Gastritis

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Gastritis and Peptic Ulcer Diseases in Dogs: A Review
Article in International Journal of Current Microbiology and Applied Sciences · March 2018
DOI: 10.20546/ijcmas.2018.703.288
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Int.J.Curr.Microbiol.App.Sci (2018) 7(3): 2475-2501
International Journal of Current Microbiology and Applied Sciences

ISSN: 2319-7706 Volume 7 Number 03 (2018)
Journal homepage: http://www.ijcmas.com
Review Article https://doi.org/10.20546/ijcmas.2018.703.288
Gastritis and Peptic Ulcer Diseases in Dogs: A Review
Pankaj Kumar Patel1, Sawita Kumari Patel2, S.K. Dixit1* and R.S. Rathore2
1
Division of Medicine, 2Division of Veterinary Public Health, ICAR-Indian Veterinary
Research Institute, Izatnagar, UP-243122, India
*Corresponding author
ABSTRACT
The most common clinical condition reported in dogs is acid related diseases in the
Keywords stomach like gastric disorders due to a structural and functional defect in gastric mucosa.
The most important factor for the development of gastritis, peptic ulcer disease and gastric
Antioxidant therapy,
Gastric mucosa,
cancer in human is Helicobacter pylori. In the cases of gastric disorder lesions in canine
Helicobacter pylori, gastric mucosa is closely similar to their human counterparts. Many etiological factors are
Oxidative stress, Triple responsible for oxidative stress due to excessive generation of reactive oxygen species as a
therapy
cause of gastric mucosal damage. The bacteria exist lifelong in the stomach of the
Article Info untreated patient. This article reviews the classification, some possible etiopathogenesis,
diagnosis and possible differential diagnosis and major strategies of therapy against acid
Accepted:
disorders (Fluid therapy, proton pump inhibitors, H-2 blocker, cytoprotective) with an
20 February 2018
Available Online: update on the management of oxidative stress with antioxidant therapy (Ascorbic acid, N-
10 March 2018 acetyl cysteine, Vitamin E) and “Triple therapy” for management of Helicobacter pylori
induced gastric disorders.
Introduction occasionally coupled with the loss of body

weight, inappetence, and spells of abdominal
Gastric diseases of dogs are usually gastric pain. In most patients the cause is secondary
mucosal inflammation, ulceration, obstruction from the history, such as dietary indiscretion;
or neoplasia. Gastritis is the inflammation of the diagnosis is rarely confirmed by biopsy,
gastric mucosa and normally visualized by and treatment is symptomatic and supportive.
vomiting. Categorization and gradation of If the hyperplastic polyp (Gencosmanoglu et
canine gastritis are based on the nature of the al., 2003) or foreign body (Papazoglou et al.,
predominant cellular infiltrate and the 2003) obstructs the pyloric region of stomach
presence of architectural abnormalities (Day results onset of acute clinical signs, however
et al., 2008). Acute gastritis is clinically if foreign object stays on the body of the
characterized by the sudden onset of vomiting stomach may lead to mucosal injury and acute
(Ettinger and Feldman, 2005) whereas gastritis (Amorim et al., 2016). Fungal
chronic gastritis is clinically defined as infections and spirochetes also lead to
intermittent vomiting with duration of more gastritis (Helman et al., 1999). Chronic
than 1-2 weeks (Day et al., 2008). It gastritis is defined as the presence of
2475
intermittent vomiting for more than 1-2 weeks and 26-48 percent of dogs are
(Dowdle et al., 2003). asymptomatically affected (Wiinberg et al.,
2005). Although there is a high prevalence of
The peptic ulcer is the imperfection in the gastritis in dogs, an underlying cause is rarely
mucosal barrier that continues to the identified. In Madras veterinary college
muscularis mucosa of the stomach (Stanton teaching hospital (two semesters), out of the
and Bright, 1989). The most common clinical total reported canine patients, 16.8 % dogs
symptoms are sudden onset of acute vomiting were suffering from gastrointestinal disorders
with or without blood, dehydration, anorexia, and 0.19 % was reported from duodenal
weight loss and depression. Peptic ulcer most ulcers (Saravanan et al., 2012). In Mekelle
commonly leads to the condition of GI veterinary clinic Ethiopia, out of the total 109
hemorrhage. reported canine patients, 36 (33.0%) were
suffered from gastrointestinal tract disorders
In dogs, non-steroidal anti-inflammatory and 15 (41.7%) dogs have been shown
drugs (NSAIDs), hepatic and renal disease are vomiting (Atsbaha et al., 2014). It is the
the most common predisposing factor for the condition which can be diagnosed on the basis
formation of peptic ulceration that leads to of clinical signs, laboratory findings, and
anorexia, haematemesis, melena, dehydration, results of imaging techniques such as
anaemia and abdominal pain. Chronic ulcers radiography, ultrasonography, and endoscopy.
have varying size and are larger than normal The most important diagnostic technique for
(Brown et al., 2007). gastritis is the endoscopic examination. In the
case of gastritis mostly Helicobacter Spp.
Chronic gastric ulcers and local ulcerative organisms are isolated from gastric mucosal
neoplastic lesions are macroscopically biopsies of dogs (Wiinberg et al., 2005).
relatively similar; they can be differentiated Endoscopic reports show that the chances of
through histopathological examination formation of gastric mucosa ulcer are 48.5
(Stanton and Bright, 1989). Based on percent in canines (Parrah et al., 2013).
histological examination (relative control of
the reparative processes and the severity of Classification of gastritis
ulceration), the gastric ulcers are classified as
acute or chronic. Gastritis in dogs classified into acute or
chronic which caused by multiple etiological
Microscopically, subacute to chronic ulcers agencies such as dietary carelessness,
have granulation tissue of uneven thickness ingestion of coarse foreign bodies, plant
and ripeness, infiltrated by a mixed materials, irritant chemicals, drugs (NSAIDs,
inflammatory cell population and covered by glucocorticoids), viral diseases (e.g. canine
a thin layer of necrotic debris at the bottom parvovirus, canine distemper) and bacterial
and boundaries along with superficial infections e.g. Helicobacter spp.). Metabolic
regenerative epithelial hyperplasia (Brown et disorders frequently present with
al., 2007). haematemesis, melena, concurrent diarrhoea
and other signs of systemic illness. Acute
Review of literature gastritis is the inflammation of the mucosal
layer of the stomach which is characterised by
Incidences sudden onset of vomiting and suspected to be
related to gastric mucosal injury or
Gastric disorders are common finding which inflammation (Amorim et al., 2016). Only
35 percent cases look into chronic vomiting some reports showed the role of an infectious
2476
agent in acute gastritis (Brown et al., 2007; (eosinophilic gastroenteritis). Diffuse form of
Simpson, 2013). Chronic gastritis classify EG has Scirrhous inflammatory thickening on
based on nature of the leading cellular the gastric wall that resembles with gastric
infiltrates (eosinophilic, lymphoplasmacytic, neoplasia (Hayden and Fleischman, 1977;
granulomatous or lymphoid follicular), the Neiger, 2008; Lidbury et al., 2009). Genetic
presence of architectural abnormalities predisposition and diet are noticed for
(atrophy, hypertrophy, fibrosis, oedema, pathogenesis (Sattasathuchana and Steiner,
ulceration or metaplasia), severity (mild, 2014) but some factors like gastric parasitic
moderate or severe) (Wilcock, 2013). It can infestation by Physaloptera spp. (Neiger,
also be subclassified on the basis of distinct 2008), Gnathostoma spp. (McCarthy et al.,
histological classification, Chronic superficial 2000), Heterobilharzia americana (Rodriguez
gastritis (CSG) is the most common form of et al., 2014) and mastocytoma along with
chronic gastritis that no have understandable infiltration of eosinophils (Ozaki et al., 2002),
changes in mucosal thickening always lesions are rarely observed in Toxocara canis
associated with excessive but uneven infestation (Chira et al., 2005). Focal type
inflammatory components (Plasma cells, chronic hypertrophy occurs as a result of
neutrophils, lymphocytes) infiltrate and chronic administration of Aspirin. Focal
fibrosis of mucosa and submucosa. Clinical cystic hypertrophic gastropathy is
importance of chronic atrophic gastritis characterised by histopathologically elongated
(CAG) has occasionally reported (Simpson, and complexed mucous glands with the
2013) which is characterised by diffuse recurrent formation of the mucosal cyst.
lesions in fundus and body of the stomach and Hypertrophic glandular gastritis is frequently
reduced mucosal layer thickening as well as associated with a diffused immune
hypochlorhydria, achlorhydria and proliferative enteropathy on basenji dogs and
proportionally increased of the number of this condition also occurs in many dogs due to
mucus-producing cells within the gland Hypergastrinemia (Breitschwerdt, 1992).
(Wilcock, 2013). Chronic Giant hypertrophic gastritis (GHG) is
rarely found in dogs and characterized by
Loss of gastric glands due to atrophy of the marked thickening on the gastric wall and
gastric mucosa and combines with mucosal hypertrophy gives a cerebriform look
mononuclear infiltration, glandular atrophy, to the rugal folds which protrude into the
regenerative glandular nesting and mucosal gastric lumen (Vaughn et al., 2014). Chronic
fibrosis and loss of feedback mechanism leads hypertrophic pyloric hypertrophy is
increased serum gastrin level causes gastric hypertrophy of mucosal layer of the antro-
ulceration (Ditchfield et al., 1960; Rugge et pyloric stomach. Lesions are focal/multifocal,
al., 2002; Amorim et al., 2016). polyploidy thickening / regionally generalised
Lymphoplasmacytic gastritis (LPG) with or rugal enlargement and these lesions are lead
without coupled with hyperplasia of lymphoid to gastric outlet obstruction (Elwood et al.,
follicles, infiltration of lymphocytes and other 2010).
inflammatory cells, including Russell bodies
into the lamina propria layer of the stomach Patho-physiology of gastritis and peptic
and sometimes it may be associated with ulcer disease
Helicobacter spp. infection (Maxie, 2007;
Amorim et al., 2016). Eosinophilic gastritis The gastric mucosal layer acts as a useful
(EG) rarely reported by widespread protective wall against acidity, bacteria,
Alimentary tract hypersensitivity reaction detergents and alteration in luminal
2477
temperature. The first line of defence of includes gastric mucosal damage by physical
gastric wall is gastric secretion which agent, alterations in the chemical structure
contains acid, mucus, bicarbonate and and its renovate process (Parrah et al., 2013).
antibacterial substances. Epithelial layer on Mechanical scratch ulceration is generally
the wall of the gastric glands and gastric superficial and short-lived and superficial
mucosal layer prevents from reverse-diffusion lamina propria covered by fibrin, mucus and
of acids and is rapidly repaired by restoration scattered neutrophils (Wilcock, 2013).
after injury. The quick response showed Secretion of hydrochloric acid that creates
through gastric mucosa against stimulation of acidity catalyzes pepsinogen to the active
neurohormonal and inflammatory signals to proteolytic enzyme pepsin (Chu and Schubert,
the gastric microvasculature by increasing 2012). Hamper integrity and protective
blood supply for maintenance of gastric mechanism disturbance in mucosal layer
mucosal integrity, removal of harmful initially, increase rate of reverse diffusion of
substances, and restoration of the gastric gastric acid and pepsin lead to GI
epithelial layer (Abdel-Salam et al., 2001; inflammation and haemorrhages than
Kawano and Tsuji, 2000). Stimulation to the inflammatory components (e.g. endothelial
gastric wall by foreign materials, chemical cells, neutrophils and mast cells) become
injury, ischemia, infection, or antigens leads activated and release inflammatory mediators
to release of inflammatory components and (e.g. histamine, leukotrienes, platelet-
vasoactive substances from neutrophils, mast activating factor, proteolytic enzymes, and
cells, platelets, endothelial cells and neurons free radicals) (Henderson and Webster, 2006).
(Wallace and Ma, 2001). Several pro- Histamine promotes gastric acid secretion;
inflammatory cytokines are released as a whereas another mediator promotes vascular
response to the pathogenesis of peptic ulcer, changes (e.g. vasodilation, vasoconstriction,
like interleukin (IL)- Ib, IL-2, IL-6, IL-8 and increased capillary permeability) lead to
tumour necrosis factor (TNF)-α. IL-I, lead to oedema and translocation of inflammatory
reduce the severity of the gastroduodenal cells that plugged the capillary lumen,
injury and increase the resistance to gastric intensify initial gastric mucosal injury by
injury (Wallace et al., 1990). These dropping blood flow, ischemia, disturbed
inflammatory components stimulate acid epithelial cell layer restoration, and reduced
secretion and mucosal breakage increases the secretion of mucus and PG-E (Sorjonen et al.,
permeability of epithelial layer and altered 1983; Guilford et al., 1996). Gastric ulcers
blood flow that continues increase the risk of also have been reported in dogs, having
gastritis, gastric erosion, ulceration, hypoxia, hepatic disease, renal disease, Addison's
haemorrhage, oedema and necrosis (Jacobson, disease; shock (Parrah et al., 2013). Dogs
1992). Granuloma formation of gastric having the severe head injury, numerous
mucosa is the end result of a response to trauma, cerebral injuries and diseases of
endogenous substances and foreign objects, spinal cord leads to Gastroduodenal ulceration
such as sewing needles and infectious (Neiger and Simpson, 2000; Dowdle et al.,
diseases (Pratt et al., 2014). Transient 2003).
ulceration commonly noticed due to direct
damage of gastric wall and mucosal barrier or Etiopathogenesis of gastritis and peptic
generally ingestion of a wide range of foreign ulcer diseases
materials like coarse foods, chemicals, plants
materials, clothes etc. Gastric ulceration is Gastric foreign bodies are the most common
caused by the multi-etiological agent that cause of gastric disorders in younger dogs
2478
(Sullivan and Yool, 1998). Ingestion of are also reported as cause of gastric ulceration
exogenous toxins like a household, cleaning (Gralnek et al., 2008). Some drug has been
chemical, lead and various plants may directly damaged in the gastric mucosal layer of dogs
harm to the gastric mucosal barrier (Sass, includes glucocorticoids (Valin and Allard,
1970). In three dogs experimentally 2012) and various NSAIDs (Mathews et al.,
administration of phenol (total dose of 2430 1996). Selective inhibitors of Cyclooxygenase
mg of phenol) leads severe oral and gastric (COX)-2 (e.g. carprofen, etodolac, deracoxib,
ulceration (Gieger et al., 2000). When orally meloxicam) are used to reducing the
lead salt mixture (Chloride Br, Sulfate, 1:1:2) ulcerogenic consequence of NSAIDs in the
give orally in nine dogs at diverse doses GI tract. Even if they reduce the hazard but
(range 5-60 mg/kg body weight/day) for 14- they do not fully remove it and in many dogs
152 days gastric ulceration is induced (Hamir have reported that formation of gastric
et al.,1983). Systemic hypovolemia leads to ulceration subsequently the given of these
decrease blood flow to gastric mucosal layer, safer NSAIDs (Enberg et al., 2006). The
there is the loss of the tolerable effects of NSAIDs inhibits the enzyme COX which is
glucocorticoids in mucosal defense involved in the prostaglandin synthesis, and
mechanism and major electrolyte inhibit the synthesis of prostacyclin and
abnormalities are leads to gastritis (Henderson prostaglandin E, resulting in the loss of the
and Webster, 2006). Dogs with kidney failure gastric protective mechanism (Enberg et al.,
have infrequently shown gastric necrosis and 2006). If any change on the expression of
ulceration (Peters et al., 2005). Gastric ulcers GKN gene leads to the deficiency of GKN1 &
due to stress less commonly noticed in dogs, GKN2, results have been reported as gastric
regular and severe exercise have a higher risk inflammation, non-steroidal anti-
for occurrence of gastric ulcers in dogs and inflammatory (NSAID) induced mucosal
during sled races mostly gastric disease has injury and the development of neoplasia of
known as a causative factor of sudden death gastric mucosa (Martin et al., 2008; Nardone
in the dog (Chatelain et al., 2014). The diet et al., 2008). Another factor concerned with
containing a high amount of fat causes the pathogenesis of NSAID-induced gastric
delayed gastric emptying and hyperacidity in disorder is peroxidation of lipids of cell
the stomach, which in alone or associated membranes and damage to the cellular
with the physiological reaction of stress proteins by the formation of oxidative free
(increasing the level of serum cortisol level), radicals and proteases from activated
may influence to GI ulceration in animals neutrophils (Biswas et al., 2003). NSAIDs
(Davis et al., 2003). acts on mitochondria and uncoupling effect
on oxidative phosphorylation, disperse the
The aspirin-induced gastric disorders mitochondrial transmembrane potential and
maximally reported in antropyloric area induce mitochondrial permeability transition
administrated dogs (Reimer et al., 1999; pore (Yoshida et al., 1992; Tomoda et al.,
Ulutas et al., 2006). Administrations of a 1994; Mahmud et al., 1996; Mingatto et al.,
diversity of NSAID drugs piroxicam 2000; Davies et al., 2000; Ulutas et al., 2006)
including, aspirin, ibuprofen (Godshalk et al., leading to the release of cytochrome c from
1992; Lanza et al., 2009) naproxen and mitochondrial intermembranous space into
flunixin meglumine or ibuprofen (Godshalk et cytosol. liberated cytochrome c generates
al., 1992; Dow et al., 1990), steroidal anti- reactive oxygen species (ROS) like hydrogen
inflammatory drugs used for treatment of peroxide, thus activation of caspase 9 and
spinal and vertebral diseases (Neiger, 2000) caspase 3 pathway and peroxidation of
2479
cellular lipid membrane all resulting into al., 2011). Gastrin directly stimulates to
cellular apoptosis (Murphy et al., 2000). hydrochloric acid secretion from the parietal
cells, as well as indirectly stimulating acid
Corticosteroid predisposes the GI tract to production by releasing histamine from fundic
damage by diminishing mucus production, enterochromaffin-like cells in response to
changing the biochemical composition of compromising the protective mechanisms and
mucus, declining restoration of epithelial cell reducing the epithelial cell turnover of the
layer and intensifying acid production gastric mucosa (Hughes, 2006). Gross and
(Sorjonen et al., 1983). It has been reported histological appearances of gastric erosions
that administration of prednisolone after 1 or and ulcers are well documented, erosions
2 weeks of peptic ulcer formation leads to involve only surface epithelium with a
decreased collagen-containing tissue in the minimal inflammatory response but ulcers can
ulcer base and delayed healing (Luo et al., extend into the muscularis mucosae (Sullivan
2004). Dexamethasone has been shown and Yool, 1998).The chronic liver disease
inhibitory effects of angiogenesis at the ulcer leads to ischemia in GI mucosa that causes
margins and baseline. Administration of portal hypertension and thrombus formation
corticosteroids along with NSAIDs leads to into the gastric vessels (Stanton and Bright,
the formation of gastric mucosal lesions 1989). The renal system has been involved in
(Boston et al., 2003). Some studies had been the elimination of at least 40 % circulating
shown that support the theory that Gastrin-17, with up to 40 percent of
corticosteroids alone lead to GI mucosal circulating Gastrin-17. Hence, in renal disease
injury and hemorrhage (Rohrer et al., 1999). hampered to clearance of Gastrin-17 lead to
hypergastrinemia which induced gastric acid
The hepatic disease leads to portal production. It is the principal factor for
hypertension which causes distorted gastric vomiting and pathogenesis of gastric ulcer
blood flow, delayed epithelial turnover, formation in renal disease (Schulman and
gastric hyperacidity, and elevated serum bile Krawiec, 2000; Peters et al., 2005). Renal
acid concentration stimulate to secretion of failure leading to progressive uremia and urea
Gastrin-17, results in apoptosis of gastric diffuses from interstitial fluids to stomach,
epithelial cells (Henderson and Webster, results in damage to epithelial cell layer of
2006). Animals with mastocytosis may have gastric wall (Polzin and Osborne, 1995;
numerous all over gastric ulcers (Stanton and Guilford and Strombeck, 1996).
Bright, 1989; Ozaki et al., 2002). The mast
cell tumor produces and releases histamine, The chief gastric pathogenic Helicobacter
which binds to H2 receptors on gastric spp. in dogs are H. felis, H.bizzozeronii and
parietal cells, gives a powerful stimulant to H. heilmanniisensustricto (s.s.), while H.
acid secretion. In humans, peptic ulcer salomonis is least reported and the prevalence
formation as a result of excessive gastrin of H. cynogastricus and H. baculiformis has
production and hyperacidity caused by a not yet been studied (Amorim et al., 2016).
gastrinoma is known as the Zollinger Ellison However, H. pylori have been rarely
syndrome. This is a condition often identified in the canine stomach (Chung et al.,
characterized by the triad of 2014). There is also evidence of mixed
hypergastrinemia, hypertrophic or CAG and infections of different species (Ekman et al.,
GI ulceration. Few cases of a canine homolog 2013). Helicobacter spp. populations are
of Zollinger Ellison syndrome associated with mostly found in the fundus and body of the
gastric ulcer formation are reported (Gal et stomach (Anacleto et al., 2011). Gastrokines
2480
(GKNs) are bioactive molecules that contain the gastric mucosal barrier than severe mixed
BRICHOS domain and secreted from a inflammatory/neoplastic-like reaction and
specific cell of gastric mucosa (Menheniott et forms nodular foci, these are generally known
al., 2013). GKN1 connected with decreasing as granulomas (van der Merwe et al., 2008).
the formation of colonies and proliferation by The initial stage of inflammation, larvae
an atypical glandular cell of gastric mucosa encircled by loose connective tissue that are
and reducing of cellular viability, extremely vascularised and containing fibrin-
proliferation, and colony (Yoon et al., 2013). rich fluid, neutrophils, and foci of necrosis.
GKNs and trefoil factors (TFFs) both are Later stage, these connective tissues are
together lead to enhance cellular composed mostly of actively dividing
differentiation, cytoprotective role and fibroblasts which like embryonic appearance,
working on NF-κβ signalling pathways that sometimes similar to sarcoma (Bailey, 1963).
result anti-inflammatory effects, therefore it In Gnathostoma spinigerum infestation, adult
promotes restoration of gastric epithelial cells parasite formed solid nodules in the gastric
(Rippa et al., 2011). If any change on the submucosa and they stick out into the lumen
expression of GKN gene cause deficiency of and parasite eggs trapped by connective tissue
GKN1 & GKN2, results from gastric lead to the formation of center portion
inflammation, non-steroidal anti- granuloma (Maleewong et al., 1992). The
inflammatory (NSAID) induced mucosal Hetero bilharzia mericanais trematode
injury and the development of neoplasia of parasite leads to gastric granulomatous
gastric mucosa (Martin et al., 2008; Nardone inflammation with circumscribing trapped
et al., 2008). eggs (Rodriguez et al., 2014). Gastric
nematode infestation by Ollulanus tricuspis,
Gastric disease caused by H. pylori suppress which was commonly observed in cats
to GKNs gene expression by methylation of (Cecchi et al., 2006) also has been reported in
trefoil factor 2 (Peterson et al., 2010), lead to dogs with the sign of chronic vomiting and
Gkn1 and Gkn2 deficiency (Menheniott et al., granulomatous gastritis (Kato et al., 2015).
2013). Progressive loss of expression GKN Nematodes, Physaloptera rara, and
gene lead to progression of different phases of Physaloptera canis, an uncommon source of
disease development, started from chronic gastric ulceration related to chronic vomiting
gastritis to gastric mucosal atrophy followed (Burrows, 1983). These parasites are free
by a neoplasm of intestine due to complete moving in lumen cause a minimal
loss of GKN gene expression (Sharman et al., inflammatory reaction, but mostly they
2017; Menheniott et al., 2013). Electron attached with the gastric mucosa lead to
microscopic examination of gastric mucosa inflammation due to the formation of
showed spiral-shaped organisms in the lumen numerous minute hemorrhages (Clark, 1990).
of stomach and canaliculi of parietal cells Gastric phycomycosis characterized by
(Lee et al., 1992). Pathogenic viral infections minute non-specific changes to thickening
in dogs include parvovirus; distemper virus, mucosal folds of gastric wall with outlet
rotavirus, and coronavirus rarely causes hindrance. Granulomatous lesions have
gastritis with intestinal or systemic typical nodular, circumscribed collections of
involvement being most responsible for macrophages along with uneven lymphocytes,
patient morbidity and mortality. eosinophils, multinucleated giant cells, and
neutrophils, with or without central necrosis
Parasitic infestation is least commonly and a peripheral lymphoid cuff (Ectors et al.,
reported. The larvae of Spirocerca lupi pierce 1993). Histoplasmosis caused by the fungus
2481
Histoplasma capsulatum infected by spores (Halliwell, 1990). In acute events of

via inhalation or ingestion route. These spores inflammation free radicals may play a major
are phagocytized by macrophages and role in gastric mucosal barrier dysfunction. In
dispersed through the bloodstream or humans oxidative stress occurs during
lymphatic channel to the organ systems and exercise leads to decrease gastric and
formation of subclinical or clinical mesenteric blood flow (Qamar et al., 1987;
granulomatous condition amongst other Mastaloudis et al., 1994; Hinchcliff et al.,
organs including the GI tract (LinBlache et 2000; Otte et al., 2001; Radak et al., 2003)
al., 2011). In young aged, large-breed, male along with mitochondrial electron transport
dogs Pythiuminsidiosum may produce chain inefficiency during respiration leading
pyogenic granulomas in mucosa and reperfusion injury mediated by ROS. In the
submucosa of stomach and different places of disease condition, exercise has been activated
the GI tract (Grooters and Gee, 2002). to pro-inflammatory cascades which are able
Cryptococcus neoformans cause to trigger the leukocytes (Cooper et al., 2007).
granulomatous gastritis mimicking carcinoma
which is a factor of gastric outlet obstruction Exercise leads to neuroendocrine changes,
(Van der Gaag et al., 1991). like increases release of growth hormone may
also play a major role in the trigger to the
Different cellular defense mechanisms neutrophils (Smith et al., 1996). Neutrophil
involve for protection against the free radical penetrates into inflammatory sites and then
damage (Lewin et al., 1997). Enzymes (e.g. release superoxide anions generated by
catalase, glutathione peroxidase complex and myeloperoxidase and NADPH oxidase
superoxide dismutase) and transition-metal activities. By the help of superoxide
binding proteins (e.g. transferrin, ferritin, and dismutase activity and highly reactive
ceruloplasmin) production and action of free hydroxyl radical catalyzed by oxido-reductive
radicals. Scavengers (e.g. albumin, bilirubin, active metal ion converts Superoxide to
ascorbic acid, urates, and thiols, or hydrogen peroxide. In rats experimentally
liposoluble, such as vitamin E and coenzyme feeding of Lipid peroxides lead to change the
Q10) stop and discontinue radical chain by oxido-reductive mechanism status in gastric
increase peroxidation chain of lipid molecules mucosal cells and can suppress apoptosis and
by a react and neutralize free radicals and turnover of epithelial cells (Tsunada et al.,
convert them into more stable molecules. The 2003). Lipid peroxidation mediated by
peroxidized fatty acids are removed by reactive oxygen species (ROS) is considered
specific phospholipases, making possible the as an important cause of oxidative damage
re-acylation of the damaged molecule by an and destruction to the cell membrane,
acetyl-CoA and the respective enzyme lead changing the structural integrity and
reconstitution of normal structures. The biochemical functions of the lipid membrane
overproduction of ROS leads to the imbalance (Fridovich et al., 1978; Niki et al., 1987).
between oxidants and antioxidants at cellular Plasma MDA concentration denotes tissue
as well as systemic level. Reactive oxygen lipid peroxidation marker (Galunska et al.,
species (ROS) are major molecules of 2002). Gastrointestinal mucosa detoxifies to
oxidative stress in exceeds the threshold level the dietary lipid peroxides (Miyamoto et al.,
which is generated as primary part of 2003) and antioxidant systems may be
metabolism that lead to trigger progressive relatively exhausted by the peroxide intake,
destruction of polyunsaturated fatty acids consequently changing the cellular redox
(PUFA) and membrane destruction mechanism. In peripheral tissue, glutathione
2482
peroxidize (GSH) acts as an electron donor in by the animals is rarely reported (Cortese et
the glutathione peroxidase-catalyzed al., 2010). Gastrointestinal lymphosarcoma
reduction of organic and hydrogen peroxides. induced gastric ulceration produces anorexia,
Therefore, the oxidized glutathione formed vomiting, diarrhoea, progressive loss of body
through this reaction removed from the cell weight, dullness and depression. In NSAIDs
using NADPH-dependent reduction induced ulceration has these similar signs
mechanism by glutathione reductase (Meister with melena and paleness of the tongue has
et al., 1983; Ehrhart et al., 2003). been observed (Shaw et al., 1997).
Diagnosis Laboratory findings
History and clinical signs In gastric ulcer disease laboratory findings

indicated that clinical abnormalities are how
Gastritis and Peptic Ulcer disease are not much severe (anemia or septic abdominal
depending on breed, age or sex. The disease fluid sample) and prediction of stimulating
depends upon history of non-steroidal anti- cause e.g. (renal failure). The main findings
inflammatory drug (NSAIDs) administration, of piroxicam induced gastric ulceration are
ingestion of foreign materials, chemicals, neutrophilic leucocytosis while the. Phenol
poisons, coarse food materials and any other poisoning induced gastric ulceration has
systemic disease like hepatic disease, renal abnormal hematological changes like
disease, tumour, pregnancy gastric or neutropenia with toxic neutrophils,
secondary metastases vomiting frequency and thrombocytopenia and increased muscular
contents of vomitus like bile, food, froth, enzymes (Talbert et al., 2012). The important
blood (frank or digested) or evidence of an hormone for the maintenance of normal
ingested substance (e.g. grass, bones, foreign gastric homeostasis is Gastrin-17 (Fourmy et
material, etc).The most common clinical sign al., 2011) secreted by G cells of gastric
of gastric ulcer is acute or chronic vomiting antrum which acts with acetylcholine into
with or without hematemesis. All animals receptors of enterochromaffin cells, results in
have gastric ulcer should be vomit, but all releases of histamine. The secreted histamine
animals those are vomit blood should not binds to receptors on the surface of the
have gastric ulcers (Otto et al., 1991). The parietal cell produces c-AMP whereas
most common clinical sign in gastric disease Gastrin-17 and acetylcholine open calcium
of animals are underweight, pale mucous channel leads to stimulating effects on gastric
membrane, tachycardia from severe anaemia acid secretion from the apical H+–K+ ATPase
or shock, pain on palpation may be observed (Guarsio et al., 2009). Serum gastrin-17 has
if there is widespread of perforated ulcer and become an important biomarker for gastric
spread of contamination into the peritoneum, antrum inflammation (Fourmy et al., 2011).
vomiting, haemoptysis, melena, weight loss, The PGI and PGII are secreted into the gastric
anaemia, abdominal pain, inappetence or lumen and out of the 1 % leaked into
anorexia, oedema, septicaemia, liver disease, circulations (Griti et al., 2000). The
renal diseases, neurologic diseases. Gastric Pepsinogen I (PGI) value proportionally
and duodenal perforated ulcers show sign of decreases with the development of fundic
extensive pain of abdomen, abdominal atrophy while Pepsinogen II (PGII) has not
distension, high fever, shock and death caused shown any pattern with fundic or antral
by peritonitis. Only mild signs of abdominal atrophy (Griti et al., 2000). However, the
disease with perforated ulcers have presented decline in value of PGI to PGII ratio
2483
(PGI/PGII) has been revealed for detection of Helicobacters organisms produce urease
fundic atrophy and diagnostic biomarkers for enzyme in gastric mucosa which hydrolyzes
atrophic gastritis and patients with high risk urea to ammonia, results increase ammonia
of gastric cancer (Vaanenen et al., 2003; concentration in the gastric mucosal layer
Graham et al., 2006). The gastric diseases, leads to raises gastric pH in which bacterial
second-degree dehydration, and the sign of populations were survived (Marshall et al.,
shock have been detected by skin fold test and 1990). Rapid urea test (RUT) and modified
relative polycythemia. It must be required rapid urease (MRU) test are used for
emergency treatment with different determination of Helicobacter infection of
haematological test e.g. complete blood count gastric mucosa in gastric biopsy samples
(Total erythrocyte Count, Total leucocyte (Katelaris et al., 1992). These organisms also
Count, Total platelet count, Haemoglobin confirmed by phase microscopic examination.
concentration, Packed cell volume), Blood Oxidative stress measurement is difficult to
urea nitrogen [BUN], Serum creatinine level, perform directly because unpaired electron
Blood glucose level, AST (aspartate makes free radical very unstable and high
aminotransferase), Alanine aminotransferase reactive (hence, short half-life) thus, their
(ALT), Alkaline phosphatase (ALP) level measurement needs specific tools like,
and, if available, lactate, pH, and electrolytes electron spin resonance that can identify
levels also measured. ALT, AST, ALP and compounds with unpaired electrons. In
BUN, Serum creatinine level are the biological samples products of ROS, reactions
biochemical marker of hepatic disease and are easier to measurable through biological
renal diseases which also leads to GI assays e.g. measure the DNA adduct 8-
ulceration. hydroxy-2‟- deoxyguanosine, protein
carbonylation, and many lipid breakdown
Serum Gastrin-17 is the most important products. Sthiobarbituric acid reactive
biomarker for gastric antrum inflammation substances (TBARS), Malondialdehyde, 4-
(Fourmy et al., 2011). The reference range of hydroxy-2-nonenal, Isoprostane, Ethane,
serum Gastrin-17 concentration is 10–40 ng/L Pentane, and Lipid hydroperoxides are the
(Garcia et al., 2005; Parente et al., 2014). The most Common measurable lipid products.
serum gastrin concentration has been Antioxidants enzymes activity Catalase
markedly increased in severe gastric disorders (CAT) activity (Aebi, 1984) has been
(Garcia et al., 2005). Serological biopsy has determined (U/g Hb) after isolation and lysis
been reported that serum PG level shows to of RBCs and glutathione peroxidase (GPx)
the morphologic and functional alteration to activity were measured (mU/mg Hb) on
the gastric environment (Taggart and Samloff, whole blood. Healthy dogs have a good
1987). Serum pepsinogen A level (18 to 129 defense system against oxidative stress that
µg/L) can be used as a diagnostic marker for compensated by balanced redox mechanism
gastric diseases in the dog (Suchodolski et al., by revert the overproduction of free radicals
2002; Suchodolski et al., 2003). and come again to homeostasis. However,
most sick animals unable to show this
Additional clinico pathological tests are mechanism and it will promote the occurrence
required to detect the liver and renal diseases, of an extreme oxidative stress. This
hypoadrenocorticism, hypothyroidism, mechanism is possible by production of the
pancreatitis which may lead to gastric antioxidant agents, which prevents from
mucosal lesions. oxidative stress and lead to regeneration of
cells, taking the reduced glutathione (GSH),
2484
superoxide dismutase (SOD), catalase (CAT) perforation given with IM injection of

and glutathione peroxidase (GPx) enzymes in Pentagastrin, @ 6 micrograms/Kg body
the frontline (Bae et al.,2011; Naito et al., weight leads to elevation of the secretion of
2010). It increases the production of H2O2 in gastric juice (hyperacidity).The extent of
response to the activity of antioxidant endoscopically detected damage shows a
enzymes CAT and GPx levels are elevated. relationship with sucrose permeability. The
Catalase enzyme activity present in all tissues decrease in the permeability of sucrose is
but higher in RBCs, hepatic, renal, adipose more quickly than gastric ulcer
tissues and lower in nervous tissue converts disappearance. Sucrose permeability test is
hydrogen peroxide (H2O2) to oxygen and more responsive for widespread mucosal
water (Pacheco et al., 2009; Zamocky et al., damage than to distinct common ulceration
2008,). GPx enzyme has been used (Meddings et al., 1995).
glutathione as a substrate along with other
organic hydroperoxides and catalyzes the Diagnostic imaging
H2O2 reduction mechanism (Bae et al., 2011).
The acute stage of GI haemorrhage leads to The plain and contrast radiographs are useful
normocytic normochromic anaemia while for determining possible origin of abdominal
chronic stage of GI haemorrhage leads to disturbances (gastric foreign bodies) but may
microcytic hypochromic anaemia in iron be unsatisfactory in smart verification of
deficiency anaemia (Waldrop et al., 2003). gastric ulceration (Guarino et al., 2008). The
The acute haemorrhagic diarrhoea with ultrasonography used for recognizing foreign
increased haematocrit count and plasma bodies and masses, identification of GI
protein concentration indicates haemorrhagic perforation and used to detect drug-induced
gastroenteritis. The faecal occult blood test gastric mucosal changes and sometimes
should be done in the unclear cases of GI helpful to suggestion for the need of surgery
haemorrhage but it gives false positive results (Boysen et al., 2003). Ultrasonography of the
due to dietary causes (e.g. vegetables, fruits, gastrointestinal tract (GIT) is a valuable
red meat, fish meat) or some bacterial diagnostic imaging technique in animals
population in the alimentary tract so that it (Penninck et al., 1990). The complete
suggests that 72 hour before performing of abdominal ultrasonographic evaluation by 5,
this test meat-free diet fed to the patients. It is 7.5 and/or 10 MHz transducers has been
generally used for coagulation defects that are performed in all age dogs, gastric lesions are
not the primary cause of GI haemorrhage but considered by gastric wall thickening, wall
noticeable intensifying blood loss e.g. layering and contents of gastric lumen. Poor
rodenticide toxicity or clotting factor Gastric motility is also considered if the
deficiencies. The Total Platelet count is a very peristaltic movement of the stomach is one or
useful measure of coagulation defects. In less contraction per minute. Ultrasonography
dogs, immune-mediated thrombocytopenia of gastric ulcer can be suspected by the
(ITP) is the common factor of GI presence of gastric wall thickening associated
haemorrhage. If no any cause of ulceration with a wall defect (crater), gastric fluid
has been found then electrolyte level can be accumulation, reduced motility, and
estimated and ACTH stimulation test should constantly accumulation of microbubbles at
be done because it has been reported that the crater site (Tomooka et al., 1989;
hypo adrenocorticism coupled with GI Smithuis et al., 1989). Ultrasonographic
haemorrhage in dogs (Medinger et al., 1993). findings of the gastric epithelial tumor are
The dogs have gastric ulceration and gastric wall thickening, pseudolayering,
2485
poorly echogenic wall and regional or distant the lumen or inflammatory pain in the
lymphadenopathy (Penninck et al., 1998). esophagus reveals star grazing behavior and
Endoscopy is the most sensitive diagnostic clinical signs that are the regurgitation of
and prognosis of a diversity of gastrointestinal food, excessive salivation, dysphagia,
diseases. Endoscopic examination is frequent tries to swallow, anorexia, and
important for the diagnosis and provides the progressive weight loss (Frank et al., 2012).
perfect diagnosis by direct gastric mucosal The anesthesia-induced gastro-esophageal
visualization, biopsy collection, decided to reflex leads to esophagitis which is the most
prognosis and therapeutic benefits (Shaheen common cause of esophageal pain (Poier et
et al., 2010). For the diagnosis of gastric al., 2014). Omeprazole is used for the
mucosal lesions endoscopic examination can treatment of the stargazing behavior of dogs
be protected, non-invasive, exact and without due to esophagitis because it enhances gastric
risk of dehiscence or peritonitis for evaluation pH (Tolbert et al., 2011). The Bravo pH
of the color and gastric mucosal integrity of monitoring system calculates Gastro-
gastric mucosal layer (Happe et al., 1983; Esophageal reflux, Nuclear scintigraphy,
Grooters et al., 1994). positive contrast esophagogram and
fluoroscopy method (GER) in canines
Differential diagnosis (Tolbert et al., 2011). If the dog is suffering
from obsessive-compulsive disorder, reveals
Ingestion of specific foods (mainly protein) signs of excessive licking to foreign objects
induces immune-mediated response leads to continuously like floor, wall, furnitures, lead
the sudden onset of gastrointestinal symptoms to nauseous sensation and discomforts
due to pruritus of the GIT known as food without GIT disorders (Overall et al., 2002;
allergy in dogs (Webb and Twedt, 2003). In Bonnet et al., 2012) should be treated with
the starting phase of the gastric neoplasm no combination of serotonergic drug with
clinical sign appears, thus it can be diagnosed behavioral therapy (Overall and Dunham,
at later stages in most cases, therefore, the 2002).If the lipolysis mechanism has been
higher mortality rate has been reported disturbed lead to the generation of an
(Tesensuren et al., 2006). The endoscopic excessive amount of ketone bodies which
examination of gastric neoplasm reveals hampers the blood buffer system and
cauliflower shape cell mass in the gastric wall development of acidemia with diabetic
and therapy based on clinical signs has not ketoacidosis (Kerl, 2001). The disturbed
been responded. The biochemical lipolysis mechanism will also lead to GI
examinations reveal elevation of serum disturbances and produce polyurea,
creatinine level, the activity of gastric polydipsia, anorexia, vomiting, progressive
enzymes and serum arginase activity while weight loss, haematuria, pollakiuria, shock
the level of the total protein concentration and death of the dogs is generally due to a
especially albumin level reduces (Meram and severe metabolic acidosis or complications to
Tarakçıoğlu, 2000). The male dogs mostly the vital and visceral organs (Hume et al.,
suspected for gastric carcinoma generally 2006). If the pH is less than 7.10, bicarbonate
originated from pylorus and microscopic and insulin therapy for the treatment of DKA
examination showed diffused penetration of is recommended (Causmaecker et al., 2009).
inadequate differentiated neoplastic cells The most important clinical sign of the
coupled with scirrhous reaction and gives haemorrhagic gastroenteritis is acute onset of
appearance of typical „„signet ring‟‟ cells vomiting, profuse bloody diarrhoea,
(Brown et al., 2007). Due to obstruction of dehydration, and depression. The puppies
2486
having age between six weeks to six months and Sherding, 2005). Reflux of duodenal
are more susceptible, but more severe in an contents (bile, pancreatic juice etc) into the
age of less than six-month young dogs or old stomach can damage the gastric mucosal
dogs (Sutton et al., 2013). In young one GI barrier (Rodriguez et al., 1997). In the drug-
system and Cardiac system are mostly induced ulcerations, NSAIDs and other
affected but only GI system is maximally steroidal drugs should be stopped; if
affected in adult dogs. The parvovirus has medication is necessary for therapy of
been identified with the help of ELISA and specific disease then it will be considered. GI
PCR. In the condition of shock, rapid infusion protectants in combination used for therapy
(over 10-20 minutes) of a bolus of 10- containing H-2 receptor antagonists
20ml/kg BW of lactated Ringers solution (cimetidine, ranitidine, famotidine), proton
should be administered because lactate has pump inhibitors (omeprazole, pantoprazole),
been further converted into bicarbonate in the cytoprotectants (sucralfate) and synthetic
liver. prostaglandins (misoprostol). Cimetidine is
the first H2 receptor antagonist used in dogs
Therapy and it is administered 3-4 times daily dose of
@ 2.5-5 mg/lb body weight for suppressing
Principles of therapy gastric acid secretion (Ephgrave et al., 1987).
Even so, there is only mild to moderate
The Principles of therapy of gastritis and inhibition of acid secretion over a 24 hours
peptic ulcer diseases are following (a) period. The fact that it works clinically for
Withdrawal of food for prevents stimulation ulcer therapy suggests that even partial
of gastric glands. (b) Removal of the suppuration of gastric acid secretion is
etiological factor that is the hepatic failure, beneficial for the healing of most gastro-
hepatic bacterial infection, NSAIDs or duodenal ulcers. In the GI haemorrhage and
corticosteroid therapy.(c) Ulcer healing vomiting in significantly ill dogs, it must be
supported by- i) stabilization of the considered dose and route of drug
cardiovascular system and preserve mucosal administration because oral route can the drug
perfusion by appropriate fluid therapy ii) absorption. Ranitidine @2mg/kg IV q 12 hr
diminishing gastric acidity iii) shielding from has not been shown a major effect on gastric
ulcer by cytoprotective agents (iv) correcting acid suppression (Bersenas et al., 2005).
secondary circumstances (dehydration, Proton pump inhibitors are the most potent
anemia, weight loss).(d) After the stabilized, agents for suppression of gastric acid
the perfusion in the patient than broad- secretion by the inhibition of the gastric
spectrum antibiotics or combination of H+/K+- ATPase enzyme (the proton pump),
antibiotic therapy has been started. which leads to failing the gastric secretion and
rising the intragastric mucosal pH (Miner et
Fluid therapy with gastric mucosal therapy al., 2003; Scott et al., 2002). Mainly clinically
available proton pump inhibitors (PPI) are
Dehydration, relative polycythemia, omeprazole, esomeprazole, lansoprazole,
Hypokalemia, and hyponatremia are rabeprazole, and pantoprazole (Miner et al.,
commonly found in dogs after vomiting and 2003). Omeprazole is the first PPI that used
diarrhoea. Immediate correction of clinically in 1988 at Losec in Europe, and in
hypokalemia with antispasmodics is required 1990 at Prilosec in the United States.
because hypokalemia leads to hindrance in Esomeprazole commonly used with
gastric emptying (Rebar et al., 2001; Bichard omeprazole that is very much effective for
2487
inhibition of gastric acid secretion (Andersson encourage epithelialization of gastric mucosa

et al., 2000). The esomeprazole (40 mg) is (Kuwayama et al., 1991). Sucralfate is a non-
more effective than lansoprazole (30 mg) for absorbable aluminum salt of sucrose
healing erosive esophagitis and heartburn octasulfate compound that used as an optional
condition. For intragastric acid control extra to H2 antagonists for treating peptic
intravenously once-daily dosing with ulcers, because when ulcerative clinical signs
esomeprazole provides faster and more are noticeable It is more effective in NSAID-
prominent healing results than intravenously induced ulceration than other drugs such as
once-daily dosing with pantoprazole (Wilder sucralfate and H2 receptor antagonists, so it is
et al., 2004).In the patients with signs of choice of drug for NSAIDs producing ulcers
GERD esomeprazole presents faster and (Lanza et al., 2009). Acid-reducing drugs are
greater acid control results to longer period work on cellular level metabolism to inhibit
maintain the intragastric mucosal pH than hydrogen ion secretion (e.g. prostaglandins)
lansoprazole, omeprazole, pantoprazole, and (Lanza et al., 2009). Intravenous
rabeprazole (Rohss et al., 2004). Famotidine administration of metoclopramide @1-
@ 0.5mg/kg IV q12hr, omeprazole @1mg/ kg 2mg/kg/24hr act as dopamine- antagonists
orally q24hr) and pantoprazole @ 1mg/kg IV that raise the threshold activity level of
q24hr each have a notable property of the chemoreceptor trigger zone in vomiting center
gastric acid secretion in dogs. Omeprazole and decrease visceral nerve input that
acts as a Proton pump inhibitor that inhibits prevents vomiting (Sawant et al., 2004). If the
the H+-K+ ATPase pump and the production GI ulceration is coupled with the acute
of hydrochloric acid from gastric parietal abdominal pain of unclear etiology, opioid
cells. Omeprazole enhances regulations of analgesics should be administered for
GKNs and produces anti-inflammatory stabilization of GIT motility as well as relieve
effects, gastric homeostasis and tumor pain suffering. Antispasmodic drugs (e.g.
suppression (Kang et al., 2001; Menheniott et dicyclomine) can also be administered.
al., 2013; Xing et al., 2012). Omeprazole
inhibits c-AMP pathway of hydrogen ion Triple therapy
generation and leads to prevent ulcer
formation and enhance ulcer healing by In considerable GI haemorrhage, broad-
increasing of gastric mucosal circulation and spectrum antibiotics should be administered
mucosal epithelial cells migration. The for check the formation of bacterial colonies
median value of 24-hour intragastric pH on in the gastric mucosa as well as systemic
days 2 and 6 were significantly higher when translocation of the bacterial population. The
dogs were given famotidine, pantoprazole, or culture of samples and Antibiotic sensitivity
omeprazole than dogs were given ranitidine test should be done before started antibiotic
(Bersenas et al., 2005). Misoprostol is an therapy. Single Antibiotics does not gives
analog of PGE2 gives at the doses of 0.5 to significant effect against Helicobacter spp.
2.3μg/lb body weight twice in a day. In Because rapidly development of drug
NSAID induced ulceration, misoprostol may resistance “Triple therapy” is effective against
provide additional benefit with sucralfate and Helicobactor organism; this contains three
H2 antagonist therapy. Prostaglandin E is antibiotic combinations or a combination of
contraindicated in hypotensive animals two antibiotics and one acid reducing agent
because it may lead to increasing of gastric like omeprazole or H2 receptor antagonist
damage. These drugs shield healthy and (Bichard and Shreding, 2005). In H. pylori
uncovered mucosa from more harm and induced gastric disease, progressive
2488
diminution of GKNs gene expression is (Hall et al., 2006; Ogawa et al., 2008; Hesta
known through disease progression chronic et al., 2009). Ascorbic acid reduces oxidative
condition to oncogenic transformation (Choi damage to the gastric mucosal layer by
et al., 2013). Removal of H. pylori organisms scavenging ROS and attenuating the H.
from stomach leads to restoration of normal pylori-induced inflammatory cascade leads to
tissue level for proper expression of GKNs decreased incidence of gastric carcinoma and
gene (Nardone et al., 2007). Gastric bleeding from peptic ulcer disease (Aditi et
Helicobactor infection treated with “Triple al., 2012). During scavenging of free oxygen
therapy” consisting anioxycillin 20 mg/kg radicals by ascorbic acid produces 2-fold
BID, metronidazole 10 mg/kg BID and greater amount of ascorbyl radicals in the H.
bismuth subcitrate 6 mg/kg BID orally for pylori-infected gastric mucosa (Drake et al.,
two to four weeks. Alternative eradication 1998). Vitamin C is also an important dietary
therapy with tetracycline 20 mg/kg BID and antioxidant because it significantly decreases
omeprazole 0.7 mg/kg OD administered the adverse effect of reactive oxygen species
orally for next 10 and 14 days was given after (ROS) that is a source of oxidative damage to
triple therapy for eradication of subsequently the cell components like, lipids membrane,
persisting helicobacter organism (Happonen DNA, and proteins (Maestro et al., 1980;
et al., 2000). Triple therapy with amoxycillin, Iheanacho et al., 1993). Vitamin C is the only
metronidazole and famotidine also antioxidant required for complete protection
successfully eradicate gastric Helicobactor of endogenous lipids from noticeable
infection in dog and cat (Simpson et al., oxidative damage induced by ROS (Polidori
2000). et al., 2004). Before the reaction and
oxidation of lipoprotein lipids, Ascorbate
Antioxidant therapy seizes the activity of ROS. If serum
concentration of Vitamin C has been down,
It is difficult to prevent the generation of ROS the remaining antioxidants cannot be able to
but the proper strategies prevent the gastric provide complete protection from ROS, leads
mucosal damage and fastening of recovery to oxidative stress and initiate lipid
from oxidative stress. In the diet of sled dog, peroxidation (Ulutas et al., 2006).
ROS scavengers such as vitamin E have been
used to diminish cellular damage due to N- Acetylcysteine works have mucolytic as
exercise (Hinchcliff et al., 2000). Some well as antioxidant effect and reduce
antioxidants are used to protect colonization of Helicobacter organism in
gastrointestinal mucosa and apical epithelial gastric mucosa (Huynh et al., 2000). N-
membrane. In rats, the Cacao Liquor water- acetylcysteine increases liver blood flow and
soluble crude polyphenols (CWSP) has been improves liver function and renal function, as
shown radical scavenging ability as well as well as hepatorenal syndrome, lead to reduce
reduce ethanol-induced gastric lesions severity of systemic induced gastritis (Holt et
(Osakabe et al., 1998). The normal blood al., 1999; Rank et al., 2000). Silymarin
level of vitamin-C is 3.2-8.9m/ L in dogs, significantly affects the serum SGPT, SGOT,
(Hishiyama et al., 2006). Vitamin -C is Alkaline phosphatase activities, serum urea
necessarily required for absorption of and creatinine levels and maintains
antioxidants like N- acetylcysteine, and alpha- malondialdehyde level (MDA) as an
tocopherol in young dogs while in geriatric antioxidant in liver and kidney (El-Maddawy
patient, the oral dosage of Vitamine C gives et al., 2012).
minor antioxidant and immunological effects
2489
Others and renal diseases (uraemia), otherwise it may

lead to intensifying the condition.
New synthetic flavonoid derivatives
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How to cite this article:
Pankaj Kumar Patel, Sawita Kumari Patel S.K. Dixit and Rathore, R.S. 2018. Gastritis and
Peptic Ulcer Diseases in Dogs: A Review. Int.J.Curr.Microbiol.App.Sci. 7(03): 2475-2501.
doi: https://doi.org/10.20546/ijcmas.2018.703.288
2501
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Gastritis and Peptic Ulcer Diseases in Dogs: A Review

Pankaj Patel Shivendra Kumar Dixit

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Gastritis and Peptic Ulcer Diseases in Dogs: A Review

Introduction occasionally coupled with the loss of body

Histoplasma capsulatum infected by spores (Halliwell, 1990). In acute events of

Diagnosis Laboratory findings

History and clinical signs In gastric ulcer disease laboratory findings

superoxide dismutase (SOD), catalase (CAT) perforation given with IM injection of

inhibition of gastric acid secretion (Andersson encourage epithelialization of gastric mucosa

Others and renal diseases (uraemia), otherwise it may

Cooper, D. M., Radom-Aizik, S., Schwindt, case complicated by avitaminosis C.

Continuing Education for the Practicing flunixin, butorphanol, and

methylprednisolone sodium succinate. Shaheen, M., Zaman, A., and Muhee, A.

Stanton, M. E., and Bright, R. M. 1989. mitochondrial dysfunction and its

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