Impaired endogenous fibrinolytic capacity in prehypertensive men.

Prehypertension (blood pressure (BP) 120-139/80-89 mm Hg) is associated with an increased risk for future atherothrombotic events. Although the mechanisms underlying this elevated risk are not completely understood, one possibility is that prehypertension is associated with impaired endothelial fibrinolytic capacity. We tested the hypothesis that vascular endothelial release of tissue-type plasminogen activator (t-PA) is impaired in prehypertensive men. Net endothelial release of t-PA was determined, in vivo, in response to intrabrachial infusions of bradykinin (12.5, 25, 50 ng per 100 ml tissue per min) and sodium nitroprusside at (1.0, 2.0, 4.0 µg per 100 ml tissue per min) in 42 middle-age and older men: 16 normotensive (BP range: 100-119/57-79 mm Hg); 16 prehypertensive (BP range: 120-139/76-89 mm Hg); and 10 hypertensive (BP range: 140-150/74-100 mm Hg). Net release of t-PA antigen was ~25% lower (P<0.05) in the prehypertensive (-0.9 ± 0.8 to 42.4 ± 5.3 ng per 100 ml tissue per min) compared with the normotensive (0.5 ± 1.0 to 53.9 ± 6.5 ng per 100 ml tissue per min) men. There was no significant difference in t-PA release between the hypertensive (-1.8 ± 1.6 to 40.8 ± 6.6 ng per 100 ml tissue per min) and prehypertensive groups. Sodium nitroprusside did not significantly alter the t-PA release in any group. These data indicate that endothelial t-PA release is diminished in prehypertensive men. Further, the level of impairment in t-PA release seen with clinical hypertension is already apparent in the prehypertensive state. Impaired endothelial fibrinolytic function may underlie the increased atherothrombotic risk associated with BP in the prehypertensive range.

Randomized, controlled trial of budesonide and prednisone for the treatment of idiopathic inflammatory bowel disease in dogs.

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

Association of hepatic necrosis with trimethoprim sulfonamide administration in 4 dogs.

Hepatic necrosis in association with trimethoprim-sulfonamide (TMS) combination therapy was diagnosed in 4 dogs based on history, clinical presentation, and examination of histopathologic specimens collected postmortem. Duration of TMS therapy prior to onset of clinical signs ranged from 4 to 30 days. The dose of TMS ranged from 18 mg/kg to 53 mg/kg bid. Despite supportive medical therapy, all dogs died or were euthanized due to hepatic failure. This report highlights the potential for hepatotoxicity during TMS therapy. Duration of therapy, type of TMS combination, and dose did not appear related to the development of toxicity. The low number of dogs affected suggests an idiosyncratic drug reaction.

Long-term complications of diabetes mellitus, Part II: Gastrointestinal and infectious.

Numerous gastrointestinal and infectious diseases are associated with long-standing and often poorly controlled DM in humans. Although not as well documented in veterinary patients, the veterinary practitioner must always have an index of suspicion for the possibility of these complications. Because the clinical signs of a number of these problems are identical, proper diagnostic procedures need to be used to differentiate among the gastrointestinal and even infectious problems. In all cases, stringent blood glucose control is the common denominator in effective treatment. Other agents can be used both to assist in short-term control and for long-term therapy.

Monoclonal gammopathy in a dog with plasmacytic gastroenterocolitis.

Monoclonal gammopathy associated with plasmacytic gastroenterocolitis was diagnosed in a dog. Treatment consisted of immunosuppressive drugs and dietary manipulation. The gammopathy resolved. Fifteen months after initial diagnosis, the dog had a relapse of intestinal disease and recurrence of the gammopathy. After inducing a second remission, the gammopathy again resolved.