• CIBDAI ;
  • Corticosteroids;
  • Diarrhea;
  • Endoscopy;
  • Vomiting


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References


Budesonide has been used to treat inflammatory bowel disease (IBD) in dogs, but no controlled studies have been performed to evaluate efficacy of this treatment.


To compare budesonide and prednisone for induction therapy of IBD in dogs by using IBD activity index scores and evaluating frequency and severity of owner-reported adverse effects.


Forty client-owned dogs with newly diagnosed idiopathic IBD were enrolled between April 2001 and January 2004; 34 dogs completed the 6 week study.


Double-blinded, randomized controlled trial. Dogs were randomized to receive either pure powder-based budesonide (3–7 kg: 1 mg PO q24h, 7.1–15 kg: 2 mg PO q24h, 15.1–30 kg: 3 mg PO q24h, >30 kg: 5 mg PO q24h) for 6 weeks or prednisone (1 mg/kg PO q12h × 3 weeks then 0.5 mg/kg PO q12h × 3 weeks). IBD activity index (IBDAI) scores were determined at diagnosis and after 6 weeks of treatment. Pet owners completed weekly questionnaires regarding clinical signs and incidence and severity of adverse effects.


Significant differences in remission rates (>75% decrease in IBDAI scores) were not observed with a remission rate of 78% in the budesonide group and 69% in the prednisone group (P = .70). Frequency of adverse effects was similar between the 2 groups.

Conclusions and Clinical Importance

There was no demonstrable difference in remission rates or incidence of adverse effects between prednisone and budesonide for induction therapy of IBD in dogs.


alkaline phosphatase


alanine aminotransferase


complete blood count


canine inflammatory bowel disease activity index


inflammatory bowel disease

Idiopathic inflammatory bowel disease (IBD) is a common cause of signs of chronic gastrointestinal disease in the dog.[1-5] Idiopathic IBD is differentiated from food responsive and antibiotic responsive causes of chronic enteropathy by lack of response to dietary or antibiotic therapies alone. The definitive cause of idiopathic IBD is unknown. However, current evidence suggests that affected individuals have an altered interaction between the mucosal immune system and intestinal microbes with aggressive host immune responses resulting in chronic intestinal inflammation.[5-10] Treatment for idiopathic IBD typically requires immunosuppressive drugs.[3] Many dogs are treated with a combination of therapies.[3, 11]

Corticosteroids are commonly prescribed for the treatment of IBD in dogs.[1, 3, 9] In a retrospective study of 80 dogs with IBD, prednisolone was the most frequently prescribed medication having been administered alone or in combination to 61% of animals.[12] Several studies have shown prednisone to be beneficial in the treatment of IBD in dogs.[3, 8, 11] In humans with IBD (Crohn's disease and ulcerative colitis), corticosteroids are also a mainstay of therapy.[3, 9, 13-16]

Unfortunately, systemic corticosteroids are often associated with adverse effects.[1, 9, 14-18] Commonly reported adverse effects of systemic corticosteroids in dogs include polyphagia, polyuria, polydipsia, restlessness, panting, and behavior changes. Long-term effects of corticosteroids can include obesity, vacuolar hepatopathy, muscle atrophy and weakness, ligament rupture, urinary tract infection, pyoderma, and development of diabetes mellitus. These adverse effects can negatively affect quality of life for animals even if clinical signs of IBD are controlled.[9, 17, 18]

Budesonide is a nonhalogenated glucocorticoid that was developed for use in human patients with IBD to limit systemic adverse effects. In humans, budesonide has a high ratio of topical to systemic activity because of high first pass metabolism in the liver and is therefore associated with fewer adverse effects than systemic corticosteroids.[9, 13, 14, 17, 19] Many studies in humans have shown budesonide to be as effective as prednisone for induction therapy of IBD.[9, 13, 15-17, 19-21]

Budesonide has been used in veterinary medicine to treat animals with IBD but no controlled studies have been published to evaluate efficacy of this treatment. A recent uncontrolled study evaluated the use of budesonide for induction therapy of IBD in a small population of dogs and found budesonide therapy to be effective with no adverse effects.[18] Two previous studies have evaluated the effects of budesonide on the pituitary adrenocortical axis. Both studies showed pituitary adrenal axis suppression, but neither study showed other subjective or objective systemic effects.[9, 17]

The goal of this study was to compare the efficacy of budesonide therapy to conventional prednisone therapy for induction therapy of histopathologically confirmed IBD using IBDAI scores. Additionally, the incidence and severity of owner-observed corticosteroid related adverse effects were compared between treatment groups.

Materials and Methods

  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References

This was a double-blinded, randomized, controlled trial conducted by Animal Medical Specialists at the Veterinary Referral Center of Colorado from April 2001 to April 2004 using client-owned animals. All clients gave written informed consent. Investigators were blinded to the treatment assignment until the conclusion of the 6-week study period.

Inclusion Criteria

To be included in the study, dogs had to be at least 3 kg body weight and had to meet previously published criteria for diagnosis of idiopathic IBD: persistent (>3 weeks duration) or recurrent gastrointestinal signs, inadequate response to dietary and symptomatic therapies alone, thorough diagnostic evaluation with exclusion of other causes of gastroenteritis, and histopathological evidence of mucosal inflammation.[3, 5, 11] Diet and antibiotic trials were performed before entry into the study by either the referring veterinarian or attending clinician with the choice of diet, antibiotic, and trial duration based on the discretion of the attending clinician. Deworming was not required for entry into the study.

Minimal diagnostic evaluation for all dogs before entry into the study included CBC, serum biochemistry profile, urinalysis, abdominal ultrasound, fecal direct smear and zinc sulfate flotation for parasites, and histopathologic review of mucosal biopsy specimens obtained via gastroduodenoscopy, colonoscopy or both. Dogs having signs of upper gastrointestinal disease only (vomiting, small bowel diarrhea, anorexia, weight loss) underwent gastroduodenoscopy whereas dogs having only signs of lower gastrointestinal disease (frequent, urgent defecation or both, mucoid feces, hematochezia, tenesmus) underwent colonoscopy. Dogs having mixed signs of gastrointestinal disease underwent both procedures. Endoscopy was performed by one of the study authors (K.J.D., S.L.W., D.S.W.). Multiple biopsy specimens were obtained with the total number at the clinician's discretion.

Histologic examination was performed by a single board certified pathologist who was blinded as to treatment group but not as to time point within the study. The samples were classified by identifying the dominant population of inflammatory cells (lymphoplasmacytic, eosinophilic, and pyogranulomatous) and using a 4-point scale to indicate severity of inflammation (normal, mild, moderate, or severe).

Some dogs received additional diagnostic tests including ACTH stimulation testing, serum trypsin like immunoreactivity, and serum assays for folate and cobalamine at the clinician's discretion.

Exclusion Criteria

Dogs were excluded from the study if they had received corticosteroids, other immune modulating medications (ie, cyclosporine, azathioprine, sulfasalazine), or nonsteroidal anti-inflammatory medications within 30 days of evaluation. Dogs were also excluded if another cause for gastrointestinal signs besides idiopathic IBD was identified during the initial evaluation or if any histopathologic diagnosis other than IBD was obtained either at enrollment or at repeat biopsy at 6 weeks.

Randomization and Treatment

Once diagnosed with idiopathic IBD, dogs were randomized by means of a computer generated schedule into one of 2 treatment groups. Randomization and drug dispensation were performed by a study technician who was blinded to dog characteristics other than body weight. Dogs in the prednisone group received prednisone PO at a dosage of 1 mg/kg q12h × 3 weeks then 0.5 mg/kg q12h × 3 weeks. Dogs in the budesonide group received a compounded preparation of powder based budesonide1 in capsule form with dosage based on body weight as follows: 3–7 kg: 1 mg budesonide q24h; 7.1–15 kg: 2 mg budesonide q24h; 15.1–30 kg: 3 mg budesonide q24h; and >30 kg: 5 mg budesonide q24h. This dosage of budesonide was continued for the 6-week duration of the study. The entire volume of medication was dispensed at enrollment into the study. Dosing was based on enrollment weight with no adjustments in medication dosage made for weight changes over the course of the study.

No other medications were administered for treatment of IBD during the 6-week study period. Antibiotics were administered for other conditions (urinary tract infection, pyoderma) if indicated. Dogs were continued on the same diet that they had been fed at the time of evaluation for the study; dietary changes were not allowed during the study period.


Owners were contacted either in person or by phone on a weekly basis and asked to complete a verbal questionnaire (Table 1) regarding their pet's clinical signs and attitude. Dogs were examined by one of the study authors (K.J.D., S.L.W., D.S.W.) at 3 weeks and 6 weeks after initiation of treatment. CBC, biochemistry profile, and urinalysis were repeated at 3 weeks and 6 weeks. Gastrointestinal endoscopy and biopsies of the intestine with histopathology were repeated at 6 weeks.

Table 1. Weekly client questionnaire regarding patient clinical signs and attitude.

1. Has your dog had any episodes of vomiting in the past week? (Yes or No)

1b. If yes, how many episodes have occurred?

1c. If yes, please describe the vomitus (ie, food, bile, presence of blood).

2. Has your dog had any episodes of diarrhea in the past week? (Yes or No)

2b. If yes, how many episodes have occurred?

2c. If yes, please describe the consistency of the diarrhea? (Slightly soft, Very soft, or Liquid)

2d. Is there blood or mucus in the feces? (Yes or No)

2e. Is your dog straining to defecate? (Yes or No)

2f. How many feces per day is your pet having on average?

3. How would you describe your dog's quality of life since starting treatment using a scale of 1–10 with 1 being significant decline in quality of life, 5 being no change, and 10 being significantly improved?

4. Is your dog's water consumption normal, decreased from normal, or increased from normal?

4b. If increased or decreased from normal, is the change mild, moderate, or marked?

5. Is your dog's appetite normal, decreased from normal, or increased from normal?

5b. If increased or decreased from normal, is the change mild, moderate or marked?

6. Is your dog urinating with normal frequency, decreased frequency, or increased frequency?

6b. If increased or decreased from normal, is the change mild, moderate, or marked?

7. Is your dog having any urinary accidents or urinary incontinence? (Yes or No)

7b. If so, how frequently do the accidents or incontinence occur?

8. Is your dog's energy level normal, decreased from normal, or increased from normal?

8b. If increased or decreased from normal, is the change mild, moderate, or marked?

9. Have you noted any panting or changes in your dog's breathing? (Yes or No)

9b. If yes, please describe

10. Have you noted any other changes in your dog since starting treatment?

10b. If yes, please describe

Information from the client questionnaire and medical record regarding the dog's attitude, appetite, vomiting, feces consistency, and feces frequency was used to calculate the CIBDAI at enrollment and 6 weeks. The CIBDAI scores were calculated as described.[11] The CIBDAI scores were calculated by one of the study authors (T.L.D.) who was not involved in case management and was blinded as to the dog's treatment group. Clinical remission was defined as a 75% reduction in the CIBDAI score from the pretreatment value.[3]

One of the study authors (T.L.D.) also compiled a list of adverse effects noted by the pet owner for each dog and the severity of adverse effects based on the client questionnaires and clinician notes. Corticosteroid adverse effects were considered to include polydipsia, polyuria, excessive panting, urinary incontinence, muscle weakness and atrophy, lethargy, and temperament change. Appetite changes were not included as many of these patients had decreased appetite associated with their gastrointestinal disease. Adverse effects were considered mild if they were noted by the owner but not considered to have a negative effect on the dog's quality of life. Adverse effects were considered moderate if the owner felt that the adverse effects were having some negative effect on the dog's quality of life but still felt that the benefit of the treatment outweighed the adverse effects. Adverse effects were considered severe if the owner felt that there was a significant enough negative impact on the dogs's quality of life that the treatment could not be continued long term.

Data Analysis and Statistics

Statistical analysis was performed by a biostatistician with the use of statistical software.2 Differences were deemed to be significant if P < .05. Baseline values continuous in nature (including age, duration of signs, baseline CIBDAI scores, WBC, neutrophils, lymphocytes, eosinophils, PCV, ALP, ALT, blood glucose, albumin, cholesterol, urine specific gravity, and body weight) were evaluated by a one-way ANOVA, including treatment group (prednisone or budesonide) as the only fixed factor in the statistical model. Baseline biopsy scores were assessed as ordinal outcomes using Wilcoxon's rank sum test. Remaining baseline observations were evaluated using Fisher's exact test.

The incidence and severity of adverse effects as reported by pet owners were assessed using Fisher's exact test. Values continuous in nature and observed over time (3 or 6 weeks, including CIBDAI scores, ALP, ALT, albumin, urine specific gravity and body weight) were evaluated by a repeated measures ANOVA, including treatment group, time, and the group by time interaction as fixed factor in the statistical model. Within group time effects and group effects at 3 or 6 weeks were compared without multiplicity adjustments to the P-value. Where the assumption of normality was grossly violated, transformations were applied to stabilize the residuals. Biopsy scores were evaluated by time and treatment using methods appropriate for ordinal data. The number of dogs in remission at 6 weeks was evaluated using Fisher's exact test.


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References

Baseline Characteristics at Inclusion

Forty dogs were enrolled into the study, with 20 dogs assigned to the prednisone group and 20 dogs assigned to the budesonide group. Four dogs in the prednisone group did not complete the study. Two dogs were withdrawn by their owners because of severe steroid related adverse effects. A 3rd dog was withdrawn because of severe steroid related adverse effects and development of a hepatopathy. The 4th dog was excluded because of poor owner compliance with medication administration and follow-up. Two dogs in the budesonide group did not complete the study. One dog was diagnosed with intestinal lymphoma at the time of repeat gastroduodenoscopy and histopathology at 6 weeks and was therefore excluded from the study. One dog was withdrawn by its clinician at 3 weeks because of severe persistent gastrointestinal signs so that additional therapies could be implemented. Overall, 34 dogs completed the study.

The groups were similar in age and weight with a variety of represented breeds in both groups (Table 2). The dogs in the budesonide group had a longer duration of clinical signs but this difference was not statistically significant. CIBDAI scores were similar between groups. There was a higher proportion of dogs having lymphoplasmacytic versus mixed or eosinophilic inflammation in the budesonide group; this difference approached but did not reach statistical significance (P = .056). The median total white blood count and neutrophil count was significantly higher in the prednisone group.

Table 2. Baseline characteristics of 40 dogs with idiopathic IBD in the intent to treat population (mean [SD] or number and percentage).
 Prednisone Group (n = 20)Budesonide Group (n = 20)P-Value
  1. a

    4 missing values.

  2. b

    4 missing values.

Age (years)5.9 (3.6)5.0 (2.3).36
Weight (kg)22.5 (13.2)21.9 (13.2).89
MC12 (60%)10 (50%).75
MI0 (0%)1 (5%)1.0
FS8 (40%)9 (45%)1.0
FI0 (0%)0 (0%)1.0
Boxer2 (10%)0 (0%).49
German Shepherd1 (5%)1 (5%)1.0
Golden Retriever0 (0%)2 (10%).49
Jack Russell Terrier1 (5%)1 (5%)1.0
Keeshond0 (0%)2 (10%).49
Labrador Retriever1 (5%)2 (10%)1.0
Shar-pei1 (5%)1 (5%)1.0
Mixed breed4 (20%)2 (10%).66
Other10 (50%)9 (45%)1.0
Clinical signs
Vomiting14 (70%)14 (70%)1.0
Diarrhea15 (75%)13 (65%).73
Inappetence11 (55%)12 (60%)1.0
Weight loss13 (65%)10 (50%).52
Duration of signs (months)9.4 (13.8)18.1 (18.3).10
Baseline CIBDAI scores8.3 (3.1)7.5 (2.5).38
Endoscopy findings
Hyperemia10 (50%)10 (50%)1.0
Edema2 (10%)7 (35%).13
Increased friability7 (35%)3 (15%).27
Increased granularity16 (80%)14 (70%).72
Erosions/ulcerations1 (5%)3 (15%).61
Lymphoplasmacytic7 (35%)14 (70%).06
Lymphoplasmacytic and suppurative2 (10%)0 (0%).49
Lymphoplasmacytic and eosinophilic8 (40%)6 (30%).74
Eosinophilic3 (15%)0 (0%).23
Baseline biopsy score2 (1–3)2 (1–3).90
WBC (/μL)14,600 (9720)8,870 (4620).023
Neutrophils (/μL)12,000 (9400)6,670 (4750).028
Lymphocytes (/μL)1,770 (826)1600 (606).47
Eosinophils (/μL)312 (524)272 (295).77
PCV (%)49.6 (5.8)47.7 (6.9).34
ALP (IU/L)133 (179)119 (220).82
ALT (IU/L)76 (102)45 (26).20
Blood glucose (mg/dL)97 (20)105 (20).19
Albumin (g/dL)3.1 (0.9)3.1 (0.9).78
Number of hypoalbuminemic dogs5 (25%)6 (30%)1.0
Cholesterol (mg/dL)176 (66)197 (73).35
Urine specific gravity1.033a (0.4)1.028b (0.4).26


Both treatments were effective in treatment of IBD with a significant (P < .0001) reduction in CIBDAI scores in both groups and similar overall remission rates between groups (Table 3). There was a significant improvement in albumin concentration from 0 weeks to 6 weeks in the budesonide group (P = .0038) but not in the prednisone group. There was a significant increase in both ALT and ALP from baseline at 6 weeks in both groups. The ALT was significantly higher at 6 weeks for dogs in the prednisone group as compared to the budesonide group (P = .0055).

Table 3. Comparison of selected variables between baseline and 6 weeks for each study group and between study groups at 6 weeks (mean [SD] or number and percentage).
 Prednisone GroupBudesonide GroupPrednisone versus Budesonide at 6 weeks
Baseline6 WeeksP-ValueBaseline6 WeeksP-ValueP-Value
CIBDAI score8.8 (3.3)2.5 (3.4)<0.00017.5 (2.6)1.3 (2.0)<.0001.22
Number patients in remissionn/a11/16 (68.8%)n/an/a14/18 (77.8%)n/a.70
Body weight (kg)22.4 (11.9)23.4 (12.1)0.07920.4 (12.1)20.1 (11.8).70.44
Albumin (g/dL)2.9 (1.0)3.2 (0.8)0.143.2 (0.9)3.7 (0.9).0038.096
Urine specific gravity1.034 (0.3)1.032 (0.3)0.641.029 (0.4)1.034 (0.02).25.71
ALT (IU/L)80.3 (113.6)403.2 (422.7)<0.000141.3 (22.7)86.2 (81.8).038.0055
ALP (IU/L)132.7 (195.9)534.4 (602.1)0.000899.7 (202.4)324.7 (524.5).011.24
Biopsy score2.3 (0.6)1.6 (1.0)0.0332.2 (0.8)1.6 (1.0).058.88

The majority of dogs in both groups were reported to have corticosteroid related adverse effects (Table 4). For most dogs in both groups, adverse effects were felt to be mild. Polyuria was reported more frequently in the prednisone group; this difference approached but did not reach statistical significance (P = .056). There was no difference in the incidence of any of the other adverse effects and no statistical difference in severity of adverse effects between groups.

Table 4. Incidence and severity of adverse effects as reported by pet owners.
Adverse EffectPrednisone Group n = 20 (%)Budesonide Group n = 20 (%)P-Value
Polydipsia16 (80)10 (50).096
Polyuria14 (70)7 (35).056
Urinary incontinence1 (5)2 (10)1.0
Excessive panting11 (55)8 (40).53
Muscle weakness or atrophy3 (15)1 (5).61
Temperament change1 (5)0 (0)1.0
Lethargy6 (30)2 (10).23
Overall severity of adverse effects
None2 (10)4 (20).66
Mild12 (60)15 (75).51
Moderate3 (15)1 (5).61
Severe3 (15)0 (0).23


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References

Budesonide has been used in dogs for treatment of allergic dermatitis (topically), chronic inflammatory airway disease (aerosol), and IBD, but there are no controlled studies evaluating the efficacy of oral budesonide therapy for IBD in dogs.[17, 18, 22, 23] This study demonstrates that budesonide is effective for the treatment of IBD and is generally well tolerated although the incidence of adverse effects was not lower for dogs receiving budesonide as compared to dogs receiving prednisone.

Budesonide is a very potent glucocorticoid, being 15 times more potent than prednisolone. It has a good distribution to mucosal surfaces because it is highly water soluble. It penetrates well into local tissue cells where it is converted into a highly lipophilic ester which is gradually hydrolyzed releasing active budesonide; this allows for a prolonged local anti-inflammatory effect. The active form of budesonide has high affinity for intracellular glucocorticoid receptors.[9, 18, 24, 25]

We used a pure powder-based formulation of budesonide in this study. Because dogs often have involvement of the upper portion of the gastrointestinal tract contributing to clinical signs of IBD, the sustained release product might not be as desirable in dogs as in humans. Additionally, the pure powder-based formulation is significantly more cost effective than the commercially available micronized formulation. The micronized formulation is only commercially available in 3 mg capsules3 so compounding is required for smaller veterinary patients regardless of which formulation is used.

The budesonide dosage used in this study was empirical. Various dosages for oral budesonide have been reported in the veterinary literature with the most commonly reported dosage being 3 mg/m2.[17, 18, 25] Other studies have used 9 mg/dog[24] or 2 mg for dogs less than 18 kg and 3 mg for dogs greater than 18 kg.[9] Because there have not been other controlled studies evaluating the efficacy of budesonide in treating inflammatory bowel disease, the most appropriate dosage in dogs is still unknown.

In humans, high dosages of budesonide are typically used for induction of remission in both adults and children with standard induction dosage being 9 mg/d.[9, 13, 19-21] In 1 study, a dosage of 3 mg/d in adult humans with Crohn's disease was not effective in inducing remission.[9, 19] This might suggest that current veterinary dosages are too low given that pharmacokinetics of budesonide appear similar between humans and dogs.[18, 23]

When calculated on a mg/kg body weight basis, the budesonide dosage in this study ranged between 0.11 and 0.27 mg/kg with a mean and median dosage of 0.16 mg/kg. Given that budesonide is 15 times as potent as prednisone, this budesonide dosage equates to a prednisone dosage of 2.4 mg/kg/d.[25] Based on this data, dogs in the budesonide group received similar corticosteroid dosages as dogs in the prednisone group for the first 3 weeks of the study but approximately 2.4 times as much corticosteroid in the second half of the study. This is an important consideration in that budesonide appeared to be well tolerated at this dosage but was providing a relatively higher amount of corticosteroid. Unfortunately, the relatively higher corticosteroid dosage did not result in a significantly higher efficacy for budesonide than prednisone but it is possible that a larger trial or trial of longer duration might demonstrate a difference.

Previous studies evaluating oral budesonide in dogs have demonstrated suppression of the hypothalamic-pituitary-adrenal axis.[9, 17] Interestingly, none of the previous studies evaluating oral budesonide in dogs have demonstrated elevations in liver enzymes or glucocorticoid associated adverse effects whereas both were noted in our study.[9, 17, 18] The previous studies involved use of both the pure powder and the controlled release formulation and both normal healthy dogs and dogs with IBD so it is unlikely that the use of the powder formulation or use in a study population with inflammatory bowel disease contributed to these findings.[9, 17, 18] Additionally, in humans the absorption of budesonide was not shown to be affected by the severity of inflammatory bowel disease, so it would not seem likely that dogs with IBD would have more adverse effects that normal dogs.[9] However, further comparisons may be warranted as more rapid absorption of budesonide was noted in a study of dogs with IBD than in a study in which budesonide was administered to healthy dogs. The 2 studies did use different dosages of budesonide.[18, 26]

It is possible that reporting of adverse effects by owners in this study population was biased since owners were aware that their pet was being treated with a steroid medication although blinded as to which steroid. It is interesting to note that many pet owners reported polydipsia and polyuria as an adverse effect but there was no change in urine specific gravity for patients in either group between baseline and 6 weeks.

Although the overall incidence of adverse effects was similar between the 2 treatment groups, it is important to note that severe adverse effects were only reported within the prednisone group with none of the dogs in the budesonide group reported as having severe adverse effects; however, this difference was not statistically significant. It may be that a larger population of dogs would be necessary to demonstrate a significant difference in adverse effect severity.

Two dogs were withdrawn from the prednisone group by their owners solely because of glucocorticoid-related adverse effects (polydipsia, polyuria, lethargy, and weakness, and in 1 dog reflex dyssynergia). A 3rd dog was withdrawn because of severe steroid adverse effects and hepatopathy. Unfortunately, the owners of this dog declined work-up for the hepatopathy but it did resolve with discontinuation of prednisone and administration of antibiotics, SAM-e, ursodiol, and vitamin E. This dog's IBD was later successfully treated with budesonide.

This study did have several limitations. Although the dogs had undergone food and antibiotic trial therapies before entry into the study, these trial therapies were not standardized. Many of the dogs had undergone trial therapies at the referring veterinarian before being referred for endoscopy, and medical records were often incomplete so it was difficult to assess the adequacy of the trials. However, all dogs were continued on their previous diet throughout the study and additional therapies besides the study drug were not allowed. Therefore, it is not likely that the lack of standardized trial therapies influenced the outcomes between treatment groups.

This study was limited to a duration of 6 weeks. A study of longer duration would be needed to assess the efficacy of budesonide as a maintenance treatment. Corticosteroid related adverse effects often become more apparent and less tolerable with a longer duration of treatment. After induction therapy for IBD with prednisone, gradual dosage tapering is generally recommended to limit adverse effects, but some animals relapse as the dosage is decreased. It is possible that budesonide may be more or less tolerated with long term use than prednisone.

The biggest limitation of this study is the small number of enrolled dogs, which limits the power of the statistical analysis. There were also a larger number of dogs with eosinophillic inflammation in the prednisone group, which could have affected response to the treatment, and the dogs in the prednisone group had higher white blood counts and neutrophil counts than dogs in the budesonide group, which could indicate that they were a sicker population of dogs. However, CIBDAI scores were similar at baseline between groups, and remission rates for both group are similar to those reported for previous studies involving treatment of idiopathic IBD.[2, 3, 8]

In conclusion, this study demonstrates that budesonide may be an effective alternative to prednisone for induction therapy of IBD but may not necessarily be associated with fewer glucocorticoid adverse effects. Larger trials would be recommended to further evaluate the use of budesonide for induction and maintenance therapy of IBD and to best determine the most appropriate dosage and formulation of budesonide for animals. Further evaluation of the incidence and severity of adverse effects through the use of more objective parameters would also be recommended.


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References

The authors thank Dr Steven Radecki for assistance with the statistical analysis and Dr Barbara Powers for assistance with the histopathology.

Funding: This study was funded by a grant from the Morris Animal Foundation.

Conflict of Interest: Authors disclose no conflict of interest.

  1. 1

    Wise Pharmacy, Littleton, CO

  2. 2

    SAS version 9.3, SAS Institute, Cary, NC

  3. 3

    Entocort EC, AstraZeneca, Wilmington, Del


  1. Top of page
  2. Abstract
  3. Materials and Methods
  4. Results
  5. Discussion
  6. Acknowledgments
  7. References