Comparison of oral prednisone and prednisone combined with metronidazole for induction therapy of canine inflammatory bowel disease: a randomized-controlled trial.

BACKGROUND: Although prednisone and metronidazole are commonly used to treat canine inflammatory bowel disease (IBD), no randomized-controlled trials have been performed. HYPOTHESIS: Combination drug therapy with prednisone and metronidazole will be more effective than prednisone alone for treatment of canine IBD. Reduction in disease severity will be accompanied by decreased canine IBD activity index (CIBDAI) scores and serum C-reactive protein (CRP) concentrations. ANIMALS: Fifty-four pet dogs diagnosed with IBD of varying severity. METHODS: Dogs were randomized to receive oral prednisone (1 mg/kg; n = 25) or prednisone and metronidazole (10 mg/kg; n = 29) twice daily for 21 days. Clinical (CIBDAI) scores and serum CRP were determined at diagnosis and after 21 days of drug therapy. The primary efficacy measure was remission at 21 days, defined as a 75% or greater reduction in baseline CIBDAI score. RESULTS: Differences between treatments in the rate of remission (both exceeding 80%) or the magnitude of its change over time were not observed. CRP concentrations in prednisone-treated dogs were increased because of many dogs having active disease. Both treatments reduced CRP in comparison with pretreatment concentrations. An interaction between CIBDAI and CRP was identified in 42 of 54 dogs (78%), whereas 8 of 54 dogs (15%) showed disagreement between these indices. CONCLUSIONS AND CLINICAL IMPORTANCE: Prednisone is as effective as combined treatment with prednisone and metronidazole for induction therapy of canine IBD. CRP may be normal or increased in dogs with IBD and may be useful in assessing the response of individual dogs to treatment along with changes in the CIBDAI.

Fluorescence in situ hybridization confirms clearance of visible Helicobacter spp. associated with gastritis in dogs and cats.

BACKGROUND: The results of studies examining the role of Helicobacter spp. in the pathogenesis of canine and feline gastritis are inconclusive. Furthermore, data evaluating the effectiveness of medical therapy for eradication of Helicobacter infection are limited. AIM: To detect Helicobacter spp. in mucosal biopsies of dogs and cats diagnosed with gastritis, with fluorescence in situ hybridization (FISH). ANIMALS: Three dogs and 2 cats with signs of chronic gastrointestinal disease. METHODS: Dogs and cats infected with Helicobacter spp. were treated with triple antimicrobial therapy and fed an elimination diet for 21 days. Helicobacter spp. status in endoscopic (3 dogs, 1 cat) or surgical biopsies (1 cat) of gastric mucosa was compared pre- and posttreatment in each animal by histology, FISH analysis, and polymerase chain reaction (PCR). RESULTS: Gastritis of varying severity with intraglandular spiral bacteria was observed in all animals. Pretreatment diagnostic tests confirmed the presence of mucosal Helicobacter spp. in all animals by FISH and histopathology and in 4/5 animals by PCR. Rapid resolution of vomiting episodes was observed in all animals. Gastric biopsies performed after triple therapy revealed clearance of visible Helicobacter spp. by histopathology and negative FISH analysis, as well as PCR in all animals. CONCLUSIONS AND CLINICAL IMPORTANCE: Application of FISH to routine biopsy specimens enabled rapid and specific identification of Helicobacter spp. within the gastric mucosa of dogs and cats. Although medical therapy was useful in resolution of clinical signs and clearance of visible Helicobacter spp. in gastric biopsies, gastric inflammation persisted.

Prognostic value of the signal-averaged electrocardiogram and a prolonged QRS in ischemic and nonischemic cardiomyopathy.

Studies of electrocardiographic predictors of mortality in patients with chronic heart failure have reached varying conclusions. Differences in the characteristics of the patients studied may explain the conflicting results regarding both a prolonged QRS and an abnormal signal-averaged electrocardiogram (SAE). We therefore investigated the impact of the etiology of heart failure on the prognostic importance of a prolonged QRS and an abnormal SAE in 200 patients with heart failure. Patients were categorized according to etiology of heart failure and electrocardiographic parameters. The mortality of patients with a prolonged QRS was compared with mortality in those with both abnormal and normal SAEs. This was done for the entire group, and separately for those with ischemic and those with nonischemic cardiomyopathy. The mean follow-up was 18.8 months. Nonischemic patients with a prolonged QRS had significantly worse survival than other patients. However, nonischemic patients with an abnormal SAE did not have a worse prognosis than patients with a normal SAE. One-year survival of patients with a prolonged QRS was 71%, compared with 98% in patients with a normal and 87% in patients with an abnormal SAE (p < 0.05). In contrast, a prolonged QRS was not a predictor of poor prognosis in patients with ischemic cardiomyopathy (81% one year mortality). Patients with ischemic cardiomyopathy and an abnormal SAE tended to have a poorer survival than patients with a normal SAE (73% and 81% one year mortality, respectively). Thus, the etiology of heart failure affects the prognostic importance of both a prolonged QRS and an abnormal SAE.

The hemodynamic actions of the antiarrhythmic agent ipazilide fumarate in patients with congestive heart failure.

Ipazilide fumarate is an investigational antiarrhythmic agent with Vaughan Williams class I and III actions, including prolongation of both ventricular refractoriness and action potential duration. Because of the frequent use of antiarrhythmic agents in patients with heart failure, we investigated the hemodynamic effects of oral administration of 400, 200, and 100 mg of ipazilide fumarate in 15 patients with congestive heart failure. There was a marked hemodynamic response to ipazilide, with the peak effect noted 2 hours after drug administration. In patients who received 400 mg ipazilide, the mean cardiac index was decreased by 0.5 L/min/m2 at 2 hours (p < 0.05). After 200 and 100 mg ipazilide, the decreases were a more modest 0.3 and 0.1 L/min/m2, respectively. The mean arterial pressure also decreased in a dose- and time-dependent manner, although this did not reach statistical significance for any of the doses. Left ventricular filling pressure, right atrial pressure, and heart rate were not altered by ipazilide. Plasma concentrations of ipazilide peaked 90 minutes after administration of 100 or 200 of the drug, but peak concentrations were noted 3 hours after administration of 400 mg. The hemodynamic response correlated with the plasma concentration of ipazilide determined contemporaneously. We conclude that, as with most antiarrhythmic agents, single-dose administration of ipazilide fumarate can cause clinically significant hemodynamic deterioration.

Effects of intravenous magnesium sulfate on arrhythmias in patients with congestive heart failure.

Intravenous magnesium is an effective treatment for ventricular tachycardia of some etiologies, and in patients with congestive heart failure low serum magnesium concentrations are associated with frequent arrhythmias and high mortality. This suggests that magnesium administration may decrease the frequency of ventricular arrhythmias in patients with heart failure. We therefore assessed the impact of an intravenous magnesium infusion upon the frequency of ventricular premature depolarizations in 40 patients with New York Heart Association (NYHA) class II to IV heart failure and serum magnesium < or = 2.0 mg/dl. Within 1 week of a baseline 6-hour ambulatory electrocardiographic recording, an infusion of 0.2 mEq/kg of MgSO4 was given over 1 hour and a repeat 6-hour recording was obtained. There was an inverse relationship between the change in magnesium concentration and the change in frequency of premature ventricular depolarizations; premature ventricular depolarizations declined by 134 +/- 207 hr-1 in patients in whom serum magnesium concentration increased > or = 0.75 mg/dl, but increased by 72 +/- 393 hr-1 in patients with a change < 0.75 mg/dl (p < 0.05). For all patients, the frequency of premature ventricular depolarizations was 283 +/- 340 hr-1 pretreatment and 220 +/- 269 hr-1 following magnesium infusion (p = 0.21). Patients with > or = 300 premature ventricular depolarizations hr-1 demonstrated a decrease from 794 +/- 309 to 369 +/- 223 hr-1 (p < 0.001). Intravenous magnesium administration decreased the frequency of couplets from 233 +/- 505 to 84 +/- 140 (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)