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EQUINE VETERINARY EDUCATION / AE / MAY 2015
Review Article
Rethinking equine gastric ulcer syndrome: Part 2 – Equine squamous gastric ulcer syndrome (ESGUS)
B. W. Sykes* and J. M. Jokisalo† BW Sykes Consultancy, Upper Orara, New SouthWales, Australia; and †Animagi Equine Hospital, Hyvinkää, Finland. *Corresponding author email:
bensykes21@hotmail.com
Keywords: horse; stomach; omeprazole; ranitidine; neutraceuticals
Summary It has recently been highlighted that significant differences in prevalence, risk factors and the response to treatment exist between ulceration of the squamous gastric mucosa and ulceration of the glandular gastric mucosa in the horse. In the first article in the series, the term equine squamous gastric ulcer syndrome (ESGUS) was used to describe disease of the squamous gastric mucosa with clinical signs and diagnosis discussed. The purpose of this article is to review the pathophysiology, risk factors, prevalence, treatment and prevention of ESGUS.
Introduction
Ulceration of the squamous mucosa of the horse has been recognised as a highly prevalent condition for nearly 30 years (Hammond et al. 1986) and numerous studies have investigated the factors that contribute to the development of disease, its prevalence, risk factors, treatment and prevention. The term equine squamous gastric ulcer syndrome (ESGUS) was proposed in the first article of this series to describe disease of the squamous mucosa (Sykes and Jokisalo 2014). It is recognised that, under the term ESGUS, further distinction into primary and secondary squamous disease is warranted as discussed below.
Pathophysiology
Horses are constant secretors of gastric acid (Campbell- Thompson and Merritt 1987) and the median pH of the ventral stomach of 3.0 over a normal 24 h period reflects this (Husted et al. 2008). Under normal conditions the consumption of roughage creates a basketball-sized bolus of feed in the stomach that acts as a buffer to absorb gastric acidity. As a result the gastric pH at the level of cardia has a median value of approximately 7.0 (Husted et al. 2008). Squamous ulceration occurs, fundamentally, as a result of
increased exposure of a tissue with limited defence mechanisms to highly acidic gastric contents (Lorenzo- Figueras and Merritt 2002). Endogenous production of hydrochloric acid is likely the dominant aggressive agent, as discussed below, although duodenal bile salts may also play a role (Berschneider et al. 1999). Any disruption of the normal stratification of gastric pH results in an increased risk of ESGUS and damage occurs rapidly with evidence of acid injury evident within 30 min of exposure in vitro (Widenhouse et al. 2002). The fermentation of short-chain fatty acids consumed in the diet are likely also to contribute to squamous mucosal injury (Nadeau et al. 2003). However, the high rate of ESGUS healing observed with omeprazole treatment, and in the absence of risk factor reduction, (Murray et al. 1997; Andrews
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et al. 1999b; MacAllister et al. 1999; Doucet et al. 2003; Lester et al. 2005; Sykes et al. 2014b, 2014d) provides indirect evidence that gastric acid is the dominant erosive agent and that the role of short-chain fatty acids and duodenal bile salts are likely to be less important. Equine squamous gastric ulcer syndrome can occur as a
primary disease in otherwise healthy animals, primarily associated with management impositions as discussed below, or as a secondary disease consequent to the delayed gastric outflow. While both ESGUS and EGGUS (equine glandular gastric ulcer syndrome) are common in certain populations, such as Thoroughbred racehorses (Begg and O’Sullivan 2003; Sykes et al. 2014b), no relationship exists between the presence of ESGUS and EGGUS within affected animals at a population level (Murray et al. 2001; Begg and O’Sullivan 2003) and the majority of ESGUS is primary in origin. However, the authors have occasionally observed severe ESGUS in horses with concurrent severe EGGUS in animals that otherwise would be considered to be at low risk of ESGUS. As such, the authors believe that, although a link is not demonstrable at a population level, the possibility that EGGUS can cause ESGUS in certain animals should not be discounted. For the purposes of this article the discussion will focus on primary ESGUS recognising that management of secondary ESGUS is dependent on appropriate treatment of any underlying disease as well as addressing any ulceration that may be present.
Prevalence and risk factors
The prevalence of ESGUS mirrors exercise intensity with the risk of disease increasing as the intensity of work increases. The highest prevalences have been reported in Thoroughbred racehorses, with >70% of animals affected across a wide range of studies (Murray et al. 1996; Vatistas et al. 1999b; Begg and O’Sullivan 2003; Bell et al. 2007) and in competing endurance horses with 93% of animals affected (Tamzali et al. 2011). Standardbred racehorses are also commonly affected (63–87% of animals [Rabuffo et al. 2002; Dionne et al. 2003]). However, ESGUS is not solely a disease of high performance horses and it is seen across a wide range of other horse types with 69% of horses used for a variety of purposes affected in a recent Danish study (Luthersson et al. 2009a). Prevalences of ESGUS of 58 and 40% have also been reported in show (McClure et al. 1999) and western performance (Bertone 2000) horses, respectively. It has recently been suggested that the above prevalences may overstate the prevalence of clinically significant disease as many animals classified as having EGUS may only have mild lesions of questionable clinical relevance (Cate et al. 2012). The authors generally consider grades 1–2/4
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