Changes

==Risk Factors==

==Risk Factors==

===Exercise===

===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.(Hartmann and Frankeny 2003)in (Nadeau 2009).  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 et al (2 1999) were able to induce and maintain EGUS in racehorses in fast work without the use of NSAIDs or fasting before exercise (Vatistas et al 2 1999).  There is also evidence that light to heavy training for just 8 days is suffcient to induce gastric ulcers.<ref>White, G, McClure, S.R, Siifferman, R, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration.  ''J Am Vet Med Assoc'', 230(11):1680-2.</ref>  Furthermore, the higher prevalence of gastric ulcers at post mortem in racehorses in training compared to those in retirement adds wait to the hypothesis that exercise is an important risk factor for EGUS.(Hammond et al. (1986)It is thought that exercise increases the exposure of the squamous mucosa to acid as the stomach is compressed by the abdominal viscera and diaphragm (Lorenzo-Figueras and Merritt 2002).

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.(Hartmann and Frankeny 2003)in (Nadeau 2009).  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 et al (2 1999) were able to induce and maintain EGUS in racehorses in fast work without the use of NSAIDs or fasting before exercise (Vatistas et al 2 1999).  There is also evidence that training for just 8 days is suffcient to induce gastric ulcers.<ref>White, G, McClure, S.R, Siifferman, R, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration.  ''J Am Vet Med Assoc'', 230(11):1680-2.</ref>  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.(Hammond et al. (1986)It is thought that exercise increases the exposure of the squamous mucosa to acid as the stomach is compressed by the abdominal viscera and diaphragm during excessive movement (Lorenzo-Figueras and Merritt 2002).

===Housing and Transport===

===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<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>  '''Transport''' has also been shown to induce squamous mucosal ulceration(71 in Sanchez)

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 situation 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>  '''Transport''' has also been shown to induce squamous mucosal ulceration(71 in Sanchez)

===Diet===

===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<ref>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.</ref>  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)

'''Feed deprivation''' encourages gastric ulceration in two ways: (1) it precludes 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<ref>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.</ref>  Ponies fed a '''concentrate diet''' had a greater 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===

===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)

Conditions that produce abdominal pain and/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===

===NSAIDs===

As in [[Gastric Ulceration - all species|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,<ref>Andrews, F.M, Reinemeyer, C.R, Longhofer, S.L (2009) Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. ''Vet Ther'', 10(3):113-20.</ref>therapeutic doses of NSAIDs may be sufficient to induce EGUS.  Other studies have suggested that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally(Monreal et al. 2004) and that combination treatment with phenylbutazone and flunixin meglumine may be more dangerous than phenylbutazone alone.(Reed et al. 2006)

As in [[Gastric Ulceration - all species|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,<ref>Andrews, F.M, Reinemeyer, C.R, Longhofer, S.L (2009) Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. ''Vet Ther'', 10(3):113-20.</ref>therapeutic doses of NSAIDs may be sufficient to induce EGUS.  Other studies have suggested that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally(Monreal et al. 2004) and that combination treatment with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone.(Reed et al. 2006) The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa(MacAllister et al. 1993 in Jonssen)(Furr and Murray 1989; Kuinaran and Bhuvanakumar 1994 in Vatisats 2 1999), they may look different endoscopically from ulcers that occur naturally,(Jonssen 2006) and they appear to heal spontaneously.(Jones 1983; MacAllister and Sangiah 1993 in Vatisats 2 1999)  Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.(Vatistas et al. 3994b; Murray et al. 1996; Vatistas 1998 in Vatistas 2 1999)  

 

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)

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). (Vatistas 2 1999)

===Temperament===

===Temperament===