Equine Gastric Ulcer Syndrome (EGUS) is common terminology that most veterinarians and horse owners are far too familiar with. The term has been around for the past 20 years and was originally coined by a panel of experts in the field at a time when vets and horse owners were just starting to learn about diseases within the equine stomach.
Gastroscopes used in the original studies were only 2.5m in length, allowing visualisation of only the squamous mucosa within the stomach. This led to an inherent bias in our understanding of EGUS towards disease of the squamous mucosa. When gastroscopes evolved and increased in length, veterinarians were able view the glandular mucosa, which in turn resulted in increased recognition of glandular disease. This necessitated a review of the terminology and in more recent times EGUS has been reclassified as an over-arching umbrella term that simply describes ulcerative, erosive, inflammatory, and hyperkeratotic diseases of the stomach.
Identified distinct differences between diseases of the squamous versus glandular mucosa include pathophysiology, prevalence, risk factors, treatment, management, and prevention. The term EGUS is now divided into Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD) with A/Prof Ben Sykes, a leading EGUS researcher, describing them as “Like the odd couple. They just live together in the same apartment but are not related to each other. As such we can’t extrapolate from one disease for another.”
EGGD presents with inflammatory and erosive lesions due to breakdown of the muco-bicarbonate layer which normally protects the glandular area from acid burn. The specific causes why this defence mechanism breaks down are not well understood but risk factors have been associated through A/Prof Sykes’ and others’ research.
EGGD prevalence is less well documented than ESGD prevalence but it has been reported as between 47-65% in Australian Thoroughbred racehorses and 27-33% in competing endurance horses (Sykes et al. 2015). A retrospective study in the United Kingdom reported EGGD in 54% of leisure horses and 64% in sport horses presented for gastroscopy (Hepburn, 2014). These findings support the clinical impression that EGGD is more prevalent in riding horse populations than racehorse populations and the majority of the EGGD lesions in all the above studies were located within the pyloric antrum.
EGGD Risk Factors
The risk factors for EGGD are very different to ESGD and less well described. While non-steroidal anti-inflammatory drugs (NSAIDs) used at higher doses may cause EGUS (both ESGD and EGGD), the impact of them at normal therapeutic doses is less clear. No evidence exists to date to support the role of Helicobacter infection in EGGD, in contrast to peptic ulcer disease in people.
There is minimal data to support the role of diet with EGGD, unlike ESGD, however, exercise does play a role in EGGD albeit appearing to be a different mechanism than for ESGD. A Canadian showjumper study conducted by Pederson et al (2018) found that horses exercised 6-7 days a week were approximately 3.5 times more likely to develop EGGD than horses exercised 5 days or less per week. Similarly, an Australian and UK racehorse study by A/Prof Sykes et al (2019) found horses exercised 5-7 days a week were approximately 10 times more likely to have EGGD than horses exercised 4 days or less per week. This shows the importance of rest days for glandular gastric health and current prevention recommendations include 3 rest days per week to allow mucosal recovery and repair from exercised induced injury.
The association of stress and ESGD has been discussed for many years but the term can be quite unclear at the best of times, with minimal evidence to support a role for stress in the causation of ESGD. However, there is a growing body of evidence to support behavioural stress as being central to EGGD risk. A study within Switzerland by Scheideger et al (2017) investigated the stress response in horses with EGGD through stimulating the release of cortisol via adrenocorticotrophic hormone (ACTH). Horses with EGGD had more pronounced stress responses when compared to horses without EGGD. A/Prof Sykes explains that further research is warranted in following the population of horses over a period of time as we don’t know if this response was cause or effect.
Another study in Finland by Mönki et al (2016) suggested that an increased number of riders or handlers increased the risk of EGGD. This discovery comes back to the concept of behavioural stress as horses are routine animals, and they can engage or bond with individuals differently. As such a change in riders or handlers may be a behavioural stressor. The same study found a breed disposition for EGGD amongst Warmbloods.
EGGD Clinical signs
It is difficult to establish clinical signs of EGGD at a population level, explains A/Prof Sykes but a range of behavioural manifestations are observed and a link with poor performance has been established. Racehorses performing below expectation were approximately 4 times more likely to have EGGD in one study (Sykes et al. 2019), and in a Canadian study by Pederson et al. (2018) horses competing internationally were 9 times less likely to have EGGD than horses competing nationally. However, it is important to note that poor performance can be due to multiple factors and that EGUS is only one differential in the work up of poor performance.
A/Prof Sykes explains that oral omeprazole alone is not as consistently effective in treating EGGD compared to its effects in ESGD (Sykes et al. 2017). Accordingly, a combination treatment protocol involving omeprazole and sucralfate is generally advised. Alternatively, misoprostol has also shown to be an effective treatment through enhancing the protective mechanisms of the glandular mucosa.
EGGD Prevention and Management
In terms of prevention and management it is important to address the risk factors by including 2-3 rest days per week, increasing environmental enrichment, removing potential stressors such as musculoskeletal pain, and including a digestive health supplement.
While searching for a high-quality product he could use and recommend, A/Prof Sykes found GastroAID was the only product on the Australian market that aligned with the findings of his research (Sykes et al. 2014). Not only is GastroAID backed by independent research, including his own, it has scientifically proven high-quality ingredients that are all clearly listed on the label, is Australian made, is manufactured to GMP standards and conforms to ISO quality standards.
GastroAID Recovery is Kelato’s premium supplement targeting both foregut and hindgut health formulated to aid horses recovering from EGUS or support horses during high risk periods. It is unique due to the combination of antacids and “coating agents” pectin and lecithin that provide an enhanced “alkaline slime” barrier for the squamous mucosa and supplement the natural defence mechanisms of the glandular mucosa. For hindgut health, the prebiotic and live yeast probiotic work together to maintain a healthy environment, stimulate the growth of beneficial microbes and enhance feed conversion efficiency.
How does it work?
- Moderates Gut Transit Time (optimal feed conversion efficiency)
- Neutralises Gastric Acid
- Coats Stomach Lining
- Strengthens Stomach Lining
- Blocks Harmful Bacteria
- Promotes Beneficial Microbes
GastroAID Everyday is an economical supplement formulated to maintain the health and function of the total digestive tract. Its daily use acknowledges the importance of optimal digestive health and function for a healthier, happier horse. It is particularly beneficial for hindgut health due to the unique, powerful prebiotic and two live yeast probiotics.
How does it work?
- Controls Stomach Acidity
- Promotes Healthy Stomach Lining
- Inhibits Harmful Bacteria
- Improves Intestinal Integrity
- Promotes Beneficial Microbes
- Enhances the Body’s Defences
When managing EGGD, A/Prof Sykes brings to light the importance of taking a holistic approach including managing the environment and emotional wellbeing of the horse to reduce the prevalence of disease.
Hepburn RJ 2014, ‘Endoscopic examination of the squamous and glandular gastric mucosa in sport and leisure horses: 684 horses (2005–2011)’ [abstract]. Proc 11th International Equine Colic Research Symposium, vol.5.
Mönki, J, Hewetson, M & Virtala, A-MK 2016, ‘Risk Factors for Equine Gastric Glandular Disease: A Case-Control Study in a Finnish Referral Hospital Population’, Journal of Veterinary Internal Medicine, vol. 30, no. 4, pp. 1270 – 1275.
Pederson, SK, Cribb, AE, Windeyer, MC, Read, EK, French, D & Banse, HE 2018, ‘Risk Factors for Equine Glandular and Squamous Gastric Disease in Show Jumping Warmbloods’, Equine Veterinary Journal, vol. 50, no. 6, pp. 747 – 751.
Scheidegger, MD, Gerber V, Bruckmaier, RM, van der Kolk, JH, Burger D & Ramseyer, A 2017, ‘Increased Adrenocrotical Response to Adrenocorticotropic Hormone (ACTH) in Sport Horses with Equine Glandular Gastric Disease (EGGD), The Veterinary Journal, vol. 228, pp. 7 – 12.
Sykes, BW, Bowen, M, Habershon-Butcher, JL, Green, M & Hallowell, GD 2019, ‘Management Factors and Clinical Implications of Glandular and Squamous Gastric Disease in Horses’, Journal of Veterinary Internal Medicine, vol. 33, no. 1, pp. 233 – 240.
Sykes BW, Hewetson M, Hepburn, RJ, Luthersson, N & Tamzali, Y 2015, ‘European College of Equine Internal Medicine Consensus Statement – Equine Gastric Ulcer Syndrome in Adult Horses’, Journal of Veterinary Internal Medicine, vol. 29, no. 5, pp. 1288 – 1299.
Sykes, BW, Sykes KM & Hallowell, GD 2014, ‘Efficacy of a Combination of Apolectol, Live Yeast (Saccharomyces cerevisiae [CNCM I-1077]), and Magnesium Hydroxide in the Management of Equine Gastric Ulcer Syndrome in Thoroughbred Racehorses: A Blinded, Randomized, Placebo-Controlled Clinical Trial’, Journal of Equine Veterinary Medicine, vol. 34, pp. 1274 – 1278.
Sykes, BW, Underwood, C, Greer, R, McGowan, CM & Mills, PC 2017, ‘The Effects of Dose and Diet on the Pharmacodynamics of Omeprazole in the Horse’, Equine Veterinary Journal, vol. 49, no. 4, pp. 525 – 531.