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NOT associated with ''Helicobacter pylori'' and not typically associated with ''Gasterophilus''
NOT associated with ''Helicobacter pylori'' and not typically associated with ''Gasterophilus''
==Risk Factors==
==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===
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<ref>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.</ref>
===Diet===
Gastric ulceration may be induced by alternately feeding and fasting
horses (Murray 1994).(Vatistas 2 1999)
A high grain low roughage diet is a risk factor in EGUS. High roughage diets provide hours of chewing and the production of salivary bicarbonate that bathes the stomach and protects against gastric ulcers. Metayer et al. (2004), found that small low starch meals empty from the stomach significantly faster than large high starch meals. Since high starch diets are fermented to VFAs and lactic acid, large high starch meals should be avoided in horses prone to gastric ulceration (Taharaguchi et al. 2004; Boswinkel et al. 2007). 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).
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)
In an investigated standardbred population in the Netherlands the amount of concentrate fed is not an important predisposing factor.(Prevalence)
Equine Vet J. 2009 Sep;41(7):625-30.
Risk factors associated with equine gastric ulceration syndrome (EGUS) in 201 horses in Denmark.
Luthersson N, Nielsen KH, Harris P, Parkin TD.
OBJECTIVES: To investigate the prevalence of EGUS in a population of Danish horses, during winter when the horses had been housed and fed for at least 8 weeks and to analyse the influence of feed, work level and environment on the risk of EGUS of > or = grade 2 in severity. CONCLUSION AND POTENTIAL RELEVANCE: This study has confirmed that components of the diet, readily modifiable, may have an important impact on the risk of EGUS in the nonracehorse. 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.
Significant factors for the development of gastric ulceration included the feeding of concentrates and faster exercise (Vatistas 1998). In addition, withholding feed before exercise was a modifying factor that, although not causing gastric ulceration, may have decreased time of onset.(Vatistas 2 1999) Murray determined that alternately withholding feed for 24 h followed by feeding for 24 h induced ulceration of the squamous mucosa that appeared endoscopically similar to naturally occurring ulcers (Murray 1994). However, such a severe form of feed deprivation does not occur in horses in training, in which horses may be fasted for 4 h before training exercise, although the period of feed withdrawal may be longer prior to a race. The results of our study tend to support the concept from other studies that feed deprivation is not necessary for the development of gastric ulceration (Vatistas 1998). The stabling of horses from pasture has been documented to increase the severity of gastric ulceration (Murray and Eichorn, 1996). All horses in the present study were stabled and this may have had some influence on the development of gastric ulceration. Evidence for the role grain is predominantly anecdotal, but there has been one study that demonstrated an increased prevalence of gastric ulceration in ponies fed a concentrate diet compared to ponies fed hay alone 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)
It seems reasonable to suggest that any condition
that influences food intake might contribute to the development
of gastric ulcers in horses.(Sandin 2000)
It has been suggested that a high-grain, low-hay diet would increase the incidence of ulcers (Hammond et al. 1986). In cannulated horses, Nadeau et al. (2000) showed that bromegrass hay produced significantly lower gastric pH and higher frequency of gastric ulcers than did alfalfa hay-grain. Deprivation of feed for repeated periods has also been shown to cause gastric ulcers (Murray 1994a). (Jonssen 2006)
===Other ailments===
Considering the intestinal lesions, gastric ulceration was found in 42% of horses with large bowel lesions and in 31% with small bowel lesions. The association between intestinal lesions and ulcers within the stomach might suggest that gastric ulcers are often part of a larger gastrointestinal disease complex. In man, it is usual to find that disturbed activity in the autonomic nervous system affects both intestine and stomach (Fielding 1977). Murray (1989) reported an association between glandular ulcers and clinical disorders in foals and a similar relationship could also be true for mature horses. It has also been established that colic is associated with gastric ulcers in horses (Murray 1989, 1992; Furr and Murray 1989). In our study, colic disturbances were significantly (P<0.001) associated with gastric ulcers in bivariate analysis. This finding further suggests a relationship between gastric ulcers and clinical signs of colic. Whether gastric ulceration was the cause or the consequence of colic in our study has not been established. A variety of conditions involving abdominal pain (Murray
1992) have also been associated with gastric ulceration in horses. Abdominal pain or inappetance for any reason probably reduces appetite and, consequently, diminishes feed intake. Feed deprivation generally results in increased stomach acidity (Murray and Schusser 1993), since the absence of protein reduces buffering capacity. Moreover, gastric juice is more readily transported in an empty stomach and, as a consequence, flushed over the vulnerable squamous mucosa resulting in gastric ulceration. Therefore, any condition that considerably influences food intake might, hypothetically, contribute to the development of gastric ulcers in horses.(Sandin 2000)
Stress, due to concurrent disease, has been documented to increase the prevalence of peptic ulcer disease in neonatal foals (Furr et al. 1992).(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).
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==
==Clinical syndrome==