Effect of levothyroxine administration on hemostatic analytes in Doberman Pinschers with von Willebrand disease.

Levothyroxine administration has been suggested to be an effective treatment for canine von Willebrand disease (vWd), but evidence supporting this treatment is lacking. Effects of levothyroxine administration were evaluated in 8 euthyroid Doberman Pinschers with plasma von Willebrand factor (vWf) concentrations < 15%, characteristic of type 1 vWd. Levothyroxine (0.04 mg/kg PO q12h) and placebo were administered for 30 days in a 2-period, 2-treatment, double-blinded, crossover design with a 30-day washout period between treatments. Buccal mucosal bleeding time (BMBT), plasma vWf concentration (vWf: Ag), vWf collagen binding activity (vWf:CBA), factor VIII coagulant activity (FVIII:C), and serum concentrations of total thyroxine (T4), free thyroxine (fT4), 3,5,3'-triiodothyronine (T3), and thyroid-stimulating hormone (TSH) were measured on days 0, 2, and 30 of each treatment period. The 8 dogs (1 male, 7 females) had markedly low plasma vWf:Ag (mean, 8.9%; reference range, 70-180%) and vWf:CBA (mean, 11.1%; reference range, >70%). Response to placebo versus levothyroxine treatment was not significantly different between groups at day 0, 2, or 30 for BMBT, vWf:Ag, vWf:CBA, and FVIII:C. Serum T4, fT4, and T3 concentrations were significantly higher and serum TSH significantly lower in the levothyroxine-treated group than in the placebo group at days 2 and 30. Administration of levothyroxine at 0.04 mg/kg caused laboratory evidence of hyperthyroidism but did not affect plasma FVIII:C and vWf:Ag concentrations or vWf-dependent collagen binding and BMBT. The results of this study failed to identify a direct action of levothyroxine supplementation on plasma vWf concentration or activity in euthyroid Doberman Pinschers with vWd.

Effects of Carolina rinse solution, dimethyl sulfoxide, and the 21-aminosteroid, U-74389G, on microvascular permeability and morphology of the equine jejunum after low-flow ischemia and reperfusion.

OBJECTIVE: To evaluate effects of Carolina rinse solution, dimethyl sulfoxide (DMSO), and 21-aminosteroid, U-74389G, on microvascular permeability and morphology of the equine jejunum after low-flow ischemia and reperfusion. ANIMALS: 20 healthy adult horses. PROCEDURE: Under anesthesia, full-thickness biopsy specimens of a distal portion of the jejunum were obtained for baseline measurements. In addition to a control segment, 2 jejunal segments were identified as sham-operated or experimental segments. Experimental segments underwent 60 minutes of low-flow ischemia and 3.5 hours of reperfusion. Treatments were as follows: U-74389G (3 mg/kg, IV; 6 horses), DMSO (20 mg/kg, IV; 6) diluted in 1 L of saline (0.9% NaCl) solution, local perfusion (via jejunal artery) of Carolina rinse solution (0.5 mL/kg; 4), and local perfusion of lactated Ringer's solution (0.5 mL/kg; 4). RESULTS: Jejunal microvascular permeability was significantly lower after treatment with Carolina rinse solution or DMSO, compared with U-74389G or lactated Ringer's solution treatments. After DMSO treatment, serosal- and submucosal-layer edema was significantly increased in experimental segments, compared with control or sham-operated segments; however, edema increases were significantly less than for lactated Ringer's solution or U-74389G treatments. Significant decreases in intestinal wet weight-to-dry weight ratio were found following Carolina rinse solution or DMSO treatments, compared with lactated Ringer's solution or U-74389G treatments. Edema formation and leukocyte infiltration in jejunal segments of horses treated with lactated Ringer's solution or U-74389G were increased, compared with Carolina rinse solution or DMSO treatments. CONCLUSIONS AND CLINICAL RELEVANCE: Carolina rinse solution and DMSO may be protective against ischemia-reperfusion injury in the equine jejunum.

SNOMED representation of explanatory knowledge in veterinary clinical pathology.

BACKGROUND: The Systematized Nomenclature of Medicine (SNOMED) is an established standard nomenclature for the expression of human and veterinary medical concepts. Nomenclature standards ease sharing of medical information, create common points of understanding, and improve data aggregation and analysis. OBJECTIVES: The objective of this study was to determine whether SNOMED adequately represented concepts relevant to veterinary clinical pathology. METHODS: Concepts were isolated from 3 different types of clinical pathology documents: 1) a textbook (Textbook), 2) the Results sections of industry pathology reports (Findings), and Discussion sections from industry pathology reports (Discussion). Concepts were matched (mapped) by 2 reviewers to semantically-equivalent SNOMED concepts. A quality score of 3 (good match), 2 (problem match), or 1 (no match) was recorded along with the SNOMED hierarchical location of each mapped concept. Results were analyzed using Cohen's Kappa statistic to assess reviewer agreement and chi-square tests to evaluate association between document type and quality score. RESULTS: The percentage of good matches was 48.3% for the Textbook, 45.4% for Findings, and 47.5% for Discussion documents, with no significant difference among documents. Of remaining concepts, 40% were partially expressed by SNOMED and 14% did not match. Mean reviewer agreement on quality score assignments was 76.8%. CONCLUSIONS: Although SNOMED representation of veterinary clinical pathology content was limited, missing and problem concepts were confined to a relatively small area of terminology. This limitation should be addressed in revisions of SNOMED to optimize SNOMED for veterinary clinical pathology applications.

Factor X deficiency in a Jack Russell terrier.

Deficiency in factor X (Stuart-Prower factor) was identified in a 7-month-old spayed female Jack Russell Terrier following recurrent bleeding episodes. Various relatives were screened for factor X deficiency and low and subnormal levels were identified in the father and paternal grandmother, respectively. Factor X deficiency has been previously documented in a family of American Cocker Spaniels, in which the inheritance pattern appeared to be an autosomal dominant trait with variable expression. This is the first report describing this coagulopathy in the Jack Russell Terrier.