to differentiate gastritis from neoplasia or fungal infection and to diagnose submucosal or muscular hypertrophy. The results of gastric ultrasonography can help to forewarn the clinician of these possibilities and are complement to the endoscopic findings.
Gastric sections should be stained with H&E for evaluation of cellularity and architecture, and modified Steiner stain for gastric spiral bacteria. Further special stains, such as Gomori’s methenamine silver, are indicated if pyogranulomatous inflammation is present to detect fungi. Masson’s trichrome can be used to highlight gastric fibrosis, whereas sirius red and alcian blue help to reveal eosinophils and mast cells, respectively. Immunocytochemistry can be employed to help distinguish lymphoma from severe lymphocytic gastritis. Mucin staining has been performed in Lundchunds with gastric atrophy and showed an abnormal presence of mucus neck cells and pseudo-pyloric metaplasia.
The interpretation of gastric biopsies has important implications for patient care because biopsy findings are often used to guide treatment. For example, moderate lymphoplasmacytic gastritis without Helicobacter spp. infection is often treated with corticosteroids, whereas mild lymphoplasmacytic gastritis may be treated with a change in diet. As the histopathologic evaluation of gastric biopsies has not been standardized, the prudent clinician should carefully review histologic sections to get a feel for the pathologist’s interpretation. Even with optimum evaluation similar histologic changes can be observed in patients with different underlying etiologies, so well-structured treatment trials often form the basis of an etiologic diagnosis.
Treatment of gastritis initially centers on the detection and treatment of underlying metabolic disorders and the removal of drugs, toxins, foreign bodies, parasites, and fungal infections.
Ollulanus tricuspis is a microscopic worm (0.7 to 1 mm long, 0.04 mm wide) that infects the feline stomach. Its predominant cat-to-cat transmisison is through ingestion of vomitus. It can also undergo internal autoinfection with worm burdens reaching up to 11, 000 per stomach. Mucosal abnormalities range from none, to rugal hyperplasia, and nodular (2 to 3 mm) gastritis.
Histologic findings include lymphoplasmacytic infiltrates, lymphoid follicular hyperplasia, fibrosis, and up to 100 / hpf globular leukocytes. Ollulanus spp. are not detected by fecal examination and require evaluation of gastric juice, vomitus, or histologic sections for larvae or worms. Gastric lavage and xylazine-induced emesis have been described to aid diagnosis. Treatment with fenbendazole 10 mg / kg PO SID 2d may be effective.
Physalloptera spp. are about 2 to 6 cm long worms that are sporadically detected in the stomachs of dogs and cats. Physalloptera rara are most commonly described and appear to be primarily a parasite of coyotes. Diagnosis is difficult as worm burden is often low and the eggs are transparent and difficult to see in sugar floatation. Treatment with pyrantel pamoate (5 mg / kg PO:dogs single dose; cats two doses 14 days apart) may be effective. Control of infection may be difficult due to the ingestion of intermediate hosts, such as cockroaches and beedes, and paratenic hosts, such as lizards and hedgehogs.
Given the difficult diagnosis of Ollulanus and Physalloptera spp., empirical therapy with an anthelminthic such as fenbendazole may be warranted in dogs and cats with unexplained gastritis.
Gastric infection with Gnathostoma spp. (cats), Spirocerca spp. (dogs), and Aonchotheca spp. (cats) has been associated with gastric nodules that have been treated by surgical resection of affected gastric tissue.
The presence of transmural thickening of the gastric outflow tract and histology that indicates pyogranulomatous inflammation raise the possibility of infection with fungi such as Pythium insidiosum. Special staining (Gomoris methenamine silver), culture, serology, and PCR of infected tissues can be used to help confirm the diagnosis. Treatment consists of aggressive surgical resection combined with itraconazole (10 mg / kg PO SID) and terbinafine (5 to 10 mg / kg PO SID) for 2 to 3 months post-surgery. ELISA titers of pre- and post-treatment samples may show a marked drop during successful treatment and drugs can be stopped. Medical therapy is continued for another 2 to 3 months if titers remain elevated. The prognosis is poor and fewer than 25% of afflicted animals are cured with medical therapy alone.
The general lack of knowledge of the pathogenicity of gastric Helicobacter spp. has meant that veterinarians are faced with the dilemma of either treating or ignoring spiral bacteria observed in biopsies from patients with chronic vomiting and gastritis. In light of their pathogenicity in man, ferrets, cheetahs, and mice, it would seem prudent that eradication of gastric Helicobacter spp. is attempted prior to initiating treatment with immunosuppressive agents to control gastritis. However, this must be decided on an individual basis. For example, in the patient with a lvmphoplasmacytic infiltrate of the stomach and small intestine with a concomitant gastric Helicobacter spp. infection, should one treat for inflammatory bowel disease, Helicobacter, or both?
The author recommends treating only symptomatic patients that have biopsy-confirmed Helicobacter spp. infection and gastritis. Current treatment protocols are based on those found to be effective in humans infected with Helicobacter pylori. An uncontrolled treatment trial of dogs and cats with gastritis and Helicobacter spp. infection showed that clinical signs in 90% of 63 dogs and cats responded to treatment with a combination of metronidazole, amoxicillin, and famotidine, and that 74% of 19 animals re-endoscoped had no evidence of Helicobacter spp. in gastric biopsies.
Unfortunately these promising results regarding the eradication of Helicobacter spp. have not been borne out by more controlled studies in asymptomatic Helicobacter-infected dogs and cats. Treatment combinations that have been critically evaluated are (1) amoxicillin (20 mg / kg PO BID 14d), metronidazole (20 mg / kg PO BID 14d), and famotidine (0.5 mg / kg PO BID 14d) in dogs; (2) clarithromycin (30 mg PO BID 4d), metronidazole (30 mg PO BID 4d), ranitidine (10 mg PO BID 4d), and bismuth (20 mg PO BID 4d) (CMRB) in H. heilmannii infected cats and (3) azithromycin (30 mg PO SID 4d), tinidazole (100 mg PO SID 4d), ranitidine (20 mg PO SID 4d) and bismuth (40 mg PO SID 4d)(ATRB) in H. heilmannii-infecled cats. Re-evaluation of infection status at 3 days (dogs) or 10 days (cats) after treatment revealed six of eight dogs and 11 of 11 CMRB and four of six ATRB-treated cats to be Helicobacter spp. free on the basis of histology and urease testing (dogs) or C-urea breath test (dogs and cats). However, at 28 days (dogs) or 42 days (cats) after completing antimicrobial therapy, eight of eight dogs and four of eleven cats that received CMRB, five of six cats that received ATRB were found to be re-infected. A transient effect of combination therapy (amoxicillin 20 mg / kg PO TID 2Id, metronidazole 20 mg / kg PO TID 21d, and omeprazole 0.7 mg PO SID 2Id) on bacterial colonization has also been observed in six cats with H. pylori infection.
Further analysis of gastric biopsies from infected dogs and H. pylori infected cats using PCR and Helicobacter-specific primers revealed persistence of Helicobacter DNA in gastric biopsies that appeared negative on histology and urease testing. These studies suggest that antibiotic regimens that are effective against H. pylori in people may only cause transient suppression, rather than eradication, of gastric Helicobacter spp. in dogs and cats.
The author has recendy employed the combination of amoxicillin (20 mg / kg PO BID), clarithromycin (7.5 mg / kg PO BID) and metronidazole (10 mg / kg PO BID) for 14 days to eradicate Helicobacter pylori infection in cats. Further controlled trials of antibiotic therapy in infected dogs and cats, particularly symptomatic patients with gastritis and Helicobacter spp. infection, are clearly required before guidelines regarding the treatment of gastric Helicobacter spp. in dogs and cats can be made.
Chronic Gastritis of Unknown Cause
Lymphocytic plasmacytic gastritis of unknown cause is common in dogs and cats. It may be associated with similar infiltrates in the intestines, particularly in cats (who should also be evaluated for the presence of pancreatic and biliary disease). The cellular infiltrate varies widely in severity and it may be accompanied by mucosal atrophy or fibrosis, and less commonly hyperplasia.
Patients with mild Iymphoplasmacytic gastritis are initially treated with diet. The diet is usually restricted in antigens to which the patient has been previously exposed, such as a lamb-based diet if the patient has previously been fed chicken and beef, or contains hydrolyzed proteins (usually chicken or soy) that may be less allergenic than intact proteins. Many of these diets are also high in carbohydrate and restricted in fat, which facilitates gastric emptying, and may contain other substances such as menhaden fish oil or antioxidants that may alter inflammation.
The test diet is fed exclusively for a period of about 2 weeks while vomiting episodes are recorded. If vomiting is improved a challenge with the original diet is required to confirm a diagnosis of food intolerance. The introduction of a specific dietary component to the test diet, such as beef, is required to confirm dietary sensitivity. If vomiting is unresponsive the patient may be placed on a different diet for another 2 weeks, usually the limit of client tolerance, or started on prednisolone (1 to 2 mg / kg / day PO, tapered to every other day at the lowest dose that maintains remission over 8 to 12 weeks).
Patients with moderate to severe Iymphoplasmacytic gastritis are usually started on a combination of a test diet and prednisolone. If the patient goes into remission they are maintained on the test diet while prednisolone is tapered and potentially discontinued. Antacids and mucosal protectants are added to the therapeutic regimen if ulcers or erosion are detected at endoscopy or if hematemesis or melena is noted.
If gastritis is unresponsive to diet, prednisolone, and antacids, additional immunosuppression may be indicated. Gastric biopsies should be carefully re-evaluated for evidence of lymphoma. In dogs immunosuppression is usually increased with azathioprine (PO 2 mg / kg SID for 5d then EOD, on alternating days with prednisolone). Chlorambucil may be a safer alternative to azathioprine in cats (PO) and has been successfully employed in the management of inflammatory bowel disease and small cell lymphoma. Prokinetic agents such as metoclopramide, cisapride, and erythromycin can be used as an adjunct where delayed gastric emptying is present. These are discussed below.
Diffuse eosinophillic gastritis of undefined etiology is usually approached in a similar fashion to Iymphoplasmacytic gastritis. The presence of eosinphilia, dermatologic changes, and eosinophilic infiltrates may be even more suggestive of dietary sensitivity. In cats it should be determined if it is part of a hypereosinophilic syndrome. Treatment for occult parasites, dietary trials, and immunosuppression can be carried out as described above. Focal eosinophilic granulomas can be associated with parasites or fungal infection that should be excluded prior to immunosuppression with corticosteroids.
Atrophic gastritis in dogs and cats is often associated with a marked cellular infiltrate. In people atrophy is associated with Helicobacter spp. infection and inflammation, and immune-mediated destruction. Gastric disease is often not discovered until the patient presents with pernicious anemia secondary to cobalamin deficiency caused by a lack of gastric intrinsic factor. In people, atrophic gastritis, intestinal metaplasia of the gastric mucosa, and hypochlorhydia are thought to precede the development of gastric cancer. The host inflammatory response is also thought to contribute to the development of atrophy and pro-inflammatory IL-1β and IL-10 gene polymorphisms in people are associated with increased inflammation, gastric atrophy, hypochlorhydria, and gastric cancer.
Atrophic gastritis has been infrequently described in dogs and cats but does share some similarities with people. Atrophy has been associated with gastric adenocarcinoma in Lundehunds and in dogs with Iymphoplasmacytic gastritis of undetermined cause atrophy correlates with the expression of mRNA for IL-1 B and IL-10 and the presence of neutrophils. However, there is no clear evidence that Iymphoplasmacytic gastritis progresses to atrophy and gastric cancer in dogs or cats, and the role of Helicobacter spp. or antigastric antibodies in the development of atrophy in dogs and cats remains to be determined.
In contrast to humans, dogs and cats with atrophic gastritis have not been reported to develop cobalamin deficiency. This is probably because the pancreas, rather than the stomach, is the main source of intrinsic factor in these species. Achlorhydria has been described in dogs and may enable the proliferation of bacteria in the stomach and upper small intestine, although this has not been proven. The treatment of atrophic gastritis has received limited attention, but Helkobacter spp. eradication and immunosuppression have been effective in people.
Hypertrophy in the fundic mucosa is uncommon and is often part ol the breed-specific gastropathies or gastroenteropathies mentioned above. Concurrent hypergastrinemia should prompt consideration of underlying hepatic or renal disease, achlorhydria, or gastrin-producing tumors, which should be pursued appropriately. Basenji gastoenteropathy is variably associated with fasting hypergastrinemia and exaggerated secretin stimulated gastrin, and anecdotal reports suggest that affected basenjis may respond to antimicrobial therapy. Antral hypertrophy of brachycephalic dogs causes outflow obstruction and is treated with surgery.