Equine gastric ulcer syndrome

Horses form ulcers in the mucosa of the stomach, leading to pain, decreased appetite, weight loss, and behavioral changes.

[1] The esophagus and dorsal stomach is made of stratified squamous epithelium, which is only weakly protected from the effects of hydrochloric acid, and those cells deeper in the layer of tissue transport hydrogen ions intracellularly, leading to death.

[1] The glandular portion produces hydrochloric acid and enzymes such as pepsinogen, as well as bicarbonate and mucus that helps prevent self-digestion.

[1][2] Mucosal blood flow is also an important factor in glandular epithelium health, since it provides oxygen and nutrients to the cells and helps to remove excess hydrogen ions.

Additionally, the horse's saliva provides a chemical buffer for the acidic pH and is produced during constant chewing and swallowing, which is encouraged by high roughage.

The duodenum is protected by its motility which removes HCl, glands in its surface that produce mucins, and products from the pancreas, including bicarbonate, to help neutralize the acidity.

[2][7] These horses have stressful lives compared to non-competitive animals, which includes travel, frequent change of environment, and high workload.

Additionally, their diet often consists of a higher proportion of grain relative to roughage, to account for their increased caloric requirements.

Horses undergoing treatment for other medical problems, such as illness or lameness, are also at increased risk, due to the stress of the disease and because they are often confined and placed on long-term non-steroidal anti-inflammatory drugs (NSAIDs).

[2][8] Ulcers in foals are often "silent", producing no clinical signs, and usually occur in the squamous portion of the stomach in animals four months old and younger.

[10] The process of gastric ulceration is similar to esophageal reflux in people (heartburn), where acid damages the epithelium of the esophagus.

[13] Diagnosis is often made based on history, clinical signs, and response to treatment, but the best diagnostic tool involves endoscopic visualization of the stomach in a process called gastroscopy.

Currently in the US, the only FDA approved method of treatment is through the use of the proton pump inhibitor omeprazole,[2] which has been shown to decrease the secretion of hydrochloric acid.

[3] Prophylactic use of both omeprazole and H2 antagonists such as ranitidine, cimetidine, and famotidine can be used to help prevent gastric ulcer formation when the horse will be placed into a stressful situation, such as travel or showing.

[1] H2 antagonists are cheaper and will decrease stomach acid production but require more frequent administration compared to PPIs, usually every eight hours.

[3] Dietary management is critical: increasing roughage provides a physical barrier to help protect the stomach as well as encourages salivation.

Horses prone to gastric ulcers should have access to hay or grass as much as possible, ideally constantly, and meal feeding should be kept to a minimum.

Possible reasons for this may include colic-induced stress, feed deprivation when treating a refluxing colic, and medication that may compromise the gastric environment.

Specifically, horses that presented with duodentis-proximal jejunitis has a significantly higher presence of gastric ulcers than other types of colic.