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lesions unlikely to cause clinical signs in contrast to grades 3–4/4 lesions, although strong evidence to support this opinion is lacking. In line with this, only 10% of Standardbred racehorses had lesions ≥grade 3/4, despite an overall ESGUS prevalence of 44% (Dionne et al. 2003) and only 36 and 48% of Thoroughbred racehorses had lesions ≥grade 3/4, despite overall ESGUS prevalences of 74 and 78%, respectively (Begg and O’Sullivan 2003; Marqués et al. 2011). As such, the authors believe that prevalences stated above should be interpreted with caution as they may not truly reflect the prevalence of animals with potentially clinically significant disease. The prevalence of ESGUS in horses at rest is variable but it is
typically lower and when observed tends to be less severe. However, the authors have observed severe (grades 3-4/4) ESGUS in some individual horses at pasture and consider that ESGUS should not be discounted as a differential diagnosis simply because a horse does not meet the ‘typical’ risk profile. A large number of management changes are imposed
upon horses with the commencement of training, many of which have been documented to increase the risk of ESGUS. These include exercise (Lorenzo-Figueras and Merritt 2002), high concentrate/low roughage diets (Nadeau et al. 2000), fasting (Murray and Eichorn 1996), transport (McClure et al. 2005a), stall confinement (Murray and Eichorn 1996), the administration of hypertonic electrolytes (Holbrook et al. 2005) and intermittent access to water (Luthersson et al. 2009b). Induction of ESGUS can be rapid occurring within 7 days in some studies (Vatistas et al. 1999a; McClure et al. 2005a) and the risk of disease increases with time in work (Habershon- Butcher et al. 2012).
Management and treatment
Given the central role that management plays in the development of ESGUS, it is logical that removing or at least reducing the impact of various risk factors should reduce the risk of disease. This is supported by a study in endurance horses where the prevalence of ESGUS was 48% during the inter-season period compared with 93% during the competition season (Tamzali et al. 2011). The provision of access to hay, or alternative forms of roughage, should restore the normal pH stratification of the stomach; however, straw on its own is an unsuitable candidate as the provision of straw as the sole roughage source has been demonstrated to be a risk factor for disease (Luthersson et al. 2009b). It has been further suggested that including multiple forage sites may be beneficial as it may increase the time spent grazing (Hepburn 2011). A reduction in the soluble carbohydrate content of meals should reduce the impact of secondary volatile fatty acid injury, while the addition of corn oil appears to have the dual benefit of increasing caloric intake (allowing a reduction in carbohydrate content) and directly decreasing gastric acid production (Cargile et al. 2004). Based on the identified risk factors other specific management measures that may be beneficial include increasing the availability of turnout, ensuring ad libitum access to water and the feeding of a small, roughage based meal 30–60 min prior to exercise. To the authors’ knowledge, the efficacy of management
changes have not been specifically documented in the peer reviewed literature and the high prevalence (48%) of ESGUS observed in endurance horses during the noncompetition season (Tamzali et al. 2011) suggests that a reduction in work alone is not enough to prevent the disease. Theoretically, removal of the horse from the risk factors that caused disease
in the first place and re-establishment of a normal pH gradient in the stomach should result in healing. However, anecdotally it appears that even when removal from the risk factors is possible, acid suppression therapy is often required to restore a normal appetite so that enough roughage is consumed to re-establish the pH gradient in the stomach allowing healing to occur, especially in horses with weight loss and/or decreased appetite. Further, the ability to remove risk factors, such as exercise and concentrate diets, is often limited thus the use of acid suppression therapy remains a cornerstone in the management of ESGUS. Pharmaceutical treatment of ESGUS focuses on
suppression of acid production. A variety of drugs have been used for this purpose but omeprazole remains the most effective (Lester et al. 2005) and best studied. In a study comparing the likelihood of ESGUS being present only commercial omeprazole decreased the risk below that of a placebo, in contrast to buffers, sucralfate, H2-receptor antagonists (ranitidine and cimetidine) and compounded omeprazole, none of which had any demonstrable benefit (Orsini et al. 2003). Omeprazole impairs the H+, K+ ATPase (proton) pump that secretes HCl (Fellenius et al. 1981) and does not directly contribute to healing. Instead the squamous mucosa has an enormous proliferative capacity and the removal of ongoing insult is sufficient for the tissues to heal in the majority of cases. Several factors warrant consideration in regards to the response to omeprazole therapy including the formulation and dose used and the timing of administration. To date, little attention has been given to the effect of
formulation with Gastrogard (Merial, Duluth, GA, USA)1, the formulation predominately used globally, due to it being patent protected in most markets. However, the patent has recently expired and interest in different formulations has increased. Omeprazole is acid labile and it is generally regarded that some formof protection is necessary to prevent degradation of the drug within the acidic environment of the stomach (Merritt et al. 2003). Gastrogard1 utilises a buffered paste formulation to achieve this protection (Merritt et al. 2003) compared with other formulations that utilise enteric-coated granules suspended within a paste to achieve the same objective (Sykes et al. 2014b). The manufacturers of enteric-coated formulations claim superior bioavailability and it appears that a modest benefit may be present with the bioavailability of a commercially available enteric-coated formulation (Gastrozol, Virbac, Milperra, NSW, Australia)2 reported to be 1.26 times greater than that of Gastrogard1 (Birkmann et al. 2014). Recently, a plain, unbuffered formulation of omeprazole has been released onto the European market with a claim of bioequivalence to Gastrogard1 (Morgan 2010). Further work into the relative bioavailability of different formulations is ongoing but preliminary results suggest that modest effects of formulation are present (Sykes et al., unpublished data). Gastrogard1 is the best studied at its registered dose of
4 mg/kg bwt per os s.i.d. for 28 days as recommended by the 1999 EGUS Council (Andrews et al. 1999a) with ESGUS healing rates of 70–77% consistently reported (Murray et al. 1997; Andrews et al. 1999b; MacAllister et al. 1999; Doucet et al. 2003; Lester et al. 2005). Recently, the use of lower doses of an enteric-coated formulation (Gastrozol)2 has been evaluated and, under certain conditions, doses as low as 1 mg/kg bwt have been shown to be as efficacious as 4 mg/kg bwt in the treatment of ESGUS (Sykes et al. 2014b). Similarly, Gastrozol2 at
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