Equine Glandular Gastric Disease (EGGD) refers to ulceration in the ventral glandular region of the horse’s stomach. This condition was previously less heard of than Equine Squamous Gastric Disease, primarily because the original endoscopes used in horses were only 2.5 meters long and as such were unable to reach the pyloric antum, where most glandular ulceration occurs, for visualization.
With the advent of the three meter endoscope, however, more complete observation of the entire equine stomach is possible, and subsequent research has shown that the incidence of glandular ulceration is higher than previously believed.
The pathophysiology, risk factors, and treatment response for glandular ulceration in the horse differs from those of squamous ulceration, and the presence or absence of one does has no bearing on the presence or absence of the other. As such, it is critical to perform completely thorough gastroscopy to identity possible glandular ulceration when EGUS is suspected, and prescribe treatment accordingly.
Pathophysiology of Equine Glandular Gastric Disease
Whereas acidic content of the stomach “splashing” on the unprotected mucosal lining above the margo plicatus is the mechanism believed to lead to squamous ulceration in the horse, the glandular region below the margo plicatus is designed to be exposed to the highly acidic contents. The glandular mucosa is lined with gastric mucus, a complex mixture of glycoproteins, water, electrolytes, lipids, and antibodies that provide natural protection from continually secreted acids.
It is believed that the glandular ulceration, then, results from the breakdown of this protective lining, exposing the glandular mucosa to damaging acids. While there is no conclusive research indicating exactly what leads to the breakdown of this defense mechanism in the horse, NSAID use and bacterial agents have been found to be causes in humans. Studies have shown that ulceration can be induced in horses with NSAIDs given at doses 50% higher than recommended, but none have been found at clinical doses given for 15 days. This indicates that the potential risk with short-term NSAID use is low, but that long-term use may increase risk for EGGD.
Presentation and Symptoms of EGGD
Recent studies show a range of EGGD incidence, from 47% and 62% reported in racehorses in Australia, 57% in a mixed population of horses in Denmark, 27% and 33% in endurance horses, and as much as 67% in a variety of horse types in abattoir studies. A study was also done using thoroughbred racehorses to attempt to identify risk factors for EGGD. They found that risk increased with the horse’s gender, different trainers, no grass turnout, horses not fed haylage, horses fed unprocessed grain, horses in direct contact with each other, infrequently fed a complete diet, fast exercise on fewer days of the week, and those that went swimming. However, unlike with ESGD, time in work was not a significant factor for increased EGGD risk.
Because EGGD can be present regardless of intensity of exercise, or lack thereof, it should be a differential for any horse demonstrating clinical signs of gastric ulceration. As with ESGD, symptomatic horses may display:
- loss of appetite,
- difficulty maintaining weight or weight loss,
- changes in hair coat,
- poor behavior,
- stereotypies such as cribbing, weaving, or wood chewing.
Remember that girthiness and diarrhea are symptomatic of a hindgut condition. So if they are also present when EGGD, and/or ESGD, has been confirmed by gastroscopy, further differential and treatment for the hindgut are required.
Differential Diagnosis of Equine Squamous Gastric Disease
Gastroscopy continues to be the only reliable method for the differential diagnosis of gastric ulceration in horses. A thorough examination of the entire stomach is essential to confirm the presence of glandular ulceration and grade it accordingly. It’s critical to examine both the squamous and glandular regions of the stomach completely, as the causative factors and treatment response vary between EGGD and ESGD.
|Grade||Squamous Mucosa||Glandular Mucosa|
|0||The epithelium is intact and there is no appearance of hyperkeratosis (yellow appearance to the mucosa)||The epithelium is intact and there is no hyperemia (reddening) of the mucosa|
|1||The mucosa is intact, but there are areas of hyperkeratosis||The mucosa is intact, but there are areas of hyperemia|
|2||Small single, or multifocal lesions||Small single, or multifocal lesions|
|3||Large single, or multifocal lesions, or extensive superficial lesions||Large single, or multifocal lesions, or extensive superficial lesions|
|4||Extensive lesions with areas of apparent deep ulceration||Extensive lesions with areas of apparent deep ulceration|
Treatment for EGGD
Omeprazole, the gold standard treatment for squamous ulceration, has more limited effect on glandular ulceration in horses. Recent studies have found only a 25% rate of healing with 28-35 days of omeprazole treatment in EGGD. This is a drastic decrease from a 78% rate of healing for squamous ulceration over the same treatment interval. Omeprazole treatment may actually suppress acid production for less than 12 hours, which provides enough relief to promote healing in the squamous region but not in the glandular. And because the bacterial involvement may be causative in the ulceration, antibiotic therapy may be necessary for healing to occur.
Omeprazole is still recommended in the treatment of EGGD, but it must be supplemented with mucosal protectants as well as antibiotics if bacterial involvement is suspected. Options for mucosal protection include:
- Sulcrafate – adheres to ulcerated mucosa, stimulates mucus secretion, and enhances blood flow.
- Pectin-lecithin – increases total mucus concentration.
These should not be used as standalone treatments, however, and should always be used in tandem with omeprazole.
However, it is important to note in 23% of horses, worsening was observed despite omeprazole therapy, and that gastric hyerplasia may be present in a percentage of cases and as such omeprazole is not advised.
Changes in management, especially feeding a high-roughage, low-concentrate diet, is highly beneficial to treatment, and possibly prevention, of EGGD.
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