Equine Gastric Ulcer Syndrome: Clinical Notes
1. Omeprazole: how soon acid suppression starts
Acid suppression starts within hours of the first dose, but the full effect takes about 3–5
days of daily dosing.
After a single dose (4 mg/kg PO)
Why the full effect takes days
Practical points
2. Intermittent omeprazole for prevention
Daily low-dose prophylaxis is well supported. True intermittent oral dosing (every other day, or a few days a week) has essentially no published efficacy data, and the data on gaps in dosing point against it.
What the evidence supports
Daily low dose works. 1–2 mg/kg PO once daily prevented new ulcers and recurrence in horses in race training (Andrews 1999, McClure 2005, White 2007 with 285 racehorses, Endo 2012).
A 2019 meta-analysis (Mason et al., EVJ) pooled 7 RCTs with 566 horses. Ulcers occurred in 23% of omeprazole-treated horses vs 77% on sham, a risk ratio of 0.28.
The ECEIM consensus endorses 1 mg/kg daily in high-risk horses, particularly during high-risk periods.
“High-risk periods” is the sanctioned form of intermittency. That means daily dosing through shipping, shows, stall rest or NSAID courses, then stopping. It is not skipping days during an ongoing risk.
What argues against skipping days
Suppression doesn’t carry over. At 4 mg/kg, inhibition is already falling by 24 h. New pumps are synthesized continuously, so a missed day lets acid output recover substantially.
Recurrence after short gaps is fast.
Shan et al. 2023 studied Hong Kong Thoroughbreds on 2.4 g daily. A 3-day withholding period brought squamous disease back to 83% prevalence, statistically no different from pre-treatment. A 1-day withhold left it at 25%.
The authors report lesions recurring within 3 days.
Rebound hyperacidity from hypergastrinemia is the proposed reason. Serum gastrin rises about 2.5-fold within a week on omeprazole and returns to baseline 2–4 days after stopping (Clark et al. 2023).
The loading lag works against on/off schedules. Full effect takes about 5 days of daily dosing, so a horse dosed every other day may never reach steady-state suppression.
Practical takeaways
For event-based protection, start daily dosing about 5 days ahead and continue through the risk period.
When stopping, step management up immediately: forage before exercise, alfalfa, lower starch. Some use a buffering supplement during the withdrawal window, though that evidence is thinner and partly industry-linked.
Tapering isn’t supported. Clark et al. found no lasting gastrin effect.
Sources:
Mason et al. 2019 meta-analysis (EVJ) – summary
White et al. – prevention with omeprazole 1 mg/kg (AAEP 2003, IVIS)
Shan et al. 2023 – withholding periods and ESGD recurrence (Animals)
Clark et al. 2023 – gastrin after omeprazole discontinuation (JVIM)
Sundra et al. 2024 – 5- vs 7-day injectable omeprazole (EVJ)
Sykes et al. 2015 – three-dose comparison (EVJ)
3. Squamous vs glandular disease
The two are different diseases that happen to share an organ. That’s why the ECEIM consensus split “EGUS” into equine squamous gastric disease (ESGD) and equine glandular gastric disease (EGGD).
Anatomy
The squamous (non-glandular) mucosa covers the dorsal third or so of the stomach. It is a continuation of the esophageal stratified squamous epithelium, with no mucus/bicarbonate layer and no intrinsic acid defense.
The glandular mucosa (cardiac, fundic and pyloric) makes up the rest. It secretes acid and protects itself with mucus, bicarbonate, prostaglandins and mucosal blood flow.
The margo plicatus divides them. Most squamous lesions sit along it, especially on the lesser curvature.
Squamous disease (ESGD)
Mechanism: acid injury. The epithelium has no defenses, so damage depends on how much acid reaches it.
Drivers:
Exercise: abdominal pressure pushes acidic contents up onto the squamous mucosa (“acid splashing”).
Feed deprivation, which removes the fibrous mat and saliva buffering.
High-starch meals, through volatile fatty acids.
Intermittent water access, stall confinement, transport.
Who gets it: racehorses (prevalence up to 80–100% in training), performance horses, and foals.
Grading: 0–4 scale.
Treatment response: good. Omeprazole at 4 mg/kg heals about 70–80% in 28 days. It is also well prevented by 1–2 mg/kg daily plus management.
Classification: primary (no underlying disorder) vs secondary (outflow obstruction, e.g., pyloric stenosis).
Glandular disease (EGGD)
Mechanism: a breakdown of mucosal defenses, not excess acid alone. Acid matters mainly once the barrier fails. Proposed contributors include:
Reduced prostaglandin-mediated blood flow, which is why NSAIDs are a factor.
Stress and cortisol.
Altered microbiota (Helicobacter is not proven).
Location: mostly the pyloric antrum, and less often the cardia or fundus.
Who gets it: risk factors are less clear and more individual. They include the number of riders or handlers, work days per week, temperament or stress, and sport horses as well as racehorses. Prevalence is roughly 30–65% depending on the population.
Description: lesions are described rather than graded, because severity doesn’t predict clinical signs. The terms used are focal, multifocal or diffuse; flat, depressed or raised; hemorrhagic, fibrinosuppurative or hyperemic. “Gastritis” is avoided unless histology confirms inflammation.
Treatment response: poorer and slower. Omeprazole alone heals only about 25–40% at 28 days.
Adding misoprostol (5 µg/kg PO BID), which restores prostaglandin- mediated defense, gives better results. Several studies show it is superior to omeprazole plus sucralfate.
Long-acting injectable omeprazole also does well.
Courses are typically 4–8+ weeks, with re-scoping.
Recurrence is common, and prevention data are sparse.
Practical consequences
Scope the pylorus. Many glandular lesions sit in the antrum and are missed if you don’t pass the scope through it. A full exam needs a 3 m scope and a proper fast.
The lesions don’t predict each other. A horse can have a normal squamous mucosa and significant glandular disease, so a “clean” margo plicatus doesn’t clear the stomach.
Clinical signs overlap. Both cause poor appetite, weight loss, poor performance, girthiness, behavior change and recurrent colic. Signs don’t distinguish them, so endoscopy is required.
NSAIDs matter more for glandular disease. Consider a COX-2-selective drug such as firocoxib when anti-inflammatories are needed in a horse with EGGD.
The rebound and withholding problems above apply mainly to squamous disease. The Hong Kong withholding study, for example, found no withholding effect on glandular lesions.
The consensus reference is Sykes et al., ECEIM Consensus Statement on Equine Gastric Ulcer Syndrome in Adult Horses, J Vet Intern Med 2015;29:1288–1299. It is the best single source if you want to cite one.
4. Single doses, and omeprazole with NSAIDs: hindgut and right dorsal colitis
A single dose given when a client thinks the horse is “off” is not effective treatment. It suppresses acid for about 24 hours, so it might ease a horse with active squamous ulcers for a day. It won’t heal anything, and nothing supports it as prevention. Its main effect is probably to delay the exam, and it can blur gastroscopy findings if the horse is scoped a day or two later. An “off” horse needs a diagnosis rather than a tube of paste. On the hindgut, the evidence splits cleanly between omeprazole alone and omeprazole with an NSAID.
Omeprazole alone: no measurable hindgut effect so far
Tyma et al. 2019 (AJVR) gave 4 mg/kg daily for 28 days to healthy horses. Fecal microbiota composition and diversity didn’t differ from sham at any time point. Gastric fluid microbiota changed, but too inconsistently to interpret.
Cerri et al. 2020 (JVIM) also found the fecal microbiome stable. The glandular mucosal microbiota shifted as pH rose, but not in a consistent direction.
Both studies were small and used healthy horses, so neither can rule out an effect in sick, hospitalized or NSAID-treated horses.
Omeprazole with phenylbutazone: this is where the concern is
Ricord et al. 2021 (EVJ) randomized horses to placebo, phenylbutazone (4.4 mg/kg q12h), or phenylbutazone plus omeprazole (4 mg/kg q24h) for 7–14 days.
Omeprazole did protect against phenylbutazone-induced glandular disease.
But 6 of the 8 intestinal complications occurred in the combination group: diarrhea, colic, impaction and enterocolitis/typhlocolitis.
The authors concluded that caution is warranted when co-prescribing the two drugs.
NSAIDs on their own shift the fecal microbiota. Whitfield-Cargile et al. 2018 (PLoS ONE) showed this for both phenylbutazone and firocoxib.
The proposed mechanism comes mostly from human and rodent work. NSAID injury beyond the stomach is driven partly by the gut flora. Acid suppression changes which bacteria and bile acids reach the distal gut, and in rats a PPI made NSAID small-intestinal injury worse (Wallace et al. 2011, Gastroenterology).
No equine study I’m aware of shows that omeprazole raises the incidence of right dorsal colitis specifically. The signal comes from one small experimental study plus a plausible mechanism. That’s enough to change habits, though not enough to call it established.
Practical implications
Drop the reflex “bute plus GastroGard” pairing. Reserve omeprazole during NSAID therapy for horses with documented or high-risk gastric disease.
Use the lowest effective NSAID dose and duration. Consider firocoxib when GI protection is the goal.
On longer NSAID courses, monitor total protein and albumin. A falling albumin is often the earliest sign of RDC.
If gastroprotection is needed during NSAID use, misoprostol is a reasonable alternative, since it targets prostaglandin loss directly. Watch for its own GI side effects: loose manure and colic.
Sources:
Tyma et al. 2019 – omeprazole and fecal/gastric microbiota (AJVR)
KER summary of Cerri et al. 2020 (JVIM)
Ricord et al. – omeprazole with phenylbutazone (EquiManagement summary)
Ricord et al. – LSU repository record
KER – Using omeprazole and phenylbutazone in horses
Whitfield-Cargile et al. 2018 – COX inhibitors and fecal microbiota (PLoS ONE)
Mayo Clinic Proceedings – NSAIDs, PPIs and GI injury in stomach vs small intestine
5. Behavior and acupuncture points as indicators
Behavior has some correlation with ulcers, but not enough to diagnose from. Acupuncture point sensitivity has essentially no validation.
Behavior and ulcers
The overall picture is that most behavior changes can’t tell an ulcer horse from a non-ulcer horse. They make more sense as reasons to scope, or as a way to track response to treatment.
Girthiness is the strongest link. It is reported in about 25% of horses with squamous disease and about 31% with glandular disease (Gough et al. 2020, 2022).
Millares-Ramirez & Le Jeune (2019) scoped 13 girthy horses and found ulcers in 12.
All 12 improved on omeprazole, and 10 resolved completely.
The reverse doesn’t hold: about 70–75% of ulcerated horses are not girthy.
Ridden behavior tracks healing. Pineau et al. (2024) found strong correlations between ulcer scores and the Ridden Horse Pain Ethogram. Those scores fell as lesions healed over 12 weeks. This is the best direct evidence linking aversive ridden behavior to the disease.
Ground behaviors and facial expression are poor markers.
Hewetson et al. (2021) found no association between glandular disease and owner-reported behavior on the ground.
The Horse Grimace Scale didn’t differ with ulcer presence or severity (Agne et al. 2023).
Squamous disease shows up more in eating. Changes in eating and unexplained weight loss are more consistently tied to squamous disease. A “nervous” temperament is also more common in horses with it (McClure 1999).
Glandular healing often doesn’t match the owner’s report. Behavior frequently doesn’t resolve when the scope shows healing (Gough 2022; Sundra 2024). The behavior may have another pain source, or may have become learned.
One preliminary signature is worth watching. McDonnell’s group (Animals 2025) reviewed 24-hour video and gastroscopy on 30 horses, blinded and retrospective. Frequent deep abdominal stretching, plus nuzzling, nipping or gazing at the area behind the elbow, was present in all 24 horses with gastric disease. Four of the 6 horses without it had no lesions. The study is small, but it is a more specific behavior than “grumpy.”
Confounders are common. Most poorly performing horses have more than one problem: 84% of poor-performance racehorses had more than one possible cause (Morris & Seeherman 1991).
Sykes & Lovett (2025) recommend a 7-day omeprazole trial while the horse stays in work.
If there’s no response, they suggest a 5–7 day phenylbutazone trial, sincemany such horses turn out to have musculoskeletal pain.
They count a partial response as evidence that the ulcers are contributing.
Acupuncture points
The traditionally cited “ulcer points” are BL-20 and BL-21 (the spleen and stomach association points, over the last ribs), CV-12, and ST-7.
The supporting evidence is weak. It is mainly Alfaro’s 2014 study of 259 horses, which reported a 100% match between point sensitivity and lesion location.
That study had a single examiner, no blinding and no controls, and only 2 of its horses actually had ulcers. Its own figures are internally inconsistent.
Where this leaves the “off” horse
Behavior is a reasonable reason to scope, and a useful way to measure response to treatment.
Point palpation and grimace scoring shouldn’t decide whether a horse has ulcers.
If a client already treats on suspicion, an empirical trial is defensible only when it is structured. That means a full treatment dose for at least 7 days, with defined behaviors scored before and after. A single dose when the horse “seems off” isn’t a structured trial.
Sources:
Sykes & Lovett 2025 – Can all behavioral problems be blamed on EGUS? (Animals)
The Horse – McDonnell et al. 2025 behavioral signature study
Agne et al. 2023 – Horse Grimace Scale does not detect pain in EGUS
Alfaro 2014 – Acupuncture point sensitivity and lesion location in 259 horses (AJTCVM)
6. Management: diet, housing, exercise, stress and temperament
Management is where most of the prevention benefit is, and it is also where squamous and glandular disease diverge most. Diet and feeding pattern drive squamous disease. Exercise load, stress and temperament drive glandular disease.
Diet (mainly a squamous lever)
Forage: ad lib, or at least 1.5 kg dry matter per 100 kg BW per day.
Gaps without forage: don’t let them exceed about 4–6 hours. Gaps longer than 6 hours are among the strongest risk factors in the epidemiology. Slow feeders and haynets help stretch feeding time.
Starch: keep it under about 1 g/kg BW per meal and under about 2 g/kg BW per day.
For a 500 kg horse, that is under about 500 g of starch per meal.
At 30–40% starch in a sweet feed, that means only about 1.5 kg of feed per meal.
Prefer low-starch, fat- and fiber-based concentrates. Feed more, smaller meals rather than one or two big ones.
Alfalfa: include some, as hay or chaff. Its protein and calcium buffer acid, and it is consistently protective for squamous disease.
Forage before work: feed a small amount of hay or alfalfa about 20–30 minutes before exercise. The fiber mat limits acid splash onto the squamous mucosa when the abdomen compresses.
Avoid straw as the only forage. Make sure water is always available, including in paddocks. Both of these were independent risk factors in Danish data.
Oil and supplements: corn oil and supplements such as pectin-lecithin, sea buckthorn or buffers have mixed, mostly small or industry-funded evidence. They’re reasonable as adjuncts, especially in the window after stopping omeprazole, but not as substitutes for the points above.
Diet (mainly a squamous lever)
Maximize pasture turnout. Stall confinement plus intermittent feeding reliably induces squamous ulcers within days in experimental models. Reduced turnout is also associated with glandular disease.
Social contact matters. Being able to see and touch other horses reduces stress. Isolation stalls, and frequent changes of neighbors or groups, work against you.
Exercise
Glandular disease tracks frequency of work. In racehorses, working 5–7 days a week carried more glandular risk than 1–4 days. Show jumpers showed the same pattern.
Build in rest days.
Use turnout as “work” on light days.
Avoid stacking long sessions.
Squamous disease tracks intensity. Faster work means more abdominal pressure and more acid splash.
Keep sustained trot and canter moderate; recommendations suggest under about 40 minutes a day.
Always feed forage beforehand.
Always feed forage beforehand.
Stress and temperament
The physiology supports a real link. International eventing and endurance horses with moderate glandular disease had a larger cortisol response to ACTH stimulation than those with mild disease (Scheidegger et al. 2017). Salivary cortisol in warmbloods is higher at competitions than at home. A “nervous” disposition is more common in horses with squamous disease (McClure 1999).
Known stressors to manage:
Transport, which induces ulcers experimentally.
Competition venues.
Multiple riders or handlers.
Frequent changes of barn, group or routine.
Weaning, and social disruption generally.
Weaning, and social disruption generally.
Mitigations:
One consistent rider and handler where possible.
A travel companion, and hay and water en route.
A travel companion, and hay and water en route.
Pre-event prophylaxis started about 5 days ahead, not the morning of.
Matching temperament to the job
No study tests temperament–job matching directly, so this section is reasoning from the risk factors above. In practice the decision goes one of two ways: pick a horse whose disposition suits the job’s stress profile, or change the job (frequency, travel, number of riders) to suit the horse.
Racing
Main exposure: High intensity, work 5–7 days a week, stalling, meals high in starch.
Disease emphasis: Both, with squamous predominating.
Fit and adjustments: Hard to avoid. Focus on forage before work, alfalfa, low starch, rest days, and prophylaxis through high-risk periods.
Eventing and endurance
Main exposure: Long hauls, competition venues, prolonged work.
Disease emphasis: Both, with glandular disease high (about 60–80% in elite horses).
Fit and adjustments: A settled, adaptable traveler is an advantage. Plan travel routines and use event-period prophylaxis.
Show jumping and dressage on the show circuit
Main exposure: Frequent travel, stalling at shows, daily schooling.
Disease emphasis: Glandular.
Fit and adjustments: A reactive horse may cope better with a lighter show schedule. Keep turnout at home and rest days.
Lesson and school horses
Main exposure: Multiple riders, irregular demands.
Disease emphasis: Glandular.
Fit and adjustments: Choose a calm, tolerant temperament. Cap daily rides and limit the number of different riders per horse.
Pleasure and trail horses
Main exposure: Usually low, unless stalled and fed concentrates.
Disease emphasis: Squamous, from management.
Fit and adjustments: Most temperaments do fine here. Fix the feeding pattern and turnout.
Broodmares, weanlings and sales prep
Main exposure: Social disruption, weaning, sales stalling and feeding.
Disease emphasis: Both.
Fit and adjustments: Wean gradually with a companion, and change diet slowly during sales prep.
The practical sequence for an at-risk or recurrent horse
- Fix forage: amount, the gaps between feedings, and alfalfa.
- Cut starch per meal.
- Increase turnout and social contact.
- Add rest days and shorten intense sessions.
- Reduce handler, rider and travel stressors.
- Then add targeted pharmacology for defined high-risk periods.
job or workload is a legitimate medical recommendation.
7. Compounded omeprazole and combination therapies
Formulation decides whether omeprazole works. The drug is destroyed by acid, so a
product that doesn’t protect it delivers far less than its label dose, and compounded
powders and pastes have repeatedly failed that test.
Why formulation matters
Omeprazole degrades quickly in acid, moisture and heat. It needs an alkaline vehicle (pH above about 7.8) or an enteric coating to get through the stomach to the small intestine, where it is absorbed.
Even the approved paste has an oral bioavailability of only about 10%, so there is little margin for loss.
A plain powder mixed into feed or water has no protection, and dosing with feed reduces absorption further.
Evidence against compounded products
Efficacy: Nieto et al. 2002 (JAVMA) gave 32 racehorses in training a compounded suspension or the approved paste, both at 4 mg/kg, then switched them. The paste healed ulcers; the suspension did not. Lesions recurred in horses moved from paste to the suspension. Serum omeprazole peak and exposure (AUC) were significantly lower with the suspension.
Potency: Stanley & Knych 2011 (AAEP) assayed five compounded pastes against the approved product.
At day 0 the compounded pastes ranged from about 63% to over 100% of label; the approved paste was about 99%.
Consistency: Wallace 2017 (ACVIM abstract, manufacturer-funded) radiographed syringes of compounded and unapproved over-the-counter products. They showed incomplete fill, air pockets and uneven mixing; the approved paste did not.
Clinical consequences
Treatment failure looks like refractory disease. A horse on an underdosed product may be labeled a non-responder, scoped repeatedly, kept on treatment longer, or moved to second-line drugs it didn’t need.
Prevention fails silently. Low-dose prophylaxis already runs close to the effective threshold, so a weak product can leave a horse unprotected during shipping or competition.
Regulation: FDA guidance on compounding from bulk drug substances for animals (GFI #256) generally does not support compounding copies of an approved drug, and lower cost is not an accepted clinical reason. AAEP recommends using only PCAB-accredited compounding pharmacies when compounding is genuinely needed.
Overseas data don’t transfer. Registered gastro-resistant and long-acting injectable products studied in Australia and Europe (for example Sykes 2015, Sundra 2024) are licensed, quality-controlled formulations. Their results don’t validate a US compounded powder or injection with the same active ingredient.
Combination therapies
Omeprazole plus sucralfate: sucralfate binds the ulcer bed best in an acid environment, so a PPI may blunt it, and it binds other drugs in the gut.
In Varley et al. 2019 (EVJ), 63 sport horses with glandular disease healed in 72% of cases on misoprostol (5 µg/kg PO BID) vs 20% on omeprazole 4 mg/kg SID plus sucralfate 12 mg/kg BID.
Misoprostol: the best-supported drug for glandular disease. Evidence that adding omeprazole improves on misoprostol alone is limited.
Compounded multi-drug pastes (for example omeprazole with sucralfate, misoprostol or antacids in one syringe) are untested.
H2 blockers and antacids: ranitidine was withdrawn from the US market in 2020 over NDMA contamination. Adding an H2 blocker to a PPI adds nothing useful. Antacids buffer for only about 1–2 hours and should not stand in for a PPI.
Omeprazole with NSAIDs: see section 4. The combination was linked to intestinal complications in Ricord et al. 2021.
Practical recommendations
Cherry Creek Equine protocol
Sources:
Nieto et al. 2002 – paste vs compounded suspension (JAVMA), summary
The Horse – Compounding study: know what you’re getting
Stanley & Knych 2011 – pharmaceutical equivalence of omeprazole preparations (AAEP, IVIS)
EquiManagement – Wallace 2017 compounded and OTC omeprazole products
Varley et al. 2019 – misoprostol vs omeprazole-sucralfate for EGGD (EVJ)