Efficacy of omeprazole paste for prevention of recurrence of gastric ulcers in horses in race training

OBJECTIVE: To determine whether omeprazole oral paste administered at a dosage of 0.5 or 1 mg/kg (0.23 or 0.45 mg/lb), PO, every 24 hours would effectively prevent the recurrence of gastric ulcers in horses in race training. DESIGN: Prospective study. ANIMALS: 135 horses. PROCEDURES: Horses with gastric ulcers were treated with omeprazole at a dosage of 4 mg/kg (1.8 mg/lb), PO, every 24 hours for 28 days. Horses in the dose selection portion of the study were sham dose treated or received 0.5 or 1 mg of omeprazole/kg, PO, every 24 hours for an additional 28 days. Horses in the dose confirmation portion of the study were sham dose treated or received 1 mg of omeprazole/kg, PO, every 24 hours for an additional 28 days. Gastric ulcers were scored before and after the preventive phase of the study (day 28 to day 56) via gastroscopy, and ulcer scores were compared. RESULTS: Sham-dose-treated horses and horses receiving 0.5 mg of omeprazole/kg had significantly higher ulcer scores than did horses receiving 1 mg of omeprazole/kg. There was a significant difference between the proportion of horses receiving 1 mg of omeprazole/kg (38/48 179%]) that remained ulcer free and the proportion of sham-dose-treated horses (7/44 [16%]) that remained ulcer free. CONCLUSIONS AND CLINICAL RELEVANCE: Omeprazole oral paste administered at a dosage of 1 mg/kg, PO, every 24 hours for 28 days was effective for prevention of recurrence of gastric ulcers in horses in race training.     

Comparison of paste and suspension formulations of omeprazole in the healing of gastric ulcers in racehorses in active training

OBJECTIVE: To compare effects of a commercially available omeprazole paste and a compounded omeprazole suspension on healing of gastric ulcers in Thoroughbred racehorses in active training. DESIGN: Randomized controlled trial. ANIMALS: 32 horses with gastric ulcers. PROCEDURE: Horses were assigned to 2 groups on the basis of endoscopic gastric ulcer severity. Group-1 horses were treated with omeprazole suspension for 30 days and with omeprazole paste for an additional 30 days. Group-2 horses were treated with omeprazole paste for 30 days and omeprazole suspension for an additional 30 days. Serum omeprazole concentrations were measured in 4 additional healthy horses after administration of a single dose of each formulation. In all instances, omeprazole was administered at a dose of 4 mg/kg (1.8 mg/lb), p.o.. RESULTS: Ulcer severity scores on day 0 were not significantly different between groups. On day 30, ulcer severity score was significantly decreased, compared with day-0 score, in group-2 but not in group-1 horses. On day 60, ulcer severity score was significantly decreased, compared with day-0 and day-30 scores, in group-1 horses. In group-2 horses, ulcer severity score on day 60 was significantly lower than the day-0 score but was not significantly different from the day-30 score. Maximum observed serum omeprazole concentration and area under the concentration-time curve were significantly higher after administration of the paste versus the suspension formulation. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that although administration of the commercially available paste omeprazole formulation was effective in promoting healing of gastric ulcers in these horses, administration of the compounded omeprazole suspension was ineffective.     

Effects of intravenously administered esomeprazole sodium on gastric juice pH in adult female horses

Background: Gastric ulcers are common in horses and treatment of horses that cannot be administered oral medication can be problematic. Objectives: To evaluate the efficacy of esomeprazole sodium administered intravenously on gastric juice pH and gastric ulcer scores in horses. Animals: Twelve adult female Quarter Horses. Methods: 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. Results: 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. Conclusions and Clinical Importance: 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.     

Evaluation of urine sucrose concentration for detection of gastric ulcers in horses

OBJECTIVE: To evaluate the use of sucrose permeability testing to detect ulcers in the gastric squamous mucosa of horses. ANIMALS: 13 adult horses ranging from 5 to 19 years of age. PROCEDURE: Following induction of gastric ulcers by intermittent feed deprivation, horses underwent sucrose permeability testing (administration of sucrose by nasogastric intubation followed by collection of urine at 2 and 4 hours after intubation) and gastric endoscopy. Squamous ulcers were assigned a severity score (range, 0 to 3) by use of an established scoring system. Horses were subsequently administered omeprazole for 21 days, and sucrose testing and endoscopy were repeated. Pair-wise comparisons of urine sucrose concentration were made between horses with induced ulcers before and after omeprazole treatment. Urine sucrose concentrations also were compared on the basis of ulcer severity score. RESULTS: Urine sucrose concentrations and ulcer severity scores were significantly higher in horses with induced ulcers before omeprazole treatment than after treatment. Urine sucrose concentrations were significantly higher for horses with ulcer severity scores > 1. Use of a cut-point value of 0.7 mg/mL revealed that the apparent sensitivity and specificity of sucrose permeability testing to detect ulcers with severity scores > 1 was 83% and 90%, respectively. Results were similar after adjusting sucrose concentrations for urine osmolality. CONCLUSIONS AND CLINICAL RELEVANCE: Urine sucrose concentration appears to be a reliable but imperfect indicator of gastric squamous ulcers in horses. Sucrose permeability testing may provide a simple, noninvasive test to detect and monitor gastric ulcers in horses.     

Efficacy of a paste formulation of omeprazole for the treatment of naturally occurring gastric ulcers in training standardbred racehorses in Canada

The efficacy of a paste formulation of the H+, K+, -ATPase inhibitor omeprazole was evaluated in standardbred racehorses for the treatment and prevention of gastric ulcers. Twenty standardbred racehorses in training, aged 2 to 9 years, were enrolled from 2 training centres in this field trial. Endoscopic examinations confirmed the presence of gastric ulcers in all horses, prior to allocation and treatment and on day 0. Lesions were scored on a scale of 0 to 3 (intact epithelium to extensive ulceration). Replicates were formed, based on training level and location. Within replicates, 1 horse was assigned to group 1 and 3 horses were assigned to group 2, randomly. Horses in group 1 were sham-dosed controls. Horses in group 2 were given omeprazole paste orally at 4 mg/kg bodyweight (BW)/day from day 0 to day 27 and 2 mg/kg BW/day of omeprazole paste orally from day 28 to day 57. Follow-up endoscopies were conducted on post treatment days 28 and 58 or 59. Physical examinations, including BWs, were conducted on all horses prior to treatment and on days 13 or 14, 28, 42 or 43, and 58 or 59. Horses treated with omeprazole had significantly (P < 0.01) more improvement in gastric lesion scores than did controls at day 28 and at study termination on days 58 or 59. All of the omeprazole-treated horses were improved relative to baseline ulcer score at both examinations, and 73.3% were healed (lesion score of 0) at both examinations. None of the controls improved at any point during the study. When the dose was reduced to 2 mg/kg BW, 80% of the horses showed no recurrences or worsening in gastric ulcers. It was concluded that omeprazole paste at 4 mg/kg BW orally, once daily is highly effective in healing gastric ulcers in standardbred racehorses in training and that a dose of 2 mg/kg BW orally, once daily, effectively prevents the recurrence of gastric ulcers in most horses.     

Effects of short-term light to heavy exercise on gastric ulcer development in horses and efficacy of omeprazole paste in preventing gastric ulceration

OBJECTIVE: To determine the effects of 8 days of light to heavy exercise on gastric ulcer development in horses and determine the efficacy of omeprazole paste in preventing gastric ulceration. DESIGN: Randomized, controlled, multicenter clinical trial. ANIMALS: 102 horses with normal-appearing gastric mucosa on endoscopic examination that were in light to heavy training. PROCEDURES: Horses at 4 trial locations were allocated into replicates and sham dosed orally (empty syringe) or treated with a paste formulation of omeprazole (1 mg/kg [0.45 mg/ lb], PO) once daily for 8 days. Training regimens varied among locations and included early training for western performance events; walking, trotting, and cantering in a mechanical exerciser; and race training (2 locations). Prevalences of gastric ulceration at the completion of the 8-day treatment period were compared between groups. RESULTS: At the end of the 8-day treatment period, the proportion of omeprazole-treated horses free from gastric ulceration (88%) was significantly higher than the proportion of sham-dosed horses free from gastric ulceration (27%). CONCLUSIONS AND CLINICAL RELEVANCE: Results showed that horses in light to heavy training for as short as 8 days were at risk of developing gastric ulcers and that administration of omeprazole paste decreased the incidence of gastric ulcers.     

Prevalence of gastric ulcers in show horses.

OBJECTIVE: To determine prevalence and risk factors for gastric ulcers in show horses. DESIGN: Field survey. ANIMALS: 50 horses in active training that had been transported to at least 1 event in the 30 days prior to endoscopy. PROCEDURE: Interview of owner, physical examination, serum biochemical analysis, CBC, and gastric endoscopy were performed. RESULTS: Gastric ulceration was detected in 58% of the horses. Horses with a nervous disposition were more likely to have ulceration than quiet or behaviorally normal horses. Horses with gastric ulceration had significantly lower RBC counts and hemoglobin concentrations than those without ulceration. CONCLUSIONS AND CLINICAL RELEVANCE: Show horses have a high prevalence of gastric ulceration. Lower RBC counts and hemoglobin concentrations may be the result of chronic gastric ulceration.     

Comparison of endoscopic,necropsy and histology scoring of equine gastric ulcers

Equine gastric ulcer syndrome (EGUS) represents a major health problem in performance horses. Much debate exists regarding endoscopic gastric ulcer scoring systems and their ability accurately to predict severity or depth of gastric ulcers. The purpose of this study was to evaluate the ability of an endoscopist to count gastric ulcers and predict gastric ulcer severity or depth using 2 endoscopic scoring systems and compare them to the same gastric ulcers see on necropsy and histopathology. Endoscopic examination of the stomach was performed under general anaesthesia on 23 mixed breed yearling horses, after feed was withheld for 24 h. Gastric ulcers were scored using 2 systems, number/severity-scoring (N/S) and practitioner simplified (PS) systems. After endoscopy, the horses were subjected to euthanasia and the stomach mucosa examined blindly and scored again at necropsy using above scoring systems. Representative gastric ulcers were then placed in 10% formalin and processed routinely for histopathology. The gastric ulcers were scored using a histopathology system (HSS) based on ulcer depth. Number scores in the N/S scoring system and PS on endoscopic and necropsy examinations were compared using Friedman 2 way analysis of variance. Where significant differences between variables were found a post hoc analysis was conducted using a Tukey's Studentised range (HSD) test. Severity scores using the N/S (ENGS) and PS scores recorded for the stomach via endoscopy and scores from HSS were evaluated for significant association using a Mantel-Haenszel Chi-square and Pearson moment correlation coefficient analysis. Significance was P < 0.05. All horses had gastric ulcers in the nonglandular mucosa via endoscopic examination and at necropsy examination. Mean nonglandular ulcer number (ENGN) score was significantly (P = 0.0024) lower on endoscopic examination compared to the score at necropsy (NNGN); whereas PS scores were not significantly different on endoscopy when compared to necropsy examination. A significant but weak association was found between ENGS and HSS (3.89, P = 0.048; r = 0.453, P = 0.045) and no correlation was found between PS and HSS (1.2, P = 0.272; r = 0.117; P = 0.622). Only 1/23 horses had glandular ulcers observed via endoscopic examination whereas, 6/23 horses had glandular ulcers at necropsy and on histopathology. The prevalence of EGUS is high in stalled yearling horses. The endoscopist may underestimate the number of gastric ulcers and may not be able accurately to predict the severity or depth of those ulcers present in the nonglandular equine stomach. Furthermore, the endoscopist may miss glandular gastric ulcers.     

Prevalence of gastric ulceration in Swedish Standardbreds in race training

REASONS FOR PERFORMING STUDY: There is little information about the prevalence of gastric ulcers in Standardbred trotters and potential correlations between ulcers and various traits, e.g. age, sex, performance, temperament and feeding regimens, need further elucidation. OBJECTIVES: The prevalence of ulcers in the gastric squamous mucosa of Swedish Standardbreds was estimated and the associations between ulcer score and age, sex, performance, temperament and feeding regimens were determined. METHODS: Eighty Swedish Standardbreds in active race training, trained by 9 different trainers, underwent gastroscopy. Information on age, gender, status of training, performance over the last 4 months compared with the trainer's expectations before that period, behaviour, eating habits, feed type, bedding type, time spent outdoors per day and medical treatment during the last month was collected. Gastroscopy was performed and lesions in the squamous gastric mucosa were scored from 0 to 4 (0 = no lesions; 4 = > 5 lesions with haemorrhage, > 10 lesions with no haemorrhage, or a large area of diffuse loss of surface epithelium). RESULTS: Twenty-four (30%) of the horses had no lesions in the squamous mucosa, 22 (27.5%) had a score of 1; 21 (26.2%) score 2; 9 (11.2%) score 3; and 4 (5%) score 4. Horses that were in preparatory training and those that had raced during the last month were significantly more affected than horses that were fit for racing but had not raced during the last month, using a logistic regression model with trainer incorporated as a random effect. CONCLUSIONS: The study confirmed a high prevalence of ulcers in the gastric squamous mucosa of Standardbreds in race training. Of the studied parameters only status of training showed a significant association with gastric ulcers of the squamous mucosa. POTENTIAL RELEVANCE: Gastric ulceration is a common disease and diagnosis should be made by endoscopic examination of the gastric mucosa, since parameters such as age, gender, performance, behaviour, eating habits provide only weak clues as to which horses might be affected. Further studies are needed to determine the aetiology of the syndrome and to find ways to reduce, if possible, the frequency of gastric ulcers.     

Endoscopic evaluation of the gastroduodenal mucosa to determine the safety of short-term concurrent administration of meloxicam and dexamethasone in healthy dogs

OBJECTIVE: To evaluate the safety, with respect to the development of gastric ulcers and erosions, of concurrent administration of meloxicam and dexamethasone for 3 days to healthy dogs. ANIMALS: 20 conditioned purpose-bred research Beagles. PROCEDURE: Seven days prior to treatment, dogs were anesthetized for endoscopic evaluation of the upper portion of the gastrointestinal tract (ie, the gastric and duodenal mucosa). Five regions of the gastroduodenal area were scored by 2 investigators. Dogs were randomly assigned to 1 of 4 treatment groups as follows: saline-saline, dexamethasone-saline, saline-meloxicam, and dexamethasone-meloxicam groups. On days 1, 2, and 3, dogs received either dexamethasone or saline (0.9% NaCl) solution injections SC twice daily. On days 2, 3, and 4, dogs received either meloxicam or saline solution injections SC once daily. On day 2, dogs were anesthetized for a sham surgery (ie, electrostimulation). On day 5, the gastroduodenal area of each dog was reevaluated by use of endoscopic evaluation and histologic examination of biopsy specimens. RESULTS: The total endoscopic score of the dexamethasone-meloxicam group was significantly greater than the scores of the other groups. The dexamethasone-saline group had a mean cumulative score that was significantly greater than the saline-meloxicam or saline-saline groups. Endoscopic scores of the saline-meloxicam group were not significantly different from scores of the saline-saline group. No significant differences in histologic findings were found between groups. CONCLUSIONS AND CLINICAL RELEVANCE: In healthy dogs, meloxicam appears to be safe with regard to adverse effects on the gastrointestinal tract. Concurrent administration of dexamethasone and meloxicam is more likely to cause gastric erosions than meloxicam administration alone.     

The effect of porcine hydrolysed collagen on gastric ulcer scores,gastric juice pH,gastrin and amino acid concentrations in horses

Gastric ulcers are common in horses. The purpose of this study was to test the effect of porcine hydrolysed collagen (PHC) on gastric ulcer scores and gastric juice pH in horses. We hypothesise that PHC-administration will result in improved gastric lesion scores and act synergistically with omeprazole to improve treatment efficacy. Thoroughbred horses (n = 10) were studied in a 2-period, 2-treatment crossover design, where the PHC (45 g) was administered twice daily. Horses were treated for 56 days. Gastroscopy was performed and gastric juice pH measured on Days 0, 14, 28, 42, 49 and 56. Nonglandular gastric ulcer number (NGN) and severity (NGS) and glandular ulcer number (GN) and glandular severity (GS) scores were assigned by an investigator masked to treatment and serum gastrin and amino acid concentrations. By Day 42, 2 weeks after discontinuing omeprazole treatment, NGN and NGS scores returned to pretreatment values and serum gastrin was higher when compared to values measured on Day 28. By Day 49, after the feed-deprivation period, NGN and NGS were similar to pretreatment values. By Day 56, mean NGN score was significantly lower in PHC-treated horses, compared to controls. Mean gastric juice pH significantly increased in both groups on Day 28 and the pH was significantly (P = 0.0127) higher in the PHC-treated horses. Serum amino acid concentrations were not significantly different 2 h after feeding PHC and hydroxyproline was not detected. Serum gastrin concentration did not increase 2 h after feeding in the PHC-fed horses. The PHC fed to horses enhanced the effects of omeprazole on increased gastric juice pH, inhibited gastrin secretion after feeding and resulted in fewer nonglandular ulcers after long-term feeding (56 days) in stall-confined horses undergoing intermittent feeding.     

The effects of phenylbutazone on the morphology and prostaglandin concentrations of the pyloric mucosa of the equine stomach

Phenylbutazone, a nonsteroidal anti-inflammatory drug known to produce gastric ulcers, was administered intravenously (13.46 mg/kg body weight) daily to 12 horses. Horses were euthanatized daily after 24, 48, 72, and 96 hours following the initial injection. Eight untreated horses served as controls. Small multifocal pyloric erosions were seen after 24 hours and then progressed in severity over time. The erosions were characterized by sloughing of the surface epithelium, subepithelial bleb formation, necrosis of the lamina propria, degeneration of the walls of subsurface capillaries, and microthrombosis of the capillaries of the pyloric mucosa. Large numbers of neutrophils with abundant fibrin and cellular debris were present at the erosion sites. Eroded pyloric mucosa and adjacent macroscopically intact mucosa were examined ultrastructurally. In both the macroscopically eroded mucosa and multifocally in the adjacent macroscopically uneroded mucosa, there was cellular swelling of the endothelium, pericytes, and smooth muscle cells of arterioles. In capillaries and post-capillary venules, the endothelium ranged from swollen to lysed and necrotic. Extensive extravasation of erythrocytes and edema were seen. These lesions were not seen in the control horses. Phenylbutazone produces a microvascular injury that is associated with the formation of pyloric erosions in horses. The pyloric mucosa of six horses was assayed for prostacyclin and prostaglandin E2 at 48 and 96 hours following the initial injection. There was no statistically significant difference between prostaglandin concentrations in the mucosa of control and treated horses. It was concluded that there was little correlation between pyloric mucosal prostaglandin concentrations and pyloric erosions after 48 hours.     

Efficacy of omeprazole paste for prevention of gastric ulcers in horses in race training

OBJECTIVE: To determine the minimal effective dosage of omeprazole oral paste for the prevention of naturally occurring ulcers in horses starting race training. DESIGN: Prospective study. ANIMALS: 175 horses. PROCEDURE: Horses in the dose selection portion of the study were sham dose treated or received 1 mg (0.45 mg/lb) or 2 mg (0.9 mg/lb) of omeprazole/kg, PO, every 24 hours for 28 days or 4 mg of omeprazole/kg (1.8 mg/lb; loading dose), PO, every 24 hours for 4 days, then 1 or 2 mg of omeprazole/kg, PO, every 24 hours for 24 days. Horses in the dose confirmation portion of the study were sham dose treated or received 1 mg of omeprazole/kg, PO, every 24 hours for 28 days. Gastric ulcer scores at the beginning and end of the study were compared. RESULTS: Sham-dose-treated horses had significantly higher ulcer scores than did horses treated with any of the omeprazole dosages evaluated. Among horses treated with omeprazole, there was no significant interaction of dose (1 or 2 mg/kg) and loading dose; therefore, the lowest effective dose (1 mg/kg) was evaluated in the dose confirmation portion of the study. In the dose confirmation study, 4 of 39 (10%) sham-dose-treated horses remained ulcer free, which was significantly different from the proportion of horses (31/38 [82%]) receiving 1 mg of omeprazole/kg that remained ulcer free. CONCLUSIONS AND CLINICAL RELEVANCE; Results indicated that omeprazole administered at a dosage of 1 mg/kg, PO, every 24 hours for 28 days was effective for prevention of gastric ulcers in horses starting race training.     

Lower gastric ulcerogenic effect of suxibuzone compared to phenylbutazone when administered orally to horses

The objective was to compare the gastrointestinal and general toxicity of suxibuzone (SBZ) to that of phenylbutazone (PBZ) when administered orally in horses. Fifteen healthy horses were allocated to three treatment groups. One group received a high dose of PBZ for two weeks; the second group was given an equimolecular dosage of SBZ; and a third group received placebo. Horses were daily monitored, and blood samples were collected before and during the study. On day 18, complete post-mortem examinations were performed.One horse treated with PBZ showed clinical signs of NSAID toxicosis. Small oral ulcers were also detected in other two horses from the PBZ group and in two horses from the SBZ group. There were no statistical differences in the blood parameters among groups. Ulcers in the stomach's glandular mucosa were observed in all horses of the PBZ group, while only two horses of the SBZ group showed ulcerations. PBZ horses had a significant higher ulcerated area, and gastric ulcers were significantly deeper than those in the SBZ and placebo groups. No other lesions were found in any other tissue. In conclusion, SBZ causes significantly lower gastric ulcerogenic effect than PBZ when administered orally at equimolecular doses in horses.     

Effect of a pelleted supplement fed during and after omeprazole treatment on nonglandular gastric ulcer scores and gastric juice pH in horses

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.     

Effects of intravenously administrated omeprazole on gastric juice pH and gastric ulcer scores in adult horses

The study was performed to evaluate the efficacy of omeprazole powder in sterile water, administered intravenously, on gastric juice pH in adult horses with naturally occurring gastric ulcers. Omeprazole (0.5 mg/kg, IV) was administered once daily for 5 days to 6 adult horses with gastric ulcers. Gastric juice was aspirated through the biopsy channel of an endoscope and pH was measured before and 1 hour after administration of omeprazole on day 1, and then before and after administration of omeprazole on day 5. Gastric ulcer scores were recorded on day 1 before administration of omeprazole and on day 5, 23 hours after the 4th daily dose. Gastric juice pH and ulcer scores were compared between the times. When compared with the pre-injection value (2.01 +/- 0.42), mean +/- SD gastric juice pH was significantly higher when measured 1 hour after administration of the initial dose (4.35 +/- 2.31), and before (5.27 +/- 1.74) and 1 hour after (7.00 +/- 0.25) administration of omeprazole on day 5. Nonglandular gastric ulcer number score significantly decreased from a mean +/- SD of 3.2 +/- 0.80 to 2.0 +/- 1.1, but nonglandular gastric ulcer severity score remained the same. Few glandular ulcers were seen in the study, and scores did not change. Because of its potent and long duration of action on gastric juice pH, this intravenous formulation of omeprazole may show promise for treatment of equine gastric ulcer syndrome (EGUS) in horses with dysphagia, gastric reflux, or other conditions that restrict oral intake of omeprazole paste. Aspiration of gastric juice and measurement of pH can be of use to determine whether the desired pH > 4.0 has been reached after omeprazole treatment.     

Assessment of Gastric Ulceration and Gastrin Response in Horses with History of Crib-Biting

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.     

Evaluation of diet as a cause of gastric ulcers in horses

OBJECTIVE: To measure pH, volatile fatty acid (VFA) concentrations, and lactate concentrations in stomach contents and determine number and severity of gastric lesions in horses fed bromegrass hay and alfalfa hay-grain diets. ANIMALS: Six 7-year-old horses. PROCEDURE: A gastric cannula was inserted in each horse. Horses were fed each diet, using a randomized crossover design. Stomach contents were collected immediately after feeding and 1, 2, 3, 4, 5, 6, 7, 8, 10, 12, and 24 hours after feeding on day 14. The pH and VFA and lactate concentrations were measured in gastric juice Number and severity of gastric lesions were scored during endoscopic examinations. RESULTS: The alfalfa hay-grain diet caused significantly higher pH in gastric juice during the first 5 hours after feeding, compared with that for bromegrass hay. Concentrations of acetic, propionic, and isovaleric acid were significantly higher in gastric juice, and number and severity of nonglandular squamous gastric lesions were significantly lower in horses fed alfalfa hay-grain. Valeric acid, butyric acid, and propionic acid concentrations and pH were useful in predicting severity of nonglandular squamous gastric lesions in horses fed alfalfa hay-grain, whereas valeric acid concentrations and butyric acid were useful in predicting severity of those lesions in horses fed bromegrass hay. CONCLUSIONS AND CLINICAL RELEVANCE: An alfalfa hay-grain diet induced significantly higher pH and VFA concentrations in gastric juice than did bromegrass hay. However, number and severity of nonglandular squamous gastric lesions were significantly lower in horses fed alfalfa hay-grain. An alfalfa hay-grain diet may buffer stomach acid in horses.     

Use of force plate analysis to compare the analgesic effects of intravenous administration of phenylbutazone and flunixin meglumine in horses with navicular syndrome

OBJECTIVE: To use force plate analysis to evaluate the analgesic efficacies of flunixin meglumine and phenylbutazone administered i.v. at typical clinical doses in horses with navicular syndrome. ANIMALS: 12 horses with navicular syndrome that were otherwise clinically normal. PROCEDURE: Horses received flunixin (1.1 mg/kg), phenylbutazone (4.4 mg/kg), or physiologic saline (0.9% NaCI; 1 mL/45 kg) solution administered IV once daily for 4 days with a 14-day washout period between treatments (3 treatments/horse). Before beginning treatment (baseline) and 6, 12, 24, and 30 hours after the fourth dose of each treatment, horses were evaluated by use of the American Association of Equine Practitioners lameness scoring system (half scores permitted) and peak vertical force of the forelimbs was measured via a force plate. RESULTS: At 6, 12, and 24 hours after the fourth treatment, subjective lameness evaluations and force plate data indicated significant improvement in lameness from baseline values in horses treated with flunixin or phenylbutazone, compared with control horses; at those time points, the assessed variables in flunixin- or phenylbutazone-treated horses were not significantly different. CONCLUSIONS AND CLINICAL RELEVANCE: In horses with navicular syndrome treated once daily for 4 days, typical clinical doses of flunixin and phenylbutazone resulted in similar significant improvement in lameness at 6, 12, and 24 hours after the final dose, compared with findings in horses treated with saline solution. The effect of flunixin or phenylbutazone was maintained for at least 24 hours. Flunixin meglumine and phenylbutazone appear to have similar analgesic effects in horses with navicular syndrome.