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Therapeutics for Equine Gastric Ulcer Syndrome
Abstract
Equine gastric ulcer syndrome (EGUS) is an umbrella term used to describe ulcers in the nonglandular squamous and glandular mucosa, terminal esophagus, and proximal duodenum. Gastric ulcers in the squamous and glandular regions occur more often than esophageal or duodenal ulcers and likely have a different pathogenesis. At present, omeprazole is accepted globally as the best pharmacologic therapy for both regions of the stomach; however, the addition of coating agents and synthetic prostaglandins could add to its effectiveness in treatment of EGUS. Dietary and environmental management are necessary for prevention of recurrence.
... Proton pump inhibitors (PPIs) and other suppressors of gastric acid secretion are used extensively in both humans and animals with suspected disorders of the upper gastrointestinal (GI) tract. 1 Omeprazole is the mainstay treatment of gastric ulcers in humans, dogs, and horses. 1,2 It is a potent inhibitor of gastric acid secretion, blocking the hydrogen-potassium-ATPase (proton pump) of gastric parietal cells, and allowing gastric pH to increase. 2 In equine practice, omeprazole is used to treat gastric ulcers and also commonly administered empirically for prevention of gastric disease, even without an established diagnosis. ...
... 1,2 It is a potent inhibitor of gastric acid secretion, blocking the hydrogen-potassium-ATPase (proton pump) of gastric parietal cells, and allowing gastric pH to increase. 2 In equine practice, omeprazole is used to treat gastric ulcers and also commonly administered empirically for prevention of gastric disease, even without an established diagnosis. 3 In human patients, treatment with PPIs is associated with profound changes in the gut microbiome and increased risk of enteric infections by Clostridioides difficile (formerly Clostridium difficile), Salmonella spp, Shigella spp, or Campylobacter spp. 4 There is increased incidence of respiratory and hematogenous infections in those patients. ...
... C0: control period, Day 0; C7: control period, Day 7; A0: administration period, Day 0; A7: administration period, I G U R E 7 Bar charts illustrate the 20 most abundant genera found in the feces and their cumulated relative abundance (%) in each of the 8 horses included in the study. Each bar represents a horse(1)(2)(3)(4)(5)(6)(7)(8). C0: control period, Day 0; C7: control period, Day 7; A0: administration period, Day 0; A7: administration period, ...
Background
Omeprazole administration is associated with changes in gastric and fecal microbiota and increased incidence of Clostridioides difficile enterocolitis in humans and dogs.
Hypothesis/Objectives
Study purpose was to assess the effect of omeprazole on gastric glandular and fecal microbiota in healthy adult horses.
Animals
Eight healthy horses stabled on straw and fed 100% haylage.
Methods
Prospective controlled study. Transendoscopic gastric glandular biopsies, gastric fluid, and fecal samples were obtained from each horse twice at a 7‐day interval before the administration of omeprazole. Samples were taken on the same horses before and after a 7‐day administration of omeprazole (4 mg/kg PO q24h). pH was assessed on fresh gastric fluid and other samples were kept at −20°C until analysis. Bacterial taxonomy profiling was obtained by V1V3 16S amplicon sequencing from feces and gastric glandular biopsies. Analysis of alpha, beta diversity, and comparison between time points were performed with MOTHUR and results were considered significant when P < .05.
Results
Gastric pH increased significantly after 7 days of omeprazole administration (P = .006). Omeprazole did not induce significant major changes in composition of fecal or gastric glandular microbiota, however, after administration, certain microbial genera became more predominant in the gastric glandular mucosa (lower Simpson's evenness, P = .05). Only the genus Clostridium sensu strictu_1 had a significant shift in the glandular gastric mucosa after omeprazole administration (P = .002). No population shifts were observed in feces.
Conclusions and Clinical Importance
Oral administration of omeprazole could have fewer effects in gastrointestinal microbiota in the horse compared to other species.
... The pathogenesis of ESGD involves an acidic attack to the squamous mucosa, with feeding practices and high exercise volume considered as important risk factors [4]. In addition, it can occur in foals with pyloric stenosis due to a delayed gastric emptying [5]. On the other hand, the pathogenesis of EGGD remains unknown, but it is believed to be caused by breakdown of the gastric glandular mucosal defense mechanisms. ...
... On the other hand, the pathogenesis of EGGD remains unknown, but it is believed to be caused by breakdown of the gastric glandular mucosal defense mechanisms. Stress, infection with bacteria, nonsteroidal anti-inflammatory drugs (NSAIDs), and inhibition of protective prostaglandins have been proposed as possible causes [4,5]. ...
In this report, the measurement of salivary biomarkers as an aid for diagnosis of equine gastric ulcer syndrome (EGUS) was studied. A comprehensive panel of 23 salivary analytes was measured in the saliva of horses affected by EGUS and compared to healthy animals and horses with other diseases clinically similar to EGUS but with a negative diagnosis at gastroscopic examination. A total of 147 horses were included in the study and divided into heathy population (n = 12), the EGUS group (n = 110), and the group of horses with other diseases (n = 25). From the 23 analytes studied, 17 showed increased values in EGUS horses when compared to healthy ones, and uric acid, triglycerides, and calcium were significantly increased in horses with EGUS compared to the group of other diseases. The receiver operating characteristic curve analyses showed a modest but significant discriminatory power of those three analytes to identify EGUS from other diseases with similar symptoms. The discriminatory power enhanced when the results of the three analytes were combined. In conclusion, the results showed that selected salivary analytes could have potential use as biomarkers in horses with EGUS.
... 13 Omeprazole is a substituted benzimidazole proton-pump inhibitor (PPI) and has been the mainstay of treatment of gastric ulcers in horses and human subjects for many years. 32 Omeprazole suppresses gastric acid secretion by inhibition of the hydrogen/potassium ATP pump in parietal cells, resulting in an increased intragastric pH. Sucralfate is an aluminium complex sulphated polysaccharide in combination with octasulfate and aluminium hydroxide. ...
... Sucralfate exerts gastroprotectant effects through multiple mechanisms of action, including improved mucosal blood flow, interaction with fibroblast and epidermal growth factors, improved angiogenesis and epithelialisation, inactivation of pepsin and adsorption of bile acids. [32][33][34][35][36] Our long-term goal is to make better evidence-based clinical recommendations for ulcer prophylaxis. The objective of this study was to evaluate the efficacy of either omeprazole or sucralfate given as monotherapy for the prevention of gastric lesions in fasted horses treated with NSAIDs. ...
Background
Equine gastric ulcer syndrome (EGUS) is a common and significant cause of morbidity in horses, with a range of clinical signs, including inappetence, colic and poor performance. Hospitalised horses are exposed to factors that may induce EGUS, including fasting and nonsteroidal anti‐inflammatory drug (NSAID) administration, and may be at risk for development of squamous (ESGD) and glandular gastric disease (EGGD). Prophylactic anti‐ulcer medication is often prescribed for these patients, but drug selection is complicated by different aetiology and response to treatment of ESGD and EGGD.
Objectives
To establish the efficacy of sucralfate or omeprazole used prophylactically in horses exposed to a combined feed‐fast and NSAID administration EGUS induction protocol. We hypothesised that these drugs would be equally effective for prevention of gastric lesions in the experimental cohort.
Study design
Randomised crossover experimental design.
Methods
Horses (n = 14) received either omeprazole (1 mg/kg PO q24h) or sucralfate (20 mg/kg PO q8h) while undergoing the feed‐fast/NSAID protocol, allowed an 8‐week washout period, and then administered the alternate treatment. Serial gastroscopy, ultrasound and haematology documented treatment effects.
Results
ESGD and EGGD score increased over time under both treatments. There was a significant effect of treatment on EGGD scores (P < .001), with post‐treatment EGGD scores higher for horses receiving sucralfate (median 3; IQR 2.25,3) than omeprazole (1; 1,1). The effect of treatment on ESGD scores just achieved significance (P = .05), with post‐treatment ESGD scores higher for sucralfate (4; 3,4) than omeprazole (2; 2,3).
Main limitations
This study was performed in healthy horses, and response to treatment may differ in horses with clinical illness. Additional investigation in a larger population may be required to detect significant differences in other clinical parameters.
Conclusions
Omeprazole was superior to sucralfate for mitigating gastric lesion severity in healthy horses exposed to a feed‐fast/NSAID model.
... 13 Although mucosal ulcers may heal spontaneously, 15 this is uncommon in horses in training or racing, and medical treatment is therefore required: omeprazole, a proton pump inhibitor, is considered the drug of choice for prevention and treatment of squamous ulceration, acting by suppressing acid secretion. 1,5,11,[16][17][18][19][20][21][22] However, pharmacological treatment is expensive and may require prolonged administrations: therefore, interest in nutraceutical supplements with anti-ulcerogenic properties has increased and numerous studies have been carried out to evaluate their effectiveness in preventing and treating gastric ulceration. 13,15,[23][24][25][26][27][28][29] supplement designed to protect gastric mucosa, containing pectin, soy lecithin, zinc oxide and Castanea sativa Mill. ...
... Gastric ulceration is commonly associated with a poor body condition 1,5,11,20,21,42 ; different studies have reported an increase in body weight after treatment, associated with an improvement in ulcer grades 13,16,23,41 . However, the results of the present study showed no significant difference in body weight before and after the treatment period, neither in the treatment group nor in the control group. ...
Introduction:
Equine squamous gastric disease (ESGD) may require prolonged treatments with acid suppressants; therefore, interest in nutraceutical supplements with anti-ulcerogenic properties has increased. This study aims to investigate the efficacy of Trophogast pellet for the treatment of ESGD in endurance horses.
Material and methods:
Fifteen endurance horses were included based on their gastroscopic examination and randomly assigned to a treatment group, receiving Trophogast pellet for 30 days together with management changes, or to a control group, only subjected to management modifications. At the end of treatment, gastroscopy was repeated. Scores were assigned according to the Equine Gastric Ulcer Council scoring system. All horses were weighed at the beginning and at the end of the study. ESGD grades and weight before and after treatment were compared.
Results:
At enrolment, median ESGD score in the treatment group was 2, while in the control group it was 1. After the treatment period, a significant decrease in ESGD grade was observed in the treatment group (median 1, p = 0.0078), while there was no change in the control group (median 2). No significant weight change was observed in either group.
Conclusion:
Trophogast pellet was effective at promoting healing of mild ESGD in endurance horses.
... In veterinary species, the PPIs have been recognized as the most potent suppressors of gastric acid (3). Drugs of the PPI class such as omeprazole have been thoroughly investigated as a treatment for gastric ulceration in horses (4). Abomasal ulceration is the manifestation of gastric ulceration in ruminant species (5), which can be caused by disease, stress, or as an adverse effect of some medications, such as nonsteroidal anti-inflammatory drugs. ...
... A 1 mg/kg dosage of pantoprazole (Pantoprazole sodium for injection, AuroMedics Pharma LLC, East Windsor, NJ) was administered intravenously to each goat. Blood samples were collected at 0, 10, 20, 30, and 45 min after collection as well as 1, 1.5, 2, 3,4,8,12,18,24, and 36 h after drug administration. Blood samples were placed into a lithium heparin tubes after collection, and then immediately spun down and transferred to cryogenic vials placed into storage at −80 • C until analysis. ...
Background: Ruminant species are at risk of developing abomasal ulceration, but there is a lack of pharmacokinetic data for anti-ulcer therapies, such as the proton pump inhibitor pantoprazole, in goats.
Objective: The primary study objective was to estimate the plasma pharmacokinetic parameters for pantoprazole in adult goats after intravenous administration. A secondary objective was to describe the pharmacokinetic parameters for the metabolite, pantoprazole sulfone, in goats.
Methods: Pantoprazole was administered intravenously to six adult goats at a dose of 1 mg/kg. Plasma samples were collected over 36h and analyzed via reverse phase high performance liquid chromatography for determination of pantoprazole and pantoprazole sulfone concentrations. Pharmacokinetic parameters were determined by non-compartmental analysis.
Results: Plasma clearance, elimination half-life, and volume of distribution of pantoprazole were estimated at 0.345 mL/kg/min, 0.7 h, and 0.9 L/kg, respectively following IV administration. The maximum concentration, elimination half-life and area under the curve of pantoprazole sulfone were estimated at 0.1 μg/mL, 0.8 h, and 0.2 hr*μg/mL, respectively. The global extraction ratio was estimated 0.00795 ± 0.00138. All animals had normal physical examinations after conclusion of the study.
Conclusion: The reported plasma clearance for pantoprazole is lower than reported for foals, calves, and alpacas. The elimination half-life appears to be < that reported for foals and calves. Future pharmacodynamic studies are necessary for determination of the efficacy of pantoprazole on acid suppression in goats.
... 24 Likewise, reduction of gastric acid secretion is also the fundamental component of gastric ulcer treatment in the dog 17 and horse. 36 Treatment options include H2-receptor antagonists, such as cimetidine, ranitidine and famotidine, or proton pump inhibitors such as omeprazole. 17,23 Sucralfate, a gastrointestinal protectant that binds to proteinaceous exudates found at ulcer sites, is also used in dogs and horses for the oral treatment of gastric ulcers. ...
... 17,23 Sucralfate, a gastrointestinal protectant that binds to proteinaceous exudates found at ulcer sites, is also used in dogs and horses for the oral treatment of gastric ulcers. 17,36 The intravenous administration of the H2-receptor antagonist famotidine was shown to be efficacious in increasing the pH of abomasal outflow digesta in adult cattle 4 as was the intramuscular administration of ranitidine. 33 The oral administration of cimetidine and ranitidine in healthy milk-fed calves resulted in immediate increase in abomasal pH in a dose-dependent fashion similar to the oral administration of ranitidine. 1, 2 It appears likely that the oral administration of drugs used to block or decrease gastric acid production are contraindicated in adult cattle because of potential inactivation by the rumen flora. ...
Introduction:
This study included 94 cows aged 2.1 to 12.0 years (5.2 ± 2.05 years) that were examined at a referral clinic because of type-1 abomasal ulcer. The most common clinical findings were poor general health status (94%), partial or complete anorexia (93%), congested scleral vessels (89%), decreased skin surface temperature (76%), decreased or absent faecal output (72%), abdominal guarding (59%), tachypnoea (56%), rumen atony (53%) and positive percussion and simultaneous auscultation and/or ballottement and simultaneous auscultation on the right side (53%). The most common laboratory findings were hypokalaemia (68%), positive base excess (60%) and azotaemia (51%). The chloride concentration of rumen fluid was increased in 48% of the cows. The diagnosis of type-1 ulcer was made during laparotomy and/or postmortem examination. One or more concurrent diseases were diagnosed in 97% of the cows. Seventy-eight (83%) cows were euthanased immediately after the initial examination, during laparotomy or after unsuccessful treatment, and eight (8.5%) cows died, and all were examined postmortem. Eight (8.5%) cows were discharged and six of these made a complete recovery.
... Perforated peptic ulcer (PPU) is a severe complication of PUD, and people with PPU also have severe abdomen with a high risk of long-term illness and fatality [2]. Proton pump inhibitors such as omeprazole, pantoprazole, lansoprazole are widely recognized worldwide as the best pharmacological therapy for both gastric and duodenal ulcers of the stomach [3] Helicobacter pylori (H. pylori) are the most common cause of peptic ulcers, along with the long-term consumption of nonsteroidal anti-inflammatory drugs (NSAIDs) like sodium naproxen and ibuprofen (Advil, Motrin IB, others). ...
Backgrounds
Peptic ulcer disease (PUD) is a common gastrointestinal tract disease characterized by mucosal damage secondary to pepsin and gastric acid secretion. This study evaluated the five-year recurrence rate for patients with PUD and risk factors contributing to PUD relapses.
Methods
From 2016 through 2021, all patients with endoscopy-proved PUD were identified by reviewing medical records (Best-Care system). Possible risk factors including smoking, nonsteroidal anti-inflammatory drugs (NSAIDs), aspirin, alcohol, caffeine, and steroids were analyzed by multivariate analysis. Treatment outcomes, 5-year recurrence rate, and mortality rate were assessed.
Results
Among 223 patients, there were 187 (83.8%) diagnosed with endoscopy-proved PUD and 36 (16.2%) diagnosed with clinical PUD. Among them, 126 (56.5%) patients were males, and the mean age was 62±2 years. The five years recurrence rate of PUD was 30.9%. There was no significant difference in the recurrence rate between the duodenal ulcer (33.3%) and the gastric ulcer (28.8%). By univariate analysis, the use of steroids and NSAID and Helicobacter pylori (H. pylori) infection were potential risk factors for PUD (P < 0.005). The common complication of PUD was gastrointestinal bleeding (34.1%). Patients who had a complicated PUD were associated with a higher rate of recurrence (45.9%) compared to the uncomplicated PUD (19.2%) (P > 0.05).
Conclusion
Our findings demonstrated that the five years recurrence rate of PUD was 30.9%. The use of steroids and NSAID and H. pylori infection were risk factors for recurrence of PUD. PUD places a significant burden on health care systems. Therefore, a multicenter prospective study is needed for effective management to prevent recurrence and complications of PUD.
... 69 The addition of alfalfa to the forage, up to 25% of the daily intake, can be helpful by providing additional buffering capacity to the gastric contents. 35,70 Horses with cyathostomiasis or other colonic inflammatory disorders require a diet that achieves mechanical and functional rest for the colon. 71 Immature cool-season grasses and good-quality pelleted complete feeds are easily digested, low in bulk, and low in insoluble fibers, and should be fed little and often. ...
Weight loss occurs when the supply of energy is insufficient to meet the energy needs of an individual. The energy supply may be reduced by inadequate provision of feed, inadequate consumption, reduced digestion and absorption, or disruption in metabolic processing. Increased energy expenditure occurs with exercise and during cold temperatures, pregnancy, and lactation. Underlying clinical disease, particularly chronic inflammation, neoplasia, and protein-losing conditions, can cause weight loss or exacerbate existing weight loss. A methodical approach to weight-loss investigation and treatment is necessary, because of the often multifactorial nature of this condition.
... This may be possible to achieve given the feeding methods that were described, for instance, access to ad libitum forage fed to the individual's needs which would be monitored by staff, specialist concentrate feed, tailored to each horse and their level of work, fed three to four times a day and pasture turnout. Such an approach should mean there would rarely be an absence of food in the horse's stomach buffering the presence of acid which is always present in the glandular region of the stomach [37]. ...
The purpose of the study was to explore the perceptions held by British racing industry stakeholders of factors influencing racehorse welfare. Ten focus groups were held across the UK with a total of 42 stakeholders from a range of roles within racehorse care including trainers, stable staff and veterinarians. Participants took part in three exercises. Firstly, to describe the scenarios of a ‘best life’ and the minimum welfare standards a horse in training could be living under. Secondly, to identify the main challenges for racehorse welfare and thirdly, to recall any innovative or uncommon practices to improve welfare they had witnessed. Using thematic analysis, eight themes emerged from the first exercise. Two strands, factors that contribute to maintaining health and the horse-human relationship ran through all eight themes. Across all themes horses living the ‘best life’ were perceived as being treated as individuals rather than being part of a ‘one size fits all’ life when kept under minimum welfare standards. Health was both perceived as the main challenge to welfare as well as one open to innovative practices such as improved veterinary treatments. Data obtained, informed by the knowledge and expertise of experienced stakeholders, combined with practical animal welfare science will be used to develop the first British racehorse welfare assessment protocol.
The presence of intestinal parasites influences equines' well-being and working performance. However, the scenario of parasitism in working horses in the lowlands of Nepal is yet to be explored. The present study aimed to reveal the prevalence and diversity of intestinal parasites (protozoa and helminths) and to list the zoonotic species in working horses in the lowlands of Nepal. Fresh fecal samples (N=102) from horses were collected at two locations (Chitwan and Birgunj) in the lowlands of Terai and were transferred to the research laboratory. Coproscopy was carried out via direct wet mount, formalin ethyl acetate (FEA) sedimentation, saturated salt flotation, and acid-fast staining techniques. Coproscopy revealed an overall prevalence rate of 90.2% (92/102) with 15 known diverse species of parasites (Protozoa: 5 and Helminths: 10) and an unknown coccidian, out of which eight possess zoonotic potential. The prevalence and diversity of intestinal parasites were higher in adult than in young animals (90.7%; 15 spp. vs. 88.9%; 11 spp.) The overall prevalence of helminths was double that of protozoa (89.2% vs. 43.1%). Furthermore, polyparasitism was much more prevalent than monoparasitism (85.3% vs 4.9%). Co-infection with two parasite species (37%) was higher in young horses. In comparison, triplet infection (34%) was higher in adults, and a maximum concurrency of up to six species of parasites at a time was recorded. Following it, the differences in the prevalence rate of parasites based on the predictor of risks, like sex, grazing, domestication type, nature of the floor, and medication practices, were statistically significant. Working horses in the lowlands of Terai harbored a significant variety of intestinal parasites with important prevalence. Since eight of the reported parasitic species were zoonotic, infected horses pose a zoonotic risk to the owners. Therefore, timely deworming, pasture management, and reduction in working pressure are highly recommended.
Over the last 10 years there has been increasing awareness and subsequently recorded cases of equine gastric ulcer syndrome and with this comes an increased interest in appropriate nutrition and feed management. This review presents a systematic approach to assessing the ration of a horse at risk of or diagnosed with equine gastric ulcer syndrome and demonstrates the ample evidence upon which to base nutritional recommendations for horses with equine squamous gastric disease, and to a lesser extent, equine glandular gastric disease, with an emphasis on forage. Careful selection and management of the forage ration should be the first step in designing a suitable ration, followed by selection of an appropriately low starch and sugar (less than 2 g per kg body weight per day and 1 g per kg body weight per meal) complementary feed.
Objective:
To quantify phytochemicals using liquid chromatography and mass spectroscopy (LCMS) analysis and explore the therapeutic effect of Aesculus hippocastanum L. (AH) seeds ethanolic extract against gastric ulcers in rats.
Methods:
Preliminary phytochemical testing and LCMS analysis were performed according to standard methods. For treatment, the animals were divided into 7 groups including normal control, ulcer control, self-healing, AH seeds low and high doses, ranitidine and per se groups. Rats were orally administered with 10 mg/kg of indomethacin, excluding the normal control group (which received 1% carboxy methyl cellulose) and the per se group (received 200 mg/kg AH seeds extract). The test group rats were then given 2 doses of AH seeds extract (100 and 200 mg/kg, respectively), while the standard group was given ranitidine (50 mg/kg). On the 11th day, rats in all groups were sacrificed, and their stomach was isolated to calculate the ulcer index, and other parameters such as blood prostaglandin (PGE2), tissue superoxide dismutase (SOD), catalase (CAT), malonyldialdehyde (MDA), and glutathione (GSH). All isolated stomach tissues were analyzed for histopathological findings.
Results:
The phytochemical examination shows that the AH seeds contain alkaloids, flavonoids, saponins, phenolic components, and glycosides. LCMS analysis confirms the presence of quercetin and rutin. The AH seeds extract showed significant improvement in gastric mucosa conditions after indomethacin-induced gastric lesions (P<0.01). Further marked improvement in blood PGE2 and antioxidant enzymes, SOD, CAT, MDA and GSH, were observed compared with self-healing and untreated ulcer-induced groups (P<0.01). Histopathology results confirmed that AH seeds extract improved the mucosal layer and gastric epithelial membrane in treated groups compared to untreated ulcer-induced groups.
Conclusions:
LCMS report confirms the presence of quercetin and rutin in AH seeds ethanolic extract. The therapeutic effect of AH seeds extract against indomethacin-induced ulcer in rat model indicated the regenerated membrane integrity, with improved cellular functions and mucus thickness. Further, improved antioxidant enzyme level would help to reduce PGE2 biosynthesis.
Over the last 10 years there has been increasing awareness and subsequently recorded cases of equine gastric ulcer syndrome and with this comes an increased interest in appropriate nutrition and feed management. This review presents a systematic approach to assessing the ration of a horse at risk or diagnosed with equine gastric ulcer syndrome and demonstrates the ample evidence upon which to base nutritional recommendations for horses with equine squamous gastric disease, and to a lesser extent, equine glandular gastric disease, with an emphasis on forage. Careful selection and management of the forage ration should be the first step in designing a suitable ration, followed by selection of an appropriately low starch and sugar (less than 2g per kg body weight per day and 1g per kg body weight per meal) complementary feed. There is still more to learn about the role of supplements in the prevention and treatment of equine gastric ulcer syndrome, thus these should currently be viewed as an adjunct to an appropriate base diet and not as an isolated solution.
Objectives:
To evaluate the clinical effect of magnesium aluminum carbonate combined with rabeprazole-based triple therapy in the treatment of patients with Helicobacter pylori-positive gastric ulcer associated with hemorrhage.
Methods:
A total of 80 patients with Helicobacter pylori-positive gastric ulcer associated with hemorrhage admitted to the Baoding First Central Hospital from January 2019 to December 2020 were selected and randomly divided into two groups, with 40 cases in each group. The control group were given rabeprazole-based triple therapy, while the experimental group were treated with magnesium aluminum carbonate on the basis of the control group. The changes of symptoms and signs such as abdominal pain, abdominal distension, nausea, vomiting and hematochezia were compared between the two groups before and after treatment. Serological changes of the gastric mucosal microenvironment, such as the serum levels of extracellular regulatory protein kinase (ERK), superoxide dismutase (SOD) and epidermal growth factor receptor (EGFR), were compared between the two groups. Moreover, the differences in the results of gastroscopy between the two groups before and after treatment were compared and analyzed.
Results:
The scores of gastrointestinal symptoms in the experimental group after treatment were significantly improved compared with the control group (p=0.00). The levels of ERK and EGFR in the experimental group were significantly lower than those in the control group (ERK, p=0.01; EGRF, p=0.00), while the level of SOD was significantly increased (p=0.02). After treatment, the total effective rate of ulcer healing in the experimental group was 82.5%, which was significantly better than 60% in the control group (p=0.03). After treatment, moderate to severe gastric mucosal inflammation in the experimental group decreased to 10%, significantly better than that in the control group (decreased to 30%) (p=0.03).
Conclusion:
Magnesium aluminum carbonate combined with rabeprazole-based triple therapy is preferred for the treatment of patients with Helicobacter pylori-positive gastric ulcer associated with hemorrhage. With such a highly effective treatment regimen, the internal environment and blood supply of gastric mucosal cells can be significantly improved, gastric mucosal inflammation and gastrointestinal symptoms can be ameliorated, and the healing of ulcer surfaces can be accelerated.
Sturgeon cartilage, which is rich in chondroitin sulfate (CS), is usually discarded during sturgeon utilization. In this paper, CS was isolated from large hybrid sturgeon skull and backbone and named SCS and BCS, respectively. Their structures were investigated via Fourier transform infrared (FT-IR) spectroscopy, nuclear magnetic resonance (NMR) spectroscopy and high performance liquid chromatography (HPLC). The average molecular weights of SCS and BCS were ∼30-44 kDa. Disaccharide analysis indicated that SCS and BCS had similar chemical structures and were composed of ΔUA-[1→3]-GalNAc (ΔDi0S, 14.71%, 16.04%), ΔUA-[1→3]-GalNAc-4s (ΔDi4S, 32.01%, 37.78%) and ΔUA-[1→3]-GalNAc-6s (ΔDi6S, 53.27%, 46.18%). The gastroprotective effect of SCS and BCS were studied using a rat model of ethanol-induced gastric ulcers. Both SCS and BCS had apparent gastroprotective activity and their ulcer inhibition rate reached ∼35%-45%, which was similar to that of omeprazole (∼41%). These results provide useful strategies for the high-value utilization of sturgeon cartilage.
Equine gastric ulcer syndrome (EGUS) affects various categories of horses worldwide. This syndrome is now divided into two different diseases, based on the presence of lesions on either the squamous (Equine Squamous Gastric Disease, ESGD) or the glandular (Equine Glandular Gastric Disease, EGGD) mucosa. Diagnosis is based on the evaluation of the presence of gastric lesions with gastroscopic examination. As a gastroscopy can be considered expensive by clients, therapy is started often on the basis of clinical signs only. The aim of this study was to validate a questionnaire to detect the risk of developing ESGD or EGGD. The owners of 418 horses that were submitted to gastroscopic evaluation were asked to answer a questionnaire on risk factors for ESGD and EGGD. Horses were divided into three groups based on the results of the questionnaire and their risk of developing gastric lesions. In our population the survey was not useful to detect the presence and the severity of the lesions detected during gastroscopic examination, however answers to some of the questions did correlate with the development of gastric lesions. The questionnaire could therefore be a useful tool to evaluate the risk of ESGD or EGGD. Having owners periodically complete the survey could also make them more aware of changes in the conditions of the horses that could lead to gastric lesions. This could then help them seek advice from veterinarians on how to manage this potential risk.
To investigate the effects of formononetin on rats with gastric ulcer and further to explore its possible mechanism. Rats were randomly divided into sham operation group (Sham), model group (Model), omeprazole control group (Omeprazole) and formononetin in different dose groups (FOR-L, FOR-M, FOR-H). Rats model with gastric ulcer were established by 100% glacial acetic acid. Hematoxylin-eosin (H&E) staining was used to observe the pathological morphology of gastric mucosa. Immunohistochemistry and enzyme-linked immunosorbent assay (ELISA) were used to detect the level of inflammatory and angiogenesis related factors. The expressions of nuclear factor kappa-B (NF-κB) signaling pathway-related proteins were detected by western blot. Formononetin and omeprazole could ameliorate the pathological morphology of gastric mucosa in gastric ulcer rats. Compared with Model group, the levels of tumor necrosis factor (TNF)-α, Interleukin (IL)-1β, IL-6, myeloperoxidase (MPO), human endothelin (ET)-1 and p-P65 protein in formononetin treatment and omeprazole groups were significantly decreased (p < 0.05). Moreover, formononetin could increase the content of vascular endothelial growth factor (VEGF), nitric oxide (NO) and the levels of CD34, tight junction proteins (ZO-1 and occludin) and p-IκBα in a dose-dependent manner. Formononetin can ameliorate gastric ulcer in rats by inhibiting inflammation and promoting gastric mucosal angiogenesis, and its mechanism maybe related to NF-κB signaling pathway.
Proton pump inhibitors such as omeprazole reduce nutrient digestibility in humans. This study determined the effect of omeprazole on the digestibility of diets containing limestone or marine-derived calcium (BMC) and to assess changes in blood parameters associated with gastric acid production and calcium status in horses. Thoroughbreds were used to evaluate the digestibility of diets containing different calcium sources with or without omeprazole over four 21-day periods. Each 21-day period had a 15-day diet adaptation phase followed by a 6-day collection phase, consisting of a 5-day total fecal collection period and a final day for gastroscopy and blood sampling. Horses were fed the same diet with either 60 g/d BMC or 50 g/d limestone, so the total diet provided ∼45 g calcium. Horses on omeprazole were given GastroGard once daily for the final 14 day of each 21-day period, which supplied 3.91 ± 0.17 mg/kg BW/d of omeprazole. On day 21, blood samples were taken and gastric fluid pH was measured 8 hour after omeprazole administration. Omeprazole had a profound effect on gastric fluid pH in omeprazole-treated horses compared with nontreated horses. Serum gastrin doubled in omeprazole-treated horses compared with nontreated horses. Omeprazole and calcium source did not affect digestibility of phosphorus, magnesium, potassium, sodium, iron, copper, zinc, or manganese but did affect calcium digestibility. Omeprazole reduced apparent calcium digestibility from 52.0% to 41.4% in limestone and from 55.1% to 46.5% in BMC, equalling a 20.3% and 15.6% decrease in calcium digestibility in the limestone and BMC, respectively. Mineral source had a significant effect on calcium digestibility with BMC at 50.8% and limestone at 46.7%.
Equine gastric ulcer syndrome (EGUS) is a pathological condition affecting the glandular and squamous regions of the stomach. It is characterized by non‐specific clinical signs, behavioural changes or can also be found without any overt clinical manifestations. Nutritional factors such as intermittent feeding, high sugars and starch intake, large amounts of straw as forage and prolonged time without access to forage have all been associated with an increased risk of equine squamous gastric disease (ESGD). The aim of this study was to investigate which nutritional practices are commonly seen in clinical ESGD cases in Belgium. Medical records of 27 horses referred to the equine nutritional service at Ghent University (2013–2018) due to equine gastric ulcer lesions were reviewed. Twenty‐one healthy horses referred for dietary evaluation during the same period were selected as control cases (CC). Dietary evaluation was performed on an individual basis. Forage/concentrate ratio on dry matter basis, forage content in the diet, total dietary sugars and starch intake per day and per meal were analysed. Retrospective descriptive and statistical analyses were performed. Significantly, higher amounts of forage intake (%DM per BW) in the CC vs. ESGD group were noted (p ≤ .05) with average values of 1.39 (SD ± 0.27) and 1.27 (SD ± 0.70) respectively. There were no significant differences for sugars and starch intake in g/kg BW/day (p = .18). However, the sugars and starch intake per meal (g/kg BW/meal) in the CC group (average value 1.06, SD ± 0.56) was significantly (p < .001) lower than in the EGUS group (average value 1.85 SD ± 0.78). Forage intake below the recommended absolute minimum value as well as high sugars and starch intake were most commonly associated with EGUS in the present case series. An adequate diet formulation taking into account these main nutritional factors is therefore essential to avoid gastric problems in horses.
Malabsorption syndrome results in impaired nutrient digestion/absorption. Diagnostic tests in horses are focused on reduced carbohydrate absorption demonstrated by abnormal oral glucose tolerance test. However, to determine the definitive diagnosis a biopsy should be performed. The objective was to evaluate the progress of horses believed to be suffering from malabsorption syndrome without other infectious conditions, following institution of appropriate dietary advice. Medical records of 15 horses admitted to the equine hospital of Ghent University (2014–2017) were reviewed. All horses had received corticosteroid treatment and individual dietary advice. All horse owners were contacted in 2017 for a follow-up. Most horses (86 per cent) had tolerated the recommended diets well and gained weight. Owners noticed the greatest improvements at three and six months after starting the diet. Adequate dietary formulation may therefore be a valuable adjunct to medical treatment. However, it may take several months before increases in bodyweight and condition are seen.
The chemical characterization and protective role against ethanol-induced gastric ulcerated rats of a polysaccharide fraction from Bletilla striata (BSP) collected by ultrafiltration membrane approach were evaluated. This BSP faction was consisted of mannose and glucose at a molar ratio of 2.4:1 approximately, with a molecular weight of 146 KDa. FT-IR, NMR and XRD spectra indicated that BSP faction contained α-Man and β-Glc residues with low overall crystallinity. The polysaccharide exhibited significant scavenging activities of ABTS and FRAP, as well as non-toxicity against human gastric epithelial GES-1 cells. Oral administration with 100 mg/kg of BSP for 3 days continuously could significantly prevent the formation of ethanol-induced gastric mucosal lesion. It could also reduce the levels of pro-inflammatory cytokines, including TNF-α, IL-1β, IL-6, and IL-18, and MPO activity in gastric tissue. Additionally, the BSP faction exhibited antioxidant activity, increased the content of PEG2 as a defensive factor, and suppressed MAPK/NF-κB signaling pathway in gastric tissue. These results indicated that the gastroprotective activity of BSP faction could be attributed to the reduction of pro-inflammatory cytokines and oxidative stress and the inhibition of MAPK/NF-κB pathways. Our results provided substantial evidence that BSP could be a promising phytomedicine for gastric ulcer prevention.
A case of a mule foal with cerebellar Purkinje cell degeneration is described. A one-day-old mule foal was presented with lateral recumbency, obtunded mentation, poor metabolic status (general weakness, congestive mucous membranes, tachycardia, weak pulse, hypomotility and hypothermia) and cerebellar signs. After receiving medical treatment, the foal’s overall condition markedly improved but severe cerebellar ataxia and intention tremors were still present. Three weeks later, physical examination was normal but neurological signs had worsened and the foal was subjected to euthanasia. Postmortem findings revealed lesions consistent with corticocerebellar Purkinje cell degeneration. This is the first case report describing this condition in a mule.
Background
Equine gastric ulcer syndrome (EGUS) is common in adult horses, particularly those involved in performance disciplines. Currently, detection of EGUS by gastroscopy is the only reliable ante mortem method for definitive diagnosis; however it is unsuitable as a screening test because it is expensive, time consuming, and is not readily available to most veterinarians. Sucrose permeability testing represents a simple, economical alternative to gastroscopy for screening purposes, and the feasibility of this approach in the horse has been previously reported. The aim of this study was to determine the diagnostic accuracy of blood sucrose as a screening test for EGUS in a large group of adult horses with and without naturally occurring gastric disease. ResultsOne hundred and one adult horses with or without naturally occurring gastric ulceration were studied. The diagnostic accuracy of blood sucrose for diagnosis of gastric lesions (GL), glandular lesions (GDL), squamous lesions (SQL), and clinically significant lesions (CSL) at 45 and 90 min after administration of 1 g/kg of sucrose via nasogastric intubation was assessed using receiver operator characteristics (ROC) curves and calculating the area under the curve (AUC). For each lesion type, sucrose concentration in blood was compared to gastroscopy, as the gold standard, and sensitivities (Se) and specificities (Sp) were calculated across a range of sucrose concentrations. Ulcer grading was performed blindly by one observer; and the results were validated by comparing them with that of two other observers, and calculating the level of agreement. Cut-off values were selected manually to optimize Se. The prevalence of GL, GDL, SQL, and CSL was 83, 70, 53 and 58% respectively. At the selected cut-offs, Se ranged from 51 to 79% and Sp ranged from 43 to 72%, depending upon the lesion type and time of sampling. Conclusions
Blood sucrose is neither a sensitive or specific test for detecting EGUS in this population of adult horses with naturally occurring gastric ulceration. Further studies aimed at evaluating the performance characteristics of the test in different study populations are warranted. Given the limitations of endoscopy, due consideration should also be given to alternative methods for comparison of blood sucrose with a gold standard.
Reasons for performing the study: A previous study demonstrated that a dose effect between 1.6 and 4.0 mg/kg bwt of omeprazole per os s.i.d. is present in the treatment of equine gastric ulceration. In the same study, healing of glandular ulceration appeared inferior to healing of squamous ulceration. However, several limitations were recognised in that study and further investigation is warranted. Objectives: To further investigate the presence of a dose relationship in the treatment of gastric ulceration under conditions that may favour omeprazole efficacy such as administration prior to exercise and after a brief fast, and potential differences between the response of squamous and glandular ulceration to omeprazole therapy. Study design: A blinded, randomised, dose–response clinical trial. Methods: Sixty Thoroughbred racehorses with grade ≥2/4 squamous and/or glandular ulceration were identified by gastroscopy. Horses were randomly assigned to receive either 1.0, 2.0 or 4.0 mg/kg bwt of enteric coated omeprazole per os s.i.d. 1–4 h prior to exercise. Gastroscopy was repeated at approximately 28 days. Results: The lower doses studied (1.0 and 2.0 mg/kg bwt) were noninferior to the reference dose (4.0 mg/kg bwt) in the treatment of squamous ulceration. Healing was greater in squamous ulceration than glandular ulceration (86% vs. 14%; P<0.0001). Improvement in ulcer grade was more likely in squamous lesions than glandular lesions (96% vs. 34%; P<0.0001). Worsening of the glandular ulcer grade was observed in 36% of horses. Conclusions: The results of this study suggest that, under the conditions studied, where omeprazole is administered before exercise and following a brief fast, doses of omeprazole as low as 1 mg/kg bwt per os s.i.d. may be as effective as higher doses. The proportion of glandular ulceration that heals with 28 days of omeprazole therapy is less than that of squamous ulceration.
Gastric ulcers are common in horses. The purpose of this study was to test the effect of a commercially available supplement, SmartGut® Ultra pellets (SmGU) on gastric ulcer scores and gastric juice pH after omeprazole treatment in stall-confined horses. Eight Thoroughbred horses were studied in a 2-period, 2-treatment crossover design, where the SmGU (40 g, twice daily) was mixed in grain feed. Horses were stall-confined and treated with the supplement or control for 6 weeks, consisting of 2 weeks (Days 1–14) omeprazole treatment, 2 weeks (Days 14–28) following discontinuation of omeprazole treatment, one week (Days 28–35) alternating feed deprivation to induce or worsen existing ulcers and a one week (Days 35–42) recovery period. Gastroscopy was performed and gastric juice pH measured on Days 0, 14, 28, 35 and 42. Gastric ulcer lesion number (NGN) and severity (NGS) scores were assigned to each horse by an investigator (F.M.A.) masked to treatment. On Day 0 before treatment, mean NGN and NGS scores and gastric juice pH were not different (P>0.05) between treatment groups. By Day 14, mean NGN and NGS scores decreased (P<0.05) in both treatment groups. By Days 28 and 35, mean NGN score significantly increased in the untreated control horses but not the SmGU-treated horses. By Day 42, mean NGN and NGS scores were not different in either group and were significantly lower than Day 0. Mean gastric juice pH was higher in both groups on Day 14 as a result of omeprazole treatment when compared with other days. SmartGut® Ultra supplement added to the feed prevented the worsening of gastric ulcer number 2 weeks after omeprazole treatment, without altering the gastric juice pH. Supplementation with SmGU might aid in protection of the nonglandular stomach from recurrence of ulcers after omeprazole treatment in stall-confined horses undergoing intermittent feeding.
Interest in Equine Gastric Ulcer Syndrome (EGUS) has recently increased in part due to a growing awareness of the differences between squamous and glandular disease. The pathophysiology and epidemiology of squamous and glandular disease are different and recently it has been shown that the response of glandular gastric ulceration to monotherapy with omeprazole is poor. Given these differences it has been recommended that specific treatment guidelines be formulated for equine glandular disease and that adjunctive therapies be investigated. Along these lines it has been suggested that the addition of antimicrobials may enhance healing. The objective of this study was to investigate whether the addition of trimethoprim-sulphadimidine to omeprazole therapy would result in superior healing of naturally occurring equine glandular ulceration compared with omeprazole monotherapy.
Combination therapy of omeprazole plus trimethoprim-sulphadimidine could not be demonstrated to be superior to omeprazole monotherapy. Healing of the glandular mucosa was observed in 7/15 (47%; 95% CI 24 to 71%) and 3/13 (23%; 95% CI 7% to 50%) of horses in the TMPS and OMEP groups, respectively (OR = 1.8; 95% CI 0.32 to 10.0; p = 0.67). Improvement of the glandular mucosa was observed in 12/15 (80%; 95% CI 56 to 94%) and 9/13 (69%; 95% CI 42 to 89%) of horses in the TMPS and OMEP groups, respectively (OR = 2.9; 95% CI 0.6 to 15.0; p = 0.25).
The results of the present study do not support the addition of trimethoprim-sulphadimidine to therapeutic protocols for equine glandular ulceration. Several limitations were present in the study and the use of antimicrobials as an adjunctive treatment warrants further investigation. However, given the potential deleterious consequences associated with the indiscriminate use of antimicrobials, the inclusion of antimicrobials in treatment regimes for EGUS is not justified until their efficacy is further validated.
The objectives of this study were to evaluate the effects of two commercial feed supplements, Egusin 250® [E-250] and Egusin SLH® [E-SLH], on gastric ulcer scores, gastric fluid pH, and blood gas values in stall-confined horses undergoing feed-deprivation.
Nine Thoroughbred horses were used in a three-period crossover study. For the three treatment groups, sweet feed was mixed with E-250, E-SLH, or nothing (control group) and fed twice daily. Horses were treated for 21 days, then an additional 7 days while on an alternating feed-deprivation model to induce or worsen ulcers (period one). In periods two and three, horses (n=6) were treated for an additional 7 days after feed-deprivation. Gastroscopies were performed on day -1 (n=9), day 21 (n=9), day 28 (n=9) and day 35 (n=6). Gastric juice pH was measured and gastric ulcer scores were assigned. Venous blood gas values were also measured.
Gastric ulcers in control horses significantly decreased after 21 days, but there was no difference in ulcer scores when compared to the Egusin® treated horses. NG gastric ulcer scores significantly increased in E-250 and control horses on day 28 compared to day 21 as a result of intermittent feed-deprivation, but no treatment effect was observed. NG ulcer scores remained high in the control group but significantly decreased in the E-SLH- and E-250-treated horses by day 35. Gastric juice pH values were low and variable and no treatment effect was observed. Mean blood pCO2 values were significantly increased two hours after feeding in treated horses compared to controls, whereas mean blood TCO2 values increased in the 24 hour sample, but did not exceed 38 mmol/l.
The feed-deprivation model increased NG gastric ulcer severity in the horses. However, by day 35, Egusin® treated horses had less severe NG gastric ulcers compared to untreated control horses. After 35 days, Egusin® products tested here ameliorate the severity of gastric ulcers in stall-confined horses after feed stress.
The present study evaluated the effect of different levels of energy restriction on metabolic parameters in obese ponies. Relative weight changes, markers of lipid metabolism and oxidant/antioxidant balance were monitored. A total of eighteen obese (body condition score ≥ 7/9) Shetland ponies were studied over a 23·5-week trial, which was divided into three periods. The first period involved a 4-week adaptation period in which each animal was fed 100 % of their maintenance energy requirements needed to maintain a stable obese body weight (MERob). This was followed by a 16·5-week weight-loss period in which ponies were assigned to receive either 100 % (control group, CONTROL), 80 % (slow weight-loss (SLOW) group) or 60 % (rapid weight-loss (RAPID) group) of their MERob. During the 3-week end-phase period, all ponies were again fed 100 % of their MERob. Relative weight loss was higher in the RAPID group (P< 0·001) compared with the SLOW group. No linear relationship was found as a doubling of the percentage of energy restriction was accompanied by a tripling of the percentage of weight loss. Relative weight gain afterwards in the end-phase period was higher in the RAPID group (P< 0·001) compared with the SLOW and CONTROL groups. During the weight-loss period, TAG and NEFA concentrations were highest in the RAPID group, as were α-tocopherol and ferric-reducing ability of plasma concentrations. After 8 weeks of weight loss, the concentrations of advanced oxidation protein products were higher in the RAPID group compared with the SLOW and CONTROL groups (P< 0·001). In conclusion, the level of energy restriction influences the extent of changes in oxidant/antioxidant balance. Practically, more severe energy restriction regimens may be associated with a greater regain of weight after the restriction period.
The objective of this study was to evaluate the effect of a commercial feed supplement containing pectin-lecithin on squamous mucosa ulceration in horses exposed to an experimental ulceration model. Five mares were treated while five mares were controls for this crossover, blinded study. The mares were fed concentrates and hay and were stabled with a two-hour turn out per day for a period of four weeks. The pectin-lecithin complex was fed for the duration of the study on the treated group. At the end of a four-week period, all mares underwent a seven-day alternating feed deprivation (week 5). The study was repeated again after a four-week washout period. Gastroscopy was performed on days 1, 28 and 35 of the study and was digitally recorded. Independent evaluation of the recordings and scoring of the lesions using the Equine Gastric Ulcer Syndrome (EGUS), severity and number scores were performed by three experienced gastroscopists. The prevalence and severity of squamous ulcers significantly increased after intermittent feed deprivation (P<0.001). No significant effect of the treatment was observed (P>0.05). In this study, the addition of a commercially available pectin-lecithin complex to the feed of horses for five weeks did not prevent or minimise the risk for gastric ulceration of the squamous mucosa.
Sea buckthorn berries (Hippophae rhamnoides) are rich in vitamin C and E, carotenoids, flavonoids, fatty acids, plant sterols, lignans, and minerals. A feed supplement containing sea buckthorn berries might have efficacy in treatment and prevention of gastric ulcers in horses.
To test the efficacy of a commercially available formulation of sea buckthorn berries and pulp (SeaBuck SBT Gastro-Plus) for treatment and prevention of gastric ulcers in stall-confined horses.
Eight Thoroughbred and Thoroughbred-cross horses (3-10 years of age, 5 geldings and 3 mares, 380-600 kg body weight).
This study was a 2-period crossover in which all horses received no treatment (untreated controls; n = 8) and treatment (SeaBuckSBT Gastro-Plus, 4 ounces [35.6 g berries and pulp], twice daily; n = 8) mixed with a pelleted complete feed (18% crude fiber; 9% starch; 14% crude protein). Horses were treated for 4 weeks followed by a 1-week (d28-d35) alternating feed-deprivation period to induce or worsen existing ulcers. Gastroscopic examinations were performed on days 0, 28, and 35. Gastric juice pH was measured and gastric ulcer number and severity scores were assigned by a masked investigator.
Mean nonglandular gastric ulcer scores significantly (P < .05) increased in all horses after day 28, as a result of intermittent feed deprivation. Mean nonglandular gastric ulcer number (P = .84) and severity (P = .51) were not significantly different between SBT-treated and untreated control horses. However, mean glandular ulcer number (P = .02) and glandular ulcer severity (P = .02) were significantly lower in the SBT-treated horses compared with the untreated control at week 5.
SeaBuck SBT Gastro-Plus liquid fed to horses did not show efficacy in treatment or prevention of naturally occurring nonglandular ulcers in horses; however, glandular ulcer scores were significantly lower in SBT-treated horses after feed deprivation. Thus, SBT might have efficacy in prevention of glandular ulcers in horses housed in stalls and undergoing intermittent feeding.
The goal of this study was to gather more clinical information about the relationship between Helicobacter species and gastric ulceration in horses. Twenty seven privately owned patients were selected for the clinical study. All horses were gastroscopically examined and biopsies were taken from the glandular mucosa. Stomach biopsies were examined using a PCR assay specific for Helicobacter pylori and/or Helicobacter equorum. In addition, faecal samples from thirteen horses were examined using a PCR assay specific for H. equorum. Twenty five horses (25/27; 93%) had lesions in their stomach. Gastric biopsies from twenty two horses were examined using the H. pylori specific PCR and the ure gene was detected in three of them (3/22; 14%). H. equorum DNA was not found in the stomach of any of the ten horses examined. H. equorum was diagnosed in only one faecal sample from the thirteen horses examined (1/13; 8%) and that case was not associated with gastric pathology. This study shows the possibility of sporadic detection of the ure gene in the equine stomach affected by mucosal ulceration.
Gastric ulcers are common in horses and treatment of horses that cannot be administered oral medication can be problematic.
To evaluate the efficacy of esomeprazole sodium administered intravenously on gastric juice pH and gastric ulcer scores in horses.
Twelve adult female Quarter Horses.
Esomeprazole sodium (0.5 mg/kg IV) was administered once daily to 8 horses (treatment group) and saline (5 mL IV) was administered to 4 horses (control group) for 13 consecutive days. Gastroscopy was performed and gastric juice pH and gastric ulcer score were recorded before and 1 hour after the administration of esomeprazole sodium or saline on days 1 and 5, then on day 14, 23 hours after the 13th daily dose of esomeprazole sodium or saline.
When compared with values before treatment, gastric juice pH was higher in esomeprazole sodium-treated horses after treatment (4.25 ± 2.39 versus 6.43 ± 1.18; P = .002). Also, gastric juice pH was higher (P = .001) in esomeprazole sodium-treated horses compared with saline-treated control horses on day 5 and on day 14 values. Gastric ulcers were seen in 5/12 (43%) horses in the study.
Esomeprazole sodium shows promise for treatment of gastric ulcers in horses with signs of dysphagia, gastric reflux, or other conditions that restrict oral intake of the current Federal Drug Administration-approved omeprazole paste.
Zinc has been reported to exert a gastroprotective action against various experimental gastric lesions suggesting that this trace element is involved in the integrity of the gastric mucosa. Compounds containing zinc, such as polaprezinc, were developed in Japan and used as an antiulcer drugs in the treatment of human peptic ulcer disease. However, the precise mechanism of Zn(2+) containing compounds and their effects on mucosal integrity, gastroprotection and ulcer healing remain unclear. We have determined the efficacy of zinc hydroaspartate, a compound containing Zn(2+), in the mechanism of gastric secretion and ulcer healing in rats with chronic gastric ulcers induced by acetic acid (initial ulcer area = 28 mm(2)). Rats with gastric ulcers were randomized into two groups: A) with gastric fistulas (GF) and B) without gastric fistulas and received a daily treatment with zinc hydroaspartate (32-130 mg/kg-d i.g.) for 3, 7 and 14 days. At the termination of each treatment, the area of gastric ulcers were examined by planimetry, the gastric blood flow (GBF) at ulcer margin was assessed by laser Doppler flowmetry and H(2)-gas clearance methods. The venous blood was withdrawn for a measurement of plasma gastrin levels by radioimmunoassay (RIA). The concentration of Zn(2+) in the gastric juice and mucosa at the ulcer margin were determined by differential pulse anodic stripping voltammetry (DPASV) and flame atomic absorption spectrometry (FAAS) methods and the gastric biopsy samples were taken for histopathological assessment of the quality of ulcer healing. The ulcers healed gradually, with the ulcer area in the vehicle control rats being diminished by 15%, 48% and 78% upon ulcer induction at 3, 7 and 14 days, respectively. Zinc hydroaspartate dose-dependently inhibited the area of gastric ulcer, the dose reducing this area by 50% (ID(50)) being about 60 mg/kg-d. The mucosal concentration of Zn(2+) significantly was unchanged from the baseline immediately after ulcer induction (day 0) and at day 3 but then it rose significantly at day 7 after ulcer induction. Treatment with zinc hydroaspartate (65 mg/kg-d i.g.), which significantly raised the gastric luminal and mucosal levels of Zn(2+), significantly accelerated ulcer healing at day 7 upon ulcer induction. The GBF, which reached a significantly higher value at the ulcer margin than the ulcer bed, was significantly increased in rats treated with zinc hydroaspartate compared with vehicle-controls. The gastric acid output was significantly inhibited in GF rats with gastric ulcer at day 3 then restored at day 14 followed by a significant rise in the plasma gastrin levels. Treatment with zinc hydroaspartate significantly inhibited gastric secretion and also significantly raised the plasma gastrin level when compared to vehicle-control rats. We concluded that 1) trace micronutrients such as Zn(2+) could be successfully measured in the gastric juice and gastric mucosa during ulcer healing; 2) compounds chelating of Zn(2+) can exert a beneficial influence on the ulcer healing via Zn(2+) mediated increase in gastric microcirculation, antisecretory activity and gastrin release, which may enhance the cell proliferation and differentiation during ulcer healing, ultimately exerting a trophic action on the ulcerated gastric mucosa.
A role for Zn(2+) in accelerating wound healing is established, yet, the signaling pathways linking Zn(2+) to tissue repair are not well known. We show that in the human HaCaT keratinocytes extracellular Zn(2+) induces a metabotropic Ca(2+) response that is abolished by silencing the expression of the G-protein-coupled receptor GPR39, suggesting that this Zn(2+)-sensing receptor, ZnR, is mediating the response. Keratinocytic-ZnR signaling is highly selective for Zn(2+) and can be triggered by nanomolar concentrations of this ion. Interestingly, Zn(2+) was also released following cellular injury, as monitored by a specific non-permeable fluorescent Zn(2+) probe, ZnAF-2. Chelation of Zn(2+) and scavenging of ATP from conditioned medium, collected from injured epithelial cultures, was sufficient to eliminate the metabotropic Ca(2+) signaling. The signaling triggered by Zn(2+), via ZnR, or by ATP further activated MAP kinase and induced up-regulation of the sodium/proton exchanger NHE1 activity. Finally, activation of ZnR/GPR39 signaling or application of ATP enhanced keratinocytes scratch closure in an in vitro model. Thus our results indicate that extracellular Zn(2+), which is either applied or released following injury, activates ZnR/GPR39 to promote signaling leading to epithelial repair.
The use of anti-ulcer medication in the neonatal intensive care unit (ICU) is common due to the concern for development of catastrophic gastric ulcer disease. In man, however, the use of acid-suppressive medication has been shown in some studies to be a substantial risk factor for the development of Clostridium difficile-associated diarrhoea (CDAD), bacteraemia and neonatal sepsis. The purpose of the study reported herein is to evaluate the influence of anti-ulcer medications on the development of diarrhoea in the neonatal foal. The use of anti-ulcer medication does not alter the incidence of diarrhoea in foals treated in an ICU. The records of 1710 foals from 6 different equine hospitals were examined and the use of anti-ulcer drugs was recorded. The presence of in-hospital acquired diarrhoea, CDAD, Clostridium perfringens-associated diarrhoea, neonatal sepsis and salmonellosis were documented. In addition, the presence of gastric ulceration, duration of hospital stay and short-term outcome were examined. The use of anti-ulcer medications increased the odds of in-hospital diarrhoea by 2.0 (95% CI 1.4-2.9; P < 0.0001), relative to the use of no anti-ulcer medication. There was no significant association of anti-ulcer medication with CDAD (P = 0.3189) (OR 2.0; 95% CI 0.4-9.5). Further, results indicated that decreased prevalence of gastric ulceration was not associated with use of anti-ulcer drugs among foals in the study for which these data were known (P = 0.5522). Use of anti-ulcer drugs increases the odds of developing diarrhoea, and may not reduce the incidence of gastric ulceration in hospitalised equine neonates. The use of anti-ulcer drugs in neonatal foals being treated in a hospital setting should be carefully evaluated on an individual basis to determine if such use is warranted.
Equine gastric ulcer syndrome is common in domesticated horses, especially those performing in athletic endeavours. However, the prevalence of equine gastric ulcer syndrome in feral populations of horses is not documented. This study investigated the prevalence and severity of squamous and glandular gastric ulceration in an abattoir population of horses in the UK. Both squamous and glandular ulceration were more prevalent in domesticated horses when compared to the feral horses studied.
The aim of this study was to explore the efficacy of multi-layered haynets and multiple presentation of haynets to increase time spent on feed intake behaviour at night (13. h observation). For preliminary assessment two horses performing the oral stereotypy of crib-biting were included. Six horses received the same amount of forage during a 22-day, cross-over study where treatment consisted of either forage presentation in a single small-holed haynet (SH) or the forage was divided between 3 haynet combinations hung up simultaneously. = multiple haynets (MH). The three haynets presented simultaneously consisted of (a) MH single haynet (same as SH), (b) MH double layered haynet and (c) MH triple layered haynet. Multiple haynets were presented, in random order, on three sides of the stable. Horses were filmed using a video surveillance camera with infrared light source. Behaviour was observed for at least 4 nights per treatment (one night during the acclimatisation period [nights 2-4] and three nights during the end period [nights 7-11]). The observation period commenced at 16.30-17.00. h (point of haynets being presented) until 06.00. h (all horses) or 9.00. h (2 crib-biting horses) the next morning. Data were analysed for normal distribution and ANOVA between haynets, paired t-tests between treatments and Pearson correlation were used (SPSS. 17.00; 2012). There was a significant effect of type of haynet (p<. 0.001) on intake time per kg forage (min/kg for SH: 39; MH all (data combined): 51; MH Single: 27; MH Double: 67; MH Triple: 78; overall sem. 8.9). The overall time budget (minutes per observation hour) showed a significant difference between treatments for eating from haynet, standing still, locomotion and drinking. Horses finished eating from SH haynets at around 01.38. am (±1.05. h s.d.), were last observed at the double net at 03.00. am and at the triple net at 05.12. am (±1.25. h s.d.). Based on these results, providing 6. kg of forage in 3 double-layered, 2.5. cm haynets spread around the stable could potentially lead to an increased feeding time of 2. h per night compared to a single 2.5. cm holed haynet containing 6. kg. From the continuous observation data a clear visual difference in crib-biting pattern and therefore motivation to perform crib-biting emerged between the two stereotypic horses.
Reasons for performing study
Gastric ulceration is an important cause of morbidity in horses. Currently, gastroscopy is the only reliable antemortem method for definitive diagnosis; however, it is unsuitable as a screening test because it is expensive, invasive and time‐consuming. Sucrose permeability testing represents a simple, economical, non‐invasive alternative to gastroscopy for screening purposes, and the feasibility of this approach in the horse has been reported [1].
Objectives
To determine the diagnostic accuracy of blood sucrose as a screening test for gastric ulceration.
Study design
Cross‐sectional design.
Methods
One hundred and one adult horses with and without naturally occurring gastric ulcers were studied. The diagnostic accuracy of blood sucrose for detection of gastric ulcers at 45 and 90 min after administration of 1 g/kg bwt of sucrose via nasogastric intubation was assessed with ROC curves and calculating the area under the curve ( AUC ). Sucrose concentration in blood was compared with gastroscopy as the gold standard; and sensitivities ( S e) and specificities (Sp) were calculated across a range of sucrose concentrations. Cut‐off values were selected manually to optimise sensitivity.
Results
The prevalence of gastric ulcers was 83%. The AUC ± 95% CI for blood sucrose concentration when used to distinguish between horses with and without gastric ulcers at 45 and 90 min was 0.592 (0.441–0.744) and 0.615 (0.469–0.761) respectively. Sucrose concentrations of 4.70 μmol/l at 45 min; and 4.57 μmol/l at 90 min were selected as optimal cut‐offs. Using these cut‐offs, S e ranged from 64.4% to 77%; and Sp ranged from 42.9% to 50%.
Conclusions
Blood sucrose is neither a sensitive nor specific test for detecting gastric ulcers in adult horses with naturally occurring ulcers.
Acknowledgements
We thank S andy L ove, S atu S ankari, A nna‐ M aija V irtala, N oah C ohen, A llen R ousell, K aisa A altonen, A nne S jöholm and J ouni J unnila.
Ethical animal research: The study protocol was approved by the National Animal Experiment Board of F inland (Eläinkoelautakunta ELLA ). For client‐owned animals, the informed consent of the owner was obtained. Source of funding: This study was funded by the Faculty of Veterinary Medicine, University of Helsinki, F inland. Competing interests: None declared.
Reasons for performing the studyA previous study demonstrated that a dose effect between 1.6 and 4.0 mg/kg bwt of omeprazole per os s.i.d. is present in the treatment of equine gastric ulceration. In the same study, healing of glandular ulceration appeared inferior to healing of squamous ulceration. However, several limitations were recognised in that study and further investigation is warranted.Objectives
To further investigate the presence of a dose relationship in the treatment of gastric ulceration under conditions that may favour omeprazole efficacy such as administration prior to exercise and after a brief fast, and potential differences between the response of squamous and glandular ulceration to omeprazole therapy.Study designA blinded, randomised, dose-response clinical trial.Methods
Sixty Thoroughbred racehorses with grade ≥2/4 squamous and/or glandular ulceration were identified by gastroscopy. Horses were randomly assigned to receive either 1.0, 2.0 or 4.0 mg/kg bwt of enteric coated omeprazole per os s.i.d. 1-4 h prior to exercise. Gastroscopy was repeated at approximately 28 days.ResultsThe lower doses studied (1.0 and 2.0 mg/kg bwt) were noninferior to the reference dose (4.0 mg/kg bwt) in the treatment of squamous ulceration. Healing was greater in squamous ulceration than glandular ulceration (86% vs. 14%; P<0.0001). Improvement in ulcer grade was more likely in squamous lesions than glandular lesions (96% vs. 34%; P<0.0001). Worsening of the glandular ulcer grade was observed in 36% of horses.Conclusions
The results of this study suggest that, under the conditions studied, where omeprazole is administered before exercise and following a brief fast, doses of omeprazole as low as 1 mg/kg bwt per os s.i.d. may be as effective as higher doses. The proportion of glandular ulceration that heals with 28 days of omeprazole therapy is less than that of squamous ulceration.
It has recently been highlighted that significant differences in prevalence, risk factors and the response to treatment exist between ulceration of the squamous gastric mucosa and ulceration of the glandular gastric mucosa in the horse. In the first article in the series, the term equine squamous gastric ulcer syndrome (ESGUS) was used to describe disease of the squamous gastric mucosa with clinical signs and diagnosis discussed. The purpose of this article is to review the pathophysiology, risk factors, prevalence, treatment and prevention of ESGUS.
It has recently been highlighted that significant differences exist between ulceration of the squamous gastric mucosa and ulceration of the glandular gastric mucosa in the horse. The first article in this series discussed terminology, clinical signs and diagnosis and the second reviewed ulceration of the squamous gastric mucosa in detail. The purpose of this article, the third and last in the series, is to review the pathophysiology, risk factors, prevalence, treatment and prevention of ulceration of the glandular gastric mucosa.
To date, prevention of Equine Gastric Ulcer Syndrome (EGUS) has relied upon management changes or pharmaceutical agents. The identification of an alternative means of prevention would be useful. Therefore, the objective of this study was to evaluate the combination of Apolectol®, a live yeast (Saccharomyces cerevisiae (CNCM I-1077)) and magnesium hydroxide for the prevention of development of, or exacerbation of existing, EGUS in Thoroughbred racehorses. Twenty-four Thoroughbred racehorses without significant gastric ulceration (grade ≤ 2/4) were identified on gastroscopy. Treated horses received 95 g Apolectol®, 2 g S. cerevisiae and 20 g magnesium hydroxide 1 – 4 hours prior to exercise. Control horses received 95 g of a feed pellet as a placebo. Gastroscopy was repeated at 24–27 days. There was no change in squamous (p=0.45) or glandular (p=1.0) ulcer grade over time in horses in the treatment group. In the placebo group ulcer grade increased in both the squamous (p=0.04) and glandular (p=0.19) mucosa, but only reached significance in the squamous mucosa group. Worsening of the ulcer grade was more likely in the placebo group in the glandular (p=0.04), but not squamous (p=0.10) mucosa. The combination studied may be an effective prophylactic against EGUS development or exacerbation.
Equine gastric ulcer syndrome (EGUS) is a common condition in the horse. A series of recent articles highlighting differences in healing of squamous and glandular ulceration have reinvigorated interest in the condition. The purpose of this series of articles is to review the current thinking on EGUS with particular emphasis on the differences between diseases of the squamous and glandular mucosae. This article, the first will review the terminology, clinical signs and diagnosis of EGUS in the horse.
Reasons for performing the study
A recent study suggested that the duration of acid suppression achieved with once‐daily administration of omeprazole is as short as 12 h and that administration of omeprazole prior to exercise may be superior compared with administration at other times of the day in the treatment of equine gastric ulcer syndrome ( EGUS ).
Objectives
The primary objective of the study was to investigate whether the administration of omeprazole prior to exercise resulted in better healing of EGUS compared with administration post exercise. A secondary objective was to investigate the differences between the response of squamous and glandular EGUS to omeprazole therapy.
Study design
A randomised, blinded, clinical trial.
Methods
Twenty‐five horses with grade ≥2/4 squamous EGUS were identified by gastroscopy. The glandular mucosa was also scored. Horses were randomly assigned to receive 4.0 mg/kg bwt of omeprazole per os once daily either 1–4 h prior to high‐intensity exercise ( PRE group; 13 horses) or 1–4 h after exercise ( POST group; 12 horses). Gastroscopy was repeated at approximately 25 days.
Results
No differences were observed between the pre‐ and post exercise treatment groups. Overall, healing was observed in 80% of squamous ulcers vs. 21% of glandular ulcers (P = 0.0002), and improvement was seen in 96% of squamous ulcers vs. 53% of glandular ulcers (P = 0.001). Worsening was observed in the glandular mucosa of 13% of horses.
Conclusions
The results of this study suggest that the timing of administration does not affect ulcer healing. Furthermore, the study demonstrates that the response of glandular ulceration to omeprazole therapy is inferior to that of the squamous mucosa.
Studies on omeprazole have reported that doses as low as 0.7 mg/kg PO are potent suppressors of acid production. Yet, to date, no studies have compared treatment efficacy of different doses in clinical cases of equine gastric ulceration. Furthermore, no studies have been performed to compare the healing response of the squamous and glandular mucosa to acid suppression therapy.
To compare: 1) The efficacy of 2 doses of omeprazole in the treatment of primary squamous and glandular gastric ulceration and 2) the healing response of primary squamous and glandular gastric ulceration to acid suppression therapy.
A blinded, randomised, dose-response clinical trial.
Twenty Thoroughbred racehorses with grade ≥ 2/4 glandular ulceration were identified on gastroscopy. Seventeen horses also had grade ≥ 2/4 squamous ulceration. Horses were randomly assigned to one of 2 groups. Horses received either 2.0 g (high dose - 4.0 mg/kg) or 0.8 g (low dose - 1.6 mg/kg) of oral omeprazole per os once daily. Gastroscopy was repeated at 28 - 35 days.
A dose response was present with healing more likely to occur in the high dose (4.0 mg/kg) group than the low dose (1.6 mg/kg) group, for both squamous (p = 0.003) and glandular (p<0.0001) ulceration. Data analysis did not support our hypothesis that the lower dose would have similar effects (i.e. be non-inferior) to the higher dose when considering ulcer healing and ulcer improvement. Improvement was more likely with the high dose for the squamous (p = 0.03) but not glandular (p = 0.13) mucosa. The percentage of glandular ulcers that improved was less than squamous ulcers (p = 0.008).
The results suggest that a dose response exists for the treatment of both squamous and glandular ulcers. Improvement of glandular ulcers was not as complete as observed with squamous ulcers and current EGUS treatment recommendations may not be appropriate for glandular disease.
It was hypothesized that horses exhibiting crib-biting (CB) have a greater degree of gastric mucosal damage and higher serum gastrin response to concentrate feeding than non-crib-biting (NCB) horses. Eighteen mature horses, 9 CB and 9 NCB, were used to determine prevalence and severity of gastric mucosal damage and effect of concentrate feeding on circulating gastrin. Horses were maintained on pasture with free access to hay and fed a pelleted concentrate diet twice daily. Number of crib-bites and duration of cribbing bouts were recorded in a 24-hour period. Endoscopic examinations (EE) of the squamous mucosa were performed and gastric fluid sampled after 24 to 28 hour feed removal. Following EE, horses were returned to pasture for 72 hours. Blood was collected following 12-hour feed removal (0 minutes), and at 60 and 120 minutes after consuming 1 kg of concentrate. Mean number of crib bites in 24 hours was 1,558 ± 303 with CB peaking prior to and during the afternoon feeding (3:30 PM, P < .05). There were no differences in the number or severity of ulcers, prevalence of hyperkeratosis, or baseline gastric pH between CB and NCB. Serum gastrin concentration at 60 and 120 minutes was greater (P < .05) and tended to be greater (P < .06), respectively, in CB than in NCB horses following feeding of concentrate. Crib-biting behavior in horses maintained on pasture was not associated with gastric mucosal damage; however, consumption of concentrate feed resulted in greater serum gastrin concentration in CB horses.
Only little is known about behaviour and stress responses in horses with gastric ulceration, despite the high prevalence of this condition. Our objectives in the present study was to (i) describe the severity of gastric ulceration in horses, housed under relatively standardised conditions, and (ii) to investigate whether horses with severe glandular gastric ulceration have increased baseline and response concentration of stress hormones and behave differently than control horses. We investigated stomachs of 96 horses at one stud, and compared an ulcer group (n = 30; with severe lesions in the glandular mucosa) to paired controls (n = 30; free from gastric ulcers). Baseline and response concentrations of faecal cortisol metabolites (FCM), heart rate and behaviour were measured in a novel object test (NOT, Day 1) and behaviour during postponed feeding (PF, Day 2). Glandular lesions occurred in 55.2% and non-glandular lesions in 40.6% of the horses. The amount of starch in the feed (P = 0.006) and paternal stallion (P = 0.031) influenced ulceration in the non-glandular region only; it should be noted that our study does not allow for separating hereditary from environmental influences, as offspring may be e.g. trained differently dependent on breeding line. Ulcer horses pawed more (P < 0.001) and ate quicker (P = 0.050) during PF. Although displayed by ulcers horses only during PF, we failed to demonstrate a significant association between glandular gastric ulceration and crib-biting/weaving; the total number of horses with these types of abnormal behaviour was low (n = 5). Behaviour and heart rate did not differ between groups in the NOT. Baseline concentration of FCM was similar (P = 0.79), however, ulcer horses responded stronger to novelty than controls (26% higher FCM; P = 0.018). We conclude that the prevalence of gastric ulcers was high, and our results suggest different factors affecting ulceration in the glandular versus the non-glandular region of the horse stomach. Obvious external signs (e.g. poor body condition) identifying ulcer horses were absent. Horses with severe glandular ulcers had a higher stress hormone response to novelty, thus they were more stress sensitive. Consequently, management evoking stress in horses should be reduced to dampen the development of glandular ulceration, or to protect horses with this condition.
The goal of this study was to determine the prevalence of gastric ulcers in horses with acute abdominal crisis (colic) and to examine the temporal effect of hospitalization on ulcer development in equine patients treated for colic. In addition, other factors that may be associated with gastric ulceration were also explored. The study design was a prospective original study incorporating 169 horses that presented to the George D. Widener Hospital for examination. One hundred and twelve horses presenting with the chief complaint of colic were included in the study group, and 57 horses that presented for non-colic or nonemergency complaints were evaluated and included as case controls. Gastroscopy was performed on equine patients presenting with the chief complaint of colic or horses presenting for reasons other than colic (control); mucosal changes were scored 0 to 3. Additionally, horses presenting for colic were gastroscopically evaluated twice during a 5-day period. Medical records were reviewed for history, clinical findings, laboratory results, and treatment. Seventy-six of 112 horses presenting with the chief complaint of colic had gastric ulceration compared with 41 of 57 horses in the control group. There was a significant association between age of the patient and chief complaint (ie, colic vs control) and between breed and chief complaint. There was no association between gastric ulcer score and chief complaint (colic vs control). Thirty-eight of the 112 horses presenting with colic deteriorated in ulcer score while hospitalized. Using a Pearson chi-squared test, there was no statistically significant association between gastric ulceration with age, breed, or sex. Horses with gastric ulceration in the colic group had lower packed cell volumes compared with horses presenting with colic without gastric ulcers, and this was statistically significant (P < .001). The high incidence of gastric ulceration in the study and control groups supports the reports of other investigators that gastric ulcers in horses, no matter the presenting complaint, are widespread. There was a significant association between breed and chief complaint (P = .005); however, breed and outcome of gastric ulceration were not related (Thoroughbreds were the least likely breed to present for colic). Although a trend in increasing gastric ulceration was seen in hospitalized colic patients, it was not statistically significant. This suggests that horses that are hospitalized may be at increased risk for developing gastric ulcers because of stress, feed deprivation, and administration of treatment. Thus, horses that present for colic should be gastroscopically evaluated if clinical signs raise the index of suspicion for gastric ulceration.
Thoroughbred and Standardbred horses in race training were selected at random and examined for gastric ulcers. The mucosa of the stomach was examined by endoscopy and was scored for ulcers on a scale of 0 (no ulcers, normal mucosa) to 3 (severe ulceration with at least five deep lesions). A total of 79 horses were examined; 37 of these horses had one to four follow-up examinations, and 42 horses had only an initial gastroscopic examination. On the first examination, 33 of 79 (42%) horses had normal mucosa (ulcer score=0), and 22 of 79 (28%) had ulcers with an ulcer score of 2 or greater. Seven horses (9%) had severe gastric ulceration (ulcer score=3). The average ulcer score for all 79 horses on initial examination was 1.1 and 1.2 for the 37 horses with follow-up gastroscopic examination. Males (including male castrates) had slightly higher ulcer scores (1.2) than females (1.0), and 2-year-old horses had lower ulcer scores (0.7) than horses older than 3 years (1.4), but these differences did not reach statistical significance. Each of these average scores was significantly (P < .05) greater than zero. For the 37 horses with follow-up examinations, the males had higher scores (1.6) than females (0.7), and 2-year-old horses had higher ulcer scores (1.0) than 3-year-old horses (0.7) and lower ulcer scores than horses older than 3 (1.8), which were statistically significant. Follow-up examinations revealed ulcer scores ranging from 0 to 3; 23 of 37 (63%) horses had an ulcer score of 2 or greater, and 4 of 37 (12%) horses had severe ulcer disease. Average ulcer scores were significantly higher at subsequent examinations than at the initial examination. Risk of gastric ulceration increases with the length of time horses are in race training.
A necropsy was performed on over 500 horses from a Texas abattoir for the presence of gastric and colonic ulceration. A first group of 365 horses from a variety of sources was examined, and 55% were found to have gastric ulcers, while 44% exhibited colonic ulcers. A second group of 180 performance horses was also examined, and 87% were shown to have gastric ulcers, while 63% exhibited colonic ulcers. The second study included a correlated guaiac-based fecal occult blood test (gFOBT), which was shown to have high specificity but a fairly low sensitivity resulting in several false negatives.
The regulation of gastric secretion is of crucial impor-tance to the equilibrium of the gastroenteric system. Despite the large number of factors involved in the causes of peptic illnesses, pH ¼ 4 is considered the threshold between physiologic and deleterious effects of stomach acid secretion. With the aim of maintaining pH greater than 4, proton-pump inhibitors, such as eso-meprazole magnesium (NEXIUM), have shown excel-lent results in the control of acid secretion. Aimed at examining the action of this drug in the control of pH levels of gastric secretion in thoroughbreds, a single dose of 40 or 80 mg of esomeprazole magnesium was administered daily, and pH was determined serially for 5 consecutive days. The results obtained corroborated the efficacy of esomeprazole magnesium in the control of gastric pH at both doses tested, with 100% of the mean pH being greater than 5. Moreover, no statistical difference was noted between the two doses tested.
A variety of inflammatory gastrointestinal diseases are associated with altered zinc metabolism or deficiency. Acute and chronic diarrheal disorders may cause deficiency because of increased losses, altered immunity or decreased absorption. When the small intestinal barrier is altered by inflammation, zinc supplementation may be beneficial not only in correcting the deficiency but also because it improves the small bowel mucosal capacity of absorbing water and electrolytes. Zinc is known to have antioxidant properties being a membrane stabilizer, scavenging reactive oxygen metabolites and regulating cytokine synthesis through the activation of transcription factors and this has relevant potential in inflammatory bowel diseases. Moreover, the element stimulates tissue healing and repair in experimental ulcers directly through promoting cell proliferation, protein synthesis and growth factors production and scavenging free radicals. Interest is growing in supplementary therapies with elements and vitamins but current research suggests great caution and to balance the benefits and dangers of uncontrolled administration, since zinc can also stimulate an increased acute phase response and this can exacerbate chronic relapsing diseases. Zinc plays an important role in inflammation. The metal has catalytic, co-catalytic and structural functions in many zinc-dependent enzymes of the body through the regulation of gene expression. Moreover, the involvement of zinc finger proteins in the genetic expression of growth factors has been established. Zinc stabilizes cellular membranes especially interacting at the SH levels and preventing depolarization of phospholipids. The effects on cellular immunity and especially on the activity of serum thymulin and natural killer cells, T-lymphocyte proliferation and interleukin-2 production are also well-known. A growing body of evidence suggests a role for zinc in antioxidant defence systems. The metal has only one stable oxidation state (divalent) and is not affected by free radicals or oxidative stress. It may act as a scavenger of radical products through the synthesis of enzymes such as superoxide dismutase (SOD) and metallothionein (MT) or it may affect cytokine-activated transcription factors. J. Trace Elem. Exp. Med. 13:33–39, 2000. © 2000 Wiley-Liss, Inc.
†California Veterinary Diagnostic Laboratory Service, California 95616, California 91024, USA.
Although gastric ulcers have been identified relatively frequently in racing Thoroughbreds, there have been no large scale studies to determine their effect on health and performance. Two hundred and two Thoroughbred horses in active race training were selected by the attending veterinarians for gastro-endoscopic examination. Images of the stomach mucosa were stored in a digitised format for subsequent evaluation. The number of ulcers and a score of severity were determined. Gastric ulceration of the squamous mucosa was identified in 82% of horses. Seventy-three (39%) horses displayed clinical signs consistent with gastric ulceration. Increasing Furr and Murray Score was associated with poor hair coat (P = 0.03), colic (P = 0.03), and increasing serum creatinine concentration (P = 0.029). There were no associations between haematology and serum biochemistry values (other than serum alkaline phosphatase concentration and serum creatinine concentration) and gastric ulceration. Our study confirmed the relatively high incidence of gastric ulceration in Thoroughbred horses involved in active race training. Gastric ulceration is a potential, but rare, cause of overt colic, but may produce more subtle detrimental effects on a horse's condition. It is concluded that the diagnosis of gastric ulceration should be based on an endoscopic examination of the stomach, although future studies are required to elucidate further the aetiology and clinical significance of gastric ulceration.
Equine gastric ulceration syndrome (EGUS) is commonly recognised in Thoroughbred racehorses. Although EGUS has previously been associated with reduced athletic performance, no objective studies have been reported.
This case report describes 4 racehorses referred for investigation of poor athletic performance where EGUS was the only abnormal finding during a thorough investigation of all body systems. All horses showed considerable improvement in performance following treatment with omeprazole. Therefore, this is the first report in which evidence is presented suggesting a direct link between EGUS and decreased performance, other causes of poor performance having been excluded.
Zinc is an important element in wound healing. Zinc compounds hasten the healing of gastric ulcers, by an unknown mechanism(s). We studied the effect of the induction of zinc deficiency on gastric ulcer healing. Rats were given a control or zinc-deficient diet for six weeks and then subjected to the induction of acetic acid-induced chronic gastric ulcers. Four days later, zinc-deficient rats were divided into two groups. In the first group, the zinc-deficient diet was continued. In the second group, the diet was changed to the control diet. Zinc-deficient rats had a mean serum zinc concentration approximately 70% of that in controls. Zinc deficiency did not affect the formation of gastric ulcers; however, it reduced cell proliferation by day 4 and delayed ulcer healing. Zinc supplementation brought zinc to control levels within a week, but failed to reverse the delay in ulcer healing. We conclude that zinc is crucial for healing of gastric ulcers, especially at the early stage.
The use of anti-ulcer medication in the neonatal intensive care unit (ICU) is common due to the concern for development of catastrophic gastric ulcerdisease. In man, however, the use of acid-suppressive medication has been shown in some studies to be a substantial riskfactorfor the development of Clostridium difficile-associated diarrhoea (CDAD), bacteraemia and neonatal sepsis.
The purpose of the study reported herein is to evaluate the influence of anti-ulcer medications on the development of diarrhoea in the neonatalfoal.
The use of anti-ulcer medication does not alter the incidence of diarrhoea in foals treated in an ICU.
The records of 1710 foals from 6 different equine hospitals were examined and the use of anti-ulcer drugs was recorded. The presence of in-hospital acquired diarrhoea, CDAD, Clostridium perfringens-associated diarrhoea, neonatal sepsis and salmonellosis were documented. In addition, the presence of gastric ulceration, duration of hospital stay and short-term outcome were examined.
The use of anti-ulcer medications increased the odds of in-hospital diarrhoea by 2.0 (95% CI 1.4-2.9; P < 0.0001), relative to the use of no anti-ulcer medication. There was no significant association of anti-ulcer medication with CDAD (P = 0.3189) (OR 2.0; 95% CI 0.4-9.5). Further, results indicated that decreased prevalence of gastric ulceration was not associated with use of anti-ulcer drugs among foals in the study for which these data were known (P = 0.5522).
Use of anti-ulcer drugs increases the odds of developing diarrhoea, and may not reduce the incidence of gastric ulceration in hospitalised equine neonates.
The use of anti-ulcer drugs in neonatal foals being treated in a hospital setting should be carefully evaluated on an individual basis to determine if such use is warranted.
Gastroscopic examinations were performed in 62 Thoroughbred broodmares (33 pregnant, 29 non-pregnant) at one breeding farm to investigate the prevalence of gastric ulceration. Age, pregnancy status, race earnings, last race start, herd size, medical history, number of live foals, breeding years, feed type and number of feedings were recorded, plus coat condition and body condition score were determined. Twenty-one mares were re-evaluated after foaling, and the foaling date, foal weight at birth and placenta weight were recorded.The overall prevalence of gastric ulcers was 70.9%, with a median ulcer score of 3.0 (range: 2–5). Most ulcers were present on the squamous portion of the stomach, while two mares had glandular ulcers. There were no differences in the presence, location and severity of gastric ulcers between pregnant and non-pregnant mares. Furthermore, there were no significant associations between the variables measured and the presence of gastric ulceration. The prevalence of gastric ulceration in this specific population of horses was higher than expected and further investigation is warranted to determine the factors that contributed to this finding.
Seventy-two lactic acid producing bacterial isolates (excluding streptococci) were cultured from the gastrointestinal tract of six horses. Two of the horses were orally dosed with raftilose to induce lactic acidosis and laminitis while the remaining four were maintained on a roughage diet. Near complete 16S rDNA was amplified by PCR from the genomic DNA of each isolate. Following RFLP analysis with the restriction enzymes MboI, HhaI and HinfI, the PCR products from the IS isolates that produced L- and/or D-lactate were subsequently cloned and sequenced. DNA sequence analysis indicated that the majority of the isolates were closely related to species within the genus Lactobacillus, including Lactobacillus salivarius, Lactobacillus mucosae and Lactobacillus delbrueckii. Four isolates were closely related to Mitsuokella jalaludinii. Lactic acid producing bacteria (LAB) from the equine gastrointestinal tract was dominated by representatives from the genus Lactobacillus, but also included D-lactate-producing bacteria closely related to M. jalaludinii. Identification and characterization of LAB from the equine gastrointestinal tract should contribute to our understanding and management of fermentative acidosis, ulceration of the stomach and laminitis. (c) 2005 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved.
The prevalence (up to 93% in Thoroughbred racehorses) and severity of equine gastric ulceration syndrome (EGUS) has been associated with type of training and differing management practices. However, there have been few studies to confirm these findings in nonracehorses in Europe.
To investigate the prevalence of EGUS in a population of Danish horses, during winter when the horses had been housed and fed for at least 8 weeks and to analyse the influence of feed, work level and environment on the risk of EGUS of > or = grade 2 in severity.
A total of 201 horses, not in active race-training, were evaluated, representing 23 different stables from all 5 regions within Denmark. All horses were considered to be healthy and not on medical treatment for EGUS. Endoscopically observed ulcer lesion scores were based on the number present (0-4) and severity (0-5). Univariate and multivariable mixed effects logistic regression models were developed using EGUS score as the dependent variable. An ulceration severity score of > or = 2 was regarded as being clinically significant. Separate models were developed for horses with ulcers in either the glandular or nonglandular regions of the stomach graded > or = 2 (EGUS > or = 2) and for those horses that had nonglandular ulcers graded > or = 2 (NG > or = 2).
In this population, 53% (107/201) of horses were graded as having EGUS > or = 2 with 95 (47%) horses having NG > or = 2. Three variables were significantly (P<0.05) associated with EGUS > or = 2: straw being the only forage available; exceeding 2 g/kg bwt of starch intake/day or >1 g/kg bwt/meal; and water not being available in the turn out paddock. Risk of NG > or = 2 significantly increased when straw was the only forage available, 1 g/kg bwt of starch/meal was exceeded, water was not available in the turnout paddock and the interval between forage feeding was >6 h.
This study has confirmed that components of the diet, readily modifiable, may have an important impact on the risk of EGUS in the nonracehorse. Differences in the multivariable models produced for all ulcers and nonglandular ulcers support differences in the aetiology of ulcers in different locations of the stomach.