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==Introduction==

 

 

 

==Description==

The term ''''Equine gastric ulcer syndrome (EGUS)'''' encompasses a number of disease complexes<ref name="Merritt">Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric

The term ''''Equine gastric ulcer syndrome (EGUS)'''' encompasses a number of disease complexes<ref name="Merritt">Merritt, A M (2009) Appeal for proper usage of the term ʻEGUSʼ: Equine gastric

ulcer syndrome.  ''Equine Vet J'', 41(7):616.</ref> associated with ulceration of the oesophageal, gastric or duodenal mucosa<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> in horses.  When such damage is caused by acidic gastric juice, the defect is described as a ''''peptic ulcer''''.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  The non-glandular (squamous, proximal or orad) region of the equine stomach is lined by stratified squamous mucosa and a glandular mucosa lines the distal (aborad) portion.  Ulceration of either, or both<ref>Andrews, F.M, Bernard, W.V, Byars, T.D ''et al.'' (1999) Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 1:122-134.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> regions of the gastric mucosa is one of the most important problems of the equine stomach as it may limit performance<ref name="Bell">Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review.  ''N Z Vet J'', 55(1):1-12).</ref> and compromise welfare.<ref name="Martineau">Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse.  Part 1: Range of lesions present in 21 mature individuals.  ''Equine Vet J'', 41(7):638-644.</ref>  The two regions meet abruptly at the '''''margo plicatus'''''<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>, adjacent to where most ulcers occur.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Damage to these regions occurs via differing pathophysiological routes and varies in severity.  Inflammation can progress to cellular death and sloughing causing disruption of the superficial mucosa ('''erosion'''), then penetration of the submucosa down to the level of the ''lamina propria''<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>('''ulceration'''),  full thickness ulceration ('''perforation''')<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> and potentially duodenal stricture.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> The occult nature of the disease typically precludes the observation of clinical signs until severe ulceration has developed.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>

ulcer syndrome.  ''Equine Vet J'', 41(7):616.</ref> associated with ulceration of the oesophageal, gastric or duodenal mucosa<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> in horses.  When such damage is caused by acidic gastric juice, the defect is described as a ''''peptic ulcer''''.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  The non-glandular (squamous, proximal or orad) region of the equine stomach is lined by stratified squamous mucosa and a glandular mucosa lines the distal (aborad) portion.  Ulceration of either, or both<ref>Andrews, F.M, Bernard, W.V, Byars, T.D ''et al.'' (1999) Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 1:122-134.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> regions of the gastric mucosa is one of the most important problems of the equine stomach as it may limit performance<ref name="Bell">Bell, R.J, Mogg, T, Kingston, J.K (2007) Equine gastric ulcer syndrome in adult horses: a review.  ''N Z Vet J'', 55(1):1-12).</ref> and compromise welfare.<ref name="Martineau">Martineau, H, Thompson, H, Taylor, D (2009) Pathology of gastritis and gastric ulceration in the horse.  Part 1: Range of lesions present in 21 mature individuals.  ''Equine Vet J'', 41(7):638-644.</ref>  The two regions meet abruptly at the '''''margo plicatus'''''<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>, adjacent to where most ulcers occur.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Damage to these regions occurs via differing pathophysiological routes and varies in severity.  Inflammation can progress to cellular death and sloughing causing disruption of the superficial mucosa ('''erosion'''), then penetration of the submucosa down to the level of the ''lamina propria''<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>('''ulceration'''),  full thickness ulceration ('''perforation''')<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> and potentially duodenal stricture.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref> The occult nature of the disease typically precludes the observation of clinical signs until severe ulceration has developed.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>

==Prevalence==

==Prevalence==

*'''Bicarbonate:''' secreted by gastric mucosal cells.  Secretion triggered by luminal acid concentrations, mechanical irritation, and release of endogenous prostaglandins. Bicarbonate trapped in the mucous layer creates a pH gradient from physiological pH at the mucosal surface to a gastric acid pH at the luminal interface.

*'''Bicarbonate:''' secreted by gastric mucosal cells.  Secretion triggered by luminal acid concentrations, mechanical irritation, and release of endogenous prostaglandins. Bicarbonate trapped in the mucous layer creates a pH gradient from physiological pH at the mucosal surface to a gastric acid pH at the luminal interface.

*'''Epidermal growth factors:''' found in salivary gland secretions, promote DNA synthesis and proliferation of gastric mucosal cells. Also important in prostaglandin synthesis and inhibit hydrochloric acid (HCl) secretion by the parietal glands.

*'''Epidermal growth factors:''' found in salivary gland secretions, promote DNA synthesis and proliferation of gastric mucosal cells. Also important in prostaglandin synthesis and inhibit hydrochloric acid (HCl) secretion by the parietal glands.

*'''Epithelial restitution mechanisms:''' important for gastric mucosal integrity. Epithelial injury induces migration of adjacent cells to replace damaged cells within minutes without the need of new cell proliferation.  Shear forces, induced by mixing of ingesta, are counterbalanced by epithlial restoration.

*'''Epithelial restitution mechanisms:''' important for gastric mucosal integrity. Epithelial injury induces migration of adjacent cells to replace damaged cells within minutes without the need of new cell proliferation.  Shear forces, induced by mixing of ingesta, are counterbalanced by epithelial restoration.

*'''Adequate mucosal blood supply:''' required to provide the mucosa with oxygen and nutrients to produce the mucus-bicarbonate layer and to support rapid turnover of epithelial cells.  Also required to remove acid that has diffused into the mucosa.  Compromised mucosal perfusion may be important in the stress-related ulceration of neonates.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

*'''Adequate mucosal blood supply:''' required to provide the mucosa with oxygen and nutrients to produce the mucus-bicarbonate layer and to support rapid turnover of epithelial cells.  Also required to remove acid that has diffused into the mucosa.  Compromised mucosal perfusion may be important in the stress-related ulceration of neonates.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

*'''Prostaglandins:''' inhibit acid secretion, promote mucosal perfusion (through vasodilation), increase mucus and bicarbonate secretions and support mucosal cell repair.  PGE2 is especially important in these functions.

*'''Prostaglandins:''' inhibit acid secretion, promote mucosal perfusion (through vasodilation), increase mucus and bicarbonate secretions and support mucosal cell repair.  PGE2 is especially important in these functions.

*'''NSAIDs:''' as in [[Gastric Ulceration - all species|other species]], NSAIDs have been shown to cause gastric ulcers in horses.  Typically this is associated with high doses or frequent administration of '''phenylbutazone''' or '''flunixin meglumine'''.  However, although there is evidence to the contrary,<ref>Andrews, F.M, Reinemeyer, C.R, Longhofer, S.L (2009) Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. ''Vet Ther'', 10(3):113-20.</ref>therapeutic doses of NSAIDs may be sufficient to induce EGUS.  Other studies have suggested that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally<ref>Monreal, L, Sabatè, D, Segura, D, Mayós, I, Homedes, J (2004) Lower gastric ulcerogenic effect of suxibuzone compared to phenylbutazone when administered orally to horses.  ''Res Vet Sci'', 76:145-149.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>and that '''combination treatment''' with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone.<ref>Reed, S.K, Messer, N.T, Tessman, R.K, Keegan, K.G (2006) Effects of phenylbutazone alone or in combination with flunixin meglumine on blood protein concentrations in horses.  ''Am J Vet Res'', 67:398-402.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref> The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa,<ref>MacAllister, C.G, Morgan, S.J, Borne, A.T, Pollet, R.A, (1993) Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses.  ''J Am Vet Med Ass'', 202:71-77.  In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref><ref>Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists.  ''Equine Vet J Suppl'', 7:77-79.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref>Kumaran, D, Bhuvanakumar, C.K (1994) Gastro duodenal ulceration in foals - a discussion.  ''Cenfaur Mylapore'', 10:83-86. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref> they may look different endoscopically from ulcers that occur naturally,<ref name="Jonsson">Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref> and they appear to heal spontaneously.<ref>Jones, W.E (1983) Gastrointestinal ulcers [foal].  ''Equine Vet Data'', 4:305-308.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref>MacAllister, C.G, Sangiah, S (1993) Effect of ranitidine (in healing of experimentally induced gastric ulcers in ponies.  ''Am J Vet Res'', 54:1103-1107.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref> Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.<ref>Vatistas N.J, Snyder, J.R, Carlson, G.P, Johnson, B, Arther, R.M, Thurmiind, M, Lloyd, K.C.K (1994) Epidemiology study of gastric ulcerarion in the Thoroughbred race horse: 202 horses.  ''Proc Am Ass Equine Pract'', 39:125-126.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref>Murray, M.J, Schusser, G.F, Pipers, F.S, Gro:ss, S.J (1996) Factors associated with gastric lesions in Thoroughbred racehorses.  ''Equine Vet J'', 28:368-374.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref name="Vatistas thesis">Vatistas, N.J (1998) Gastric Ulceration in the Racing Thoroughbred.  ''PhD Thesis''.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref>

*'''NSAIDs:''' as in [[Gastric Ulceration - all species|other species]], NSAIDs have been shown to cause gastric ulcers in horses.  Typically this is associated with high doses or frequent administration of '''phenylbutazone''' or '''flunixin meglumine'''.  However, although there is evidence to the contrary,<ref>Andrews, F.M, Reinemeyer, C.R, Longhofer, S.L (2009) Effects of top-dress formulations of suxibuzone and phenylbutazone on development of gastric ulcers in horses. ''Vet Ther'', 10(3):113-20.</ref>therapeutic doses of NSAIDs may be sufficient to induce EGUS.  Other studies have suggested that suxibuzone causes significantly less ulcerogenic effects than phenylbutazone when administered orally<ref>Monreal, L, Sabatè, D, Segura, D, Mayós, I, Homedes, J (2004) Lower gastric ulcerogenic effect of suxibuzone compared to phenylbutazone when administered orally to horses.  ''Res Vet Sci'', 76:145-149.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>and that '''combination treatment''' with phenylbutazone and flunixin meglumine may be more risky than phenylbutazone alone.<ref>Reed, S.K, Messer, N.T, Tessman, R.K, Keegan, K.G (2006) Effects of phenylbutazone alone or in combination with flunixin meglumine on blood protein concentrations in horses.  ''Am J Vet Res'', 67:398-402.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref> The ulcers produced by NSAIDs are unusual in that they have a predilection for the glandular mucosa,<ref>MacAllister, C.G, Morgan, S.J, Borne, A.T, Pollet, R.A, (1993) Comparison of adverse effects of phenylbutazone, flunixin meglumine, and ketoprofen in horses.  ''J Am Vet Med Ass'', 202:71-77.  In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref><ref>Furr, M.O, Murray, M.J (1989) Treatment of gastric ulcers in horses with histamine type 2 receptor antagonists.  ''Equine Vet J Suppl'', 7:77-79.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref>Kumaran, D, Bhuvanakumar, C.K (1994) Gastro duodenal ulceration in foals - a discussion.  ''Cenfaur Mylapore'', 10:83-86. In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref> they may look different endoscopically from ulcers that occur naturally,<ref name="Jonsson">Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref> and they appear to heal spontaneously.<ref>Jones, W.E (1983) Gastrointestinal ulcers [foal].  ''Equine Vet Data'', 4:305-308.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref>MacAllister, C.G, Sangiah, S (1993) Effect of ranitidine (in healing of experimentally induced gastric ulcers in ponies.  ''Am J Vet Res'', 54:1103-1107.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref> Despite the well-established link bewteen NSAIDs and ulcers, NSAIDs are rarely responsible for the lesions in horses in race training.<ref>Vatistas N.J, Snyder, J.R, Carlson, G.P, Johnson, B, Arther, R.M, Thurmiind, M, Lloyd, K.C.K (1994) Epidemiology study of gastric ulcerarion in the Thoroughbred race horse: 202 horses.  ''Proc Am Ass Equine Pract'', 39:125-126.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref>Murray, M.J, Schusser, G.F, Pipers, F.S, Gro:ss, S.J (1996) Factors associated with gastric lesions in Thoroughbred racehorses.  ''Equine Vet J'', 28:368-374.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref><ref name="Vatistas thesis">Vatistas, N.J (1998) Gastric Ulceration in the Racing Thoroughbred.  ''PhD Thesis''.  In: Vatistas, N.J, Sifferman, R.L, Holste, J, Cox, J.L, Pinalto, G, Schultz, K.T (1999) Induction and maintenance of gastric ulceration in horses in simulated race training.  ''Equine Vet J Suppl'', 29:40-44</ref>

*'''Infective agents:''' ''Helicobacter spp.'' have been held responsible for the initiation and recurrence of human gastric ulcers.  ''Helicobacter equorum'' has been isolated from equine faecal samples<ref>Fox, J.G (2002) The non-''H.pylori'' helicobacters: their expanding role in gastorintestinal and systemic disease.  ''Gut'', 50:273-283.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref> and ''Helicobacter''-like DNA has been found in both foal faeces<ref>Moyaert, H, Haesebrouck, F, Dewulf, J, Ducatelle, R, Pasmans, F (2009) ''Helicobacter equorum'' is highly prevalent in foals.  ''Vet Microbiol'', 133:190-192.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> and the stomachs of mature horses.  However, such findings have been demonstrated in horses with and without gastric lesions<ref>Contreras, M, Morales, A, Garcia-Amado, M.A, DeVera, M, Bermudez, V, Gueneau, P (2007) Detection of ''Helicobacter''-like DNA in the gastric mucosa of Thoroughbred horses.  ''Letters in Appl Microbiol'', 45:553-337.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>and in clinically healthy animals.  Any link between EGUS and ''Helicobacter'' remains weak at best, although there is a suggestion that colonisation of equine gastric ulcers with ''E.coli'' may delay their healing.<ref>Al Jassim, R.A.M, Scott, P.T, Trebbin, A.L, Trott, D, Pollitt, C.C (2006) The genetic diversity of lactic acid producing bacteria in the equine gastrointestinal tract.  ''FEMS Microbiol Letters'', 248:75-81.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref>

*'''Infective agents:''' [[Helicobacter|''Helicobacter spp.'']] have been held responsible for the initiation and recurrence of human gastric ulcers.  ''Helicobacter equorum'' has been isolated from equine faecal samples<ref>Fox, J.G (2002) The non-''H.pylori'' helicobacters: their expanding role in gastorintestinal and systemic disease.  ''Gut'', 50:273-283.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref> and ''Helicobacter''-like DNA has been found in both foal faeces<ref>Moyaert, H, Haesebrouck, F, Dewulf, J, Ducatelle, R, Pasmans, F (2009) ''Helicobacter equorum'' is highly prevalent in foals.  ''Vet Microbiol'', 133:190-192.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref> and the stomachs of mature horses.  However, such findings have been demonstrated in horses with and without gastric lesions<ref>Contreras, M, Morales, A, Garcia-Amado, M.A, DeVera, M, Bermudez, V, Gueneau, P (2007) Detection of ''Helicobacter''-like DNA in the gastric mucosa of Thoroughbred horses.  ''Letters in Appl Microbiol'', 45:553-337.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>and in clinically healthy animals.  Any link between EGUS and ''Helicobacter'' remains weak at best, although there is a suggestion that colonisation of equine gastric ulcers with [[Escherichia coli|''E.coli'']] may delay their healing.<ref>Al Jassim, R.A.M, Scott, P.T, Trebbin, A.L, Trott, D, Pollitt, C.C (2006) The genetic diversity of lactic acid producing bacteria in the equine gastrointestinal tract.  ''FEMS Microbiol Letters'', 248:75-81.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref>

*'''Temperament:''' a nervous disposition has been linked with gastric ulcers<ref>McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses.  ''J Am Vet Med Ass 215:1130-1133.  In: In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref>but the same association was not seen in another study.<ref>Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthur, R.M, Thurmond, M, Zhou, H, Lloyd, L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses.  ''Equine Vet J Suppl'', 29:34-39.  In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref>   

*'''Temperament:''' a nervous disposition has been linked with gastric ulcers<ref>McClure, S.R, Glickman, L.T, Glickman, N.W (1999) Prevalence of gastric ulcers in show horses.  ''J Am Vet Med Ass 215:1130-1133.  In: In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref>but the same association was not seen in another study.<ref>Vatistas, N.J, Snyder, J.R, Carlson, G, Johnson, B, Arthur, R.M, Thurmond, M, Zhou, H, Lloyd, L.K (1999) Cross-sectional study of gastric ulcers of the squamous mucosa in Thoroughbred racehorses.  ''Equine Vet J Suppl'', 29:34-39.  In: Jonsson, H, Egenvall, A (2006) Prevalence of gastric ulceration in Swedish Standardbreds in race training.  ''Equine Vet J'', 38(3):209-213.</ref>   

*hypotensive shock (for example with blood loss, sepsis, endotoxaemia or fluid sequestration in colic)

*hypotensive shock (for example with blood loss, sepsis, endotoxaemia or fluid sequestration in colic)

*an increase in sympathetic tone (which might be related to physiological or psychological stresses) or  

*an increase in sympathetic tone (which might be related to physiological or psychological stresses) or  

*other severe disease states (such as disseminated intravascular coagulation).

*other severe disease states (such as [[DIC|disseminated intravascular coagulation]]).

Furthermore, any impairment of gastric motility (as seen with neurological imbalances, several types of colic and certain drugs) might be expected to increase the risk of ulceration.  Despite a lack of clarity, the final common pathway for EGUS appears to be the breaching of mucosal defences by acidic gastric contents.  Since horses secrete gastric HCl continuously, even in the fasted state,<ref>Campbell-Thompson, M.L, Merritt, A.M (1987) Effect of ranitidine on gastric acid secretion in young male horses.  ''Am J Vet Res'', 48:1511-1515.</ref> they are especially vulnerable to acid-associated damage.

Furthermore, any impairment of gastric motility (as seen with neurological imbalances, several types of colic and certain drugs) might be expected to increase the risk of ulceration.  Despite a lack of clarity, the final common pathway for EGUS appears to be the breaching of mucosal defences by acidic gastric contents.  Since horses secrete gastric HCl continuously, even in the fasted state,<ref>Campbell-Thompson, M.L, Merritt, A.M (1987) Effect of ranitidine on gastric acid secretion in young male horses.  ''Am J Vet Res'', 48:1511-1515.</ref> they are especially vulnerable to acid-associated damage.

*Excessive recumbency<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>

*Excessive recumbency<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>

*Mild to severe colic

*Mild to severe colic

**Mild, recurrent colic signs post-prandially<ref>Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.  ''Vet Clin North Am Equine Pract'', 25(2):283-301.</ref>

**Mild, recurrent [[Colic Diagnosis - Clinical Signs|colic signs]] post-prandially<ref>Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.  ''Vet Clin North Am Equine Pract'', 25(2):283-301.</ref>

**In one study, 49% of horses that presented for colic had gastric ulceration and those with duodenitis-proximal jejunitis had a trend towards a higher prevalence of gastric ulceration compared to those with other GI lesions.<ref>Dukti, S.A, Perkins, S, Murphy, J, Barr, B, Boston, R, Southwood, L.L, Bernard, W (2006) Prevalence of gastric squamous ulceration in horses with abdominal pain.  ''Equine Vet J'', 38:347-349.</ref>

**In one study, 49% of horses that presented for colic had gastric ulceration and those with duodenitis-proximal jejunitis had a trend towards a higher prevalence of gastric ulceration compared to those with other GI lesions.<ref>Dukti, S.A, Perkins, S, Murphy, J, Barr, B, Boston, R, Southwood, L.L, Bernard, W (2006) Prevalence of gastric squamous ulceration in horses with abdominal pain.  ''Equine Vet J'', 38:347-349.</ref>

*Changes in attitude (dullness or depression)<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>

*Changes in attitude (dullness or depression)<ref name="Orsini">Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>

'''Clinical signs in foals vary depending on age and severity:'''

'''Clinical signs in foals vary depending on age and severity:'''

*'''Neonatal foals''': many ulcers are silent, some foals only exhibit signs when ulceration has become severe.  Glandular ulcers are considered the most significant<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

*'''Neonatal foals''': many ulcers are silent, some foals only exhibit signs when ulceration has become severe.  Glandular ulcers are considered the most significant<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>.

**Poor appetite

**Poor appetite

**Diarrhoea

**Diarrhoea

**Diarrhoea

**Diarrhoea

In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  GDUD is the primary differential for ptyalism in foals, other possible diagnoses include oesophageal obstruction and ''Candida'' infection.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>

In foals with outflow obstruction distal to the common bile duct, marked reflux may be seen even with limited nursing.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Brown gastric fluid may signify bleeding ulcers or necrotizing enterocolitis. GDUD is the primary differential for ptyalism in foals, other possible diagnoses include oesophageal obstruction and ''Candida'' infection.<ref name="Merck">Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition), Merial</ref>

==Diagnosis==

==Diagnosis==

====Histamine 2 receptor antagonists====

====Histamine 2 receptor antagonists====

Parietal cells secrete HCl upon stimulation of histamine, acetylcholine or gastrin receptors.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Competitive H2 receptor antagonists have successfully elevated gastric pH and treated gastric ulcers in mature horses and foals.<ref name="Lester">Sanchez, L.C, Lester, G.D, Merritt, A.M (1998) Effect of ranitidine on intragastric pH in clinically normal neonatal foals.  ''J Am Vet Med Assoc'', 212:1407-1412.</ref><ref>Becht, J.L, Byars, T.D (1986) Gastroduodenal ulceration in foals.  ''Equine Vet J'', 18:307-312.</ref>  There appears to be a great variability among horses in their dose requirements for H2 antagonists which may be explained by individual bioavilability for these compounds.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Currently recommended doses proposed to be effective in the majority of horses<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> are:

Parietal cells secrete HCl upon stimulation of histamine, acetylcholine or gastrin receptors.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Competitive H2 receptor antagonists have successfully elevated gastric pH and treated gastric ulcers in mature horses and foals.<ref name="Lester">Sanchez, L.C, Lester, G.D, Merritt, A.M (1998) Effect of ranitidine on intragastric pH in clinically normal neonatal foals.  ''J Am Vet Med Assoc'', 212:1407-1412.</ref><ref>Becht, J.L, Byars, T.D (1986) Gastroduodenal ulceration in foals.  ''Equine Vet J'', 18:307-312.</ref>  There appears to be a great variability among horses in their dose requirements for H2 antagonists which may be explained by individual bioavailability for these compounds.<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref>  Currently recommended doses for cimetidine, ranitidine and f amotidine proposed to be effective in the majority of horses have been recommended by Sanchez.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

====Proton-pump inhibitors (PPIs)====

====Proton-pump inhibitors (PPIs)====

====Mucosal protectants====

====Mucosal protectants====

'''Sucralfate''' is a complex salt of sucrose and aluminium hydroxide.  It is thought to promote ulcer healing via several mechanisms: adherence to ulcerated mucosa, stimulation of mucus secretion, pepsin inibition, increasing PGE synthesis and enhancing the local production of epidermal growth factor.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  It has been used effectively to treat and prevent stress-induced ulcers in man and has been recommended at 10-20mg/kg three times daily for the treatment of glandular ulcers in horses.<ref>Murray, M.J (1994) Gastric ulcers in adult horses.  ''Comp Cont Educ Pract Vet'', 16:792-794,797.  In: Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>  However, the effect of sucralfate on equine squamous gastric ulcers remains inconclusive<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> and the product may be ineffective in the alkaline conditions created by acid suppression agents.<ref>Danesh, J.Z, Duncan, A, Russell, R.I, Mitchell, G (1988) Effect of intragastric pH on mucosal protective action of sucralfate.  ''Gut'', 29:1379-1385.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

'''Sucralfate''' is a complex salt of sucrose and aluminium hydroxide.  It is thought to promote ulcer healing via several mechanisms: adherence to ulcerated mucosa, stimulation of mucus secretion, pepsin inibition, increasing PGE synthesis and enhancing the local production of epidermal growth factor.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  It has been used effectively to treat and prevent stress-induced ulcers in man and has been recommended for the treatment of glandular ulcers in horses.<ref>Murray, M.J (1994) Gastric ulcers in adult horses.  ''Comp Cont Educ Pract Vet'', 16:792-794,797.  In: Orsini, J (2000) Tutorial Article Gastric ulceration in the mature horse: a review. ''Equine Vet Educ'', 12(1):24-27.</ref>  However, the effect of sucralfate on equine squamous gastric ulcers remains inconclusive<ref name="EGUC">The Equine Gastric Ulcer Council (1999) Tutorial Article: Recommendations for the diagnosis and treatment of equine gastric ulcer syndrome (EGUS).  ''Equine Vet Educ'', 11(5):262-272.</ref> and the product may be ineffective in the alkaline conditions created by acid suppression agents.<ref>Danesh, J.Z, Duncan, A, Russell, R.I, Mitchell, G (1988) Effect of intragastric pH on mucosal protective action of sucralfate.  ''Gut'', 29:1379-1385.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

====Prostaglandin analogues====

====Prostaglandin analogues====

   

   

Synthetic PGE1 analogues are believed to inihibit gastric acid secretion and enhance mucosal cytoprotection.<ref>Leandro, G, Pilotto, A, Franceschi, M ''et al.'' (2001) Prevention of acute NSAID-related gastroduodenal damage: a meta-analysis of controlled clinical trials.  ''Dig Dis Sci'', 46:1924-1936.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  '''Misoprostol''' has been an effective agent in the treatment of human gastric and duodenal ulcers and at 5µg/kg has been shown to increase gastric pH in horses.<ref>Sangiah, S, MacAllister, C.C, Amouzadeh, H.R (1989) Effects of misoprostol and omeprazole on basal gastric pH and free acid content in horses.  ''Res Vet Sci'', 47:350-354.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Although contraindicated in pregnant mares, Misoprostol may be beneficial for mucosal recovery in the face of flunixin treatment.<ref>Tomlinson, J.E, Blikslager, A.T (2005) Effects of cyclooxygenase inhibitors flunixin and deracoxib on permeability of ischaemic-injured equine jejunum.  ''Equine Vet J'', 37:75-80.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

Synthetic PGE1 analogues are believed to inihibit gastric acid secretion and enhance mucosal cytoprotection.<ref>Leandro, G, Pilotto, A, Franceschi, M ''et al.'' (2001) Prevention of acute NSAID-related gastroduodenal damage: a meta-analysis of controlled clinical trials.  ''Dig Dis Sci'', 46:1924-1936.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>  '''Misoprostol''' has been an effective agent in the treatment of human gastric and duodenal ulcers and has been shown to increase gastric pH in horses.<ref>Sangiah, S, MacAllister, C.C, Amouzadeh, H.R (1989) Effects of misoprostol and omeprazole on basal gastric pH and free acid content in horses.  ''Res Vet Sci'', 47:350-354.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref> Although contraindicated in pregnant mares, Misoprostol may be beneficial for mucosal recovery in the face of flunixin treatment.<ref>Tomlinson, J.E, Blikslager, A.T (2005) Effects of cyclooxygenase inhibitors flunixin and deracoxib on permeability of ischaemic-injured equine jejunum.  ''Equine Vet J'', 37:75-80.  In: Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

====Gastric prokinetics====

====Gastric prokinetics====

====Treatment problems====

====Treatment problems====

The prevalence of gastric ulcers in horses remains high regardless of the common use of antiulcer treatments.  This has been attributed to the expense of recommended products encouraging subtherapeutic and curtailed dosing schedules.<ref>Orsini, J.A, Haddock, M, Stine, L, Sullivan, E.K, Rabuffo, T.S, Smith, G (2003) Odds of moderate or severe gastric ulceration in racehorses receiving antiulcer medications.  ''J Am Vet Med Ass'', 223:336-339.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref>  Omeprazole and ranitidine must be administered for at least 28 days for adequate ulcer healing.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  In the USA, compounded omeprazole from bulk powders are used as a cheaper substitute for the FDA approved products. However, these formulations lack efficacy and are not regulated<ref>Nieto, J.E, Spier, S, Pipers, F.S, Stanley, S, Aleman, M.R, Smith, D.C, Snyder, J.R (2002) Comparison of paste and suspension formulations of omeprazole in the healing of gastric ulcers in racehorses in active training.  ''J Am Vet Med Ass'', 221: 1139-1143.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  A considerable challenge lies in the management of abdominal pain associated with EGUS, since the commonly used NSAIDs for pain control may worsen and even induce further ulcerative lesions.<ref>Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.''Vet Clin North Am Equine Pract'', 25(2):283-301.</ref>  Another challenge is the horse in which oral medication is prohibited.  However, Andrews and colleagues (2006) have demonstrated the efficacy of an omeprazole powder, adminstered IV in sterile water, which signifcantly increases the pH of equine gastric contents and may be useful in problem horses.<ref name="Andrews 2006">Andrews, F.M, Frank, N, Sommardahl, C.S, Buchanan, B.R, Elliott, S.B, Allen, V.A (2006) Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses.  ''J Vet Intern Med'', 20(5):1202-6.</ref>  An ongoing point of debate is the use of antiulcer medication in competition horses.  In 2000, the Bureau of '''The Fèdèration Equestre Internationale (FEI)''' permitted the use of cimetidine, ranitidine and omeprazole to prevent and treat gastric ulcers.  This decision was based on evidence that the compounds were not performance enhancing and that EGUS was such a widespread concern. However, these drugs are still listed under prohibited substances in the '''2009 Appendices of the American Endurance Ride Conference (AERC) Rules and Regulations'''.  The argument is that a horse requiring such treatment is not suffciently well to compete and should be withdrawn from competition if it needs preventative medication.  A related concern is that the AERC permits the use of hyperosmolar oral electrolyte pastes which may cause gastric ulcers.<ref>Holbrook, T.C, Simmons, R.D, Payton, M.E, MacAllister, C.G (2005) Effect of repeated oral administration of hypertonic electrolyte solution on equine gastric mucosa.  ''Equine Vet J'', 37: 501-504.</ref>  Without the protection afforded by antiulcer agents, these horses may be at considerable risk for EGUS.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>

The prevalence of gastric ulcers in horses remains high regardless of the common use of antiulcer treatments.  This has been attributed to the expense of recommended products encouraging subtherapeutic and curtailed dosing schedules.<ref>Orsini, J.A, Haddock, M, Stine, L, Sullivan, E.K, Rabuffo, T.S, Smith, G (2003) Odds of moderate or severe gastric ulceration in racehorses receiving antiulcer medications.  ''J Am Vet Med Ass'', 223:336-339.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum. ''Equine Vet J'', 41(7):611-615.</ref>  Omeprazole and ranitidine must be administered for at least 28 days for adequate ulcer healing.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  In the USA, compounded omeprazole from bulk powders are used as a cheaper substitute for the FDA approved products. However, these formulations lack efficacy and are not regulated.<ref>Nieto, J.E, Spier, S, Pipers, F.S, Stanley, S, Aleman, M.R, Smith, D.C, Snyder, J.R (2002) Comparison of paste and suspension formulations of omeprazole in the healing of gastric ulcers in racehorses in active training.  ''J Am Vet Med Ass'', 221: 1139-1143.  In: Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>  A considerable challenge lies in the management of abdominal pain associated with EGUS, since the commonly used NSAIDs for pain control may worsen and even induce further ulcerative lesions.<ref>Videla, R, Andrews, F.M (2009) New perspectives in equine gastric ulcer syndrome.''Vet Clin North Am Equine Pract'', 25(2):283-301.</ref>  Another challenge is the horse in which oral medication is prohibited.  However, Andrews and colleagues (2006) have demonstrated the efficacy of an omeprazole powder, adminstered IV in sterile water, which signifcantly increases the pH of equine gastric contents and may be useful in problem horses.<ref name="Andrews 2006">Andrews, F.M, Frank, N, Sommardahl, C.S, Buchanan, B.R, Elliott, S.B, Allen, V.A (2006) Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses.  ''J Vet Intern Med'', 20(5):1202-6.</ref>  An ongoing point of debate is the use of antiulcer medication in competition horses.  In 2000, the Bureau of '''The Fèdèration Equestre Internationale (FEI)''' permitted the use of cimetidine, ranitidine and omeprazole to prevent and treat gastric ulcers.  This decision was based on evidence that the compounds were not performance enhancing and that EGUS was such a widespread concern. However, these drugs are still listed under prohibited substances in the '''2009 Appendices of the American Endurance Ride Conference (AERC) Rules and Regulations'''.  The argument is that a horse requiring such treatment is not suffciently well to compete and should be withdrawn from competition if it needs preventative medication.  A related concern is that the AERC permits the use of hyperosmolar oral electrolyte pastes which may cause gastric ulcers.<ref>Holbrook, T.C, Simmons, R.D, Payton, M.E, MacAllister, C.G (2005) Effect of repeated oral administration of hypertonic electrolyte solution on equine gastric mucosa.  ''Equine Vet J'', 37: 501-504.</ref>  Without the protection afforded by antiulcer agents, these horses may be at considerable risk for EGUS.<ref name="Nadeau">Nadeau, J.A, Andrews, F.M (2009) ''Science: Overviews'' Equine gastric ulcer syndrome: The continuing conundrum.  ''Equine Vet J'', 41(7):611-615.</ref>

==Prognosis==

==Prognosis==

====Prophylaxis====

====Prophylaxis====

'''Omeprazole paste''' at a lower dose (1-2mg/kg) daily for 3-4 weeks.<ref name="McClure">McClure, S.R, White, G.W, Sifferman, R.L, ''et al.'' (2005) Efficacy of omeprazole paste for prevention of recurrence of gastric ulcers in horses in race training.  ''J Am Vet Med Assoc'', 226:1685-1688.</ref>

'''Omeprazole paste''' at a lower dose daily for 3-4 weeks.<ref name="McClure">McClure, S.R, White, G.W, Sifferman, R.L, ''et al.'' (2005) Efficacy of omeprazole paste for prevention of recurrence of gastric ulcers in horses in race training.  ''J Am Vet Med Assoc'', 226:1685-1688.</ref>

*Prevented ulcers in horses maintained under ulcerogenic conditions.<ref name="McClure">McClure, S.R, White, G.W, Sifferman, R.L, ''et al.'' (2005) Efficacy of omeprazole paste for prevention of recurrence of gastric ulcers in horses in race training.  ''J Am Vet Med Assoc'', 226:1685-1688.</ref><ref>McClure, S.R, White, G.W, Sifferman, R.L, ''et al.'' (2005) Efficacy of omeprazole paste for prevention of gastric ulcers in horses in race training.  ''J Am Vet Med Assoc'', 226:1681-1684.</ref><ref>White, G.W, McClure, S.R, Sifferman, R.L, Bernard, W, Doucet, M, Vrins, A, Hughes, F, Holste, J.E, ALva, R, Fleishman, C, Cramer, L (2003) Prevention of occurrence and recurrence of gastric ulcers in horses by treatment with omeprazole at 1mg/kg/day.  ''Proc Am Ass Equine Practnrs'', 49: 220-221.</ref><ref>White, G.W, McClure, S.R, Sifferman, R.L, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration.  ''J Am Vet Med Ass'', 230:1680-1682.</ref>

*Prevented ulcers in horses maintained under ulcerogenic conditions.<ref name="McClure">McClure, S.R, White, G.W, Sifferman, R.L, ''et al.'' (2005) Efficacy of omeprazole paste for prevention of recurrence of gastric ulcers in horses in race training.  ''J Am Vet Med Assoc'', 226:1685-1688.</ref><ref>McClure, S.R, White, G.W, Sifferman, R.L, ''et al.'' (2005) Efficacy of omeprazole paste for prevention of gastric ulcers in horses in race training.  ''J Am Vet Med Assoc'', 226:1681-1684.</ref><ref>White, G.W, McClure, S.R, Sifferman, R.L, Bernard, W, Doucet, M, Vrins, A, Hughes, F, Holste, J.E, ALva, R, Fleishman, C, Cramer, L (2003) Prevention of occurrence and recurrence of gastric ulcers in horses by treatment with omeprazole at 1mg/kg/day.  ''Proc Am Ass Equine Practnrs'', 49: 220-221.</ref><ref>White, G.W, McClure, S.R, Sifferman, R.L, Holste, J.E, Fleishman, C, Murray, M.J, Cramer, L.G (2007) Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration.  ''J Am Vet Med Ass'', 230:1680-1682.</ref>

*Prophylaxis in critically ill foals may not be necessary and is controversial since gastric acidity may be protective against bacterial translocation.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

*Prophylaxis in critically ill foals may not be necessary and is controversial since gastric acidity may be protective against bacterial translocation.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

*May benefit foals receiving substantial doses of NSAIDs for orthopaedic pain.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

*May benefit foals receiving substantial doses of NSAIDs for orthopaedic pain.<ref name="Sanchez">Sanchez, L.C (2010) 'Diseases Of The Stomach' in  Reed, S.M, Bayly, W.M. and Sellon, D.C (2010) '''Equine Internal Medicine''' (Third Edition), Saunders, Chapter 15.</ref>

==References==

==References==

[[Category:Gastric_Ulceration]]

[[Category:Gastric_Ulceration]]

[[Category:To_Do_-_Nina]]

 

[[Category:Stomach_Disorders_-_Horse]]

[[Category:Stomach Diseases - Horse]]

[[Category:To_Do_-_Review]]

[[Category:Expert_Review]]

[[Category:Medical Colic in the Horse]]