Diagnosis and management of equine gastric disease updates

Gastric disease remains a highly prevalent condition in all equine breeds and equestrian disciplines – particularly those that are in regular and intense work.

Despite attempts to develop blood or saliva tests, gastroscopy remains the only means of identifying the presence of the condition. Recent studies suggest a poor association between the reported clinical signs and gastroscopic evidence of gastric disease. Appreciation of the differences between diseases of the squamous and glandular portions of the stomach has grown, with a realisation that treatment for glandular disease cannot simply be extrapolated from experience of managing squamous disease.

Oral omeprazole remains the only medicine registered for the management of squamous gastric disease (ESGD); however, alternatives are increasingly used and are typically associated with better responses to treatment. No products are registered for the management of equine glandular gastric disease (EGGD).

Omeprazole monotherapy is no longer considered appropriate for the treatment of EGGD and may be used in association with sucralfate, although alternatives such as esomeprazole, extended-release injectable omeprazole or misoprostol are frequently preferred for EGGD.

Clinical signs of gastric disease

Clinical signs of gastric disease are frequently non-specific, and the presence of gastroscopic lesions does not confirm that they are the cause of the clinical complaint. Several studies have indicated that the correlation between reported clinical signs and gastroscopic lesions is poor; horses with clinical signs reportedly associated with gastric disease may have normal stomachs and lesions may be present in horses that are considered normal clinically.

It is, therefore, important that horses with gastric disease – particularly EGGD – undergo an holistic assessment with investigation of other disease and orthopaedic pain which may explain the clinical signs or be an underlying cause of secondary gastric disease.

Stress is consistently identified as a risk factor for EGGD, and it is, therefore, important that the housing and management of horses with glandular lesions is scrutinised to look for potential causes of stress. When assessing clinical responses to treatment, it is also important to consider that a poor correlation exists between reported reduction in clinical signs and improvement in the gastroscopic appearance of the stomach.

Clinical signs of gastric disease include:

• Changes in behaviour. Stereotypical behaviour has been associated with ESGD. Discomfort on girthing or touching the flanks is often highlighted as a sign of gastric disease, but evidence for this is lacking. Horses with EGGD are more stressed (assessed via cortisol responses) and may exhibit negative changes in behaviour.
• Colic – particularly post-feeding – has been associated with both ESGD and EGGD, but in the author’s experience the gastric disease has to be severe. Both ESGD and EGGD can occur secondary to colic because of fasting, reduced gastric emptying or pain and stress. EGGD may be a component of wider gastrointestinal inflammatory disease.
• Poor performance or changes in ridden performance. Objective assessments have inconsistently indicated reduced fitness in association with ESGD, and owner-reported poor performance has been associated with both ESGD and EGGD. Altered responses under saddle or a reluctance to work are commonly cited as a sign of EGGD, but this has not been well substantiated.
• Weight loss and reduced feed intake have been reported with ESGD and severe EGGD; however, this is not consistent across all studies, and both ESGD and EGGD are commonly identified in horses that are in excellent condition and horses that eat well. Recent evidence suggests that some previously reported clinical signs, such as poor coat quality and diarrhoea, are less likely to indicate gastric disease than was once suggested¹.

Diagnosis

Interest has grown in the use of blood or salivary markers for gastric disease. While differences have been identified between populations of horses with or without gastric disease, extensive overlap occurs such that reliable blood or salivary markers for diagnosing disease in individual horses do not exist currently. One might expect acute phase proteins to increase in association with gastric disease, but this is not the case and they cannot be used for its diagnosis. Faecal occult blood testing is marketed as a means of identifying gastric or intestinal disease, but has no evidence to support its use.

Gastroscopy is hailed as the only means of diagnosing gastric disease and is a safe and relatively straightforward procedure. The challenge with gastroscopy comes in agreeing what mucosal changes are indicative of disease and what lesions might be associated with clinical signs. There is good agreement over the grading of squamous lesions; however, no one truly knows which lesions are likely to be clinically significant, and in humans gastric pain may be present in the absence of visible lesions.

There is little agreement, meanwhile, over grading of glandular lesions and in determining which changes in the mucosa are likely to be clinically relevant and merit treatment. This is particularly true where discolouration of the mucosa is present in the absence of haemorrhage or fibrinosuppurative lesions, and clinicians do not agree on what constitutes mucosal erythema or an altered mucosa.

The recent convention in EGGD is to describe the location (cardia, fundus, antrum), nature (erythema, haemorrhage, fibrinosuppurative inflammation), topography (flat, raised, nodular, depressed), perceived severity (mild, moderate, marked) and extent (focal, multifocal, diffuse) of lesions. Some EGGD lesions – particularly nodular lesions – are thought to be chronic, asymptomatic and unlikely to respond to treatment. Histological examination of biopsies is rarely helpful.

Preventing gastric disease through reduction in risk factors

Factors that increase acid exposure of the squamous mucosa have consistently been identified as risk factors for ESGD and these factors primarily relate to diet and exercise. Reduced forage and/or increased sugars or starches in the diet will increase the risk of ESGD.

It used to be thought that pasture turnout reduced the risk of gastric disease; however, some recent studies have found a lower incidence of disease in horses that are brought in from pasture and housed^2,3. Stress or shortage of forage in these pasture environments may have increased the risk of gastric disease and highlights the importance of investigating the diet and management factors unique to each horse.

Dietary fibre is important in stimulating saliva and in forming feed layers within the stomach that maintain the normal pH stratification and protect the squamous mucosa. Exercise increases movement and splashing of acid within the stomach, which is potentially injurious to the squamous mucosa.

Duration of exercise is also a risk factor for EGGD, and it has been proposed that this may be due to reduction in gastric blood flow during exercise and/or the psychological stress that is associated with exercise. Stress is considered an important, and potentially the most important, factor in EGGD and this is thought to explain the associations that have been identified between EGGD and specific trainers or the number of people riding a particular horse. Investigating and aiming to eliminate causes of stress is considered critical in the prevention and management of EGGD.

Treatment of gastric disease

The most important determinant of outcome in the treatment of gastric disease is the degree to which underlying risk factors can be identified and addressed.

In the absence of fundamental management change, dietary modification and attention to any chronic pain or behavioural issues, treatment of gastric disease may fail and is highly likely to recur.

Interest is increasing around the use of behavioural therapies and potentially behaviour-modifying drugs such as trazadone to reduce stress in horses prone to EGGD. Beyond this, a range of treatment options that can be considered for gastric disease are now available.

Oral omeprazole

Oral omeprazole is the registered product and is effective in treating and preventing ESGD. Healing rates are generally high, but will be influenced by diet and management.

Recommended treatment courses have reduced in duration from the traditional four weeks, with some recent studies reporting high rates of healing after only two weeks of oral enteric-coated omeprazole (or two doses of extended-release injectable omeprazole; ERIO). Some compromise on three weeks of therapy.

Dose, as well as duration, is relevant to healing rates, and a move has been made towards lower doses of buffered omeprazole, from 4mg/kg to 2mg/kg. A dose response with diet and management is likely to occur, again affecting the likelihood of the lower dose being sufficient. Enteric-coated omeprazole products are more effective than buffered products at equivalent doses and may, therefore, be used effectively at lower doses (1mg/kg to 2mg/kg).

Appreciation has grown of the influence of diet and owner compliance on the efficacy of oral omeprazole. The absorption of omeprazole is affected by feeding and administration on an empty stomach improves bioavailability.

The absorption of enteric-coated products appears less affected by the presence of feed than the absorption of buffered products. Administration with a small amount of hard feed on an empty stomach is not the same as administration to a horse that is on ad-lib fibre and, in the author’s opinion, administration with feed may negate at least some of the benefit of the enteric encapsulation such that administration after fasting is still preferred, irrespective of the posology of the omeprazole preparation.

Oral omeprazole is considered ineffective in the treatment of EGGD when used alone, but may be effective in a proportion of cases when used in combination with oral sucralfate. Robust data to support the omeprazole/sucralfate combination remains lacking, but supportive case reports exist as well as a consensus of expert opinion that sucralfate increases the rate of healing. Treatment may need to be longer than with some of the alternatives, with courses of six to eight weeks being commonplace.

Esomeprazole

Omeprazole was the first proton pump inhibitor developed for use in human medicine, but newer drugs in the same class are now generally preferred.

Esomeprazole is absorbed more consistently and metabolised more slowly than omeprazole⁴. Compared to an equivalent dose of omeprazole, esomeprazole results in a more pronounced and consistent acid suppressive effect in man, and similar benefits have now been demonstrated in horses.

When pH was measured using indwelling monitors in the same six horses, enteric-coated esomeprazole at 2mg/kg maintained pH above 4 at the mucosal surface for 80% of a 24-hour period, compared to only 40% for oral omeprazole⁵. At half the dose, esomeprazole resulted in greater acid suppression than omeprazole in a further small study⁶.

Esomeprazole has also been found to be effective in treating ESGD when treatment with omeprazole was ineffective. Enteric-coated esomeprazole, therefore, offers advantages and may be appropriate for use in situations where diet and management are suboptimal and anticipated rates of healing with buffered omeprazole would be expected to be lower.

Given the challenges of achieving healing of EGGD with oral omeprazole (with or without sucralfate), esomeprazole offers an attractive alternative. Data to support the use of esomeprazole (with or without sucralfate) in EGGD is limited; however, it would be expected to be more effective than omeprazole – particularly if used in an enteric-coated form. The author uses enteric-coated esomeprazole at 2mg/kg to 4mg/kg for the treatment of EGGD, typically with oral sucralfate administered an hour apart.

ERIO

The highest rates of both ESGD and EGGD healing have reported following the administration of an ERIO preparation (BOVA UK) and ERIO has consistently proven more effective in studies that have compared it to oral omeprazole.

Intramuscular injection overcomes any issues with bioavailability or owner compliance with the administration of oral preparations. Administration of an ERIO preparation to six horses with implanted pH probes demonstrated the capacity of the injectable preparation to suppress acid more profoundly and consistently than when the same horses were administered oral omeprazole⁷. A risk exists of injection site reactions associated with the use of ERIO; however, it appears to be very low at around 2%^7-11. Systemic reactions have also been reported¹², likely because of inadvertent intra-arterial injection; however, pharmacovigilance data puts this risk at one in 50,000 doses.

The use of ERIO in racehorses is limited by the long withdrawal (three to four weeks) to comply with the rules or racing; no withdrawal is required for other equestrian sports. Administration every five days has been shown to be more effective than administration every seven days¹³. The author typically uses two doses for ESGD and four doses for EGGD. Anecdotally, the use of protracted courses of ERIO increases the risk of injection site reactions and is not recommended. If a response has not occurred after four doses, then it is more appropriate to consider switching to an alternative treatment, as acid suppression is unlikely to be curative. While no evidence exists to support the use of ERIO with oral sucralfate for the treatment of EGGD, this combination is logical and used widely.

Misoprostol

Misoprostol is licensed for refractory gastric disease in man and has a number of theoretical benefits, including increasing mucosal blood flow, reducing pepsin and gastric acid production, enhancing mucosal resistance to injury and increasing mucus-producing cells relative to parietal cells. In the single published study of misoprostol treatment in EGGD, 73% healing was reported in 20 horses compared to 22% in a further 20 horses treated with oral omeprazole and sucralfate in combination¹⁴.

Misoprostol is not recommended in the treatment of ESGD and may even exacerbate (or induce) the condition. Other adverse effects associated with misoprostol may include diarrhoea and abortion. The risk of human abortion and potential for drug misuse are a concern – particularly when dispensing human misoprostol tablets.

Extemporaneous misoprostol paste formulated for horses mitigates the risk of abuse and overcomes the increasing challenge of obtaining human tablets.

Misoprostol and omeprazole are sometimes used in combination; however, no evidence exists to indicate whether this offers any advantages. Mechanisms of action are potentially conflicting, so it is recommended that oral omeprazole is administered at least an hour ahead of misoprostol. Some clinicians combine misoprostol with sucralfate; however, both drugs have broadly similar mechanisms of action and no data exists to indicate that this offers an advantage over using either drug in isolation.

Glucocorticoids

EGGD is an inflammatory rather than an ulcerative condition that is typically associated with a lymphoplasmacytic infiltrate with variable neutrophilia. The use of glucocorticoids is, therefore, logical to suppress the inflammatory response; however, no evidence of their benefit exists beyond anecdotal reports of small numbers of cases.

Glucocorticoids tend to be used when other options have failed.

Antimicrobials

A single study of antimicrobials in the treatment of EGGD did not suggest that any benefit was to be found in the use of potentiated sulphonamides¹⁵. There was a phase of using antimicrobials on the basis that Helicobacter species or other bacteria might be pathogenic in EGGD; however, this was likely misguided, and in the absence of evidence of bacterial infection, the use of antimicrobials cannot be justified.

Nutraceuticals

Dietary oil is beneficial in reducing the need for sugars and starches, and may reduce gastric acidity. Recent work suggests that fish oils may actually be preferable to flax/linseed oils and may have benefits in ESGD¹⁶ .

Pectin-lecithin complexes have been shown to be potentially beneficial in ESGD and EGGD, though data is limited. Beet pulp is rich in pectin and has been shown to reduce the risk of ESGD. The probiotic Saccharomyces cerevisiae may be protective against both ESGD and EGGD – particularly in the presence of high starch diets. Limited studies of varying quality purport benefits of nutraceuticals including liquorice, aloe vera, fermented soy or rice, sea buckthorn, hyalouran and Chinese herbs¹.

Conclusions

While huge knowledge gaps remain, the management of gastric disease has developed considerably in recent years as clinicians have embraced a number of new treatment options. The greatest gap in our knowledge is probably in attributing clinical significance and knowing which horses warrant treatment for gastric disease and which do not.

ESGD and EGGD are distinct conditions that are managed differently. Proton pump inhibitors remain the mainstay for ESGD, but new actives, enteric-coated formulations and parenteral administration may help to improve management of the condition.

Treatment of EGGD remains a challenge; the improved acid suppression that is achieved with ERIO appears to result in higher rates of healing; however, some cases do not respond, and other options such as misoprostol, sucralfate and glucocorticoids may all have a place. EGGD likely represents a syndrome and, until it is better understood, there will be a degree of trial an error in managing the condition.

• Use of some of the drugs in this article is under the veterinary medicine cascade.
• This article appeared in Vet Times (28 April 2026), Vlume 56, Issue 17, Pages 12-14.

David Rendle graduated from the University of Bristol in 2001 and then worked in farm animal and equine practice before completing an internship at Liphook Equine Hospital. A three-year Horserace Betting Levy Board residency at the University of Glasgow and Liphook Equine Hospital enabled him to train as a specialist in equine internal medicine. David moved to Rainbow Equine Hospital, North Yorkshire, where he became a director and subsequently a clinical director. David now works as an independent equine medicine and therapeutics consultant.