Gastric Ulceration - Horse

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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)' is used to describe the disease complex associated with ulceration of the oesophageal, gastric or duodenal mucosa[1] in horses. When such damage is caused by acidic gastric juice, the defect is described as a 'peptic ulcer'.[1] Ulceration of either or both[2] regions of the gastric mucosa is one of the most important conditions of the equine stomach as it may limit performance[3] and compromise welfare.[4] 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[5], adjacent to where most ulcers occur.[1] 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[1](ulceration), full thickness ulceration (perforation)[5] and potentially duodenal stricture.[6] The occult nature of the disease typically precludes the observation of clinical signs until severe ulceration has developed.[1]

Prevalence

The prevalence of equine gastric ulceration has increased over the last century.[7] 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.[7] For the squamous region, reported prevalences are:

  • Racehorses 70-100%[8][9][10]
  • Racehorses in active race training 80-90% (incidence 100%)[11][12]
  • Show horses 58%[13]
  • Ponies 78%[14]
  • Endurance 67%[15]
  • Western performance horses 40%[16]
  • Thoroughbred broodmares (67-77%)[17]
  • Nonracing performance horses (17% pre-competition, 56% post-competition)[18]
  • Pleasure horses in full work ~ 60%[3]
  • Pleasure, riding lessons, showing 37%[19]
  • Foals ~25-57%[20][21][22], the incidence increases dramatically in foals with clinical signs, especially gastrointestinal signs.[1]

The prevalence and severity of ulcers increases with work intensity[6] and duration[23][24], thus racehorses in active training are more often affected[8] and in half of these, the lesions are moderate to severe.[6] In one study, all horses developed gastric ulcers within 2 weeks of entering simulated race training.[11] Lesions are thought to be chronically progressive during race training, but to regress during retirement.[8] Horses with signs of gastrointestinal distress also demonstrate an increased frequency and severity of ulcerative lesions.[1]EGUS prevalence is high in horses with bowel, liver and oesophageal lesions.[7] Among show horses, 82% of those with signs of abdominal discomfort had gastric ulcers[25] Around 30% of adult horses and about 50% of foals have mild gastric erosions which heal without treatment or clinical signs.[6] 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[5] but is most common in young horses in training and foals. Gastric ulceration is considered to be rare in horses at pasture.[27]

Pathophysiology

NOT associated with Helicobacter pylori and not typically associated with Gasterophilus Differences in the multivariable models produced for all ulcers and nonglandular ulcers support differences in the aetiology of ulcers in different locations of the stomach. (Luthersson et al 2009)

Risk Factors

Exercise

The aims of this study were to determine whether ulcers could be induced and maintained in a population of horses fed a concentrate diet, maintained in fast work and fasted before exercise. In this study ulcers developed without the administration of nonsteroidal anti-inflammatory agents or withholding of feed.(Vatistas 2 1999) The mechanism for this is that compression of the stomach by abdominal viscera and diaphragm leads to delivery of acid contents into the proximal region of the stomach (Lorenzo-Figueras and Merritt 2002). This mechanism is thought to deliver the acid to the nonglandular mucosa resulting in acid exposure and injury.Other risk factors have surfaced in a variety of recent studies. In one study of horses in Australia, horses trained in urban areas are 3.9x more likely to have gastric ulcers. Also, time in work, crib-biting, difficulty maintaining bodyweight and playing the radio in the barn were identified as other risk factors (Lester et al. 2007). On the other hand, protective factors included training on the property and turnout with other horses. Also, in another study in Standardbred mares, 7/8 horses (Gordon et al. 2006) had gastric ulcers after 8 weeks of training, compared to 0/7 horses housed similarly and not trained. Although racehorses have a high prevalence of EGUS, 56.5% of horses in endurance competition, show jumping, dressage or western performance and travel, had gastric ulcers (Hartmann and Frankeny 2003) after competition. Thus, even nonrace training and performance horses are at risk of developing EGUS and should be monitored for clinical signs(Nadeau 2009) J Am Vet Med Assoc. 2007 Jun 1;230(11):1680-2. Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration. White G, McClure SR, Sifferman R, Holste JE, Fleishman C, Murray MJ, Cramer LG. OBJECTIVE: To determine the effects of 8 days of light to heavy exercise on gastric ulcer development in horses and determine the efficacy of omeprazole paste in preventing gastric ulceration.). CONCLUSIONS AND CLINICAL RELEVANCE: Results showed that horses in light to heavy training for as short as 8 days were at risk of developing gastric ulcers and that administration of omeprazole paste decreased the incidence of gastric ulcers. Conclusions: The study confirmed a high prevalence of ulcers in the gastric squamous mucosa of Standardbreds in race training. Of the studied parameters only status of training showed a significant association with gastric ulcers of the squamous mucosa.In a post mortem study, Hammond et al. (1986) showed a significantly higher prevalence (80%) of gastric ulcers among Thoroughbreds in race training compared with horses that had retired (52%), a finding supported by other authors (Murray et al. 1989, 1996; Vatistas et al. 1999b). (Jonssen 2006)

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.(Murray and Eichorn1996).(Jonssen 2006). However, when comparing solitary stable confinement with stabling next to a companion, and finally turn out in a paddock, Husted et al. found that the environmental circumstance had no effect on mucosal acid exposure in the equine stomach[28] Transport has also been shown to induce squamous mucosal ulceration(71 in Sanchez)

Diet

Feed deprivation encourages gastric ulceration in two ways: (1) it removes the buffering capacity of protein leading to a reduced gastric pH (Murray and Schusser 1993) (2) it empties the stomach and exposes the squamous mucosa to the more mobile gastric juice.(Sandin 2000) It is predictable, therefore, that an alternating feed-fast protocol produces a consistent model of ulcer induction in the equine squamous mucosa (36, 37, 66 in Sanchez). Despite this, feed deprivation is not a prerequisite for gastric ulceration in the horse(Vatistas 1998). 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. (Nadeau 2009). This sort of diet is commonly fed to racehorses but dietary components have also been shown to influence EGUS risk in nonracehorses[29] Ponies fed a concentrate diet had a greaer prevalence of gastric ulcers than ponies fed hay alone.(Vatisats 2 1999) 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 (Metayer et al. 2004)(Taharaguchi et al. 2004; Boswinkel et al. 2007)(Nadeau 2009)

Other ailments

Conditions that produce abdominal pain or inappetance are likely to reduce food intake and predipose to gastric ulcers (Sandin 2000). This may be the reason that colic and other gastrointestinal disorders have been associated with EGUS (Murray 1989, 1992; Furr and Murray 1989(Murray 1992). Alternatively, EGUS may be part of a more general gastrointestinal disease complex.(Vatistas 2 1999) Stress induced by other clinical disorders has been reported to increase the prevalence of EGUS in neonatal foals (Furr et al. 1992) and a similar mechanism may exist for adult animals.(Vatistas 2 1999)

NSAIDs

Nonsteroidal anti-inflammatory drugs (NSAIDs: phenylbutazone, flunixin meglumine) have been shown to cause gastric ulcers in horses. This is usually related to the use of a high dose or frequent administration of NSAIDs; however, therapeutic doses have been known to cause ulcers in horses. Recently, a study was conducted comparing the ulcerogenic effects of an orally administered prophenylbutazone drug, suxibuzone, to phenylbutazone (Monreal et al. 2004). Horses treated with phenylbutazone had more ulcerated areas and deeper ulcers than those in the suxibuzone treated or placebo groups. The authors concluded that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally at equimolar doses in horses. However, a more recent study in horses given suxibuzone or phenylbutazone at therapeutic doses for 14 days showed no significant difference in gastric ulcer scores when compared to each other and control horses receiving no treatment (Andrews et al. 2009). Thus, therapeutic doses of these NSAIDs did not lead to gastric ulcers more than what was observed in the untreated control group. Another study evaluated the use of a combination of NSAIDs and gastric ulcers in horses. Phenylbutazone (2.2 mg/kg bwt per os, q. 12 h, for 5 days) or phenylbutazone (same dose) and flunixin meglumine (1.1 mg/kg bwt, i.v., q. 12 h, for 5 days) were administered to adult horses (Reed et al. 2006). In this study, total plasma protein and albumin decreased in NSAID treated horses and nonglandular gastric ulcer scores were significantly higher in horses treated with the 2 NSAID drugs. Thus, NSAIDs and a combination NSAID treatment should be approached with caution in horses. Recently, firocoxib1, a new cox-2 inhibitor NSAID was approved for treatment of lameness in horses. Gastric ulcers were not detected in horses administered firocoxib (0.1 mg/kg bwt, per os, q. 24 h, 30 days) (Anon 2005). However, firocoxib is FDA approved for the control of pain and inflammation associated with osteoarthritis in horse, thus its efficacy in horses with abdominal pain is unknown. Furthermore, currently there is no i.v. formulation of this product, so it cannot be administered orally in horses with abdominal pain and gastric reflux or dysphagia. (Nadeau 2009) Vet Ther. 2009 Fall;10(3):113-20. Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. Andrews FM, Reinemeyer CR, Longhofer SL. 

These findings suggest that when administered at the recommended label dose for 15 days, neither PBZ nor SBZ causes an increase in the number or severity of gastric ulcers over what would be expected with traditional stabling and intermittent feeding patterns. Also, PBZ-treated horses did not have more severe gastric ulcers than SBZ-treated horses, indicating that SBZ does not appear to offer an advantage over PBZ in preventing gastric ulcers when used at recommended label doses. However, ulcers in other regions of the gastrointestinal tract (e.g., right dorsal colon, duodenum) were not evaluated in horses in this study.

Administration of nonsteroidal anti-inflammatory drugs (NSAIDs) has been proven to cause ulcers in the glandular portion of the stomach (MacAllister et al. 1993), but in studies where primarily the squamous mucosa were studied, the same association was not evident (Hammond et al. 1986; Murray et al. 1989, 1996; McClure et al. 1999; Vatistas et al. 1999a; Rabuffo et al. 2002). (Jonssen 2006) However, ulcers had healed in the majority of animals which were examined endoscopically 7 days following the final period of fasting (Murray 1994). Spontaneous resolution of ulcers is uncommon clinically in horses maintained in active training. Models have also used nonsteroidal anti-inflammatory medications (NSAIDs) to produce ulcers in ponies (Jones 1983; MacAllister and Sangiah 1993). Ulcers induced by the administration of NSAIDs may have a dissimilar endoscopic appearance to naturally occurring ulcers (D.R. Thompson, personal communication) and gastric ulceration in horses in race training is rarely associated with the administration of NSAIDs (Vatistas et al. 3994b; Murray et al. 1996; Vatistas 1998). In addition, ulcers caused by NSAID administration frequently affected the glandular mucosa (Furr and Murray 1989; Kuinaran and Bhuvanakumar 1994) and tended to heal spontaneously (Jones 1983; MacAllister and Sangiah 1993). both of which occunences are infrequent in the clinical setting (Vatistas and Snyder 1997; Vatistas 1998). Spontaneous healing of ulcers, following induction of ulceration by either fasting or NSAID administration, precludes the evaluation of anti-ulcer medication.(Vatistas 2 1999)

Temperament

A nervous disposition has been linked with gastric ulcers (McClure et al. 1999) but the same association was not seen in another study (Vatistas et al. 1999a)(Jonssen 2006).

The results of our study suggest that, rather than training itself, the most stressful event may have been when horses entered their new environment..(Vatistas 2 1999)


Foals: associated with stress, hypoxia, altered gut motility and NSAIDs (PBZ and flunixin) or intercurrent disease or hospitalisation Housing, stress, boredom, training, diet Feeding practices:

  • Grain and pelleted feed asssociated with increased serum gastrin (Smyth et al 1988)
  • Eating behaviour (grazing vs feeds)
  • Feed constituents (alfalfa)
  • Individual variability

Exercise and training

  • Strenuous exercise stimulates gastrin release which has effects on HCL secretion, gastric emptying, gastric blood flow

Clinical syndrome

The clinical signs associated with gastric ulcers are often very non-sepcific, difficult to document and at times only subjective.[30] In addition, there appears to be a poor correlation between the severity of endoscopic lesions and the clinical presentation.[19] 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.[30] 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)[5]
  • Poor condition
  • Rough hair coat
  • Weight loss
  • Excessive recumbency[1]
  • Mild to severe colic
    • Mild, recurrent colic signs post-prandially[31]
    • 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.[32]
  • Changes in attitude (dullness or depression)[30]
  • Poor racing performance and reluctance to train
    • Performance improved in 4 Thoroughbred racehorses after antiulcer treatment[33]
    • Gastric ulcers have adversely affected physiological indices of performance in horses.[34]


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[5]
    • Poor appetite
    • Diarrhoea
    • Intermittent colic
    • Frequent dorsal recumbency
  • Sucklings and weanlings:[5]
    • 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):[5]
    • Bruxism
    • Colic
    • Gastrooesophageal reflux after suckling
    • Ptyalism (secondary to gastric outflow obstruction and gastroesophageal reflux)[6]
    • Diarrhoea

In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.[5] GDUD is the primary differential for ptyalism in foals, other possible diagnoses include oesophageal obstruction and Candida infection.[6]

Diagnosis

Presumptive on clinical signs and response to treatment (Sanchez) Definitive diagnosis requires endoscopy (cannot do in foals as need to starve prior to exam) 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.(BEVA)

Endoscopy

Performed under mild sedation in standing horse or foal (Sanchez) Duodenoscopy is most specific diagnostic method but is technically me chanllenegng than gastrocopy EGUS Lesion Scoring System publsihed based on consens by Equine Gastric Ulcer Council(2 in Sanchez)

Lesion Grade Description
Grade 0 Intact epithelium with no appearance of hyperaemia or hyperkeratosis
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 reddeing or inflammation may be only lesion seen in cases of early duodenal disease In older foals with GDUD, detection ofgastrci outflow obsturction is critical to therapeutic plan and appropriate prognosis (Sanchez)

Minimum endoscope length of two metres and 2.8-3.0 metre instruments are required for duodenoscopy A 3 mtre endoscope allows visualization of stomach, pyrlorus and proximal duodenum (Sanchez) Shorter scopes permit investigation fo gastric body and fundus only (Sanchez) Maximum external diameter of 9mm for neonates (Sanchez) Foals - lesions mainly in glandular epithelium Adults - margo plicatus and squamous epithelium

Abdominal radiography without contrast in foals with outflow obsturction typically rveeals very disticnt enlarged, gas-filled stomach. Liquid barium contrast will either have markedly delayed (with incomplete obstruction) oir no (complete onsbtruction) outflow. (Sanchez)

Biopsy

A transendoscopic gastric biopsy technique was recently validated for obtaining samples from the gastric glandular mucosa in the live horse.[35]Unfortunately this technique failed to produce samples of squamous mucosa that would be suitable for histopathological analysis.

Laboratory tests

The detection of occult blood in faeces has proven unreliable in the horse and currently, useful laboratory markers for EGUS are lacking.[1] Tests that require further analysis for sensitivity and specificity[5] include:

  • Urine[36] and blood[37] sucrose absorption as an assay of gastric mucosal permeability
  • Serum alpha1-antitrypsin which has been detected more frequently in foals with gastric ulceration[38]

Pathology

Treatment

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 foas with diarrhoea Histamine H2 receptor antagonists:

  • ranitidine 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)

Foals: Omeprazole 4mg/kg PO SID (preferred) Ranitidine (Zantac, Zeneca, UK) 6mg/kg TID PO, 1-2mg/kg IV BID (second choice) Sucralfate (Antepsin, Wyeth Labs, Maidenhead, UK)(intestinal mucosal protective), 2-4g total dose or 50kg per foal QID PO (in theory best effect of this compound is in acid medium so should not be given at the same time or after H2 blockers btu latest research shows it appears to work just as well if given at the same time and this reduces stress of handling), NB nto a good prophylactic Antacids not good - rebound effect Metocloprmade, gastrci decompression (foals with severe gastor0duodenal stenosis), analgesia (butorphenol or pethidine or morphine NOT NSAIDs) Supportive nursing by reducing stressors, milk and saliva have preventative effects so good feeding habits should be encouraged Corn oil (50ml q6h) reportedly anti-ulcerogenic (increases PG production) PG analogues (Misoprostenol) 5microgram/kg PO q8h

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.[6]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.[6]

Prevention

Gastroguard at lower dose (1-2mg/kg) daily for 3-4wks (100, 107-109 in Sanchez) Prophylaxis in foals controversial as gastric acidity may be protective against bacterial translocation (Sanchez). It may be beneficial in foals receiving substantial doses of NSAIDs for orthopaedic pain (Sanchez) Management: diet, training, exercise, stress (company, toys) Pasture turnout and continuous access to high quality forage especially alfalfa (Sanchez) Furthermore, recent information suggests that feeding a diet that contains 0.5 kg of grain per 100 kg bwt no more frequently than 6 h apart can reduce the risk of EGUS (Andrews et al. 2006). It has been suggested that a high-grain, low-hay diet would increase the incidence of ulcers (Hammond et al. 1986). In another study, alfalfa hay was shown to protect horses against EGUS, by increasing stomach pH. Gastric juice pH and ulcer scores were lower in horses fed a diet containing alfalfa hay compared to the same horses fed dietary brome or costal Bermuda hay (Nadeau et al. 2000; Lybbert et al. 2007). The authors concluded that alfalfa hay may be useful in addition to antiulcer treatment for prevention and treatment of squamous gastric ulcers.(Nadeau 2009)

References

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 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.
  2. ↑ 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.
  3. ↑ 3.0 3.1 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).
  4. ↑ 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.
  5. ↑ 5.0 5.1 5.2 5.3 5.4 5.5 5.6 5.7 5.8 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.
  6. ↑ 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial
  7. ↑ 7.0 7.1 7.2 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.
  8. ↑ 8.0 8.1 8.2 Hammond, C.J, Mason, D.K, Watkins, K.L (1986) Gastric ulceration in mature Thoroughbred horses. Equine Vet J, 18(4):284-287.
  9. ↑ 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
  10. ↑ 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.
  11. ↑ 11.0 11.1 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
  12. ↑ 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.
  13. ↑ 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.
  14. ↑ 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.
  15. ↑ 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.
  16. ↑ Bertone, J (2000) Prevalence of gastric ulcers in elite, heavy use western performance horses. Proc Am Assoc Equine Pract, 46:256-259.
  17. ↑ 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.
  18. ↑ 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.
  19. ↑ 19.0 19.1 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.
  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. ↑ 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.
  29. ↑ 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.
  30. ↑ 30.0 30.1 30.2 Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. Equine Vet Educ, 12(1):24-27.
  31. ↑ Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome. Vet Clin North Am Equine Pract, 25(2):283-301.
  32. ↑ 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.
  33. ↑ 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.
  34. ↑ 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.
  35. ↑ 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.
  36. ↑ 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.
  37. ↑ 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.
  38. ↑ 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.


Gastric Ulceration - all species

  • Affects the pars oesophagea (margo plicatus) in adults and foals.
  • 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.
  • In foals, the glandular area may sometimes be affected.
    • This may be e.g. stress-related, or due to used of NSAIDs.
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