Equine gastric ulcer syndrome

Last updated

Equine gastric ulcer syndrome (EGUS) is a common cause of colic and decreased performance in horses. Horses form ulcers in the mucosa of the stomach, leading to pain, decreased appetite, weight loss, and behavioral changes. Treatment generally involves reducing acid production of the stomach and dietary management. Unlike some animals, however, stomach rupture is rare, and the main goal of treating is to reduce pain and improve performance of animals used for showing or racing. [1]

Contents

Pathophysiology

The digestive system of the horse evolved for its grazing lifestyle, where it would almost constantly eat small amounts of roughage throughout the day. Unlike carnivores, who produce stomach acid during meals, horses constantly secrete acid [1] to help digest this source of grass, leading up to 9 gallons produced per day. [2] Unchecked, the stomach acid can lower the pH to levels that will damage the gastric mucosa, leading to ulcers.

The stomach is divided into two main sections: a squamous region at the upper 1/3 of the stomach near the cardiac sphincter, and a lower glandular region. These two regions are separated by a band of tissue called the margo plicatus. The pH of the stomach contents varies by location. The most dorsal part of the stomach has the highest pH, usually close to 7, dropping to a pH of 3.0–6.0 near the margo plicatus, and reaching as low as 1.5–4.0 in the glandular regions. [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] [2] This region is therefore especially vulnerable, and accounts for 80% of all gastric ulcers. [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. [1]

When a horse is on a diet high in roughage, the fibrous mat of chewed roughage provides a physical barrier and helps prevent splashing of acid up onto the squamous region of the stomach. 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. [1]

Both the esophagus and duodenum are also at risk for ulceration. Esophageal ulceration is partially prevented by the tone of the cardia sphincter to prevent reflux, as well as by saliva, which both washes the esophagus and contains mucins that can help protect its surface. 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. [1] Most duodenal ulcers occur in foals, and there appears to be an association between duodenal ulcers and enteritis in these animals. Pyloric or duodenal ulcers may result in inflammation of the duodenum so profound it blocks gastric emptying, which can cause severe gastric ulcers and occasionally esophageal ulcers. [1] Perforation secondary to ulcers, although rare, can occur both in the stomach and the duodenum, producing peritonitis. Rupture can not be predicted by ulcer severity as seen on endoscopic examination, and clinical signs are often not present until just prior to the event. [1]

Risk factors

Horses used for competitive activities, such as showing or racing are at greatest risk of gastric ulceration, with up to 60% of show horses, 60–70% of endurance horses, 75% of event horses, and 80–90% of race horses having ulcers. [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]

Up to 50% of all foals have ulcers, which may be due to decreased feedings and recumbency. [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. Glandular ulcers in foals are thought to be caused by stress, and are often seen in foals four months old and younger that are also sick or debilitated. [1] [2]

Unlike humans, Helicobacter infection has not been shown to be a definitive cause of gastric ulcers in horses. [9] Although it has not been cultured, DNA from the organism has been found in the gastric mucosa using PCR. [10] [11] Additionally, ulcers have been shown to be colonized by bacteria which may prevent healing. [12] Given that some horses do not respond to traditional therapy, it is sometimes recommended to add antibiotics to their treatment regimes. [10]

Clinical signs

The process of gastric ulceration is similar to esophageal reflux in people (heartburn), where acid damages the epithelium of the esophagus. Therefore, behaviors associated to pain are the most common clinical signs of a horse with EGUS. This commonly includes chronic intermittent colic, especially after eating, decreased appetite or sudden cessation of eating in the middle of a meal, weight loss, decreased performance, changes in attitude, and "girthiness". [1] Horses with ulcers may be difficult to keep in good condition, despite a high-quality diet. Additionally, horses may display bruxism, ptyalism, and dullness. Foals may additionally have diarrhea and display a potbelly and poor hair coat. [1] [2] Those foals with more serious ulceration are also seen to lay in dorsal recumbency and show pain when palpated just caudal to the xiphoid process. [1]

Horses may not display any clinical signs, even with severe gastric ulcers. However, gastric ulcers are usually more severe in horses displaying clinical signs. [13]

Diagnosis

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. The horse is fasted for at least 6 hours [1] prior to the procedure to help reduce the amount of feed material in the stomach. They are then sedated, and an endoscope is passed through one of the nostrils, into the esophagus, and down to the stomach. The endoscope must be at least 2 meters to visualize the non-glandular region of the stomach, and 2.5–3 meters to visualize the glandular region. [10] This is a simple and minimally invasive procedure that allows for definitive diagnosis and can be used to track healing of lesions once treatment has begun post diagnosis. [2]

Degree of ulceration is graded both on lesion number (grade 0–4, with a grade 4 for stomachs containing >10 lesions or diffuse ulceration) and lesion severity (0-5, with 5 being deep, active, hemorrhagic ulcers). The squamous and glandular regions are graded separately. [14]

Treatment and prevention

The main goal of treatment of horses with gastric ulcers is to keep the pH of the stomach >4. 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. [10] Treatment is expensive and usually requires at least a month of daily administration of the drug. To reduce costs, compounded omeprazole is occasionally used; however, the efficacy of these products are likely poor. [15] Omeprazole requires 3–5 days to reach steady-state levels in horses, so horses suffering from ulcers are often started on H2 antagonists at the same time. [1] For this reason, some veterinarians recommend beginning prophylactic treatment several days before a stressful event. It is best to exercise a horse 2–8 hours after administration of omeprazole, and it may be taken up more quickly if the horse is given a grain meal at the same time, which should improve efficacy. [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. Ranitidine has been shown to reduce ulceration when given concurrently during feed deprivation trials. [1] H2 antagonists are cheaper and will decrease stomach acid production but require more frequent administration compared to PPIs, usually every eight hours. There are no studies suggesting that H2 antagonists improve the healing of ulcers already present. [1] H2 antagonists require doses much higher than other species to block acid production in the equine stomach, possibly because so little histamine is needed to produce maximal secretion of acid. [3] This is also true for omeprazole doses, especially if given orally.

Antacids have a short duration of effectiveness, and therefore are not very practical for use in horses because the damaging acid is produced constantly rather than just at meals. Such medications would require prohibitively frequent and excessive dosing to treat ulcers in the horse if used independently of other drugs. [1]

Sucralfate is often used as an adjunctive therapy. At a pH <4, it becomes thick in consistency and it binds to gastric ulcerations preferably over squamous epithelial cells. It is not recommended as the sole treatment of EGUS because it has not been shown to have great efficacy in treating ulcers of the squamous region, and has not been studied in cases of glandular ulcers. [1] If it is used, it should not be given around the time of an H2 antagonist, because sucralfate binds best at a lower pH. [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. Specifically, feeding alfalfa hay has also been shown to decrease the severity of ulcers. [16] [17] Grain should be reduced to a level below 0.5 kg grain/220 kg body weight, [4] and ideally as much as possible. Corn oil may be beneficial, especially for horses taking NSAIDs, as it contains 40% linoleic aid, a substance that is thought to increase prostaglandin E2 (one of the protective prostaglandins) and decrease acid production. [3] Additional turnout and a reduction in training or traveling can also have positive effects. Stalled horses should be kept in as stress-free of an environment as possible, with access to hay and the ability to see other horses. NSAID use should be kept to a minimum, and use of COX-2 selective NSAIDs such as firocoxib may be preferable over other commonly used NSAIDs. [2]

Recent studies

Although oral omeprazole treatment is the licensed treatment in the majority of countries, recent studies have shown long‐acting injectable omeprazole has been demonstrated to suppress acid production more markedly, more consistently and for longer than observed in previous investigations using oral omeprazole. [18]

Development of EGUS due to Colic

While there is not a significant correlation between the presence of gastric ulcers and presentation for a documented gastrointestinal colic, [19] in horses that present with colic symptoms and have a severe lack of gastrointestinal abnormalities, severe gastric ulceration has been determined to be the source of the colic episode, given the presence of severe ulceration and the improvement in colic symptoms following treatment of ulcerations with histamine type-2 receptor antagonists. [20] [21] Additionally, hospitalization for colic episodes can significantly induce/increase gastric ulceration. Possible reasons for this may include colic-induced stress, feed deprivation when treating a refluxing colic, and medication that may compromise the gastric environment. [19] It also has been shown that medically treated colic horses were more likely to develop gastric ulcers than surgical patients. Specifically, horses that presented with duodentis-proximal jejunitis has a significantly higher presence of gastric ulcers than other types of colic. [22]

Acid rebound following PPI treatment & possible new treatments

Following treatment of ulceration using proton pump inhibitors like Omeprazole, gastric acid can rebound to post treatment pH levels, possibly leading to the development of ulcerations again. Given 2 days of withheld omeprazole treatments, gastric ulceration worsened, with 17% of horses exhibiting ulceration during treatment, and 83% exhibiting ulceration post withdrawal of treatment. [23] Acid rebound has been shown in horses for up to 7 days post treatment with proton pump inhibitors. One study found that within 3 days post treatment, ulceration returned to pre-treatment severity in some horses. [21] Tapering treatments approaching discontinuation is a good method to reduce chances of rebound for treatment of severe ulcerations, however tapering of treatment is not recommended for treatments that are less than 8 weeks in length. Instead, a break from exercise, ample forage and a calm environment is recommended for 1–2 days following discontinuation of treatment. [21]

New formulations of omeprazole treatments have recently been under study. Different pharmacokinetics imply different dosages, different buffering mechanisms and different enteric coatings, altering their bioavailability and release rate. Esomeprazole, another proton pump inhibitor has also recently come under study. It has been shown to be a good alternative to omeprazole if treatment shows no improvement. [21] Nutraceuticals have also been explored as possible treatments. Oils such as vegetable and corn oil have been shown to increase gastric pH, decreasing risk of ulceration. [21]

Related Research Articles

<span class="mw-page-title-main">Peptic ulcer disease</span> Ulcer of an area of the gastrointestinal tract

Peptic ulcer disease is a break in the inner lining of the stomach, the first part of the small intestine, or sometimes the lower esophagus. An ulcer in the stomach is called a gastric ulcer, while one in the first part of the intestines is a duodenal ulcer. The most common symptoms of a duodenal ulcer are waking at night with upper abdominal pain, and upper abdominal pain that improves with eating. With a gastric ulcer, the pain may worsen with eating. The pain is often described as a burning or dull ache. Other symptoms include belching, vomiting, weight loss, or poor appetite. About a third of older people with peptic ulcers have no symptoms. Complications may include bleeding, perforation, and blockage of the stomach. Bleeding occurs in as many as 15% of cases.

H<sub>2</sub> receptor antagonist Class of medications

H2 antagonists, sometimes referred to as H2RAs and also called H2 blockers, are a class of medications that block the action of histamine at the histamine H2 receptors of the parietal cells in the stomach. This decreases the production of stomach acid. H2 antagonists can be used in the treatment of dyspepsia, peptic ulcers and gastroesophageal reflux disease. They have been surpassed by proton pump inhibitors (PPIs). The PPI omeprazole was found to be more effective at both healing and alleviating symptoms of ulcers and reflux oesophagitis than the H2 blockers ranitidine and cimetidine.

<span class="mw-page-title-main">Zollinger–Ellison syndrome</span> Condition in which tumours stimulate excessive gastric acid production

Zollinger–Ellison syndrome is a rare disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers. Symptoms include abdominal pain and diarrhea.

Coffee ground vomitus refers to a particular appearance of vomit. Within organic heme molecules of red blood cells is the element iron, which oxidizes following exposure to gastric acid. This reaction causes the vomitus to look like ground coffee.

<span class="mw-page-title-main">Gastric acid</span> Digestive fluid formed in the stomach

Gastric acid or stomach acid is the acidic component – hydrochloric acid of gastric juice, produced by parietal cells in the gastric glands of the stomach lining. With a pH of between one and three, gastric acid plays a key role in the digestion of proteins by activating digestive enzymes, which together break down the long chains of amino acids of proteins. Gastric acid is regulated in feedback systems to increase production when needed, such as after a meal. Other cells in the stomach produce bicarbonate, a base, to buffer the fluid, ensuring a regulated pH. These cells also produce mucus – a viscous barrier to prevent gastric acid from damaging the stomach. The pancreas further produces large amounts of bicarbonate and secretes bicarbonate through the pancreatic duct to the duodenum to neutralize gastric acid passing into the digestive tract.

<span class="mw-page-title-main">Pantoprazole</span> Stomach acid suppressing medication

Pantoprazole, sold under the brand name Protonix, among others, is a medication used for the treatment of stomach ulcers, short-term treatment of erosive esophagitis due to gastroesophageal reflux disease (GERD), maintenance of healing of erosive esophagitis, and pathological hypersecretory conditions including Zollinger–Ellison syndrome. It may also be used along with other medications to eliminate Helicobacter pylori. Pantoprazole is a proton-pump inhibitor (PPI) and its effectiveness is similar to that of other PPIs. It is available by mouth and by injection into a vein.

<span class="mw-page-title-main">Famotidine</span> Medication that reduces stomach acid

Famotidine, sold under the brand name Pepcid among others, is a histamine H2 receptor antagonist medication that decreases stomach acid production. It is used to treat peptic ulcer disease, gastroesophageal reflux disease, and Zollinger-Ellison syndrome. It is taken by mouth or by injection into a vein. It begins working within an hour.

<span class="mw-page-title-main">Phenylbutazone</span> Nonsteroidal anti-inflammatory drug (NSAID)

Phenylbutazone, often referred to as "bute", is a nonsteroidal anti-inflammatory drug (NSAID) for the short-term treatment of pain and fever in animals.

<span class="mw-page-title-main">Esomeprazole</span> Medication which reduces stomach acid

Esomeprazole, sold under the brand name Nexium [or Neksium] among others, is a medication which reduces stomach acid. It is used to treat gastroesophageal reflux disease, peptic ulcer disease, and Zollinger–Ellison syndrome. Its effectiveness is similar to that of other proton pump inhibitors (PPIs). It is taken by mouth or injection into a vein.

Curling's ulcer is an acute gastric erosion resulting as a complication from severe burns when reduced plasma volume leads to ischemia and cell necrosis (sloughing) of the gastric mucosa. The condition was first described in 1823 and named after Thomas Blizard Curling, who observed ten such cases in 1842.

A Cushing ulcer, named after Harvey Cushing, is a gastric ulcer associated with elevated intracranial pressure. It is also called von Rokitansky–Cushing syndrome. Apart from the stomach, ulcers may also develop in the proximal duodenum and distal esophagus.

Colic in horses is defined as abdominal pain, but it is a clinical symptom rather than a diagnosis. The term colic can encompass all forms of gastrointestinal conditions which cause pain as well as other causes of abdominal pain not involving the gastrointestinal tract. What makes it tricky is that different causes can manifest with similar signs of distress in the animal. Recognizing and understanding these signs is pivotal, as timely action can spell the difference between a brief moment of discomfort and a life-threatening situation. The most common forms of colic are gastrointestinal in nature and are most often related to colonic disturbance. There are a variety of different causes of colic, some of which can prove fatal without surgical intervention. Colic surgery is usually an expensive procedure as it is major abdominal surgery, often with intensive aftercare. Among domesticated horses, colic is the leading cause of premature death. The incidence of colic in the general horse population has been estimated between 4 and 10 percent over the course of the average lifespan. Clinical signs of colic generally require treatment by a veterinarian. The conditions that cause colic can become life-threatening in a short period of time.

<span class="mw-page-title-main">Flunixin</span> NSAID analgesic veterinary drug

Flunixin is a nonsteroidal anti-inflammatory drug (NSAID), analgesic, and antipyretic used in horses, cattle and pigs. It is often formulated as the meglumine salt. In the United States, it is regulated by the U.S. Food and Drug Administration (FDA), and may only be lawfully distributed by order of a licensed veterinarian. There are many trade names for the product.

<span class="mw-page-title-main">Sucralfate</span> Chemical compound and gastrointestinal medication

Sucralfate, sold under various brand names, is a medication used to treat stomach ulcers, gastroesophageal reflux disease (GERD), radiation proctitis, and stomach inflammation and to prevent stress ulcers. Its usefulness in people infected by H. pylori is limited. It is used by mouth and rectally.

<span class="mw-page-title-main">Gastrinoma</span> Medical condition

Gastrinomas are neuroendocrine tumors (NETs), usually located in the duodenum or pancreas, that secrete gastrin and cause a clinical syndrome known as Zollinger–Ellison syndrome (ZES). A large number of gastrinomas develop in the pancreas or duodenum, with near-equal frequency, and approximately 10% arise as primary neoplasms in lymph nodes of the pancreaticoduodenal region.

<span class="mw-page-title-main">Cribbing (horse)</span> Stable vice in horses

Cribbing is a form of stereotypy, otherwise known as wind sucking or crib-biting. Cribbing is considered to be an abnormal, compulsive behavior seen in some horses, and is often labelled a stable vice. The major factors that cause cribbing include stress, stable management, genetic and gastrointestinal irritability.

<span class="mw-page-title-main">Vagotomy</span> Surgical procedure

A vagotomy is a surgical procedure that involves removing part of the vagus nerve. It is performed in the abdomen.

A stress ulcer is a single or multiple mucosal defect usually caused by physiological stress which can become complicated by upper gastrointestinal bleeding. These ulcers can be caused by shock, sepsis, trauma or other conditions and are found in patients with chronic illnesses. These ulcers are a significant issue in patients in critical and intensive care.

<span class="mw-page-title-main">Acid peptic diseases</span> Overview of the acid peptic diseases of the stomach and gastrointestinal tract

Acid peptic diseases, such as peptic ulcers, Zollinger-Ellison syndrome, and gastroesophageal reflux disease, are caused by distinct but overlapping pathogenic mechanisms involving acid effects on mucosal defense. Acid reflux damages the esophageal mucosa and may also cause laryngeal tissue injury, leading to the development of pulmonary symptoms.

<span class="mw-page-title-main">Antrectomy</span> Type of gastric resection surgery

Antrectomy, also called distal gastrectomy, is a type of gastric resection surgery that involves the removal of the stomach antrum to treat gastric diseases causing the damage, bleeding, or blockage of the stomach. This is performed using either the Billroth I (BI) or Billroth II (BII) reconstruction method. Quite often, antrectomy is used alongside vagotomy to maximise its safety and effectiveness. Modern antrectomies typically have a high success rate and low mortality rate, but the exact numbers depend on the specific conditions being treated.

References

  1. 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 "Log in | IVIS" (PDF). www.ivis.org. Retrieved 2024-10-18.
  2. 1 2 3 4 5 6 7 8 9 10 11 12 13 Ferraro, Gregory (October 2012). "Diagnosing and Treating Gastric Ulcers in Horses" (PDF). Center of Equine Health at UC Davis Horse Report. Archived (PDF) from the original on 2014-03-28. Retrieved October 17, 2024.
  3. 1 2 3 4 5 Merritt, Alfred (March 1, 2004). "The Equine Stomach" (PDF). AAEP. Retrieved October 17, 2024.
  4. 1 2 Andrews, Frank M.; Buchanan, Benjamin R.; Smith, Sionagh H.; Elliott, Sarah B.; Saxton, Arnold M. (2006-11-01). "In vitro effects of hydrochloric acid and various concentrations of acetic, propionic, butyric, or valeric acids on bioelectric properties of equine gastric squamous mucosa". American Journal of Veterinary Research. 67 (11): 1873–1882. doi:10.2460/ajvr.67.11.1873. PMID   17078749.
  5. ↑ Loving, Nancy (April 1, 2010). "Consequences of Stall Confinement" (PDF). Quia. Retrieved October 17, 2024.
  6. ↑ "Blister Beetles Are Toxic to Horses". Veterinary Medicine at Illinois. Retrieved 2024-10-18.
  7. ↑ Murray, M. J.; Schusser, G. R.; Pipers, F. S.; Gross, Sheila J. (September 1996). "Factors associated with gastric lesions in Thoroughbred racehorses". Equine Veterinary Journal. 28 (5): 368–374. doi:10.1111/j.2042-3306.1996.tb03107.x. ISSN   0425-1644. PMID   8894534.
  8. ↑ Murray, M. J. (1989-10-15). "Endoscopic appearance of gastric lesions in foals: 94 cases (1987-1988)". Journal of the American Veterinary Medical Association. 195 (8): 1135–1141. ISSN   0003-1488. PMID   2808108.
  9. ↑ Husted, Louise; Jensen, Tim K.; Olsen, Susanne N.; Mølbak, Lars (2010-03-19). "Examination of equine glandular stomach lesions for bacteria, including Helicobacter spp by fluorescence in situ hybridisation". BMC Microbiology. 10: 84. doi: 10.1186/1471-2180-10-84 . ISSN   1471-2180. PMC   2848230 . PMID   20298612.
  10. 1 2 3 4 Andrews, Frank (March 23, 2013). "Overview of Gastric and Colonic Ulcers" (PDF). Wayback Machine Archive. Archived from the original (PDF) on 2013-03-23. Retrieved October 17, 2024.
  11. ↑ Martinez Aranzalez, Jose (December 11, 2013). "Equine gastric ulcer syndrome: risk factors and therapeutic aspects". Revista Colombiana de Ciencias Pecuarias. Retrieved October 17, 2024.
  12. ↑ Yuki, N.; Shimazaki, T.; Kushiro, A.; Watanabe, K.; Uchida, K.; Yuyama, T.; Morotomi, M. (November 2000). "Colonization of the stratified squamous epithelium of the nonsecreting area of horse stomach by lactobacilli". Applied and Environmental Microbiology. 66 (11): 5030–5034. doi:10.1128/AEM.66.11.5030-5034.2000. ISSN   0099-2240. PMC   92416 . PMID   11055960.
  13. ↑ Murray, M. J.; Grodinsky, Carolyn; Anderson, C. W.; Radue, P. F.; Schmidt, G. R. (June 1989). "Gastric ulcers in horses: a comparison of endoscopic findings in horses with and without clinical signs". Equine Veterinary Journal. 21 (S7): 68–72. doi:10.1111/j.2042-3306.1989.tb05659.x. ISSN   0425-1644. PMID   9118110.
  14. ↑ MacAllister, C. G.; Andrews, F. M.; Deegan, E.; Ruoff, W.; Olovson, S. G. (November 1997). "A scoring system for gastric ulcers in the horse". Equine Veterinary Journal. 29 (6): 430–433. doi:10.1111/j.2042-3306.1997.tb03154.x. ISSN   0425-1644. PMID   9413714.
  15. ↑ Nieto, Jorge E.; Spier, Sharon; Pipers, Frank S.; Stanley, Scott; Aleman, Monica R.; Smith, Donald C.; Snyder, Jack R. (2002-10-15). "Comparison of paste and suspension formulations of omeprazole in the healing of gastric ulcers in racehorses in active training". Journal of the American Veterinary Medical Association. 221 (8): 1139–1143. doi:10.2460/javma.2002.221.1139. ISSN   0003-1488. PMID   12387383.
  16. ↑ Nadeau, J. A.; Andrews, F. M.; Mathew, A. G.; Argenzio, R. A.; Blackford, J. T.; Sohtell, M.; Saxton, A. M. (July 2000). "Evaluation of diet as a cause of gastric ulcers in horses". American Journal of Veterinary Research. 61 (7): 784–790. doi:10.2460/ajvr.2000.61.784. ISSN   0002-9645. PMID   10895901.
  17. ↑ "Feeding Alfalfa Hay to Exercising Horses Reduces the Severity of Gastric Squamous Mucosal Ulceration | IVIS". www.ivis.org. 2007-12-05. Retrieved 2024-10-18.
  18. ↑ Gough, Hallowell (2020). "A Study Investigating the Treatment of Equine Squamous Gastric Disease with Long-Acting Injectable or Oral Omeprazole". Veterinary Medicine and Science. 6 (2): 235–241. doi:10.1002/vms3.220. PMC   7196684 . PMID   31945806.
  19. 1 2 Rabuffo, Tara; Hackett, Eileen; Grenager, Nora; Boston, Raymond; Orsini, James (June 2009). "Prevalence of Gastric Ulcerations in Horses with Colic". Journal of Equine Veterinary Science. 29 (6): 540–546. doi:10.1016/j.jevs.2009.05.005 . Retrieved November 6, 2024.
  20. ↑ Murray, Michael (1 July 1992). "Gastric ulceration in horses: 91 cases (1987-1990)". Journal of the American Veterinary Medical Association. 201 (1): 117–120. doi:10.2460/javma.1992.201.01.117. PMID   1644631 . Retrieved 6 Nov 2024.
  21. 1 2 3 4 5 Vokes, Jessica; Lovett, Amy; Sykes, Benjamin (January 2023). "Equine Gastric Ulcer Syndrome: An Update on Current Knowledge". Animals. 13 (7): 1261. doi: 10.3390/ani13071261 . ISSN   2076-2615. PMC   10093336 . PMID   37048517.
  22. ↑ Dukti, S. A.; Perkins, S.; Murphy, J.; Barr, B.; Boston, R.; Southwood, L. L.; Bernard, W. (5 January 2010). "Prevalence of gastric squamous ulceration in horses with abdominal pain". Equine Veterinary Journal. 38 (4): 347–349. doi:10.2746/042516406777749164. PMID   16866203 . Retrieved 6 November 2024.
  23. ↑ Shan, Ran; Steel, Catherine; Sykes, Ben (31 May 2023). "The Impact of Two Recommended Withholding Periods of Omeprazole and the Use of a Nutraceutical Supplement on Recurrence of Equine Gastric Ulcer Syndrome in Thoroughbred Racehorses". Animals. 13 (11): 1823. doi: 10.3390/ani13111823 . PMC   10251805 . PMID   37889700.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.