There are still no definitive external signs that are deemed as pathognomonic for equine gastric ulcer syndrome (EGUS). Instead, a number of clinical signs have been attributed as potentially raising a cause for concern with regards to this gastric disease. These include poor appetite or ‘picky eating’, poor body condition and weight loss, poor coat condition, bruxism (teeth grinding), behavioural changes, recurrent post prandial colic and poor performance.
Despite a certain lack of clarity in some areas with regards to EGUS, there is one thing that does appear to remain more or less of a constant, the epidemiology. In most studies investigating this, warm-blooded horses such as Thoroughbreds and Arabians do show a predilection to the syndrome over and above cold-blooded (calmer horses) horses such as Shires and Clydesdales; especially in relation to ulcers in the squamous region of the stomach. This is mirrored in the fact that 80 – 90% of race horses have been found to have some degree of gastric ulceration. A risk predilection is also consistently shown in other disciplines, with up to 60% of non-racing performance horses thought to suffer from the syndrome.
In spite of this however, EGUS should not be thought of as only being a condition of elite athletes. Up to 50% of leisure horses can also be affected1, with foals also forming an important risk category. With regards to diagnosis, in 1985 gastroscopy was first described as being a viable diagnostic tool for equine gastric ulceration and still remains the only reliable method for obtaining a definitive ante-mortem diagnosis for ulcers in either the squamous or pyloric regions of the stomach. Studies have shown that if an animal has an ulcer in the pyloric region of the stomach, then it doesn’t follow that there will be ulceration of the squamous region. Likewise, just because there are no squamous ulcers visible, this does not mean that the horse could not have a pyloric region ulcer. Therefore all anatomical areas of the gastric surface must be examined.
With regards to the therapy of equine gastric ulceration, it has been stated that ‘no acid, equals no ulcers’, thereby acid suppression is the cornerstone for treatment. Consistent with this, omeprazole has been hailed as the mainstay drug of choice. Omeprazole is a proton pump inhibitor belonging to the substituted benzimidazole class of compounds. It suppresses gastric acid secretion by specific inhibition of the H+/K+ ATPase enzyme system, which is the acid pump (also known as the proton pump) at the secretory surface of the parietal cell within the gastric mucosa. Because the H+/K+ ATPase are the final step involved in control of acid secretion, omeprazole blocks secretion irrespective of stimulus. The binding of omeprazole to the H+/K+ ATPase enzyme is irreversible, with pentagastrin-stimulated gastric acid secretion being shown to be inhibited by 99% at eight hours, 95% at 16 hours and 90% at 24 hours following oral dosing of horses with 4mg/kg/day of omeprazole.
The dosing schedule of omeprazole is based upon the time it takes for the body to naturally replace the inhibited proton pumps – this is approximately 24 hours – therefore a once a day dosing protocol is sufficient. The full effect on the inhibition of acid secretion is reached by five days into the treatment course after the initial administration. Omeprazole reaches its area of effect via the blood supply to the gastric mucosa. Therefore following oral dosing it is imperative the omeprazole component of any product enters into the small intestine in concentrations adequate enough to be absorbed here and gain efficacious plasma levels. Omeprazole is generally considered to be acid labile, meaning it is easily degraded by the acidic environment of the stomach upon oral dosing. Protection from this degradation is therefore necessary in order for a product to achieve sufficient absorption of the active ingredient.
Peptizole® Oral Paste for Horses is the first licensed generic omeprazole on the GB market for use in horses. Peptizole® has proven bioequivalence to the pioneer and contains basifying/buffering agents which protect the active in the acidic stomach. This means that the absorption of omeprazole into the blood stream from the small intestine is equivalent to the pioneer and the effectiveness of the product will be the same. The paste is used at a dose rate of 4mg/kg PO SID for a treatment duration of 28 days. Use of omeprazole at this dose rate has been well studied, with consistent healing rates of up to 70-90% reported for squamous ulceration after a month of treatment.
The pharmacological approach for prevention of recurrence of gastric ulceration is similar to that of treatment, i.e. omeprazole is the active ingredient of choice, however a lowered dose rate of 1mg/kg PO SID is used.
It cannot be forgotten however, that for the treatment and especially the prevention of recurrence of gastric ulcers, the story does not end at simply utilising an effective pharmaceutical product. Management and husbandry changes alongside are complementary and can be synergistic to the clinical effects of drug therapy. Without these alterations being made on a long term basis, gastric ulceration can easily recur once an oral omeprazole product is withdrawn, even within as little as 5 days.