Equine Gastric Ulcer Syndrome: An Update on Current Knowledge

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TL;DR

Equine Gastric Ulcer Syndrome (EGUS) encompasses two distinct diseases: Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD), which differ in pathophysiology, risk factors, and treatment response. ESGD is well-understood and effectively treated with acid-suppression therapy (omeprazole), while EGGD remains poorly understood with lower healing rates and a likely multifactorial pathophysiology involving stress and management factors. Clinically, both conditions are associated with colic, poor performance, and behavioral changes, but many horses show no clinical signs, and gastroscopy remains the primary diagnostic tool despite limitations in correlating gross lesions with clinical significance.

Full summary

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**Background:** Equine Gastric Ulcer Syndrome (EGUS) has been used since 1999 to describe gastric mucosal disease in horses. In 2015, the European College of Equine Internal Medicine (ECEIM) released a consensus statement defining two distinct disease entities: Equine Squamous Gastric Disease (ESGD) and Equine Glandular Gastric Disease (EGGD). This review updates current knowledge on both conditions, highlighting progress and persistent knowledge gaps since the last large-scale review.

**Methods:** This is a narrative review synthesizing previously and recently published literature on the terminology, prevalence, risk factors, clinical signs, pathophysiology, diagnosis, grading, treatment, and prevention of ESGD and EGGD. The authors critically evaluate evidence from epidemiological studies, experimental models, and clinical trials, noting limitations such as small sample sizes and variability between populations.

**Key Results:** - **Prevalence:** ESGD prevalence varies widely: 37–52% in Thoroughbreds, 38–56% in Standardbreds, and 48% in endurance horses out of training, increasing to up to 100%, 72–88%, and 57–93% respectively when in training. EGGD prevalence ranges from 3% in Italian donkeys to 72% in Canadian showjumpers. An abattoir survey found 71% prevalence in domesticated horses vs. 30% in feral horses. - **Risk Factors:** Thoroughbred and Standardbred breeds are associated with increased ESGD risk. Exercise intensity and duration are key ESGD risk factors. For EGGD, exercising ≥5 days/week, racing below expectation, and trainer are risk factors. Nutritional risk factors (high grain/starch, low hay) are well-established for ESGD but not for EGGD. - **Clinical Signs:** Proposed signs include colic, weight loss, poor coat condition, reduced appetite, diarrhea, bruxism, behavioral changes, and poor performance. However, a recent study found no associations between owner-reported clinical signs and EGGD, and many horses with gastric disease show no signs. - **Pathophysiology:** ESGD results from increased acid exposure of the squamous mucosa due to management factors and exercise. EGGD pathophysiology remains poorly understood but is hypothesized to involve loss of normal defense mechanisms, with evidence supporting a role for stress (increased cortisol responses to novel stimuli and exogenous ACTH in affected horses). - **Treatment:** Oral omeprazole monotherapy heals 67–100% of ESGD but only 14–25% of EGGD. Long-acting injectable omeprazole achieves up to 93% EGGD healing. Combined omeprazole and sucralfate therapy is superior to omeprazole alone for EGGD. Misoprostol shows promise but requires more evidence. - **Discontinuation:** ESGD can return to pre-treatment levels within 3 days of omeprazole discontinuation. Rebound gastric hyperacidity may occur within a 48-hour window but is not prolonged; tapering is not recommended for ≤8-week treatments. - **Prevention:** Management changes (ad libitum roughage, exercise timing, adequate rest days) are foundational. Nutraceuticals (n-3 LC-PUFAs, pectin-lecithin complexes) show some evidence. Omeprazole for prevention fails in >20% of Thoroughbred racehorses and may induce its own metabolism with long-term use.

**Clinical Implications:** ESGD management is well-established with effective acid-suppression therapy, while EGGD remains challenging with lower treatment success rates. The authors emphasize that gastroscopy alone is insufficient for determining clinical significance of glandular lesions, and that histopathology, clinical signs, and treatment response should be considered together. The review highlights the need for further research into EGGD pathophysiology, the relationship between stress and disease, and effective preventative strategies, particularly during periods of increased risk such as NSAID use.