Difference between revisions of "Gastric Ulceration - Horse"

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===Mucosal protectants===
 
===Mucosal protectants===
 +
 +
 
Sucralphate, a complex salt of sucrose and aluminium hydroxide, has been used successfully to treat gastric and duodenal ulcers in man. Its main protective action is through adherence to the ulcerated surface. The
 
Sucralphate, a complex salt of sucrose and aluminium hydroxide, has been used successfully to treat gastric and duodenal ulcers in man. Its main protective action is through adherence to the ulcerated surface. The
 
aluminum and magnesium hydroxide buffering agents may have a prostaglandin-stimulating action as a heavy metal effect. The mucosal protective functions stimulated by prostaglandin E are discussed below.
 
aluminum and magnesium hydroxide buffering agents may have a prostaglandin-stimulating action as a heavy metal effect. The mucosal protective functions stimulated by prostaglandin E are discussed below.
 
Results of some recent studies of sucralphate in horses indicate questionable efficacy in the treatment of squamous ulcers.(EGUC)
 
Results of some recent studies of sucralphate in horses indicate questionable efficacy in the treatment of squamous ulcers.(EGUC)
−
Sucralphate  inhibits pepsin, enhances the protective mucusbicarbonate layer, increases local protective prostaglandins and increases binding and enhancement of local epidermal growth factor, all of which allow ulcers to heal. However, sucralphate is only indicated for gastric glandular or duodenal ulcers, not for gastric squamous ulcers. Sucralphate has no effect on the healing of gastric squamous epithelial ulcers in horses, but is effective in treating gastric glandular ulcers.  Therefore, sucralphate should not be used alone in the treatment of gastric ulcers in foals or mature horses without an endoscopic examination confirming glandular ulcers (Murray 1994). (Orsini)
+
Sucralphate  inhibits pepsin, enhances the protective mucus bicarbonate layer, increases local protective prostaglandins and increases binding and enhancement of local epidermal growth factor, all of which allow ulcers to heal. However, sucralphate is only indicated for gastric glandular or duodenal ulcers, not for gastric squamous ulcers. Sucralphate has no effect on the healing of gastric squamous epithelial ulcers in horses, but is effective in treating gastric glandular ulcers.  Therefore, sucralphate should not be used alone in the treatment of gastric ulcers in foals or mature horses without an endoscopic examination confirming glandular ulcers (Murray 1994). (Orsini)
  
 
===Prostaglandin analogues===
 
===Prostaglandin analogues===

Revision as of 12:25, 30 July 2010


 This article is still under construction.


Also known as: Gastroduodenal ulceration

Gastrointestinal ulceration
 Equine Gastric Ulcer Syndrome
 Peptic ulcer disease
 Equine Gastric Ulcer

See also: Gastric Ulceration - all species


Description

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] 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 non-glandular (proximal or orad) region of the equine stomach is lined by stratified squamous mucosa and a glandular mucosa lines the distal (aborad) portion. 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 from inflammation, to cellular death and sloughing causing disruption of the superficial mucosa (erosion), 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]
  • Pleasure, riding lessons, showing 37%[20]
  • Foals ~25-57%[21][22][23], the incidence increases dramatically in foals with clinical signs, especially gastrointestinal signs.[2]

The prevalence and severity of ulcers increases with work intensity[7] and duration[24][25], 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] Among show horses, 82% of those with signs of abdominal discomfort had gastric ulcers[26] Around 30% of adult horses and about 50% of 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[27]

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.[28]

Pathophysiology

Risk Factors

Exercise

There appears to be a high prevalence of gastric ulcers in horses performing in most disciplines including racing, endurance, show jumping, dressage and western performance.[29] Although this may be related to exercise, other confounding factors associated with these disciplines such as travel, diet, feeding regime, 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.[30] Furthermore, the higher prevalence of gastric ulcers at post mortem in racehorses in training compared to those in retirement adds weight to the hypothesis that exercise is 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. 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.[31]

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.[32] 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.[33] Transport has also been shown to induce squamous mucosal ulceration in horses.[34]

Diet

Feed deprivation encourages gastric ulceration in two ways: (1) it precludes the buffering capacity of protein leading to a reduced gastric pH[35] and (2) it empties the stomach and exposes the squamous mucosa to the more mobile gastric juice.[8] It is unsurprising, therefore, that an alternating feed-fast protocol would produce a consistent model of ulcer induction in the equine squamous mucosa.[36][37] Despite this, feed deprivation is not a prerequisite for gastric ulceration in the horse.[38] 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.[39] This sort of diet is commonly fed to racehorses but dietary components have also been shown to influence EGUS risk in nonracehorses.[40] 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.[41] High starch meals are also a risk because they are fermented to volatile fatty acids (VFAs) and lactic acid and are emptied from the stomach relatively slowly.[42][43][44]

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 have been associated with EGUS.[45] Alternatively, EGUS may be part of a more general gastrointestinal disease complex.[12] Stress induced by other clinical disorders has been reported to increase the prevalence of EGUS in neonatal foals[46] and a similar mechanism may exist for adult animals.[12]

NSAIDs

As in other species, nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to cause gastric ulcers in horses. Typicaly this is associated with high doses or frequent administration of phenylbutazone or flunixin meglumine. However, although there is evidence to the contrary,[47]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[48]and that combination treatment with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone.[49] The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa[50][51][52], they may look different endoscopically from ulcers that occur naturally,[53] and they appear to heal spontaneously.[54][55] Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.[56][57][38]

Temperament

A nervous disposition has been linked with gastric ulcers[58]but the same association was not seen in another study.[59] The physiological and psychological stresses of training, housing, boredom, travel, mixing, hospitalisation and entering new environments[12] may increase the risk of developing EGUS. In foals hypoxia may also be a risk factor.

Clinical syndrome

The clinical signs associated with gastric ulcers are often very non-sepcific, difficult to document and at times only subjective.[60] In addition, there appears to be a poor correlation between the severity of endoscopic lesions and the clinical presentation.[20] 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.[60] Cases 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[61]
    • 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.[62]
  • Changes in attitude (dullness or depression)[60]
  • Poor racing performance and reluctance to train
    • Performance improved in 4 Thoroughbred racehorses after antiulcer treatment[63]
    • Gastric ulcers have adversely affected physiological indices of performance in horses.[64]


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] 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.[39]

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[60]) 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,[60] 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.[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 the most well established and useful 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 of 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,[65] 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.[66] Lesions that appear grossly similar may have different grades on histopathology.[39] This is important as varying lesions may have different causes, requiring a range of treatment approaches.

Radiography

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.

Biopsy

A transendoscopic gastric biopsy technique was recently validated for obtaining samples from the gastric glandular mucosa in the live horse.[67]Unfortunately this technique failed to produce samples of squamous mucosa that would be suitable for histopathological analysis.

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.[68][69]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.[39] False positive results may arise from rectal trauma (e.g. recent biopsy or rectal examination) or protein losing enteropathy.[39] Other tests that require further analysis for sensitivity and specificity[6] include:

  • Urine[70] and blood[71] sucrose absorption as an assay of gastric mucosal permeability
  • Serum alpha1-antitrypsin may be released from damaged gastric tissue[39] and has been detected more frequently in foals with gastric ulceration[72]

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.[73] From their findings, a pathogenesis for the development of lesions in the squamous region was proposed:

Treatment

Histamine 2 receptor antagonists

This concept follows from the still widely held belief, ‘no acid, no ulcer’ (Fig 19). The current treatment of choice is to suppress acid production from the parietal cells. These cells release acid when any one of 3 distinct receptors (histamine, acetylcholine, gastrin) is stimulated. Currently, the most popular treatment involves an histamine receptor antagonist (H2 blocker). The proton-pump inhibitors constitute a new treatment approach that blocks acid production within the cell. This modality is receptor-independent and therefore more effective.(EGUC) Histamine receptor (H2) antagonists The 4 most popular Hz antagonists licensed in the United States for man are cimetidine, ranitidine, famotidine and nizatidine. Cimetidine has been shown to affect hepatic disposition of some drugs. Most of these compounds have been tested in the horse; cimetidine and ranitidine have been studied most extensively (Table 2). Ranitidine at a dose of 6.6 mgkg bwt q. 8 h has been demonstrated to maintain a pH level >4 when horses are allowed free access to hay.(EGUC) Horses with documented gastric ulcers respond well to treatment with histamine type-2 receptor (Hz) antagonists such as ranitidine (Furr and Murray 1989; Murray and Grodinsky 1992). The problem with treatment of gastric ulcers in horses is that individuals have different dose requirements for effective treatment. This probably relates to varying bioavailability of the drug in individual horses. The bioavailability of H2 antagonists is generally lower in horses than in man. The wide variability among horses in acid suppression achieved with H2 antagonists may be a result of other unknown factors as well; this variability is most pronounced at low doses. The medication selected, dosage and duration of treatment depend on the location and severity of lesions, clinical signs, and owner considerations., The recommended dose of oral ranitidine is 6.6 mg/kg bwt 3 times daily. The equivalent dose of cimetidine is 40-60 mg/kg/day; and of famotidine 10 mg/kg/day. Treatment is effective and alleviates clinical signs in those that are affected. Lower dosages may be effective in some horses, but the percentage of individuals that fail to respond increases as the dosage decreases.(Orsini)

Proton-pump inhibitors

This class of compounds is the newest addition to the antisecretory group. Unlike Ha-receptor antagonists, proton-pump inhibitors block the enzyme (pump) responsible for a hydrogen-potassium exchange. Blocking this enzyme exchange retards the final step in parietal cell acid production. Omeprazole, one of 2 compounds in this class currently licensed in the United States for use in man, is now licensed for use in horses. It has demonstrated an excellent efficacy and safety profile. In double-blind, placebo-controlled field trials, omeprazole paste, administered at 4 mgkg bwt was effective in eliminating or substantially reducing the severity of gastric ulcers. At this dose rate, pH >6 persisted for 24 h after the last treatment. In human medicine, omeprazole has been approved for long term and prophylactic use in patients with erosive oesophagitis. This is meaningful, because ulcers in the squamous portion of the equine stomach are most prevalent (>go%) and resemble the human form of erosive oesophagitis.(EGUC) Treatment of uncomplicated equine peptic ulcer disease Omeprazole has the advantages that: 

It is licensed for use in horses

Its efficacy has been demonstrated in controlled clinical trials Its ease of administration and once-daily dosing promotes compliance with a recommended treatment strategy.(EGUC) A newer and more effective treatment approach is inhibition of the proton pump, also Proton pump inhibitors bind irreversibly to the enzyme hydrogen-potassium adenosine triphosphate (H+, K+, ATPase) needed for secretion of hydrogen ions from parietal cells into the gastric lumen. The proton pump is the final pathway in gastric acid secretion. Maximum control of acid production is achieved regardless of the stimulus to the parietal cell. One important advantage of proton pump inhibitors is their ability to inhibit acid production for 24 h with once-a-day dosing (Papich 1993). The recommended dose of oral omeprazole is 4.0 mgkg bwt every 24 h.(Orsini)


J Vet Intern Med. 2006 Sep-Oct;20(5):1202-6. Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses. Andrews FM, Frank N, Sommardahl CS, Buchanan BR, Elliott SB, Allen VA. The study was performed to evaluate the efficacy of omeprazole powder in sterile water, administered intravenously, on gastric juice pH in adult horses with naturally occurring gastric ulcers. Because of its potent and long duration of action on gastric juice pH, this intravenous formulation of omeprazole may show promise for treatment of equine gastric ulcer syndrome (EGUS) in horses with dysphagia, gastric reflux, or other conditions that restrict oral intake of omeprazole paste. Aspiration of gastric juice and measurement of pH can be of use to determine whether the desired pH > 4.0 has been reached after omeprazole treatment.

Omeprazole, a substituted benzimidazole Omeprazole inhibits H+K+ATPase, the enzyme responsible for the final production of acid by parietal cells. In man, it has recently been shown that healing of erosive oesophagitis with antisecretory drugs is directly correlated to both the duration of acid suppression over a 24 h period and the elevation of intraoesophageal pH above 4 for at least 96% of the 24 h period (Tibbling 1993). In horses, orally administered omeprazole has been shown to increase stomach pH above 4 and to significantly inhibit gastric secretion for at least 27 h after treatment (Bough et al. 1995) In addition, omeprazole has a longer duration of action than the H2 receptor antagonists and, consequently, only requires once daily dosing (Brown and Rees 1994). No side-effects were observed in any of the horses in our study. Similarly, in 2 studies in which omeprazole was administered orally to horses over a 5 day period no adverse effects were noted (Ryberg et al. 1989; Bough et al. 1995). At the present dosage, omeprazole appears safe for use in horses, although further studies are required. As with human individuals suffering GERD (Gunasekaran and Hassall 1993), once omeprazole treatment was stopped in the horses, ulceration returned within 2 weeks. Presumably the same factors responsible for the development of ulcers in horses were still present at the end of the trial. In man, long-term treatment of GERD has been achieved by placing patents on a maintenance dose of omeprazole (Gunasekaran and Hassall 1993). Although no side-effects were observed in human patients receiving long-term omeprazole therapy (Goldberg 1992; Gunasekaran and Hassall 1993), one potential problem may be that increasing gastric pH may allow bacterial overgrowth in the small intestine by preventing the entry of organisms normally inhibited by gastric acidity. Consequently, further studies are required to determine the long-term efficacy and safety of omeprazole in horses. Acceptability of omeprazole as a paste was, in general, excellent. Omeprazole, administered once daily at the dosage in this study, was effective in reducing the severity of gastric ulcers in Thoroughbred horses in active race training. Further studies are required to determine the optimal dosage and long-term safety of omeprazole in horses. (Vatistas 1999)

Equine Vet J. 2008 Jan;40(1):41-4. The effect of omeprazole paste on intragastric pH in clinically ill neonatal foals. Javsicas LH, Sanchez LC. Omeprazole paste effectively increases intragastric pH in clinically ill neonatal foals after one dose at 4 mg/kg bwt orally.


Antacids

The use of antacids to treat EGUS in the horse has not been critically evaluated(Sanchez) 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. (Orsini)

Mucosal protectants

Sucralphate, a complex salt of sucrose and aluminium hydroxide, has been used successfully to treat gastric and duodenal ulcers in man. Its main protective action is through adherence to the ulcerated surface. The aluminum and magnesium hydroxide buffering agents may have a prostaglandin-stimulating action as a heavy metal effect. The mucosal protective functions stimulated by prostaglandin E are discussed below. Results of some recent studies of sucralphate in horses indicate questionable efficacy in the treatment of squamous ulcers.(EGUC) Sucralphate inhibits pepsin, enhances the protective mucus bicarbonate layer, increases local protective prostaglandins and increases binding and enhancement of local epidermal growth factor, all of which allow ulcers to heal. However, sucralphate is only indicated for gastric glandular or duodenal ulcers, not for gastric squamous ulcers. Sucralphate has no effect on the healing of gastric squamous epithelial ulcers in horses, but is effective in treating gastric glandular ulcers. Therefore, sucralphate should not be used alone in the treatment of gastric ulcers in foals or mature horses without an endoscopic examination confirming glandular ulcers (Murray 1994). (Orsini)

Prostaglandin analogues

Synthetic prostaglandin E1 analogues are believed to inihibit gastric acid secretion and enhance mucosal cytoprotection(127 in Sanchez). 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 (128 in Sanchez). Although contraindicated in pregnant mares, Misoprostol may be beneficial for mucosal recovery in the face of flunixin treatment.(129 in Sanchez)

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.(Sanchez) Such compounds include bethanechol, metaclopramide, erythromycin and cisapride which have been shown to hasten gastric empyting in adult horses.(EGUC) 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.(Sanchez)


Proton pump inhibitors: only omeprazole (Gastroguard) is licensed for horses. Given PO once daily (4mg/kg) for 3-4 wks, most effective drug at controlling HCl secretion (decreases basal and stimulated release). Expensive and not absorbed in foals with diarrhoea Histamine H2 receptor antagonists:

  • ranitidine (Zantac, Zeneca, UK) 7mg/kg TID for 3-4wks
  • cimetidine 25mg/kg QID for 3-4wks (cheaper but less effective so must be given more frequently)

Gastric protectants: sucralfate 10-20mg/kg TID for 2-4wks Antacids: magnesium and aluminium hydroxides (NOT recommended as have massive rebound effect) Foal tx (see medicine notes)

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(Orsini et al 2003 in Nadeau 2009). Omeprazole and ranitidine must be administered for at least 28 days for adequate ulcer healing.(Nadeau 2009) 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 (Nieto et al. 2002; Merritt et al. 2003; Orsini et al. 2003).(Nadeau 2009) 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.[74] Another challenge is the horse that cannot take oral medication. 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. An ongoing point of debate is the use of antiulcer medication in competition horses. In 2000, the Bureau of the 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.(Nadeau 2009)

Prognosis

Complications:

  • Recurrence if management not altered
  • Perforation and peritonitis (rare - foals)
  • Pyloric stenosis (rare - foals)

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.[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. In rare cases, severe gastric ulceration causes fibrosis and contracture of the stomach.[7]

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 calorifc needs are met by concentrates.(Orsini) 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.(Andrews 2006) Horses prone to, or at risk of, EGUS should be fed the minimum amount of concentrates necessary.(Nadeau 2009)
  • Stress: minimise wherever possible, provide company and toys for stabled horses.

Most of these suggestions would be difficult if not impossible to achieve for horses in race training, thus prophylactic medication should be considered.(Orsini)

Prophylaxis

Omeprazole paste at a lower dose (1-2mg/kg) daily for 3-4 weeks.(100, 107-109 in Sanchez)

  • Prevented ulcers in horses maintained under ulcerogenic conditions (White et al. 2003; McClure et al. 2005a,b,c;White et al. 2007).
  • Treating ulcers in asymptomatic performance horses may lead to improved performance.(Orsini)
  • Prophylaxis in foals controversial as gastric acidity may be protective against bacterial translocation (Sanchez).
  • May benefit foals receiving substantial doses of NSAIDs for orthopaedic pain (Sanchez)

References

  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.
  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 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.
  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).
  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
  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 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.
  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
  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.
  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.
  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
  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. ↑ 20.0 20.1 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.
  21. ↑ Wilson, J.H (1986) Gastric and duodenal ulcers in foals: a retrospective study. Proc Equine Colic Res Symp 2nd:126-128.
  22. ↑ 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.
  23. ↑ Murray, M.J (1989) Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988). J Am Vet Med Assoc, 195:1135-1141.
  24. ↑ 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.
  25. ↑ 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.
  26. ↑ 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.
  27. ↑ 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.
  28. ↑ 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.
  29. ↑ 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.
  30. ↑ 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.
  31. ↑ 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.
  32. ↑ 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.
  33. ↑ 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.
  34. ↑ 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.
  35. ↑ 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.
  36. ↑ 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.
  37. ↑ 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.
  38. ↑ 38.0 38.1 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
  39. ↑ 39.0 39.1 39.2 39.3 39.4 39.5 In: 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
  40. ↑ 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.
  41. ↑ 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.
  42. ↑ 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.
  43. ↑ 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.
  44. ↑ 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.
  45. ↑ 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.
  46. ↑ 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.
  47. ↑ 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.
  48. ↑ 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.
  49. ↑ 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.
  50. ↑ 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.
  51. ↑ 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
  52. ↑ 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
  53. ↑ Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training. Equine Vet J, 38(3):209-213.
  54. ↑ 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
  55. ↑ 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
  56. ↑ 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
  57. ↑ 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
  58. ↑ 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.
  59. ↑ 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.
  60. ↑ 60.0 60.1 60.2 60.3 60.4 Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
  61. ↑ Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome. Vet Clin North Am Equine Pract, 25(2):283-301.
  62. ↑ 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.
  63. ↑ 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.
  64. ↑ 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.
  65. ↑ 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.
  66. ↑ 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.
  67. ↑ 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.
  68. ↑ 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.
  69. ↑ 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.
  70. ↑ 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.
  71. ↑ 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.
  72. ↑ 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.
  73. ↑ 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.
  74. ↑ Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.Vet Clin North Am Equine Pract, 25(2):283-301.



  • Due to parasites - Gasterophilus (Bots).
  • Bots are not as common as they once were.
  • Look like big pink maggots.
  • Killed by Ivermectin.
  • Gasterophilus leave large ulcers in glandular regions of the stomach.
    • Ulcers / erosions are quite deep.
  • The parasites are believed to be non-pathogenic, but in large numbers they probably produce some discomfort and poor growth.
  • Carcinoma can also produce ulceration in the stomach of the horse as, in other species.
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