Overview of Omeprazole (Prilosec®) for Dogs and Cats
What is the omeprazole dose for dogs?
As you can imagine, it is also important to give your dog the right amount of omeprazole. Typically, veterinarians will calculate the dose for omeprazole (in milligrams or mg) based on the dog’s bodyweight (in kilograms or kg). This is accomplished by multiplying the omeprazole dose (in mg/kg) by the dog’s weight (in kg).
Different conditions may require a different dose of omeprazole. So it is always best to consult your veterinarian to find the dose that is right for your dog.
Your vet will also advise you on the best dosing frequency. Usually, he or she will recommend giving your dog omeprazole every 24 hours on an empty stomach for five to seven days to start out. Administering it an hour before breakfast is ideal. If your dog isn’t doing well at that dose, your vet may recommend switching to twice daily dosing (i.e. every 12 hours).
How often can I give my dog omeprazole?
Omeprazole is generally used once a day though it can take 3 to 5 days to achieve maximum effect.
Acid Reflux in Dogs
Famotidine is an acid suppressant commonly administered to dogs. Prolonged famotidine use in people results in decreased efficacy, but the effect in dogs is unknown.
To compare the effect of repeated oral administration of famotidine or placebo on intragastric pH and serum gastrin in dogs. We hypothesized that famotidine would have a diminished effect on intragastric pH on day 13 compared to day 1.
Randomized, 2‐factor repeated‐measures crossover design. All dogs received oral placebo or 1.0 mg/kg famotidine q12h for 14 consecutive days. Intragastric pH monitoring was used to continuously record intragastric pH on treatment days 1–2 and 12–13. Mean pH as well as mean percentage time (MPT) that intragastric pH was ≥3 or ≥4 were compared between and within groups by analysis of variance. Serum gastrin was measured on days 0, 3, and 12 for each treatment.
Continued administration of famotidine resulted in a significant decrease in mean pH, MPT ≥3, and MPT ≥4 (P < .0001) on day 12 and 13. This resulted in a mean decrease in pH by 1.63 on days 12 and 13 compared to days 1 and 2. Furthermore, a mean decrease of MPT ≥3 and MPT ≥4 by 33 and 45% was observed for the same time period, respectively.
Continued administration of famotidine results in a diminished effect on intragastric pH in dogs. Caution is advised when recommending long‐term, daily oral administration of famotidine to dogs.
Acid‐related disorders such as gastrointestinal (GI) erosion and ulceration or reflux‐induced esophagitis are increasingly recognized in veterinary patients. Although the cause of acid‐related disorders is often multifactorial, healing of proximal GI tissue injury is based on sustaining an increased gastric pH. In human patients with acid‐related disorders, the mean percentage of time (MPT) that the gastric pH is above 3.0 and 4.0 in a 24‐hour period predicts tissue healing.1, 2 Thus, acid suppressant drugs represent the mainstay of the medical treatment of acid‐related disorders. Two classes of acid suppressants, proton pump inhibitors (PPIs) such as omeprazole, and histamine‐2 receptor antagonists (H2RAs), such as famotidine, are commercially available.
In published studies in healthy dogs and cats, omeprazole has proven to be more effective at raising intragastric pH than famotidine and is often recommended for the treatment of erosive and ulcerative GI disease.3, 4, 5 Despite this, famotidine continues to be widely used in veterinary medicine and there might be good reasons behind this practice. Unlike omeprazole, famotidine can be given with a full meal, is relatively inexpensive, is thought to have additional tissue healing effects including increased mucus and bicarbonate secretion, and is maximally effective within hours of administration.6 Moreover, chronic administration of PPIs to dogs and cats might not be without complications. A recent meta‐analysis suggested an association between chronic PPI use and development of chronic kidney disease (CKD) in people.7 Chronic use of PPIs has also been linked to a wide range of adverse effects in people, including an increased risk for the development of community‐acquired pneumonia, Clostridium difficile‐associated diarrhea (CDAD), hypocobalaminemia, and decreased bone mineral content.8, 9, 10, 11 The development of adverse effects depends on the duration of exposure to the drug with some adverse effects occurring within days to weeks (eg, CDAD) and others developing after years of chronic use (eg, hypomagnesemia). Omeprazole administration for 60 days can result in hypergastrinemia, withdrawal‐induced rebound gastric acid hypersecretion, and potentially decreased bone mineral content in cats.12 Additionally, aggressive acid suppression is not always warranted. Therefore, famotidine, a weaker acid suppressant associated with fewer adverse effects than PPIs in people, might be a reasonable choice of acid suppression in dogs when prolonged or less potent acid suppression is desired. However, the efficacy of prolonged famotidine use has not been explored in dogs. Repeat famotidine administration might lead to diminished efficacy in dogs. The acid suppressing effects of famotidine and other H2RAs in humans can decrease with continued administration perhaps because of a reduction in the degradation of parietal cell H2‐receptors over time.6, 13 In people, this effect occurs in as little as 8 days of continuous oral treatment.14, 15, 16 Recognition of this phenomenon in dogs is needed to create successful acid suppressant therapy guidelines. In a study designed to evaluate serum gastrin concentrations in 11 dogs receiving oral famotidine at 0.5 mg/kg twice daily, gastrin was increased on day 3 but returned to normal on day 14 despite continued famotidine administration.17 Although intragastric pH was not measured in that study, these results suggest a reduction in efficacy over time.
Despite its widespread use, studies have not been undertaken to investigate for a potential for a diminishing acid suppressing effect of famotidine over time in dogs. Accordingly, the objective of this study was to determine whether continued administration of famotidine leads to a reduced effect on intragastric pH in dogs. We hypothesized that famotidine would have a diminished effect on intragastric pH on day 13 compared to day 1.
The Institutional Animal Care and Use Committee (IACUC) at the University of Tennessee approved the protocol for this study (Approval# 2456‐0516). The subjects of this study were 6 healthy adult Beagle dogs from a research colony at the University of Tennessee (4 neutered and 2 intact males), aged 4.0–5.5 years (median, 5 years), and weighing 10.5–15.3 kg (median, 13.0 kg). All dogs lacked clinical signs of GI disease and were deemed healthy on the basis of review of history and available historical blood work as well as normal physical examination, normal baseline blood work (ie, PCV, serum chemistry, serum cobalamin and folate, venous blood gas,1 and urinalysis), and negative fecal examinations by zinc and sugar sulfate centrifugation flotation methods performed at study entry. All dogs were also given 2 doses of a prophylactic broad‐spectrum anthelmintic2 2 weeks apart before the onset of the study.
In a randomized, open label, 2‐factor repeated‐measures crossover design, all dogs were PO administered placebo (250 mg lactose3 ) q12h or 15 mg famotidine4 (median, 1.15 mg/kg; range, 0.98–1.42 mg/kg) q12h with their meal. The objective was to dose famotidine as close to 1 mg/kg q12h as possible as this is the standard dose of famotidine used in our hospital for treatment of ulcerative disease. Dogs were randomized to a treatment schedule by a random number generator so that 3 dogs each were randomized to receive famotidine or placebo first. Dogs were medicated and fed5 at consistent times twice daily. Clinical signs, including change in attitude, appetite, vomiting, number of defecations, and fecal character, were recorded at least twice daily. Feces were graded from 1 to 7 by a standardized fecal scoring system.6 A washout period of 20 days separated treatment groups, with no medications administered during this time period, to prevent carryover effects.
One day before the first treatment period (day 0, baseline), dogs were sedated with dexmedetomidine7 (0.005 mg/kg) and butorphanol8 (0.4 mg/kg) IV. An IV catheter was placed, and general anesthesia was induced with propofol9 to effect. General anesthesia was maintained in dogs with sevoflurane10 in 100% oxygen after endotracheal tube placement. The entire esophagus and stomach were evaluated by endoscopy for any evidence of gross disease. Gastric biopsy samples were obtained by routine gastric endoscopic biopsy. Gastric tissue samples were fixed in 10% buffered formalin, paraffin embedded, sliced in 5‐μm sections, stained with hematoxylin and eosin, and assessed by a single board‐certified pathologist (KN). After acquisition of biopsies, a pH capsule11 was placed in the gastric fundus under endoscopic guidance as previously described.3, 18 Before use, all pH capsules and receivers were calibrated as previously described according to manufacturers instructions.3 All pH capsules were placed by the same investigator (MKT). The location of each pH capsule was kept consistent in each dog within and between treatment groups by utilizing the measurements on the capsule delivery device to measure the distance from the maxillary canine teeth to the area of capsule placement. On day 12 of both treatment periods as well as baseline (day 0) of the second treatment group, pH capsules were placed by radiographic guidance under sedation with dexmedetomidine and butorphanol, as previously described12, to eliminate the need for repeated general anesthesia. Briefly, after sedation, dogs were placed in left lateral recumbency. The pH capsule was then blindly introduced transorally into the proximal stomach. We used the recorded length of the delivery device measurement for the first capsule placed endoscopically to place the second capsule in a similar location. For radiographic assessment, location of the capsule with its delivery device in respect to the stomach was evaluated on orthogonal (lateral and ventrodorsal) abdominal radiographs after published criteria for normal radiographic anatomy of the stomach in dogs.19 Successful placement of the capsule within the fundus was ascertained by visualization of the device in the dorsal part of the stomach (at the level of or slightly dorsal to the esophageal hiatus) on the lateral view, and to the left of midline on the ventrodorsal view which corresponds to reported location of the gastric fundus on abdominal radiographs in dogs (Fig. A). The ability to visualize rugal folds in these fasted animals with a small amount of gas and no fluid or solid contents within the gastric lumen further aided in radiographic identification of the fundus. After confirmation of correct positioning, the pH capsule was adhered to the gastric mucosa with vacuum suction and a spring‐loaded pin as previously described3. The delivery device was removed. Abdominal radiographs were obtained to ensure that the capsule remained firmly adhered in the desired location (Fig. B). The sedation was reversed with atipamezole12 (0.05 mg/kg IM) after each capsule placement.
Intragastric pH recordings were obtained telemetrically at 6‐second sampling intervals for a minimum of 48 hours after capsule placement starting at baseline (day 0) and on treatment days 12. The corresponding data receivers were kept on the front of each dogs run during the data acquisition phase. When the dogs were walked or given time for play, the receivers remained with the caretaker within 6 feet of the dogs. pH data were uploaded to the computer by manufacturer software13 every 24 hour for each monitoring period. After data upload, data from the receiver were cleared and the receiver was used to obtain data for the next 24 hour. Data from day 0, a nontreatment day, was excluded from analysis. The mean pH and MPT that intragastric pH was ≥3 and ≥4 were calculated by the manufacturer software.
At baseline and on treatment days 3 and 12, 3 mL of blood was obtained via jugular venipuncture. Serum was collected from blood tubes after centrifugation at 250 × g and stored in cryovials at −80°C. After study completion, the serum was shipped on dry ice to the Gastrointestinal Laboratory at Texas A&M University for measurement of gastrin concentrations. Serum gastrin concentrations were measured with an automated chemiluminescent, enzyme‐labeled immunometric assay14 as previously described.20
A 2‐factor repeated‐measures mixed‐effects crossover design and corresponding analysis of variance (ANOVA) were performed to evaluate mean intragastric pH and MPT that intragastric pH was ≥3 and ≥4 for treatment, time (day of treatment), and period differences. To be conservative, a value of 9.9 was assigned to all gastrin data that was below the limit of detection (<10 ng/L). Serum gastrin concentration data were then rank transformed and analyzed by repeated‐measures crossover ANOVA to evaluate for treatment, time, and period differences. Heterogeneous variance structures were incorporated into each model, for both pH and gastrin data, to adjust for unequal between subjects treatment variances.21 For pH data, the interaction of treatment and time was tested to explain, when significant differences were found, how each pH measure changed over time, while dogs were under the effects of each treatment. To accomplish this, a single‐factor within‐subjects repeated‐measures ANOVA was established. In each model, a contrast was developed to see whether mean values for days 1 and 2 were statistically different than mean values for days 12 and 13 for each pH measure under each treatment. A Shapiro–Wilk W and QQ normality plots were used to evaluate normality of ANOVA residuals. Levenes equality of variances test was used to evaluate equality of treatment variances. All statistical assumptions regarding normality were met. Heterogenous variances were incorporated during model development.21