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EQUINE GASTRIC ULCERS
Bruce Kuesis, DVM
Southwest Equine Medical and Surgical Center

Over the past decade with the advent of powerful new video-endoscopy equipment a great deal of knowledge has been gained about the equine stomach. The importance of gastric ulcers as a cause of colic, weight loss, poor performance and irritability has been discovered. This has lead to intense research efforts into the multiple causes and possible therapies for Equine Gastric Ulcer Syndrome (EGUS).

The Equine Stomach:

The equine stomach is unique in that it has two distinct regions with quite different characteristics. The upper 1/3 of the stomach is termed the squamous or non-glandular stomach and anatomically is similar to the esophagus. The layers of cells that compose the inner surface or mucosa of the stomach are squamous or stacks of flat type cells. The bottom 2/3's of the stomach is similar to out stomachs and is termed the glandular or non-squamous stomach. This area of the stomach is composed of a number of cell types that are responsible for the initial digestion of feed.

Equine Gastric Ulcer Syndrome = EGUS

The physiologic structure of the squamous part of the stomach makes this area of the stomach most susceptible to EGUS. About 80 percent of the gastric ulcers in adult horses involve the squamous area of the stomach. Most ulcers that we observe endoscopically involve the squamous mucosa just above the junction of the glandular and non-glandular stomach. This junction is called the Margo Plicatus. The glandular stomach is more resistant to ulceration for a numbers of reasons. There is a buffer rich mucus-bicarbonate layer that acts as a shield for acids and harmful enzymes. The cells of the glandular mucosa are tightly bound in such a way to form a tight barrier, limiting caustic gastric contents. And, the cells undergo more rapid growth and replacement (restitution).

The causal factors leading to gastric ulceration in the horse are complex and multi-factorial. Stress, exercise and diet are risk factors that are common among horses. These factors lead to alterations that allow hydrochloric acid, volatile fatty acids, bile acids and aggressive factors are normally held in check by protective factors.

Protective factors for the equine stomach:
  1. Normal stomach blood circulation leads to production of mucus-bicarbonate layer, and normal cell replacement.
  2. Normal transit through the stomach allows the exit of caustic acids and enzymes from the stomach.
  3. Saliva and buffer production.
Aggressive factors for the equine stomach:
  1. Low pH, higher acidity. Hydrochloric acid, Volatile Fatty Acids, Bile Acids.
  2. Enzymes such as Pepsin that can inflict damage to gastric cells.
  3. Poor gastric circulation from various causes.
Risk factors for gastric ulcers include stress from various causes including training, transport, and illness. Exercise has recently been shown to be a significant risk factor for the development of EGUS by researchers from Florida. Exercise leads to contraction of the stomach and the displacement of acid rich fluid onto the squamous portion of the stomach. This is more damaging to the more susceptible squamous mucosa.
Dietary factors are very important in the development of EGUS. The ingestion of concentrated carbohydrate diets lead to the production of more volatile fatty acids which can be harmful to the stomach. Intermittent feeding programs such as two big meals a day lead to higher stomach acidity from less buffering of stomach acid. Alfalfa hay appears to be better at buffering stomach acid then other types of hay. This is due to the high concentration of calcium and protein in alfalfa which act to buffer acid.

The clinical signs of gastric ulcers differ somewhat for adult horses and foals. Common clinical signs are often vague and a number of horses have sub-clinical ulcers and do not exhibit obvious clinical signs.

Clinical signs in adult horses:
  • Colic
  • Poor appetite, picky eaters
  • Poor appearance, haircoat
  • Weight loss
  • Decreased performance, endurance
Clinical signs in foals:
  • Diarrhea
  • Colic
  • Bruxism - grinding teeth, salivation
  • Intermittent nursing behavior
  • Poor-doer, pot-belly, decreased growth
To date the most definitive diagnosis of stomach ulcers is through gastric endoscopy. Endoscopy allows for visualization and grading of the ulcers, as well as response to therapy.

Treatment of gastric ulcers is aimed at shifting the balance of protective and aggressive factors. Treatment today consists mainly of decreasing acid production. A less acidic environment allows for stomach healing. A number of acid inhibiting drugs have been used in horses.

Acid inhibiting drugs:
  1. Histamine blocking drugs. H-2 receptor blockers. Blocks histamine from stimulating acid secretion from parietal cells.
  2. Anti-acids. Act to buffer acid by binding acid.
  3. Proton pump inhibitors. Omeprazole, the active ingredient in Gastrogard. Works by inhibiting the proton pump or acid pump.
Agents to increase cell healing:
  1. Misoprostil: PGE-2 analogue increases blood flow to the mucosa and increases protective mucus production.
  2. Sucralfate: May act as a patch over the stomach. Acts to increase natural prostaglandin release.
Gastrogard is currently the only FDA approved treatment for EGUS. It is highly efficacious and when compared to other treatments based upon acid reduction is the most cost effective. A 4 mg/kg dose consistently cures almost all ulcers we identify. A 2 mg/kg dose is highly efficacious at preventing gastric ulcers for horses in stressful situations such as race training.

Prevention of EGUS is aimed at decreasing the amount of risk factors.
  1. Decreasing stress - training
  2. Diet, Diet, Diet - decrease the amount of refined carbohydrates. Increasing continuous consumption of high quality roughage is effective at decreasing stomach acidity. Alfalfa hay is better then grass hay at decreasing stomach acidity. Continuous grazing of pasture is best. Recent research identified corn oil supplementation as beneficial in ulcers healing of the glandular stomach.
  3. Avoid bute, banamine, and other nonsteroidal anti-inflammatory drugs.
  4. Feeding of nutriceutical products
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