Difference between revisions of "Gastric Ulceration - Horse"

Latest revision as of 15:59, 6 July 2012

Also known as: Gastroduodenal ulceration — Gastrointestinal ulceration — Equine Gastric Ulcer Syndrome — EGUS — Peptic ulcer disease — Equine Gastric Ulcer

Introduction

The term 'Equine gastric ulcer syndrome (EGUS)' encompasses a number of disease complexes^[1] associated with ulceration of the oesophageal, gastric or duodenal mucosa^[2] in horses. When such damage is caused by acidic gastric juice, the defect is described as a 'peptic ulcer'.^[2] The non-glandular (squamous, proximal or orad) region of the equine stomach is lined by stratified squamous mucosa and a glandular mucosa lines the distal (aborad) portion. Ulceration of either, or both^[3] regions of the gastric mucosa is one of the most important problems of the equine stomach as it may limit performance^[4] and compromise welfare.^[5] The two regions meet abruptly at the margo plicatus^[6], adjacent to where most ulcers occur.^[2] Damage to these regions occurs via differing pathophysiological routes and varies in severity. Inflammation can progress to cellular death and sloughing causing disruption of the superficial mucosa (erosion), then penetration of the submucosa down to the level of the lamina propria^[2](ulceration), full thickness ulceration (perforation)^[6] and potentially duodenal stricture.^[7] The occult nature of the disease typically precludes the observation of clinical signs until severe ulceration has developed.^[2]

Prevalence

The prevalence of equine gastric ulceration has increased over the last century.^[8] In a retrospective study of 3715 Swedish horses, ulcers were most often found in the squamous mucosa along the margo plicatus, then the glandular body, proximal squamous mucosa and antrum.^[8] For the squamous region, reported prevalences are:

Racehorses 66-93%^[9]^[10]^[11]
Racehorses in active race training 80-93% (incidence 100%)^[12]^[13]
Show horses 58%^[14]
Ponies 78%^[15]
Endurance horses 67%^[16]
Western performance horses 40%^[17]
Thoroughbred broodmares (67-77%)^[18]
Nonracing performance horses (17% pre-competition, 56% post-competition)^[19]
Pleasure horses in full work ~ 60%^[4]
Foals ~25-57%^[20]^[21]^[22]

The prevalence and severity of ulcers increases with work intensity^[7] and duration^[23]^[24], thus racehorses in active training are more often affected^[9] and in half of these, the lesions are moderate to severe.^[7] In one study, all horses developed gastric ulcers within 2 weeks of entering simulated race training.^[12] Lesions are thought to be chronically progressive during race training, but to regress during retirement.^[9] Horses with signs of gastrointestinal distress also demonstrate an increased frequency and severity of ulcerative lesions.^[2]EGUS prevalence is high in horses with bowel, liver and oesophageal lesions^[8] and in foals, the incidence increases dramatically in those with gastrointestinal signs.^[2] Among show horses, 82% of those with signs of abdominal discomfort had gastric ulcers^[25] but around 30% of adult horses and many foals have mild gastric erosions which heal without treatment or clinical signs.^[7] In 201 clinically normal horses in Denmark, 53% had EGUS with severity score >2 and older horses were more likely to have lesions in both regions of the stomach^[26]

Signalment

EGUS develops in horses of all ages^[6] but is most common in young horses in training and foals. Gastric ulceration is considered to be rare in horses at pasture.^[27]

Pathophysiology

Anatomy

In the horse, the squamous mucosa covers the lining of the oesophagus and about one third of the gastric wall. It provides a protective barrier comprising a tightly bound superifcial layer of cornified cells.^[2] This squamous epithelium has no absorptive or secretory function. The glandular region of the stomach contains mucus-secreting cells and gastric glands. The margo plicatus is analagous to the gastro-oesophageal junction in man, however it lacks the lower oesophageal sphincter that helps to prevent acidic injury of the squamous mucosa.^[6] The predilection sites for lesions in various groups are:

Neonatal foals: glandular mucosa
Healthy suckling foals younger than 50 days: squamous mucosa adjacent to margo plicatus along the greater curvature, squamous epithelial desquamation
Suckling foals older than 50 days with clinical signs: squamous mucosa along lesser curvature, squamous mucosa of fundus and adjacent to margo plicatus.
Sucklings and early weanlings: gastroduodenal ulcer disease (GDUD) – lesions in proximal duodenum, also severe lesions in squamous or glandular region
Yearlings and adults: squamous epithelium, particularly adjacent to margo plicatus, glandular and antral involvement becoming more common,^[28]^[29] severe cases of ulceration can extend dorsally into squamous fundus.^[6]

Intrinsic protective factors

Glandular mucosal defence mechanisms^[2]

Mucus: secreted by specialised mucous neck cells. This viscous, hydrophobic glycoproteinaceous gel adheres to the mucosa and resists acid and pepsin contact. Also acts as a lubricant to minimise mechanical damage.
Bicarbonate: secreted by gastric mucosal cells. Secretion triggered by luminal acid concentrations, mechanical irritation, and release of endogenous prostaglandins. Bicarbonate trapped in the mucous layer creates a pH gradient from physiological pH at the mucosal surface to a gastric acid pH at the luminal interface.
Epidermal growth factors: found in salivary gland secretions, promote DNA synthesis and proliferation of gastric mucosal cells. Also important in prostaglandin synthesis and inhibit hydrochloric acid (HCl) secretion by the parietal glands.
Epithelial restitution mechanisms: important for gastric mucosal integrity. Epithelial injury induces migration of adjacent cells to replace damaged cells within minutes without the need of new cell proliferation. Shear forces, induced by mixing of ingesta, are counterbalanced by epithelial restoration.
Adequate mucosal blood supply: required to provide the mucosa with oxygen and nutrients to produce the mucus-bicarbonate layer and to support rapid turnover of epithelial cells. Also required to remove acid that has diffused into the mucosa. Compromised mucosal perfusion may be important in the stress-related ulceration of neonates.^[6]
Prostaglandins: inhibit acid secretion, promote mucosal perfusion (through vasodilation), increase mucus and bicarbonate secretions and support mucosal cell repair. PGE2 is especially important in these functions.

Squamous mucosal defence mechanisms^[2]

The squamous mucosa has comparatively few defence mechansims:

Intercellular tight junctions and intracellular buffering systems act as barriers
Epidermal growth factor also contributes to the maintenance and repair of gastric squamous epithelium.^[30]

Other intrinsic defence mechanisms

Gastrodudodenal motility: critically ill neonatal foals can have a substantially different pH profile compared to clinically normal foals, possibly due to changes in gastric motility and acid secretion.^[31]

Intrinsic ulcerogenic factors^[32]

The most significant factors promoting gastric ulceration are HCl and a gastric pH persistently less than 4.0. Volatile fatty acids (VFAs), lactic acid and bile acids augment the changes in squamous mucosal bioelectrical properties induced by HCl (the first sign of acidic damage). VFAs and lactic acid are by-products of the bacterial fermentation of sugars found in concentrate diets.

Hydrochloric acid compromises the outer cell barrier of the squamous epithelium. It then diffuses into the cells of the stratum spinosum, inhibiting cellular sodium transport and causing cell swelling, necrosis and eventual ulceration.^[33]^[34]

VFAs: acetic, propionic, butyric and valeric acids are lipid soluble, which enables them to readily diffuse into the stratum spinosum and immediately cause the damage as described above.

Lactic acid: has been shown to increase the permeability of the squamous mucosa.^[35]

Extrinsic ulcerogenic factors (RISK FACTORS)

Exercise: there appears to be a high prevalence of gastric ulcers in horses performing in most disciplines.^[36] Although this may be related to exercise, other confounding factors related to these disciplines such as travel, diet, feeding regime, use of non-steroidal anti-inflammatory drugs (NSAIDs) and stress may be significant. However, Vatistas and co-workers (1999) were able to induce and maintain EGUS in racehorses in fast work without the use of NSAIDs or fasting before exercise.^[12] There is also evidence that training for just 8 days is suffcient to induce gastric ulcers.^[37] The higher prevalence of gastric ulcers at post mortem in racehorses in training compared to those in retirement is consistent with the hypothesis that exercise may be an important risk factor for EGUS.^[9] Strenuous exercise is known to stimulate gastrin release which has effects on HCl secretion, gastric emptying and gastric blood flow. Diversion of blood to active muscle groups may further deprive the gastric mucosa of the perfusion required for its integrity. It is also thought that exposure of the squamous mucosa to acid is increased as the stomach is compressed by the abdominal viscera and diaphragm during excercise.^[38]

Housing and Transport: housing in stables has been proposed as a risk factor for gastric ulcers, with more lesions being found in confined horses compared to those out at grass.^[39] However, when comparing solitary stable confinement with stabling next to a companion, and finally turn out in a paddock, Husted and colleagues (2008) found that the environmental situation had no effect on mucosal acid exposure in the equine stomach.^[40] Thus the reason for a higher prevalence of EGUS in stabled animals is unclear. Transport has also been shown to induce squamous mucosal ulceration in horses, by as yet, unidentified mechanisms.^[41]

Diet and feeding regime: feed deprivation encourages gastric ulceration in three ways: (1) it precludes the buffering capacity of protein leading to a reduced gastric pH,^[42] (2) it empties the stomach and exposes the squamous mucosa to the more mobile gastric juice^[8] and (3) it permits the accumulation of bile salts, which, together with HCl, cause greater squamous mucosal damage than HCl alone.^[43] It is unsurprising, therefore, that an alternating feed-fast protocol would produce a consistent model of ulcer induction in the equine squamous mucosa.^[44]^[45] Despite this, feed deprivation is not a prerequisite for gastric ulceration in the horse.^[46] Diets that are plentiful in roughage prolong the mastication process and the production of salivary bicarbonate that protects the gastric mucosa. A diet of high grain and low roughage thus predisposes to EGUS.^[32] This sort of diet is commonly fed to racehorses but dietary components have also been shown to influence EGUS risk in nonracehorses.^[47] Ponies fed a concentrate diet had a greater prevalence of gastric ulcers than ponies fed hay alone^[12] and this may be because grain and pelleted feeds are asssociated with increased serum gastrin.^[48] High starch meals are also a risk because they are fermented to VFAs and lactic acid and are emptied from the stomach relatively slowly.^[49]^[50]^[51]

Other ailments: conditions that produce abdominal pain and/or inappetance are likely to reduce food intake and predipose to gastric ulcers.^[8] This may be the reason that colic and other gastrointestinal disorders (especially those resulting in delayed gastric emptying)^[52] have been associated with EGUS.^[53] Alternatively, EGUS may be part of a more general gastrointestinal disease complex.^[12]

NSAIDs: as in other species, NSAIDs have been shown to cause gastric ulcers in horses. Typically this is associated with high doses or frequent administration of phenylbutazone or flunixin meglumine. However, although there is evidence to the contrary,^[54]therapeutic doses of NSAIDs may be sufficient to induce EGUS. Other studies have suggested that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally^[55]and that combination treatment with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone.^[56] The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa,^[57]^[58]^[59] they may look different endoscopically from ulcers that occur naturally,^[60] and they appear to heal spontaneously.^[61]^[62] Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.^[63]^[64]^[46]

Infective agents: Helicobacter spp. have been held responsible for the initiation and recurrence of human gastric ulcers. Helicobacter equorum has been isolated from equine faecal samples^[65] and Helicobacter-like DNA has been found in both foal faeces^[66] and the stomachs of mature horses. However, such findings have been demonstrated in horses with and without gastric lesions^[67]and in clinically healthy animals. Any link between EGUS and Helicobacter remains weak at best, although there is a suggestion that colonisation of equine gastric ulcers with E.coli may delay their healing.^[68]

Temperament: a nervous disposition has been linked with gastric ulcers^[69]but the same association was not seen in another study.^[70]

Stress: the physiological and psychological stresses of training, housing, boredom, travel, mixing, hospitalisation and entering new environments^[12] may increase the risk of developing EGUS. Stress induced by other clinical disorders (including hypoxia) has been reported to increase the prevalence of EGUS in the glandular mucosa of neonatal foals^[71] and a similar mechanism may exist for adult animals.^[12]

It is clear that the aetiopathogenesis of EGUS is multifactorial.^[72] What remains uncertain, is how these various risk factors interact to produce lesions in different regions of the equine gastric mucosa. Based on extrapolation from other species,^[2] it is conceivable that a reduction in mucosal blood flow might result from:

hypotensive shock (for example with blood loss, sepsis, endotoxaemia or fluid sequestration in colic)
an increase in sympathetic tone (which might be related to physiological or psychological stresses) or
other severe disease states (such as disseminated intravascular coagulation).

Furthermore, any impairment of gastric motility (as seen with neurological imbalances, several types of colic and certain drugs) might be expected to increase the risk of ulceration. Despite a lack of clarity, the final common pathway for EGUS appears to be the breaching of mucosal defences by acidic gastric contents. Since horses secrete gastric HCl continuously, even in the fasted state,^[73] they are especially vulnerable to acid-associated damage.

Clinical syndrome

The clinical signs associated with gastric ulcers are often very non-sepcific, difficult to document and at times only subjective.^[74] In addition, there appears to be a poor correlation between the severity of endoscopic lesions and the clinical presentation.^[75] The significance of gastric ulceration in horses thus remains questionable. However, there have been instances where ulcer treatment has preceded an improvement in clinical status and/or racing perfomance, suggesting that in some horses, ulcers are a considerable burden.^[74] Cases of gastric ulceration are often asymptomatic, but signs that have been attributed to these lesions in mature horses include:

Poor appetite (particularly decreased consumption of concentrates)^[6]
Poor condition
Rough hair coat
Weight loss
Excessive recumbency^[2]
Mild to severe colic
- Mild, recurrent colic signs post-prandially^[76]
- In one study, 49% of horses that presented for colic had gastric ulceration and those with duodenitis-proximal jejunitis had a trend towards a higher prevalence of gastric ulceration compared to those with other GI lesions.^[77]
Changes in attitude (dullness or depression)^[74]
Poor racing performance and reluctance to train
- Performance improved in 4 Thoroughbred racehorses after antiulcer treatment^[78]
- Gastric ulcers have adversely affected physiological indices of performance in horses.^[79]

Clinical signs in foals vary depending on age and severity:

Neonatal foals: many ulcers are silent, some foals only exhibit signs when ulceration has become severe. Glandular ulcers are considered the most significant^[6].
- Poor appetite
- Diarrhoea
- Intermittent colic
- Frequent dorsal recumbency
Sucklings and weanlings:^[6]
- Diarrhoea
- Poor appetite (off suck or partially off suck)
- Poor growth, failure to thrive
- Poor body condition
- Rough hair coat
- Potbelly appearance
- Bruxism (almost pathognomonic)
- Colic after feeding or tubing
- Chewing straw
- Dorsal recumbency

Signs of gastroduodenal ulcer disease (GDUD):^[6]
- Bruxism
- Colic
- Gastrooesophageal reflux after suckling
- Ptyalism (secondary to gastric outflow obstruction and gastroesophageal reflux)^[7]
- Diarrhoea

In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.^[6] Brown gastric fluid may signify bleeding ulcers or necrotizing enterocolitis. GDUD is the primary differential for ptyalism in foals, other possible diagnoses include oesophageal obstruction and Candida infection.^[7]

Diagnosis

A presumptive diagnosis can be based on clinical signs and response to therapy,^[6] however, a definitive diagnosis requires visualisation of the stomach. This can be achieved in the live horse using endsocopy or, alternatively, at post-mortem.^[32]

EGUS was recently discussed at the 2010 Annual meeting between the Equine Insurers Forum (EIF) and the British Equine Veterinary Association (BEVA). The EIF maintained that in order to support claims for the long term costs associated with treatment of EGUS, there would be a requirement for veterinary surgeons to make a definitive diagnosis prior to prescribing omeprazole.

Endoscopy

Oesophagogastroscopy or duodenoscopy can be performed under mild sedation (e.g. 0.6-0.8mg/kg xylazine^[74]) in the standing horse. Of these, duodenoscopy is the more specific but more technically demanding method.^[6] Endoscopic examination requires preparatory starving of the patient for 6-8hours,^[74] eliciting a certain degree of stress. As such, it is preferable not to carry out this technique in foals. Should endoscopy be necessary, any air introduced into the foal's stomach must be evacuated at the end of the procedure to avoid exacerbation of colic.^[6] In adult horses, a minimum endoscope length of two metres is essential to visualize the gastric body and fundus.^[6] A 2.8-3.0 metre endoscope is needed to observe the gastric antrum, pylorus and proximal dudoenum.^[6] In either case, fibreoptic or videoendoscopic equipment can be used.^[2] Based on a consensus, the Equine Gastric Ulcer Council (EGUC) published an EGUS Lesion Scoring System which they claimed to be simple and applicable to both regions of the equine gastric mucosa.^[2] This last point has been debated, since most of the acquired data on gastric lesions refers only to the squamous mucosa.^[1] At the time of writing however, the EGUC system appears to be widely used in practice:

Lesion Grade	Description
Grade 0	Intact epithelium with no appearance of hyperaemia (reddening) or hyperkeratosis (yellowing of the squamous mucosa)
Grade 1	Intact mucosa with areas of reddening or hyperkeratosis (squamous)
Grade 2	Small single or multifocal lesions
Grade 3	Large single or multifocal lesions or extensive superficial lesions
Grade 4	Extensive lesions with areas of deep ulceration

Diffuse inflammation may be the only lesion observed in foals with early GDUD.^[6] In contrast to other scoring systems,^[80] the EGUC approach does not include bleeding when assigning lesion grades. The justification is that the 'snapshot' provided by endoscopy may by chance identify bleeding of superficial erosions whilst missing the intermittent haemorrhage of more severe lesions.^[2] Endoscopy may assist in understanding the severity of the disease and assessing the therapeutic response, but it is not without disadvantages. Ulcer severity may be underestimated, particularly in the squamous region and glandular ulcers may be missed altogether.^[81] Lesions that appear grossly similar may have different grades on histopathology.^[32] This is important because varying lesions may have different causes, requiring a range of treatment approaches.

Other Imaging

In older foals with GDUD, detection of gastric outflow obstruction via abdominal radiography is essential to treatment and prognosis.^[6] Liquid barium will demonstrate very delayed or no outflow depending on the degree of obstruction. Without contrast medium, a large, gas filled stomach will be obvious.^[6] The need to perform contrast radiography must be weighed against the stress it would place upon the foal. If gastric rupture is suspected, abdominal ultrasound can be used to identify free fluid in the abdomen and abdominocentesis may confirm the diagnosis.^[6]

Biopsy

A transendoscopic gastric biopsy technique was recently validated for obtaining samples from the gastric glandular mucosa in the live horse.^[82]Unfortunately this technique failed to produce samples of squamous mucosa that would be suitable for histopathological analysis.

Flow chart depicting the proposed pathogenesis of ulcerative lesions of the equine squamous gastric mucosa. Created by Nina Rzechorzek, July 2010. Information sourced from Martineau et al., 2009^[83]

Laboratory tests

Currently, useful and reliable markers for EGUS are lacking.^[2] The SUCCEED® Equine Fecal Blood Test™ uses specific equine monoclonal antibodies to albumin and haemoglobin to detect occult blood in faeces.^[84]^[85]The test has a positive predictive value of 77% and a negative predictive value of 72% and thus cannot be relied upon alone to diagnose EGUS.^[32] False positive results may arise from rectal trauma (e.g. recent biopsy or rectal examination) or protein losing enteropathy.^[32] Other tests that require further analysis for sensitivity and specificity^[6] include:

Urine^[86] and blood^[87] sucrose absorption as an assay of gastric mucosal permeability
Serum alpha1-antitrypsin may be released from damaged gastric tissue^[32] and has been detected more frequently in foals with gastric ulceration^[88]

Pathology

Martineau and co-workers (2009) demonstrated that in a mixed population of horses, a wide range of lesions associated with EGUS could be found at post mortem.^[5] These included hyperkeratosis, punctate scars, diffuse erosions or ulcerations and margo injuria in the squamous region and hyperaemia, focal erosions and ulcerations in the glandular region. A novel finding was glandular metaplasia which may be evidence of a protective mechanism developing in response to acid exposure.^[5] The authors then devised a pathological scoring system - the Equine Gastritis Grading (EGG) system - which uses 5 samples of gastric mucosa taken from specific regions of the equine stomach. For each of these, the inflammatory infiltrate is graded by type, density and location, reactive changes are classified in both squamous and glandular samples and the presence or absence of infectious agents and lymphoid follicles is noted.^[83] From their findings, a pathogenesis for the development of lesions in the squamous region was proposed:

Treatment

Histamine 2 receptor antagonists

Parietal cells secrete HCl upon stimulation of histamine, acetylcholine or gastrin receptors.^[2] Competitive H2 receptor antagonists have successfully elevated gastric pH and treated gastric ulcers in mature horses and foals.^[89]^[90] There appears to be a great variability among horses in their dose requirements for H2 antagonists which may be explained by individual bioavailability for these compounds.^[2] Currently recommended doses for cimetidine, ranitidine and f amotidine proposed to be effective in the majority of horses have been recommended by Sanchez.^[6]

Proton-pump inhibitors (PPIs)

PPIs irreversibly bind to the H+K+-ATPase proton pump of the parietal cell and block the secretion of hydrogen ions. These agents are more effective than H2 antagonsists as their action is receptor-independent,^[2] blocking the final pathway of acid secretion and they have a prolonged effect allowing for once-daily dosing.^[91] Omeprazole (Gastroguard™), a subsituted benzimidazole, is currently the only PPI licensed for use in horses. At a dose rate of 4mg/kg per day omeprazole has proven effective in reducing the severity of gastric ulcers in Thoroughbred horses in active race training^[92] and no adverse effects have been observed. The paste formulation is easy to administer and is generally well accepted by horses. Omeprazole has demonstrated efficacy in the resolution of both naturally-occurring and NSAID-induced gastric ulcers in horses.^[93]^[94] A single dose has also produced an increase in gastric pH in clinically ill neonatal foals^[95] and has contributed to ulcer healing in neonates.^[93] A potential concern is that altering gastric pH may encourage bacterial overgrowth. Thus further work is needed to evaluate the long-term safety of omeprazole in horses and particularly, foals.^[92]

Antacids

The use of antacids to treat EGUS in the horse has not been critically evaluated^[6] and some believe they are contraindicated due to potential rebound effects. Furthermore, the requirement for frequent dosing of large volumes of these products (owing to their poor efficacy) makes them an unattractive, stressful and impractical alternative to omeprazole.^[74]

Mucosal protectants

Sucralfate is a complex salt of sucrose and aluminium hydroxide. It is thought to promote ulcer healing via several mechanisms: adherence to ulcerated mucosa, stimulation of mucus secretion, pepsin inibition, increasing PGE synthesis and enhancing the local production of epidermal growth factor.^[6] It has been used effectively to treat and prevent stress-induced ulcers in man and has been recommended for the treatment of glandular ulcers in horses.^[96] However, the effect of sucralfate on equine squamous gastric ulcers remains inconclusive^[2] and the product may be ineffective in the alkaline conditions created by acid suppression agents.^[97]

Prostaglandin analogues

Synthetic PGE1 analogues are believed to inihibit gastric acid secretion and enhance mucosal cytoprotection.^[98] Misoprostol has been an effective agent in the treatment of human gastric and duodenal ulcers and has been shown to increase gastric pH in horses.^[99] Although contraindicated in pregnant mares, Misoprostol may be beneficial for mucosal recovery in the face of flunixin treatment.^[100]

Gastric prokinetics

In cases of gastrooesophageal reflux, duodenal disease and delayed gastric emptying without a serious physical obstruction to gastric outflow, gastric prokinetics might be considered.^[6] Such compounds include bethanechol, metaclopramide, erythromycin and cisapride which have been shown to hasten gastric empyting in adult horses.^[2] To date only the parasympathomimetic agent bethanechol has been used as an adjunct for EGUS and cholinergic side effects are possible. Cisapride has been withdrawn from the US and UK markets over concern about its potential to cause adverse cardiac effects in man.^[6]

Treatment problems

The prevalence of gastric ulcers in horses remains high regardless of the common use of antiulcer treatments. This has been attributed to the expense of recommended products encouraging subtherapeutic and curtailed dosing schedules.^[101] Omeprazole and ranitidine must be administered for at least 28 days for adequate ulcer healing.^[32] In the USA, compounded omeprazole from bulk powders are used as a cheaper substitute for the FDA approved products. However, these formulations lack efficacy and are not regulated.^[102] A considerable challenge lies in the management of abdominal pain associated with EGUS, since the commonly used NSAIDs for pain control may worsen and even induce further ulcerative lesions.^[103] Another challenge is the horse in which oral medication is prohibited. However, Andrews and colleagues (2006) have demonstrated the efficacy of an omeprazole powder, adminstered IV in sterile water, which signifcantly increases the pH of equine gastric contents and may be useful in problem horses.^[104] An ongoing point of debate is the use of antiulcer medication in competition horses. In 2000, the Bureau of The Fèdèration Equestre Internationale (FEI) permitted the use of cimetidine, ranitidine and omeprazole to prevent and treat gastric ulcers. This decision was based on evidence that the compounds were not performance enhancing and that EGUS was such a widespread concern. However, these drugs are still listed under prohibited substances in the 2009 Appendices of the American Endurance Ride Conference (AERC) Rules and Regulations. The argument is that a horse requiring such treatment is not suffciently well to compete and should be withdrawn from competition if it needs preventative medication. A related concern is that the AERC permits the use of hyperosmolar oral electrolyte pastes which may cause gastric ulcers.^[105] Without the protection afforded by antiulcer agents, these horses may be at considerable risk for EGUS.^[32]

Prognosis

Improvement in most clinical signs should be noted within 1-3 weeks of commencing treatment. Colic or diarrhoea should resolve within 48 hours.^[6] Complications related to gastric ulcers are most frequent and severe in foals with GDUD. They include gastric or duodneal perforation, delayed gastric emptying, gastroesophageal reflux and oesophagitis, ascending cholangitis and megaoesophagus or aspiration pneumonia^[106] secondary to chronic gastroesophageal reflux. Sudden gastric perforation without prior signs occurs sporadically in foals.^[7]Ulcers in the proximal duodenum or at the pylorus can cause fibrosis and stricture. The latter complication is seen in both foals and adult horses.^[7] In mature animals, the most common complication is the recurrence of EGUS after treatment has ceased. This is typically because the inciting managemental causes have not been altered.

Prevention

Management

Diet: ideally turnout to good quality grass. Stabled horses should have continuous access to hay and should be offered this before calorific needs are met by concentrates.^[74] Alfalfa, or another high calcium or high protein forage may be preventative by increasing gastric pH.^[107]^[108] Concentrates should be fed at no more than 0.5kg per 100kg body weight and not more frequently than every 6 hours.^[104] Horses prone to, or at risk of, EGUS should be fed the minimum amount of concentrates necessary.^[32]
Stress: minimise handling wherever possible, provide company and toys for stabled horses, encourage good feeding habits of foals.^[89]

Most of these suggestions would be difficult, if not impossible, to achieve for horses in race training, thus prophylactic medication should be considered.^[74]

Prophylaxis

Omeprazole paste at a lower dose daily for 3-4 weeks.^[109]

Prevented ulcers in horses maintained under ulcerogenic conditions.^[109]^[110]^[111]^[112]

Treating ulcers in asymptomatic performance horses may lead to improved performance.^[74]
Prophylaxis in critically ill foals may not be necessary and is controversial since gastric acidity may be protective against bacterial translocation.^[6]
May benefit foals receiving substantial doses of NSAIDs for orthopaedic pain.^[6]

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References

↑ ^1.0 ^1.1 Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric ulcer syndrome. Equine Vet J, 41(7):616.
↑ ^2.00 ^2.01 ^2.02 ^2.03 ^2.04 ^2.05 ^2.06 ^2.07 ^2.08 ^2.09 ^2.10 ^2.11 ^2.12 ^2.13 ^2.14 ^2.15 ^2.16 ^2.17 ^2.18 ^2.19 ^2.20 The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet Educ, 11(5):262-272.
↑ Andrews, F.M, Bernard, W.V, Byars, T.D et al. (1999) Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet Educ, 1:122-134. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ ^4.0 ^4.1 Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review. N Z Vet J, 55(1):1-12).
↑ ^5.0 ^5.1 ^5.2 Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644. Cite error: Invalid <ref> tag; name "Martineau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Martineau" defined multiple times with different content
↑ ^6.00 ^6.01 ^6.02 ^6.03 ^6.04 ^6.05 ^6.06 ^6.07 ^6.08 ^6.09 ^6.10 ^6.11 ^6.12 ^6.13 ^6.14 ^6.15 ^6.16 ^6.17 ^6.18 ^6.19 ^6.20 ^6.21 ^6.22 ^6.23 ^6.24 ^6.25 ^6.26 ^6.27 ^6.28 Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15. Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content
↑ ^7.0 ^7.1 ^7.2 ^7.3 ^7.4 ^7.5 ^7.6 ^7.7 Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial
↑ ^8.0 ^8.1 ^8.2 ^8.3 ^8.4 Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.
↑ ^9.0 ^9.1 ^9.2 ^9.3 Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. Equine Vet J, 18(4):284-287.
↑ Vatistas, N.J, Snyder, J.R, Carlson, G, et al (1994) Epidemiological study of gastric ulceration in the thoroughbred racehorse:202 horses 1992-1993. Proc Am Assoc Equine Pract, 40:125-126
↑ Murray, M.J, Schusser, G.F, Pipers, F.S, Gross, S.J (1996) Factors associated with gastric lesions in thoroughbred racehorses. Equine Vet J, 28:368-374.
↑ ^12.0 ^12.1 ^12.2 ^12.3 ^12.4 ^12.5 ^12.6 Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44 Cite error: Invalid <ref> tag; name "Vatistas 2" defined multiple times with different content
↑ Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthruy, R.M, Thurmond, M, Zhou, H, Lloyd, K.L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses. Equine Vet J, Suppl 29:34-39.
↑ McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses. J Am Vet Med Assoc, 215:1130-1133.
↑ MacAllister, C.G, Sangiah, S, Mauromoustakos, A (1992) Effect of a histamine H, type receptor antagonist (WY 45, 727) on the healing of gastric ulcers in ponies. J Vet Int Med, 6:271-275.
↑ Nieto, J.E, Snyder, J.R, Beldomenico, P et al. (2004) Prevalence of gastric ulcers in endurance horses: a preliminary report. Vet J, 167:33-37.
↑ Bertone, J (2000) Prevalence of gastric ulcers in elite, heavy use western performance horses. Proc Am Assoc Equine Pract, 46:256-259.
↑ LeJeune, S.S, Nieto, J.E, Dechant, J.E, Snyder, J.R (2009) Prevalence of gastric ulcers in Thoroughbred broodmares in pasture: a preliminary report. Vet J, 181(3):251-5.
↑ Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. J Equine Vet Sci, 23:560-561. In:Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Wilson, J.H (1986) Gastric and duodenal ulcers in foals: a retrospective study. Proc Equine Colic Res Symp 2nd:126-128.
↑ Murray, M.J, Grodinsky, C, Cowles, R.R, et al.(1990) Endoscopic evaluation of changes in gastric lesions of Thoroughbred foals. J Am Vet Med Assoc, 196:1623-1627.
↑ Murray, M.J (1989) Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). J Am Vet Med Assoc, 195:1135-1141.
↑ Orsini, J.A, Pipers, F.S (1997) Endoscopic evaluation of the relationship between training, racing, and gastric ulcers. Vet Surg, 26:424. In: Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
↑ Murray, M.J (1994) Gastric ulcers in adult horses. Comp Cont Educ Pract Vet, 16:792-794. In:Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
↑ Murray, M. (1992) Gastric ulceration in horses: 91 cases (1987-1990). J Am Vet Med Assoc, 201:117-120. In: Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644.
↑ Luthersson, N, Nielsen, K.H, Harris, P, Parkin, T.D (2009) The prevalence and anatomical distribution of equine gastric ulcer syndrome (EGUS) in 201 horses in Denmark. Equine Vet J, 41(7):619-24.
↑ Murray, M.J (1994) Characteristics of gastric ulcer pathophysiology. Proc Am Coll Vet Intern Med, 12:610-612. In: Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.
↑ Bell, R.J.W, Kingston, J.K, Mogg, T.D, Perkins, N.R (2007) The prevalence of gastric ulceration in racehorses in New Zealand. N Z Vet J, 55:13-18. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Murray, M.J, Nout, Y.S, Ward, D.L (2001) Endoscopic findings of the gastric antrum and pylorus in horses: 162 cases (1996-2000). J Vet Intern Med, 15:401-406. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Jeffrery, S.C, Murray, M.J, Eichorn, E.S (2001) Distribution of epidermal growth factor receptor (EGFr) in normal and acute peptic-injured equine gastric squaous epithelium. Equine Vet J, 33:562-569. In: Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644.
↑ Sanchez, L.C, Lester, G.D, Merritt, A.M (2001) Intragastric pH in critically ill neonatal foals and the effect of ranitidine. J Am Vet Med Assoc, 218:907-911. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ ^32.0 ^32.1 ^32.2 ^32.3 ^32.4 ^32.5 ^32.6 ^32.7 ^32.8 ^32.9 Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615. Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content
↑ Nadeau, J.A, Andrews, F.M, Patton, C.S, Argenzio, R.A, Mathew, A.G, Saxton, A.M (2003) Effects of hydrochloric, acetic, butyric, and proprionic acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses. Am J Vet Res,64:404-412.
↑ Nadeau, J.A, Andrews, F.M, Patton, C.S, Argenzio, R.A, Mathew, A.G, Saxton, A.M (2003) Effects of hydrochloric, valeric, and other volatile fatty acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses. Am J Vet Res, 64:413-417.
↑ Andrews, F.M, Buchanan, B.R, Elliott, S.B, Al Jassim, R.A.M, McGowan, C.M, Saxton, A.M (2008) In vitro effects of hydrochloric and lactic acids on bioelectric properties of equine gastric squamous mucosa. Equine Vet J, 40:301-305.
↑ Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. J Equine Vet Sci, 23:560-561. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ White, G, McClure, S.R, Siifferman, R, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration. J Am Vet Med Assoc, 230(11):1680-2.
↑ Lorenzo-Figueras, M, Merritt, A.M (2002) Effects of exercise on gastric volume and pH in the proximal portion of the stomach of horses. Am J Vet Res, 63:1481-1487.
↑ Murray, M.J, Eichorn, E.S (1996) Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall confinement with ad libitum access to hay on gastric ulceration in horses. Am J Vet Res, 57:1599-1603.
↑ Husted, L, Sanchex, L.C, Olsen, S.N, Baptiste, K.E, Merritt, A.M (2008) Effect of paddock vs. stall housing on 24 hour gastric pH within the proximal and ventral equine stomach. Equine Vet J, 40(4):337-41.
↑ McClure, S.R, Carithers, D.S, Gross, S.J, Murray, M.J (2005) Gastric ulcer development in horses in a simulated show or training environment. J Am Vet Med Assoc, 227:775-777.
↑ Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. Equine Vet J, 25:417-421. In: Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.
↑ Berschneider, H.M, Blikslager, A.T, Roberts, M.C (1999) Role of dudodenal relfux in nonglandular gastric ulcer disease of the mature horse. Equine Vet J Suppl, 29:24-29.
↑ Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. Equine Vet J, 25:417-421. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Murray, M.J (1994) Equine model of inducing ulceration in alimentary squamous epithelial mucosa. Dig Dis Sci, 39:2530-2535. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ ^46.0 ^46.1 Vatistas, N.J (1998) Gastric Ulceration in the Racing Thoroughbred. PhD Thesis. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
↑ Luthersson, N, Nielson, K.H, Harris, P, Parkin, T.D (2009) Risk factors associated with equine gastric ulceration syndrome (EGUS) in 201 horses in Denmark. Equine Vet J, 41(7):625-30.
↑ Smyth, G.B, Young, D.W, Hammond, L.S (1988) Effects of diet and feeding on post-prandial serum gastrin and insulin concentrations in adult horses. Equine Vet J Suppl 7:56-59.
↑ Mètayer, N, Lhôte, M, Bahr, A, Cohen, N.D, Kim, I, Rousell, A.J, Julliand, V (2004) Meal size and starch content affect gastric emptying in horses. Equine Vet J, 36:434-440. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Taharaguchi, S, Okai, K, Orita, Y, Kuwano, M, Ueno, T, Taniyama, H (2004) Relation between amounts of concentrated feed given mares and gastric ulcers in foals. J Japan Vet Med Ass, 57:366-370. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Boswinkel, A.M, Ellis, A.D, Sloet van Oldruitenborgh-Oosterbaan, M.M (2007) The influence of low versus high fibre haylage diets in combination with training or pasture rest on equine gastric ulceration syndrome (EGUS). Pferdeheilkunde, 23:123-130. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Mertz, H.R, Walsh, J.H, (1991) Peptic ulcer pathophysiology. Med Clin North Am, 75:799-814. In: Sanchez, L.C (2010) 'Diseases of the stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists. Equine Vet J Suppl, 7:77-79.
↑ Andrews, F.M, Reinemeyer, C.R, Longhofer, S.L (2009) Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. Vet Ther, 10(3):113-20.
↑ Monreal, L, Sabatè, D, Segura, D, Mayós, I, Homedes, J (2004) Lower gastric ulcerogenic effect of suxibuzone compared to phenylbutazone when administered orally to horses. Res Vet Sci, 76:145-149. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Reed, S.K, Messer, N.T, Tessman, R.K, Keegan, K.G (2006) Effects of phenylbutazone alone or in combination with flunixin meglumine on blood protein concentrations in horses. Am J Vet Res, 67:398-402. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ MacAllister, C.G, Morgan, S.J, Borne, A.T, Pollet, R.A, (1993) Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses. J Am Vet Med Ass, 202:71-77. In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
↑ Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists. Equine Vet J Suppl, 7:77-79. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
↑ Kumaran, D, Bhuvanakumar, C.K (1994) Gastro duodenal ulceration in foals - a discussion. Cenfaur Mylapore, 10:83-86. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
↑ Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
↑ Jones, W.E (1983) Gastrointestinal ulcers [foal]. Equine Vet Data, 4:305-308. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
↑ MacAllister, C.G, Sangiah, S (1993) Effect of ranitidine (in healing of experimentally induced gastric ulcers in ponies. Am J Vet Res, 54:1103-1107. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
↑ Vatistas N.J, Snyder, J.R, Carlson, G.P, Johnson, B, Arther, R.M, Thurmiind, M, Lloyd, K.C.K (1994) Epidemiology study of gastric ulcerarion in the Thoroughbred race horse: 202 horses. Proc Am Ass Equine Pract, 39:125-126. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
↑ Murray, M.J, Schusser, G.F, Pipers, F.S, Gro:ss, S.J (1996) Factors associated with gastric lesions in Thoroughbred racehorses. Equine Vet J, 28:368-374. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44
↑ Fox, J.G (2002) The non-H.pylori helicobacters: their expanding role in gastorintestinal and systemic disease. Gut, 50:273-283. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Moyaert, H, Haesebrouck, F, Dewulf, J, Ducatelle, R, Pasmans, F (2009) Helicobacter equorum is highly prevalent in foals. Vet Microbiol, 133:190-192. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Contreras, M, Morales, A, Garcia-Amado, M.A, DeVera, M, Bermudez, V, Gueneau, P (2007) Detection of Helicobacter-like DNA in the gastric mucosa of Thoroughbred horses. Letters in Appl Microbiol, 45:553-337. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Al Jassim, R.A.M, Scott, P.T, Trebbin, A.L, Trott, D, Pollitt, C.C (2006) The genetic diversity of lactic acid producing bacteria in the equine gastrointestinal tract. FEMS Microbiol Letters, 248:75-81. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses. J Am Vet Med Ass 215:1130-1133. In: In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
↑ Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthur, R.M, Thurmond, M, Zhou, H, Lloyd, L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses. Equine Vet J Suppl, 29:34-39. In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
↑ Furr, M.O, Murray, M.J, Ferguson, D.C (1992) The effects of stress on gastric ulceration, T3, T4, reverse T3 and cortisol in neonatal foals. Equine Vet J, 24:37-40.
↑ Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
↑ Campbell-Thompson, M.L, Merritt, A.M (1987) Effect of ranitidine on gastric acid secretion in young male horses. Am J Vet Res, 48:1511-1515.
↑ ^74.0 ^74.1 ^74.2 ^74.3 ^74.4 ^74.5 ^74.6 ^74.7 ^74.8 Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
↑ Murray, M.J, Grodinsky, C, Anderson, C.W, Radue, P.F, Schmidt, G.R (1989) Gastric ulcers in horses: a comparison of endoscopic findings in horses with and without clinical signs. Equine Vet J Suppl, 7:68-72.
↑ Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome. Vet Clin North Am Equine Pract, 25(2):283-301.
↑ Dukti, S.A, Perkins, S, Murphy, J, Barr, B, Boston, R, Southwood, L.L, Bernard, W (2006) Prevalence of gastric squamous ulceration in horses with abdominal pain. Equine Vet J, 38:347-349.
↑ Franklin, S.H, Brazil, T.J, Allen, K.J (2008) Poor performance associated with equine gastric ulceration syndrome in four Thoroughbred racehorses. Equine Vet Educ, 20:119-124. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Nieto, J.E, Snyder, J.R, Vatistas, N.J, Jones, J.H (2009) Effect of gastric ulceration on physiologic responses to exercise in horses. Am J Vet Res, 70(6):787-95.
↑ MacAllister, C.G, Andrews F.M, Deegan E, Ruoff, W, Olovson, S.G (1997) A scoring system for gastric ulcers in horses. Equine Vet J, 29:430-433.
↑ Andrews, F.M, Reinmeyers, C.R, McCracken, M.D, Blackford, J.T, Nadeau, J.A, Saabye, L, Sotell, M, Saxton, A (2002) Comparison of endoscopic, necropsy and histology scoring of equine gastric ulcers. Equine Vet J,34(5):475-478.
↑ Rodrigues, N.L, Dore, M, Doucet, M.Y (2009) Validation of a transendoscopic glandular and nonglandular gastric biopsy technique in horses. Equine Vet J, 41(7):631-5.
↑ ^83.0 ^83.1 Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 2: a scoring system. Equine Vet J,41(7):646-51.
↑ Carter, S, Pellegrini, F.A (2006) The use of novel antibody tools to detect the presence of blood in equine feces. Company Bulletin Freedom Health LLC 1-3. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Pellegrini, F.L, Carter, S.D (2007) An equine necroscopic study to determine the sensitivity and specificity of a dual antibody test. Company Bulletin Freedom Health LLC 1-2. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ O'Connor, M.S, Steiner, J.M, Roussel, A.J, et al. (2004) Evaluation of urine sucrose concentration for detection of gastric ucleration in horses. Am J Vet Res, 65:31-39. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Hewetson, M, Cohen, N.D, Love, S, et al. (2006) Sucrose concentration in bood: a new method for assessment of gastric permeability in horses with gastric ulceration. J Vet Intern Med, 20:388-394. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Taharaguchi, S, Nagano, A, Okai, K, et al. (2007) Detection of an isoform of alpha(1)-antitrypsin in serum samples from foals with gastric ulcers. Vet Rec, 161:338-342. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ ^89.0 ^89.1 Sanchez, L.C, Lester, G.D, Merritt, A.M (1998) Effect of ranitidine on intragastric pH in clinically normal neonatal foals. J Am Vet Med Assoc, 212:1407-1412. Cite error: Invalid <ref> tag; name "Lester" defined multiple times with different content
↑ Becht, J.L, Byars, T.D (1986) Gastroduodenal ulceration in foals. Equine Vet J, 18:307-312.
↑ Papich, M.G (1993) Anti-ulcer therapy. Vet Clin N Am, 202:1465-1468.
↑ ^92.0 ^92.1 Vatistas, N.J, Snyder, J.R, Nieto, J, Thompson, D, Pollmeier, M, Holstes, J (1999) Acceptability of a paste formulation and efficacy of high dose omeprazole in healing gastric ulcers in horses maintained in race training. Equine Vet J Suppl, 29:71-76.
↑ ^93.0 ^93.1 MacAllister, C.G, Sifferman, R.L, McClure, S.R et al. (1999) Effects of omeprazole paste on healing of spontaneous gastric ulcers in horses and foals: a field trial. Equine Vet J Suppl, 77-80. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15. Cite error: Invalid <ref> tag; name "MacAllister" defined multiple times with different content
↑ Murray, M.J, Haven, M.L, Eichorn, E.S, et al. (1997) Effects of omeprazole on healing of naturally-occurring gastric ulcers in thoroughbred racehorses. Equine Vet J, 29:425-429. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Javsicas, L.H, Sanchez, L.C (2008) The effect of omeprazole paste on intragastric pH in clinically ill neonatal foals. Equine Vet J, 40(1):41-4.
↑ Murray, M.J (1994) Gastric ulcers in adult horses. Comp Cont Educ Pract Vet, 16:792-794,797. In: Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
↑ Danesh, J.Z, Duncan, A, Russell, R.I, Mitchell, G (1988) Effect of intragastric pH on mucosal protective action of sucralfate. Gut, 29:1379-1385. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Leandro, G, Pilotto, A, Franceschi, M et al. (2001) Prevention of acute NSAID-related gastroduodenal damage: a meta-analysis of controlled clinical trials. Dig Dis Sci, 46:1924-1936. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Sangiah, S, MacAllister, C.C, Amouzadeh, H.R (1989) Effects of misoprostol and omeprazole on basal gastric pH and free acid content in horses. Res Vet Sci, 47:350-354. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Tomlinson, J.E, Blikslager, A.T (2005) Effects of cyclooxygenase inhibitors flunixin and deracoxib on permeability of ischaemic-injured equine jejunum. Equine Vet J, 37:75-80. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.
↑ Orsini, J.A, Haddock, M, Stine, L, Sullivan, E.K, Rabuffo, T.S, Smith, G (2003) Odds of moderate or severe gastric ulceration in racehorses receiving antiulcer medications. J Am Vet Med Ass, 223:336-339. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Nieto, J.E, Spier, S, Pipers, F.S, Stanley, S, Aleman, M.R, Smith, D.C, Snyder, J.R (2002) Comparison of paste and suspension formulations of omeprazole in the healing of gastric ulcers in racehorses in active training. J Am Vet Med Ass, 221: 1139-1143. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.Vet Clin North Am Equine Pract, 25(2):283-301.
↑ ^104.0 ^104.1 Andrews, F.M, Frank, N, Sommardahl, C.S, Buchanan, B.R, Elliott, S.B, Allen, V.A (2006) Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses. J Vet Intern Med, 20(5):1202-6.
↑ Holbrook, T.C, Simmons, R.D, Payton, M.E, MacAllister, C.G (2005) Effect of repeated oral administration of hypertonic electrolyte solution on equine gastric mucosa. Equine Vet J, 37: 501-504.
↑ Murray, M.J, Ball, M.M, Parker, G.A (1988) Megaoesophagus and aspiration pneumonia secondary to gastric ulceration in a foal. J Am Vet Med Assoc, 192:381-383.
↑ Nadeau, J.A, Andrews, F.M, Mathews, A.M, Argenzio, R.A, Blackford, J.T, Saxton, A.M (2000) Evaluation of diet as a cause of gastric ulcers in horses. Am J Vet Res, 61:784-790. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ Lybbert, T, Gibbs, P, Cohen, N, Scott, B, Sigler, D (2007) Feeding alfalfa hay to exercising horses reduces the severity of gastric mucosal ulceration. Proc Am Ass Equine Practnrs, 53:525-526. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.
↑ ^109.0 ^109.1 McClure, S.R, White, G.W, Sifferman, R.L, et al. (2005) Efficacy of omeprazole paste for prevention of recurrence of gastric ulcers in horses in race training. J Am Vet Med Assoc, 226:1685-1688.
↑ McClure, S.R, White, G.W, Sifferman, R.L, et al. (2005) Efficacy of omeprazole paste for prevention of gastric ulcers in horses in race training. J Am Vet Med Assoc, 226:1681-1684.
↑ White, G.W, McClure, S.R, Sifferman, R.L, Bernard, W, Doucet, M, Vrins, A, Hughes, F, Holste, J.E, ALva, R, Fleishman, C, Cramer, L (2003) Prevention of occurrence and recurrence of gastric ulcers in horses by treatment with omeprazole at 1mg/kg/day. Proc Am Ass Equine Practnrs, 49: 220-221.
↑ White, G.W, McClure, S.R, Sifferman, R.L, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration. J Am Vet Med Ass, 230:1680-1682.

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[Merritt-1] 1.0 ^1.1 Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric ulcer syndrome. Equine Vet J, 41(7):616.

[EGUC-2] 2.00 ^2.01 ^2.02 ^2.03 ^2.04 ^2.05 ^2.06 ^2.07 ^2.08 ^2.09 ^2.10 ^2.11 ^2.12 ^2.13 ^2.14 ^2.15 ^2.16 ^2.17 ^2.18 ^2.19 ^2.20 The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet Educ, 11(5):262-272.

[3] Andrews, F.M, Bernard, W.V, Byars, T.D et al. (1999) Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS). Equine Vet Educ, 1:122-134. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.

[Bell-4] 4.0 ^4.1 Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review. N Z Vet J, 55(1):1-12).

[Martineau-5] 5.0 ^5.1 ^5.2 Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644. Cite error: Invalid <ref> tag; name "Martineau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Martineau" defined multiple times with different content

[Sanchez-6] 6.00 ^6.01 ^6.02 ^6.03 ^6.04 ^6.05 ^6.06 ^6.07 ^6.08 ^6.09 ^6.10 ^6.11 ^6.12 ^6.13 ^6.14 ^6.15 ^6.16 ^6.17 ^6.18 ^6.19 ^6.20 ^6.21 ^6.22 ^6.23 ^6.24 ^6.25 ^6.26 ^6.27 ^6.28 Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15. Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content Cite error: Invalid <ref> tag; name "Sanchez" defined multiple times with different content

[Merck-7] 7.0 ^7.1 ^7.2 ^7.3 ^7.4 ^7.5 ^7.6 ^7.7 Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial

[Sandin-8] 8.0 ^8.1 ^8.2 ^8.3 ^8.4 Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.

[Hammond-9] 9.0 ^9.1 ^9.2 ^9.3 Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. Equine Vet J, 18(4):284-287.

[10] Vatistas, N.J, Snyder, J.R, Carlson, G, et al (1994) Epidemiological study of gastric ulceration in the thoroughbred racehorse:202 horses 1992-1993. Proc Am Assoc Equine Pract, 40:125-126

[11] Murray, M.J, Schusser, G.F, Pipers, F.S, Gross, S.J (1996) Factors associated with gastric lesions in thoroughbred racehorses. Equine Vet J, 28:368-374.

[Vatistas_2-12] 12.0 ^12.1 ^12.2 ^12.3 ^12.4 ^12.5 ^12.6 Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44 Cite error: Invalid <ref> tag; name "Vatistas 2" defined multiple times with different content

[13] Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthruy, R.M, Thurmond, M, Zhou, H, Lloyd, K.L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses. Equine Vet J, Suppl 29:34-39.

[14] McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses. J Am Vet Med Assoc, 215:1130-1133.

[15] MacAllister, C.G, Sangiah, S, Mauromoustakos, A (1992) Effect of a histamine H, type receptor antagonist (WY 45, 727) on the healing of gastric ulcers in ponies. J Vet Int Med, 6:271-275.

[16] Nieto, J.E, Snyder, J.R, Beldomenico, P et al. (2004) Prevalence of gastric ulcers in endurance horses: a preliminary report. Vet J, 167:33-37.

[17] Bertone, J (2000) Prevalence of gastric ulcers in elite, heavy use western performance horses. Proc Am Assoc Equine Pract, 46:256-259.

[18] LeJeune, S.S, Nieto, J.E, Dechant, J.E, Snyder, J.R (2009) Prevalence of gastric ulcers in Thoroughbred broodmares in pasture: a preliminary report. Vet J, 181(3):251-5.

[19] Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. J Equine Vet Sci, 23:560-561. In:Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.

[20] Wilson, J.H (1986) Gastric and duodenal ulcers in foals: a retrospective study. Proc Equine Colic Res Symp 2nd:126-128.

[21] Murray, M.J, Grodinsky, C, Cowles, R.R, et al.(1990) Endoscopic evaluation of changes in gastric lesions of Thoroughbred foals. J Am Vet Med Assoc, 196:1623-1627.

[22] Murray, M.J (1989) Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). J Am Vet Med Assoc, 195:1135-1141.

[23] Orsini, J.A, Pipers, F.S (1997) Endoscopic evaluation of the relationship between training, racing, and gastric ulcers. Vet Surg, 26:424. In: Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.

[24] Murray, M.J (1994) Gastric ulcers in adult horses. Comp Cont Educ Pract Vet, 16:792-794. In:Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.

[25] Murray, M. (1992) Gastric ulceration in horses: 91 cases (1987-1990). J Am Vet Med Assoc, 201:117-120. In: Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: Range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644.

[26] Luthersson, N, Nielsen, K.H, Harris, P, Parkin, T.D (2009) The prevalence and anatomical distribution of equine gastric ulcer syndrome (EGUS) in 201 horses in Denmark. Equine Vet J, 41(7):619-24.

[27] Murray, M.J (1994) Characteristics of gastric ulcer pathophysiology. Proc Am Coll Vet Intern Med, 12:610-612. In: Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.

[28] Bell, R.J.W, Kingston, J.K, Mogg, T.D, Perkins, N.R (2007) The prevalence of gastric ulceration in racehorses in New Zealand. N Z Vet J, 55:13-18. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.

[29] Murray, M.J, Nout, Y.S, Ward, D.L (2001) Endoscopic findings of the gastric antrum and pylorus in horses: 162 cases (1996-2000). J Vet Intern Med, 15:401-406. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.

[30] Jeffrery, S.C, Murray, M.J, Eichorn, E.S (2001) Distribution of epidermal growth factor receptor (EGFr) in normal and acute peptic-injured equine gastric squaous epithelium. Equine Vet J, 33:562-569. In: Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse. Part 1: range of lesions present in 21 mature individuals. Equine Vet J, 41(7):638-644.

[31] Sanchez, L.C, Lester, G.D, Merritt, A.M (2001) Intragastric pH in critically ill neonatal foals and the effect of ranitidine. J Am Vet Med Assoc, 218:907-911. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.

[Nadeau-32] 32.0 ^32.1 ^32.2 ^32.3 ^32.4 ^32.5 ^32.6 ^32.7 ^32.8 ^32.9 Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615. Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content Cite error: Invalid <ref> tag; name "Nadeau" defined multiple times with different content

[33] Nadeau, J.A, Andrews, F.M, Patton, C.S, Argenzio, R.A, Mathew, A.G, Saxton, A.M (2003) Effects of hydrochloric, acetic, butyric, and proprionic acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses. Am J Vet Res,64:404-412.

[34] Nadeau, J.A, Andrews, F.M, Patton, C.S, Argenzio, R.A, Mathew, A.G, Saxton, A.M (2003) Effects of hydrochloric, valeric, and other volatile fatty acids on pathogenesis of ulcers in the nonglandular portion of the stomach of horses. Am J Vet Res, 64:413-417.

[35] Andrews, F.M, Buchanan, B.R, Elliott, S.B, Al Jassim, R.A.M, McGowan, C.M, Saxton, A.M (2008) In vitro effects of hydrochloric and lactic acids on bioelectric properties of equine gastric squamous mucosa. Equine Vet J, 40:301-305.

[36] Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses. J Equine Vet Sci, 23:560-561. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.

[37] White, G, McClure, S.R, Siifferman, R, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration. J Am Vet Med Assoc, 230(11):1680-2.

[38] Lorenzo-Figueras, M, Merritt, A.M (2002) Effects of exercise on gastric volume and pH in the proximal portion of the stomach of horses. Am J Vet Res, 63:1481-1487.

[39] Murray, M.J, Eichorn, E.S (1996) Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall confinement with ad libitum access to hay on gastric ulceration in horses. Am J Vet Res, 57:1599-1603.

[40] Husted, L, Sanchex, L.C, Olsen, S.N, Baptiste, K.E, Merritt, A.M (2008) Effect of paddock vs. stall housing on 24 hour gastric pH within the proximal and ventral equine stomach. Equine Vet J, 40(4):337-41.

[41] McClure, S.R, Carithers, D.S, Gross, S.J, Murray, M.J (2005) Gastric ulcer development in horses in a simulated show or training environment. J Am Vet Med Assoc, 227:775-777.

[42] Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. Equine Vet J, 25:417-421. In: Sandin, A, Skidell, J, Haggstrom, J, Nilsson, G (2000) Postmortem findings of gastric ulcers in Swedish horses older than age one year: a retrospective study of 3715 horses (1924–1996). Equine Vet J, 32(1):36-42.

[43] Berschneider, H.M, Blikslager, A.T, Roberts, M.C (1999) Role of dudodenal relfux in nonglandular gastric ulcer disease of the mature horse. Equine Vet J Suppl, 29:24-29.

[44] Murray, M.J, Schusser, G.F (1993) Measurement of 24-h gastric pH using an indwelling pH electrode in horses unfed, fed and treated with ranitidine. Equine Vet J, 25:417-421. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.

[45] Murray, M.J (1994) Equine model of inducing ulceration in alimentary squamous epithelial mucosa. Dig Dis Sci, 39:2530-2535. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) Equine Internal Medicine (Third Edition), Saunders, Chapter 15.

[Vatistas_thesis-46] 46.0 ^46.1 Vatistas, N.J (1998) Gastric Ulceration in the Racing Thoroughbred. PhD Thesis. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training. Equine Vet J Suppl, 29:40-44

[47] Luthersson, N, Nielson, K.H, Harris, P, Parkin, T.D (2009) Risk factors associated with equine gastric ulceration syndrome (EGUS) in 201 horses in Denmark. Equine Vet J, 41(7):625-30.

[48] Smyth, G.B, Young, D.W, Hammond, L.S (1988) Effects of diet and feeding on post-prandial serum gastrin and insulin concentrations in adult horses. Equine Vet J Suppl 7:56-59.

[49] Mètayer, N, Lhôte, M, Bahr, A, Cohen, N.D, Kim, I, Rousell, A.J, Julliand, V (2004) Meal size and starch content affect gastric emptying in horses. Equine Vet J, 36:434-440. In: Nadeau, J.A, Andrews, F.M (2009) Science: Overviews Equine gastric ulcer syndrome: The continuing conundrum. Equine Vet J, 41(7):611-615.

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@@ Line 1: / Line 1: @@
-{{unfinished}}
+{{OpenPagesTop}}
+Also known as: '''''Gastroduodenal ulceration — Gastrointestinal ulceration — Equine Gastric Ulcer Syndrome — EGUS — Peptic ulcer disease — Equine Gastric Ulcer
-{| cellpadding="10" cellspacing="0" border="1"
+==Introduction==
-| Also known as:
-|'''Gastroduodenal ulceration<br>
-'''Gastrointestinal ulceration<br>
-'''Equine Gastric Ulcer Syndrome<br>
-'''EGUS<br>
-'''Peptic ulcer disease<br>
-'''Equine Gastric Ulcer'''
-|}
-{| cellpadding="10" cellspacing="0" border="1"
-| See also:
-|'''[[Gastric Ulceration - all species]]'''
-|}
-==Description==
 The term ''''Equine gastric ulcer syndrome (EGUS)'''' encompasses a number of disease complexes<ref name="Merritt">Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric
 ulcer syndrome.  ''Equine Vet J'', 41(7):616.</ref> associated with ulceration of the oesophageal, gastric or duodenal mucosa<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> in horses.  When such damage is caused by acidic gastric juice, the defect is described as a ''''peptic ulcer''''.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  The non-glandular (squamous, proximal or orad) region of the equine stomach is lined by stratified squamous mucosa and a glandular mucosa lines the distal (aborad) portion.  Ulceration of either, or both<ref>Andrews, F.M, Bernard, W.V, Byars, T.D ''et al.'' (1999) Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).   ''Equine Vet Educ'', 1:122-134.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> regions of the gastric mucosa is one of the most important problems of the equine stomach as it may limit performance<ref name="Bell">Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review.  ''N Z Vet J'', 55(1):1-12).</ref> and compromise welfare.<ref name="Martineau">Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse.  Part 1: Range of lesions present in 21 mature individuals.  ''Equine Vet J'', 41(7):638-644.</ref>  The two regions meet abruptly at the '''''margo plicatus'''''<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>, adjacent to where most ulcers occur.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Damage to these regions occurs via differing pathophysiological routes and varies in severity.  Inflammation can progress to cellular death and sloughing causing disruption of the superficial mucosa ('''erosion'''), then penetration of the submucosa down to the level of the ''lamina propria''<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>('''ulceration'''),  full thickness ulceration ('''perforation''')<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> and potentially duodenal stricture.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> The occult nature of the disease typically precludes the observation of clinical signs until severe ulceration has developed.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>
+See also:'''[[Gastric Ulceration - all species]] — [[Colic, Gastric Causes]]'''
 ==Prevalence==
@@ Line 57: / Line 44: @@
 *'''Bicarbonate:''' secreted by gastric mucosal cells.  Secretion triggered by luminal acid concentrations, mechanical irritation, and release of endogenous prostaglandins. Bicarbonate trapped in the mucous layer creates a pH gradient from physiological pH at the mucosal surface to a gastric acid pH at the luminal interface.
 *'''Epidermal growth factors:''' found in salivary gland secretions, promote DNA synthesis and proliferation of gastric mucosal cells. Also important in prostaglandin synthesis and inhibit hydrochloric acid (HCl) secretion by the parietal glands.
-*'''Epithelial restitution mechanisms:''' important for gastric mucosal integrity. Epithelial injury induces migration of adjacent cells to replace damaged cells within minutes without the need of new cell proliferation.  Shear forces, induced by mixing of ingesta, are counterbalanced by epithlial restoration.
+*'''Epithelial restitution mechanisms:''' important for gastric mucosal integrity. Epithelial injury induces migration of adjacent cells to replace damaged cells within minutes without the need of new cell proliferation.  Shear forces, induced by mixing of ingesta, are counterbalanced by epithelial restoration.
 *'''Adequate mucosal blood supply:''' required to provide the mucosa with oxygen and nutrients to produce the mucus-bicarbonate layer and to support rapid turnover of epithelial cells.  Also required to remove acid that has diffused into the mucosa.  Compromised mucosal perfusion may be important in the stress-related ulceration of neonates.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
 *'''Prostaglandins:''' inhibit acid secretion, promote mucosal perfusion (through vasodilation), increase mucus and bicarbonate secretions and support mucosal cell repair.  PGE2 is especially important in these functions.
@@ Line 79: / Line 66: @@
 ====Extrinsic ulcerogenic factors (RISK FACTORS)====
-*'''Exercise:''' there appears to be a high prevalence of gastric ulcers in horses performing in most disciplines.<ref>Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses.  ''J Equine Vet Sci'', 23:560-561.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  Although this may be related to exercise, other confounding factors related to these disciplines such as travel, diet, feeding regime, use of non-steroidal anti-inflammatory drugs (NSAIDs) and stress may be significant.  However, Vatistas and co-workers (1999) were able to induce and maintain EGUS in racehorses in fast work without the use of NSAIDs or fasting before exercise.<ref name="Vatistas 2">Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref>  There is also evidence that training for just 8 days is suffcient to induce gastric ulcers.<ref>White, G, McClure, S.R, Siifferman, R, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration.  ''J Am Vet Med Assoc'', 230(11):1680-2.</ref>  The higher prevalence of gastric ulcers at ''post mortem'' in racehorses in training compared to those in retirement is consistent with the hypothesis that exercise may be an important risk factor for EGUS.<ref name="Hammond">Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses.  ''Equine Vet J'', 18(4):284-287.</ref>  Strenuous exercise is known to stimulate '''gastrin release''' which has effects on HCl secretion, gastric emptying and gastric blood flow.  Diversion of blood to active muscle groups may further deprive the gastric mucosa of the perfusion required for its integrity(REF).  It is also thought that exposure of the squamous mucosa to acid is increased as the stomach is compressed by the abdominal viscera and diaphragm during excercise.<ref>Lorenzo-Figueras, M, Merritt, A.M (2002) Effects of exercise on gastric volume and pH in the proximal portion of the stomach of horses.  ''Am J Vet Res'', 63:1481-1487.</ref>
+*'''Exercise:''' there appears to be a high prevalence of gastric ulcers in horses performing in most disciplines.<ref>Hartmann, A.M, Frankeny, R.L (2003) A preliminary investigation into the association between competition and gastric ulcer formation in non-racing performance horses.  ''J Equine Vet Sci'', 23:560-561.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  Although this may be related to exercise, other confounding factors related to these disciplines such as travel, diet, feeding regime, use of non-steroidal anti-inflammatory drugs (NSAIDs) and stress may be significant.  However, Vatistas and co-workers (1999) were able to induce and maintain EGUS in racehorses in fast work without the use of NSAIDs or fasting before exercise.<ref name="Vatistas 2">Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref>  There is also evidence that training for just 8 days is suffcient to induce gastric ulcers.<ref>White, G, McClure, S.R, Siifferman, R, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration.  ''J Am Vet Med Assoc'', 230(11):1680-2.</ref>  The higher prevalence of gastric ulcers at ''post mortem'' in racehorses in training compared to those in retirement is consistent with the hypothesis that exercise may be an important risk factor for EGUS.<ref name="Hammond">Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses.  ''Equine Vet J'', 18(4):284-287.</ref>  Strenuous exercise is known to stimulate '''gastrin release''' which has effects on HCl secretion, gastric emptying and gastric blood flow.  Diversion of blood to active muscle groups may further deprive the gastric mucosa of the perfusion required for its integrity.  It is also thought that exposure of the squamous mucosa to acid is increased as the stomach is compressed by the abdominal viscera and diaphragm during excercise.<ref>Lorenzo-Figueras, M, Merritt, A.M (2002) Effects of exercise on gastric volume and pH in the proximal portion of the stomach of horses.  ''Am J Vet Res'', 63:1481-1487.</ref>
 *'''Housing and Transport:'''  housing in '''stables''' has been proposed as a risk factor for gastric ulcers, with more lesions being found in confined horses compared to those out at grass.<ref>Murray, M.J, Eichorn, E.S (1996) Effects of intermittent feed deprivation, intermittent feed deprivation with ranitidine administration, and stall
@@ Line 90: / Line 77: @@
 *'''NSAIDs:''' as in [[Gastric Ulceration - all species|other species]], NSAIDs have been shown to cause gastric ulcers in horses.  Typically this is associated with high doses or frequent administration of '''phenylbutazone''' or '''flunixin meglumine'''.  However, although there is evidence to the contrary,<ref>Andrews, F.M, Reinemeyer, C.R, Longhofer, S.L (2009) Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. ''Vet Ther'', 10(3):113-20.</ref>therapeutic doses of NSAIDs may be sufficient to induce EGUS.  Other studies have suggested that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally<ref>Monreal, L, Sabatè, D, Segura, D, Mayós, I, Homedes, J (2004) Lower gastric ulcerogenic effect of suxibuzone compared to phenylbutazone when administered orally to horses.  ''Res Vet Sci'', 76:145-149.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>and that '''combination treatment''' with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone.<ref>Reed, S.K, Messer, N.T, Tessman, R.K, Keegan, K.G (2006) Effects of phenylbutazone alone or in combination with flunixin meglumine on blood protein concentrations in horses.  ''Am J Vet Res'', 67:398-402.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref> The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa,<ref>MacAllister, C.G, Morgan, S.J, Borne, A.T, Pollet, R.A, (1993) Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses.  ''J Am Vet Med Ass'', 202:71-77.  In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref><ref>Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists.  ''Equine Vet J Suppl'', 7:77-79.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref>Kumaran, D, Bhuvanakumar, C.K (1994) Gastro duodenal ulceration in foals - a discussion.  ''Cenfaur Mylapore'', 10:83-86. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref> they may look different endoscopically from ulcers that occur naturally,<ref name="Jonsson">Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref> and they appear to heal spontaneously.<ref>Jones, W.E (1983) Gastrointestinal ulcers [foal].  ''Equine Vet Data'', 4:305-308.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref>MacAllister, C.G, Sangiah, S (1993) Effect of ranitidine (in healing of experimentally induced gastric ulcers in ponies.  ''Am J Vet Res'', 54:1103-1107.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref> Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.<ref>Vatistas N.J, Snyder, J.R, Carlson, G.P, Johnson, B, Arther, R.M, Thurmiind, M, Lloyd, K.C.K (1994) Epidemiology study of gastric ulcerarion in the Thoroughbred race horse: 202 horses.  ''Proc Am Ass Equine Pract'', 39:125-126.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref>Murray, M.J, Schusser, G.F, Pipers, F.S, Gro:ss, S.J (1996) Factors associated with gastric lesions in Thoroughbred racehorses.  ''Equine Vet J'', 28:368-374.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref name="Vatistas thesis">Vatistas, N.J (1998) Gastric Ulceration in the Racing Thoroughbred.  ''PhD Thesis''.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref>
-*'''Infective agents:''' ''Helicobacter spp.'' have been held responsible for the initiation and recurrence of human gastric ulcers.  ''Helicobacter equorum'' has been isolated from equine faecal samples(Fox 2002 in Nadeau) and ''Helicobacter''-like DNA has been found in both foal faeces(Moyaert 2009 in Nadeau)and the stomachs of mature horses.  However, such findings have been demonstrated in horses with and without gastric lesions(Contreras 2007 in Nadeau) and in clinically healthy animals.  Any link between EGUS and ''Helicobacter'' remains weak at best, although there is a suggestion that colonisation of equine gastric ulcers with ''E.coli'' may delay their healing.(Al Jassim 2006 in Nadeau)
+*'''Infective agents:''' [[Helicobacter|''Helicobacter spp.'']] have been held responsible for the initiation and recurrence of human gastric ulcers.  ''Helicobacter equorum'' has been isolated from equine faecal samples<ref>Fox, J.G (2002) The non-''H.pylori'' helicobacters: their expanding role in gastorintestinal and systemic disease.  ''Gut'', 50:273-283.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref> and ''Helicobacter''-like DNA has been found in both foal faeces<ref>Moyaert, H, Haesebrouck, F, Dewulf, J, Ducatelle, R, Pasmans, F (2009) ''Helicobacter equorum'' is highly prevalent in foals.  ''Vet Microbiol'', 133:190-192.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> and the stomachs of mature horses.  However, such findings have been demonstrated in horses with and without gastric lesions<ref>Contreras, M, Morales, A, Garcia-Amado, M.A, DeVera, M, Bermudez, V, Gueneau, P (2007) Detection of ''Helicobacter''-like DNA in the gastric mucosa of Thoroughbred horses.  ''Letters in Appl Microbiol'', 45:553-337.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>and in clinically healthy animals.  Any link between EGUS and ''Helicobacter'' remains weak at best, although there is a suggestion that colonisation of equine gastric ulcers with [[Escherichia coli|''E.coli'']] may delay their healing.<ref>Al Jassim, R.A.M, Scott, P.T, Trebbin, A.L, Trott, D, Pollitt, C.C (2006) The genetic diversity of lactic acid producing bacteria in the equine gastrointestinal tract.  ''FEMS Microbiol Letters'', 248:75-81.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref>
 *'''Temperament:''' a nervous disposition has been linked with gastric ulcers<ref>McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses.  ''J Am Vet Med Ass 215:1130-1133.  In: In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref>but the same association was not seen in another study.<ref>Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthur, R.M, Thurmond, M, Zhou, H, Lloyd, L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses.  ''Equine Vet J Suppl'', 29:34-39.  In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref>
@@ Line 100: / Line 87: @@
 *hypotensive shock (for example with blood loss, sepsis, endotoxaemia or fluid sequestration in colic)
 *an increase in sympathetic tone (which might be related to physiological or psychological stresses) or
-*other severe disease states (such as disseminated intravascular coagulation (DIC)).
+*other severe disease states (such as [[DIC|disseminated intravascular coagulation]]).
-Furthermore, any impairment of gastric motility (as seen with neurological imbalances, several types of colic and certain drugs) might be expected to increase the risk of ulceration.  Despite a lack of clarity, the final common pathway for EGUS appears to be the breaching of mucosal defences by acidic gastric contents.  Since horses secrete gastric HCl continuously, even in the fasted state,(Campbell-Thompson, Merritt, 1987) they are especially vulnerable to acid-associated damage.
+Furthermore, any impairment of gastric motility (as seen with neurological imbalances, several types of colic and certain drugs) might be expected to increase the risk of ulceration.  Despite a lack of clarity, the final common pathway for EGUS appears to be the breaching of mucosal defences by acidic gastric contents.  Since horses secrete gastric HCl continuously, even in the fasted state,<ref>Campbell-Thompson, M.L, Merritt, A.M (1987) Effect of ranitidine on gastric acid secretion in young male horses.  ''Am J Vet Res'', 48:1511-1515.</ref> they are especially vulnerable to acid-associated damage.
 ==Clinical syndrome==
@@ Line 113: / Line 100: @@
 *Excessive recumbency<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>
 *Mild to severe colic
-**Mild, recurrent colic signs post-prandially<ref>Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.  ''Vet Clin North Am Equine Pract'', 25(2):283-301.</ref>
+**Mild, recurrent [[Colic Diagnosis - Clinical Signs|colic signs]] post-prandially<ref>Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.  ''Vet Clin North Am Equine Pract'', 25(2):283-301.</ref>
 **In one study, 49% of horses that presented for colic had gastric ulceration and those with duodenitis-proximal jejunitis had a trend towards a higher prevalence of gastric ulceration compared to those with other GI lesions.<ref>Dukti, S.A, Perkins, S, Murphy, J, Barr, B, Boston, R, Southwood, L.L, Bernard, W (2006) Prevalence of gastric squamous ulceration in horses with abdominal pain.  ''Equine Vet J'', 38:347-349.</ref>
 *Changes in attitude (dullness or depression)<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>
@@ Line 122: / Line 109: @@
 '''Clinical signs in foals vary depending on age and severity:'''
-*'''Neonatal foals''': many ulcers are silent, some foals only exhibit signs when ulceration has become severe.  Glandular ulcers are considered the most significant<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
+*'''Neonatal foals''': many ulcers are silent, some foals only exhibit signs when ulceration has become severe.  Glandular ulcers are considered the most significant<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>.
 **Poor appetite
 **Diarrhoea
@@ Line 146: / Line 133: @@
 **Diarrhoea
-In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  GDUD is the primary differential for ptyalism in foals, other possible diagnoses include oesophageal obstruction and ''Candida'' infection.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>
+In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  Brown gastric fluid may signify bleeding ulcers or necrotizing enterocolitis.  GDUD is the primary differential for ptyalism in foals, other possible diagnoses include oesophageal obstruction and ''Candida'' infection.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>
 ==Diagnosis==
@@ Line 155: / Line 142: @@
 ====Endoscopy====
-Oesophagogastroscopy or duodenoscopy can be performed under mild sedation (e.g. 0.6-0.8mg/kg xylazine<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>) in the standing horse.  Of these, duodenoscopy is the more specific but more technically demanding method.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  Endoscopic examination requires preparatory starving of the patient for 6-8hours,<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> eliciting a certain degree of stress.  As such, it is preferable not to carry out this technique in foals.  In adult horses, a minimum endoscope length of two metres is essential to visualize the gastric body and fundus.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  A 2.8-3.0 metre endoscope is needed to observe the gastric antrum, pylorus and proximal dudoenum.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  In either case, fibreoptic or videoendoscopic equipment can be used.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Based on a consensus, the Equine Gastric Ulcer Council (EGUC) published an EGUS Lesion Scoring System which they claimed to be simple and applicable to both regions of the equine gastric mucosa.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  This last point has been debated, since most of the acquired data on gastric lesions refers only to the squamous mucosa.<ref name="Merritt">Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric
+Oesophagogastroscopy or duodenoscopy can be performed under mild sedation (e.g. 0.6-0.8mg/kg xylazine<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>) in the standing horse.  Of these, duodenoscopy is the more specific but more technically demanding method.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  Endoscopic examination requires preparatory starving of the patient for 6-8hours,<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref> eliciting a certain degree of stress.  As such, it is preferable not to carry out this technique in foals.  Should endoscopy be necessary, any air introduced into the foal's stomach must be evacuated at the end of the procedure to avoid exacerbation of colic.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  In adult horses, a minimum endoscope length of two metres is essential to visualize the gastric body and fundus.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  A 2.8-3.0 metre endoscope is needed to observe the gastric antrum, pylorus and proximal dudoenum.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  In either case, fibreoptic or videoendoscopic equipment can be used.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Based on a consensus, the Equine Gastric Ulcer Council (EGUC) published an EGUS Lesion Scoring System which they claimed to be simple and applicable to both regions of the equine gastric mucosa.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  This last point has been debated, since most of the acquired data on gastric lesions refers only to the squamous mucosa.<ref name="Merritt">Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric
 ulcer syndrome.  ''Equine Vet J'', 41(7):616.</ref>  At the time of writing however, the EGUC system appears to be widely used in practice:
@@ Line 180: / Line 167: @@
 Diffuse inflammation may be the only lesion observed in foals with early GDUD.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  In contrast to other scoring systems,<ref>MacAllister, C.G, Andrews F.M, Deegan E, Ruoff, W, Olovson, S.G (1997) A scoring system for gastric ulcers in horses.  ''Equine Vet J'', 29:430-433.</ref> the EGUC approach does not include bleeding when assigning lesion grades.  The justification is that the 'snapshot' provided by endoscopy may by chance identify bleeding of superficial erosions whilst missing the intermittent haemorrhage of more severe lesions.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Endoscopy may assist in understanding the severity of the disease and assessing the therapeutic response, but it is not without disadvantages.  Ulcer severity may be underestimated, particularly in the squamous region and glandular ulcers may be missed altogether.<ref>Andrews, F.M, Reinmeyers, C.R, McCracken, M.D, Blackford, J.T, Nadeau, J.A, Saabye, L, Sotell, M, Saxton, A (2002) Comparison of endoscopic, necropsy and histology scoring of equine gastric ulcers.  ''Equine Vet J'',34(5):475-478.</ref>  Lesions that appear grossly similar may have different grades on histopathology.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  This is important because varying lesions may have different causes, requiring a range of treatment approaches.
-====Radiography====
+====Other Imaging====
-In older foals with GDUD, detection of gastric outflow obstruction via abdominal radiography is essential to treatment and prognosis.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  Liquid barium will demonstrate very delayed or no outflow depending on the degree of obstruction.  Without contrast medium, a large, gas filled stomach will be obvious.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  The need to perform contrast radiography must be weighed against the stress it would place upon the foal.
+In older foals with GDUD, detection of gastric outflow obstruction via abdominal radiography is essential to treatment and prognosis.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  Liquid barium will demonstrate very delayed or no outflow depending on the degree of obstruction.  Without contrast medium, a large, gas filled stomach will be obvious.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  The need to perform contrast radiography must be weighed against the stress it would place upon the foal.  If gastric rupture is suspected, abdominal ultrasound can be used to identify free fluid in the abdomen and abdominocentesis may confirm the diagnosis.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
 ====Biopsy====
@@ Line 203: / Line 190: @@
 ====Histamine 2 receptor antagonists====
-Parietal cells secrete HCl upon stimulation of histamine, acetylcholine or gastrin receptors.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Competitive H2 receptor antagonists have successfully elevated gastric pH and treated gastric ulcers in mature horses and foals.(44,85,97 in Sachez)  There appears to be a great variability among horses in their dose requirements for H2 antagonists which may be explained by individual bioavilability for these compounds.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Currently recommended doses proposed to be effective in the majority of horses<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> are:
+Parietal cells secrete HCl upon stimulation of histamine, acetylcholine or gastrin receptors.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Competitive H2 receptor antagonists have successfully elevated gastric pH and treated gastric ulcers in mature horses and foals.<ref name="Lester">Sanchez, L.C, Lester, G.D, Merritt, A.M (1998) Effect of ranitidine on intragastric pH in clinically normal neonatal foals.  ''J Am Vet Med Assoc'', 212:1407-1412.</ref><ref>Becht, J.L, Byars, T.D (1986) Gastroduodenal ulceration in foals.  ''Equine Vet J'', 18:307-312.</ref>  There appears to be a great variability among horses in their dose requirements for H2 antagonists which may be explained by individual bioavailability for these compounds.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Currently recommended doses for cimetidine, ranitidine and f amotidine proposed to be effective in the majority of horses have been recommended by Sanchez.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
-*'''Cimetidine''' 20-30mg/kg PO every 8 hours or 6.6mg/kg IV every 6 hours
-*'''Ranitidine''' 6.6mg/kg PO every 8 hours or 1.5-2mg/kg IV every 6 hours
-*'''Famotidine''' 10-15mg/kg PO every 24 hours
 ====Proton-pump inhibitors (PPIs)====
-PPIs irreversibly bind to the H+K+-ATPase proton pump of the parietal cell and block the secretion of hydrogen ions.  These agents are more effective than H2 antagonsists as their action is receptor-independent,<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> blocking the final pathway of acid secretion and they have a prolonged effect allowing for once-daily dosing.((Brown and Rees 1994). Papich 1993, Sanchez)  '''Omeprazole (Gastroguard™)''', a subsituted benzimidazole, is currently the only PPI licensed for use in horses.  At a dose rate of 4mg/kg per day omeprazole has proven effective in reducing the severity of gastric ulcers in Thoroughbred horses in active race training<ref name="Vatistas">Vatistas, N.J, Snyder, J.R, Nieto, J, Thompson, D, Pollmeier, M, Holstes, J (1999) Acceptability of a paste formulation and efficacy of high dose omeprazole in healing gastric ulcers in horses maintained in race training.  ''Equine Vet J Suppl'', 29:71-76.</ref> and no adverse effects have been observed.  The paste formulation is easy to administer and is generally well accepted by horses.  Omeprazole has demonstrated efficacy in the resolution of both naturally-occurring and NSAID-induced gastric ulcers in horses.(103.104 in Sanchez)  A single dose has also produced an increase in gastric pH in clinically ill neonatal foals<ref>Javsicas, L.H, Sanchez, L.C (2008) The effect of omeprazole paste on intragastric pH in clinically ill neonatal foals.  ''Equine Vet J'', 40(1):41-4.</ref> and has contributed to ulcer healing in neonates.<ref>MacAllister, C.G, Sifferman, R.L, McClure, S.R ''et al.'' (1999) Effects of omeprazole paste on healing of spontaneous gastric ulcers in horses and foals: a field trial.  ''Equine Vet J Suppl'', 77-80.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  A potential concern is that altering gastric pH may encourage bacterial overgrowth.  Thus further work is needed to evaluate the long-term safety of omeprazole in horses and particularly, foals.<ref name="Vatistas">Vatistas, N.J, Snyder, J.R, Nieto, J, Thompson, D, Pollmeier, M, Holstes, J (1999) Acceptability of a paste formulation and efficacy of high dose omeprazole in healing gastric ulcers in horses maintained in race training.  ''Equine Vet J Suppl'', 29:71-76.</ref>
+PPIs irreversibly bind to the H+K+-ATPase proton pump of the parietal cell and block the secretion of hydrogen ions.  These agents are more effective than H2 antagonsists as their action is receptor-independent,<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> blocking the final pathway of acid secretion and they have a prolonged effect allowing for once-daily dosing.<ref>Papich, M.G (1993) Anti-ulcer therapy.  ''Vet Clin N Am'', 202:1465-1468.</ref>  '''Omeprazole (Gastroguard™)''', a subsituted benzimidazole, is currently the only PPI licensed for use in horses.  At a dose rate of 4mg/kg per day omeprazole has proven effective in reducing the severity of gastric ulcers in Thoroughbred horses in active race training<ref name="Vatistas">Vatistas, N.J, Snyder, J.R, Nieto, J, Thompson, D, Pollmeier, M, Holstes, J (1999) Acceptability of a paste formulation and efficacy of high dose omeprazole in healing gastric ulcers in horses maintained in race training.  ''Equine Vet J Suppl'', 29:71-76.</ref> and no adverse effects have been observed.  The paste formulation is easy to administer and is generally well accepted by horses.  Omeprazole has demonstrated efficacy in the resolution of both naturally-occurring and NSAID-induced gastric ulcers in horses.<ref name="MacAllister">MacAllister, C.G, Sifferman, R.L, McClure, S.R ''et al.'' (1999) Effects of omeprazole paste on healing of spontaneous gastric ulcers in horses and foals: a field trial. ''Equine Vet J Suppl'', 77-80. In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref><ref>Murray, M.J, Haven, M.L, Eichorn, E.S, ''et al.'' (1997) Effects of omeprazole on healing of naturally-occurring gastric ulcers in thoroughbred racehorses.  ''Equine Vet J'', 29:425-429.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  A single dose has also produced an increase in gastric pH in clinically ill neonatal foals<ref>Javsicas, L.H, Sanchez, L.C (2008) The effect of omeprazole paste on intragastric pH in clinically ill neonatal foals.  ''Equine Vet J'', 40(1):41-4.</ref> and has contributed to ulcer healing in neonates.<ref name="MacAllister">MacAllister, C.G, Sifferman, R.L, McClure, S.R ''et al.'' (1999) Effects of omeprazole paste on healing of spontaneous gastric ulcers in horses and foals: a field trial.  ''Equine Vet J Suppl'', 77-80.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  A potential concern is that altering gastric pH may encourage bacterial overgrowth.  Thus further work is needed to evaluate the long-term safety of omeprazole in horses and particularly, foals.<ref name="Vatistas">Vatistas, N.J, Snyder, J.R, Nieto, J, Thompson, D, Pollmeier, M, Holstes, J (1999) Acceptability of a paste formulation and efficacy of high dose omeprazole in healing gastric ulcers in horses maintained in race training.  ''Equine Vet J Suppl'', 29:71-76.</ref>
 ====Antacids====
@@ Line 218: / Line 202: @@
 ====Mucosal protectants====
-'''Sucralfate''' is a complex salt of sucrose and aluminium hydroxide.  It is thought to promote ulcer healing via several mechanisms: adherence to ulcerated mucosa, stimulation of mucus secretion, pepsin inibition, increasing PGE synthesis and enhancing the local production of epidermal growth factor.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  It has been used effectively to treat and prevent stress-induced ulcers in man and has been recommended at 10-20mg/kg three times daily for the treatment of glandular ulcers in horses.<ref>Murray, M.J (1994) Gastric ulcers in adult horses.  ''Comp Cont Educ Pract Vet'', 16:792-794,797.  In: Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>  However, the effect of sucralfate on equine squamous gastric ulcers remains inconclusive<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> and the product may be ineffective in the alkaline conditions created by acid suppression agents.(123-125 in Sanchez)
+'''Sucralfate''' is a complex salt of sucrose and aluminium hydroxide.  It is thought to promote ulcer healing via several mechanisms: adherence to ulcerated mucosa, stimulation of mucus secretion, pepsin inibition, increasing PGE synthesis and enhancing the local production of epidermal growth factor.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  It has been used effectively to treat and prevent stress-induced ulcers in man and has been recommended for the treatment of glandular ulcers in horses.<ref>Murray, M.J (1994) Gastric ulcers in adult horses.  ''Comp Cont Educ Pract Vet'', 16:792-794,797.  In: Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>  However, the effect of sucralfate on equine squamous gastric ulcers remains inconclusive<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> and the product may be ineffective in the alkaline conditions created by acid suppression agents.<ref>Danesh, J.Z, Duncan, A, Russell, R.I, Mitchell, G (1988) Effect of intragastric pH on mucosal protective action of sucralfate.  ''Gut'', 29:1379-1385.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
 ====Prostaglandin analogues====
-Synthetic PGE1 analogues are believed to inihibit gastric acid secretion and enhance mucosal cytoprotection.<ref>Leandro, G, Pilotto, A, Franceschi, M ''et al.'' (2001) Prevention of acute NSAID-related gastroduodenal damage: a meta-analysis of controlled clinical trials.  ''Dig Dis Sci'', 46:1924-1936.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  '''Misoprostol''' has been an effective agent in the treatment of human gastric and duodenal ulcers and at 5µg/kg has been shown to increase gastric pH in horses.<ref>Sangiah, S, MacAllister, C.C, Amouzadeh, H.R (1989) Effects of misoprostol and omeprazole on basal gastric pH and free acid content in horses.  ''Res Vet Sci'', 47:350-354.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Although contraindicated in pregnant mares, Misoprostol may be beneficial for mucosal recovery in the face of flunixin treatment.<ref>Tomlinson, J.E, Blikslager, A.T (2005) Effects of cyclooxygenase inhibitors flunixin and deracoxib on permeability of ischaemic-injured equine jejunum.  ''Equine Vet J'', 37:75-80.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
+Synthetic PGE1 analogues are believed to inihibit gastric acid secretion and enhance mucosal cytoprotection.<ref>Leandro, G, Pilotto, A, Franceschi, M ''et al.'' (2001) Prevention of acute NSAID-related gastroduodenal damage: a meta-analysis of controlled clinical trials.  ''Dig Dis Sci'', 46:1924-1936.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  '''Misoprostol''' has been an effective agent in the treatment of human gastric and duodenal ulcers and has been shown to increase gastric pH in horses.<ref>Sangiah, S, MacAllister, C.C, Amouzadeh, H.R (1989) Effects of misoprostol and omeprazole on basal gastric pH and free acid content in horses.  ''Res Vet Sci'', 47:350-354.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Although contraindicated in pregnant mares, Misoprostol may be beneficial for mucosal recovery in the face of flunixin treatment.<ref>Tomlinson, J.E, Blikslager, A.T (2005) Effects of cyclooxygenase inhibitors flunixin and deracoxib on permeability of ischaemic-injured equine jejunum.  ''Equine Vet J'', 37:75-80.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
 ====Gastric prokinetics====
@@ Line 229: / Line 213: @@
 ====Treatment problems====
-The prevalence of gastric ulcers in horses remains high regardless of the common use of antiulcer treatments.  This has been attributed to the expense of recommended products encouraging subtherapeutic and curtailed dosing schedules.<ref>Orsini, J.A, Haddock, M, Stine, L, Sullivan, E.K, Rabuffo, T.S, Smith, G (2003) Odds of moderate or severe gastric ulceration in racehorses receiving antiulcer medications.  ''J Am Vet Med Ass'', 223:336-339.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref>  Omeprazole and ranitidine must be administered for at least 28 days for adequate ulcer healing.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  In the USA, compounded omeprazole from bulk powders are used as a cheaper substitute for the FDA approved products. However, these formulations lack efficacy and are not regulated<ref>Nieto, J.E, Spier, S, Pipers, F.S, Stanley, S, Aleman, M.R, Smith, D.C, Snyder, J.R (2002) Comparison of paste and suspension formulations of omeprazole in the healing of gastric ulcers in racehorses in active training.  ''J Am Vet Med Ass'', 221: 1139-1143.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>
+The prevalence of gastric ulcers in horses remains high regardless of the common use of antiulcer treatments.  This has been attributed to the expense of recommended products encouraging subtherapeutic and curtailed dosing schedules.<ref>Orsini, J.A, Haddock, M, Stine, L, Sullivan, E.K, Rabuffo, T.S, Smith, G (2003) Odds of moderate or severe gastric ulceration in racehorses receiving antiulcer medications.  ''J Am Vet Med Ass'', 223:336-339.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref>  Omeprazole and ranitidine must be administered for at least 28 days for adequate ulcer healing.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  In the USA, compounded omeprazole from bulk powders are used as a cheaper substitute for the FDA approved products. However, these formulations lack efficacy and are not regulated.<ref>Nieto, J.E, Spier, S, Pipers, F.S, Stanley, S, Aleman, M.R, Smith, D.C, Snyder, J.R (2002) Comparison of paste and suspension formulations of omeprazole in the healing of gastric ulcers in racehorses in active training.  ''J Am Vet Med Ass'', 221: 1139-1143.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  A considerable challenge lies in the management of abdominal pain associated with EGUS, since the commonly used NSAIDs for pain control may worsen and even induce further ulcerative lesions.<ref>Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.''Vet Clin North Am Equine Pract'', 25(2):283-301.</ref>  Another challenge is the horse in which oral medication is prohibited.  However, Andrews and colleagues (2006) have demonstrated the efficacy of an omeprazole powder, adminstered IV in sterile water, which signifcantly increases the pH of equine gastric contents and may be useful in problem horses.<ref name="Andrews 2006">Andrews, F.M, Frank, N, Sommardahl, C.S, Buchanan, B.R, Elliott, S.B, Allen, V.A (2006) Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses.  ''J Vet Intern Med'', 20(5):1202-6.</ref>  An ongoing point of debate is the use of antiulcer medication in competition horses.  In 2000, the Bureau of '''The Fèdèration Equestre Internationale (FEI)''' permitted the use of cimetidine, ranitidine and omeprazole to prevent and treat gastric ulcers.  This decision was based on evidence that the compounds were not performance enhancing and that EGUS was such a widespread concern. However, these drugs are still listed under prohibited substances in the '''2009 Appendices of the American Endurance Ride Conference (AERC) Rules and Regulations'''.  The argument is that a horse requiring such treatment is not suffciently well to compete and should be withdrawn from competition if it needs preventative medication.  A related concern is that the AERC permits the use of hyperosmolar oral electrolyte pastes which may cause gastric ulcers.<ref>Holbrook, T.C, Simmons, R.D, Payton, M.E, MacAllister, C.G (2005) Effect of repeated oral administration of hypertonic electrolyte solution on equine gastric mucosa.  ''Equine Vet J'', 37: 501-504.</ref>  Without the protection afforded by antiulcer agents, these horses may be at considerable risk for EGUS.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>
-Nieto, J.E., Spier, S., Pipers, F.S., Stanley, S., Aleman, M.R., Smith, D.C. and Snyder,
-, 1139-1143.
-Merritt et al. 2003; Orsini et al. 2003).<ref name="Nadeau"> In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  A considerable challenge lies in the management of abdominal pain associated with EGUS, since the commonly used NSAIDs for pain control may worsen and even induce further ulcerative lesions.<ref>Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.''Vet Clin North Am Equine Pract'', 25(2):283-301.</ref>  Another challenge is the horse in which oral medication is prohibited.  However, Andrews and colleagues (2006) have demonstrated the efficacy of an omeprazole powder, adminstered IV in sterile water, which signifcantly increases the pH of equine gastric contents and may be useful in problem horses.<ref name="Andrews 2006">Andrews, F.M, Frank, N, Sommardahl, C.S, Buchanan, B.R, Elliott, S.B, Allen, V.A (2006) Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses.  ''J Vet Intern Med'', 20(5):1202-6.</ref>  An ongoing point of debate is the use of antiulcer medication in competition horses.  In 2000, the Bureau of '''The Fèdèration Equestre Internationale (FEI)''' permitted the use of cimetidine, ranitidine and omeprazole to prevent and treat gastric ulcers.  This decision was based on evidence that the compounds were not performance enhancing and that EGUS was such a widespread concern. However, these drugs are still listed under prohibited substances in the '''2009 Appendices of the American Endurance Ride Conference (AERC) Rules and Regulations'''.  The argument is that a horse requiring such treatment is not suffciently well to compete and should be withdrawn form competition if it needs preventative medication.  A related concern is that the AERC permits the use of hyperosmolar oral electrolyte pastes which may cause gastric ulcers.(Holbrook et al. 2005)  Without the protection afforded by antiulcer agents, these horses may be at considerable risk for EGUS.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>
 ==Prognosis==
-Improvement in most clinical signs should be noted within 1-3 weeks of commencing treatment.  Colic or diarrhoea should resolve within 48 hours.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  '''Complications''' related to gastric ulcers are most frequent and severe in foals and include perforation, delayed gastric emptying, gastroesophageal reflux and oesophagitis, and megaoesophagus secondary to chronic gastroesophageal reflux. Sudden '''gastric perforation''' without prior signs occurs sporadically in foals.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>Ulcers in the proximal duodenum or at the pylorus can cause fibrosis and stricture. The latter complication is seen in both foals and adult horses.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>  In mature animals, the most common complication is the recurrence of EGUS after treatment has ceased.  This is typically because the inciting managemental causes have not been altered.
+Improvement in most clinical signs should be noted within 1-3 weeks of commencing treatment.  Colic or diarrhoea should resolve within 48 hours.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  '''Complications''' related to gastric ulcers are most frequent and severe in foals with GDUD.  They include gastric or duodneal perforation, delayed gastric emptying, gastroesophageal reflux and oesophagitis, ascending cholangitis and megaoesophagus or aspiration pneumonia<ref>Murray, M.J, Ball, M.M, Parker, G.A (1988) Megaoesophagus and aspiration pneumonia secondary to gastric ulceration in a foal.  ''J Am Vet Med Assoc'', 192:381-383.</ref> secondary to chronic gastroesophageal reflux. Sudden '''gastric perforation''' without prior signs occurs sporadically in foals.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>Ulcers in the proximal duodenum or at the pylorus can cause fibrosis and stricture. The latter complication is seen in both foals and adult horses.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>  In mature animals, the most common complication is the recurrence of EGUS after treatment has ceased.  This is typically because the inciting managemental causes have not been altered.
-Potential complications of GDUD: delayed gastric emptying, gastrooesphageal reflux, gastric or duodenal rupture, pyloric or duodenal stricture, ascending cholangitis.  Severe squamous and oesophageal ulceration and aspiration pnemonia can occur secondary to gastroesophageal reflux (24, 84-87 in Sanchez)
 ==Prevention==
 ====Management====
-*'''Diet:''' ideally turnout to good quality grass.(Murray 1994)  Stabled horses should have continuous access to hay and should be offered this before calorific needs are met by concentrates.<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>  Alfalfa, or another high calcium or high protein forage may be preventative by increasing gastric pH.(Nadeau et al. 2000; Lybbert et al. 2007; Ralston 2007)   Concentrates should be fed at '''no more than 0.5kg per 100kg body weight''' and not more frequently than every 6 hours.<ref name="Andrews 2006">Andrews, F.M, Frank, N, Sommardahl, C.S, Buchanan, B.R, Elliott, S.B, Allen, V.A (2006) Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses.  ''J Vet Intern Med'', 20(5):1202-6.</ref>  Horses prone to, or at risk of, EGUS should be fed the minimum amount of concentrates necessary.<ref name="Nadeau"> In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>
+*'''Diet:''' ideally turnout to good quality grass.  Stabled horses should have continuous access to hay and should be offered this before calorific needs are met by concentrates.<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>  Alfalfa, or another high calcium or high protein forage may be preventative by increasing gastric pH.<ref>Nadeau, J.A, Andrews, F.M, Mathews, A.M, Argenzio, R.A, Blackford, J.T, Saxton, A.M (2000) Evaluation of diet as a cause of gastric ulcers in horses.  ''Am J Vet Res'', 61:784-790.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref><ref>Lybbert, T, Gibbs, P, Cohen, N, Scott, B, Sigler, D (2007) Feeding alfalfa hay to exercising horses reduces the severity of gastric mucosal ulceration.  ''Proc Am Ass Equine Practnrs'', 53:525-526.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref>  Concentrates should be fed at '''no more than 0.5kg per 100kg body weight''' and not more frequently than every 6 hours.<ref name="Andrews 2006">Andrews, F.M, Frank, N, Sommardahl, C.S, Buchanan, B.R, Elliott, S.B, Allen, V.A (2006) Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses.  ''J Vet Intern Med'', 20(5):1202-6.</ref>  Horses prone to, or at risk of, EGUS should be fed the minimum amount of concentrates necessary.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>
-*'''Stress:''' minimise handling wherever possible, provide company and toys for stabled horses, encourage good feeding habits of foals.(44 in Sanchez)
+*'''Stress:''' minimise handling wherever possible, provide company and toys for stabled horses, encourage good feeding habits of foals.<ref name="Lester">Sanchez, L.C, Lester, G.D, Merritt, A.M (1998) Effect of ranitidine on intragastric pH in clinically normal neonatal foals. ''J Am Vet Med Assoc'', 212:1407-1412.</ref>
 Most of these suggestions would be difficult, if not impossible, to achieve for horses in race training, thus prophylactic medication should be considered.<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>
 ====Prophylaxis====
-'''Omeprazole paste''' at a lower dose (1-2mg/kg) daily for 3-4 weeks.(100, 107-109 in Sanchez)
+'''Omeprazole paste''' at a lower dose daily for 3-4 weeks.<ref name="McClure">McClure, S.R, White, G.W, Sifferman, R.L, ''et al.'' (2005) Efficacy of omeprazole paste for prevention of recurrence of gastric ulcers in horses in race training.  ''J Am Vet Med Assoc'', 226:1685-1688.</ref>
-*Prevented ulcers in horses maintained under ulcerogenic conditions (White et al. 2003; McClure et al. 2005a,b,c;White et al. 2007).
+*Prevented ulcers in horses maintained under ulcerogenic conditions.<ref name="McClure">McClure, S.R, White, G.W, Sifferman, R.L, ''et al.'' (2005) Efficacy of omeprazole paste for prevention of recurrence of gastric ulcers in horses in race training.  ''J Am Vet Med Assoc'', 226:1685-1688.</ref><ref>McClure, S.R, White, G.W, Sifferman, R.L, ''et al.'' (2005) Efficacy of omeprazole paste for prevention of gastric ulcers in horses in race training.  ''J Am Vet Med Assoc'', 226:1681-1684.</ref><ref>White, G.W, McClure, S.R, Sifferman, R.L, Bernard, W, Doucet, M, Vrins, A, Hughes, F, Holste, J.E, ALva, R, Fleishman, C, Cramer, L (2003) Prevention of occurrence and recurrence of gastric ulcers in horses by treatment with omeprazole at 1mg/kg/day.  ''Proc Am Ass Equine Practnrs'', 49: 220-221.</ref><ref>White, G.W, McClure, S.R, Sifferman, R.L, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration.  ''J Am Vet Med Ass'', 230:1680-1682.</ref>
 *Treating ulcers in asymptomatic performance horses may lead to improved performance.<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>
-*Prophylaxis in foals controversial as gastric acidity may be protective against bacterial translocation.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
+*Prophylaxis in critically ill foals may not be necessary and is controversial since gastric acidity may be protective against bacterial translocation.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
 *May benefit foals receiving substantial doses of NSAIDs for orthopaedic pain.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>
+{{Learning
+|literature search = [http://www.cabdirect.org/search.html?q=%28title%3A%28gastr*%29+OR+title%3A%28stomach%29%29+AND+title%3A%28ulcer*%29+AND+od%3A%28horses%29 Gastric Ulceration in Horses publications]
+}}
 ==References==
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+{{review}}
+{{OpenPages}}
+[[Category:Colic - Gastric Causes]]
 [[Category:Gastric_Ulceration]]
-[[Category:To_Do_-_Nina]]
-[[Category:Stomach_Disorders_-_Horse]]
+[[Category:Stomach Diseases - Horse]]
+[[Category:Expert_Review]]
+[[Category:Medical Colic in the Horse]]

Difference between revisions of "Gastric Ulceration - Horse"

Latest revision as of 15:59, 6 July 2012

Contents

Introduction

Prevalence

Signalment

Pathophysiology

Anatomy

Intrinsic protective factors

Glandular mucosal defence mechanisms^[2]

Squamous mucosal defence mechanisms^[2]

Other intrinsic defence mechanisms

Intrinsic ulcerogenic factors^[32]

Extrinsic ulcerogenic factors (RISK FACTORS)

Clinical syndrome

Diagnosis

Endoscopy

Other Imaging

Biopsy

Laboratory tests

Pathology

Treatment

Histamine 2 receptor antagonists

Proton-pump inhibitors (PPIs)

Antacids

Mucosal protectants

Prostaglandin analogues

Gastric prokinetics

Treatment problems

Prognosis

Prevention

Management

Prophylaxis

References

Navigation menu

Search

Difference between revisions of "Gastric Ulceration - Horse"

Latest revision as of 15:59, 6 July 2012

Introduction

Prevalence

Signalment

Pathophysiology

Anatomy

Intrinsic protective factors

Glandular mucosal defence mechanisms[2]

Squamous mucosal defence mechanisms[2]

Other intrinsic defence mechanisms

Intrinsic ulcerogenic factors[32]

Extrinsic ulcerogenic factors (RISK FACTORS)

Clinical syndrome

Diagnosis

Endoscopy

Other Imaging

Biopsy

Laboratory tests

Pathology

Treatment

Histamine 2 receptor antagonists

Proton-pump inhibitors (PPIs)

Antacids

Mucosal protectants

Prostaglandin analogues

Gastric prokinetics

Treatment problems

Prognosis

Prevention

Management

Prophylaxis

References

Navigation menu

Search

Glandular mucosal defence mechanisms^[2]

Squamous mucosal defence mechanisms^[2]

Intrinsic ulcerogenic factors^[32]