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- Author or Editor: Martin J. Fettman x
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Objective—To determine historical, physical examination, clinicopathologic, and postmortem findings in horses with putative uremic encephalopathy.
Animals—5 horses with renal failure and neurologic disease not attributable to abnormalities in any other organ system.
Procedure—Medical records from 1978 to 1998 were examined for horses with renal disease and neurologic signs not attributable to primary neurologic, hepatic, or other diseases. Signalment, history, physical examination findings, clinicopathologic data, renal ultrasonographic findings, and postmortem data were reviewed.
Results—Of 332 horses with renal disease, 5 met selection criteria. Historical findings, physical examination findings, clinicopathologic data, ultrasonographic data, and postmortem findings were consistent with chronic renal failure. Swollen astrocytes were detected in all 4 horses examined at necropsy.
Conclusions and Clinical Relevance—A single criterion was not determined to be pathognomonic for uremic encephalopathy in horses. Uremic encephalopathy should be considered as a differential diagnosis in horses with evidence of chronic renal failure and encephalopathic neurologic sign not attributable to other causes. Astrocyte swelling, which was common to all 4 horses examined at necropsy, may serve as a microscopic indicator of uremic encephalopathy in horses. (J Am Vet Med Assoc 2001;218:560–566)
Objective—To evaluate plasma glipizide concentration and its relationship to plasma glucose and serum insulin concentrations in healthy cats administered glipizide orally or transdermally.
Animals—15 healthy adult laboratory-raised cats.
Procedure—Cats were randomly assigned to 2 treatment groups (5 mg of glipizide, PO or transdermally) and a control group. Blood samples were collected 0, 10, 20, 30, 45, 60, 90, and 120 minutes and 4, 6, 10, 14, 18, and 24 hours after administration to determine concentrations of insulin, glucose, and glipizide.
Results—Glipizide was detected in all treated cats. Mean ± SD transdermal absorption was 20 ± 14% of oral absorption. Mean maximum glipizide concentration was reached 5.0 ± 3.5 hours after oral and 16.0 ± 4.5 hours after transdermal administration. Elimination half-life was variable (16.8 ± 12 hours orally and 15.5 ± 15.3 hours transdermally). Plasma glucose concentrations decreased in all treated cats, compared with concentrations in control cats. Plasma glucose concentrations were significantly lower 2 to 6 hours after oral administration, compared with after transdermal application; concentrations were similar between treatment groups and significantly lower than for control cats 10 to 24 hours after treatment.
Conclusions and Clinical Relevance—Transdermal absorption of glipizide was low and inconsistent, but analysis of our results indicated that it did affect plasma glucose concentrations. Transdermal administration of glipizide is not equivalent to oral administration. Formulation, absorption, and stability studies are required before clinical analysis can be performed. Transdermal administration of glipizide cannot be recommended for clinical use at this time. (Am J Vet Res 2005;66:581–588)
Objective—To determine essential fatty acid concentrations in plasma and tissue before and after supplementation with n-3 fatty acids in dogs with atopic dermatitis.
Animals—30 dogs with atopic dermatitis.
Procedure—Dogs received supplemental flaxseed oil (200 mg/kg/d), eicosapentaenoic acid (EPA; 50 mg/kg/d)-docosahexaenoic acid (DHA; 35 mg/kg/d), or mineral oil as a placebo in a doubleblind, placebo-controlled, randomized trial. Clinical scores and plasma and cutaneous concentrations of linoleic acid, arachidonic acid, α-linolenic acid (α-LLA), EPA, DHA, prostaglandin E2, and leukotriene B4 were determined.
Results—Total plasma concentrations of α-LLA and EPA increased and those of arachidonic acid decreased significantly with administration of EPADHA, and concentrations of α-LLA increased with flaxseed oil supplementation; nevertheless, there was no significant change in the concentrations of these fatty acids or eicosanoids in the skin. There was no correlation between clinical scores and plasma or cutaneous concentrations for any of the measured fatty acids or eicosanoids.
Conclusion and Clinical Relevance—Results indicated that at the dose used, neither the concentrations of fatty acids in skin or plasma nor a decrease in the production of inflammatory eicosanoids was a major factor involved in the mechanism of action in dogs with atopy that responded to fatty acid supplementation. (Am J Vet Res 2005;66:868–873)
Objective—To determine effects of various diets on the pharmacokinetics of phenobarbital and the interactive effects of changes in body composition and metabolic rate.
Animals—27 healthy sexually intact adult female Beagles.
Procedure—Pharmacokinetic studies of phenobarbital were performed before and 2 months after dogs were fed 1 of 3 diets (group 1, maintenance diet; group 2, protein-restricted diet; group 3, fat- and protein-restricted diet) and treated with phenobarbital (approx 3 mg/kg [1.4 mg/lb] of body weight, PO, q 12 h). Pharmacokinetic studies involved administering phenobarbital (15 mg/kg [6.8 mg/lb], IV) and collecting blood samples at specific intervals for 240 hours. Effects of diet and time were determined by repeated-measures ANOVA.
Results—Volume of distribution, mean residence time, and half-life (t1/2) of phenobarbital significantly decreased, whereas clearance rate and elimination rate significantly increased with time in all groups. Dietary protein or fat restriction induced significantly greater changes: t1/2 (hours) was lower in groups 2 (mean ± SD; 25.9 ± 6.10 hours) and 3 (24.0 ± 4.70) than in group 1 (32.9 ± 5.20). Phenobarbital clearance rate (ml/kg/min) was significantly higher in group 3 (0.22 ± 0.05 ml/kg/min) than in groups 1 (0.17 ± 0.03) or 2 (0.18 ± 0.03). Induction of serum alkaline phosphatase activity (U/L) was greater in groups 2 (192.4 ± 47.5 U/L) and 3 (202.0 ± 98.2) than in group 1 (125.0 ± 47.5).
Conclusions and Clinical Relevance—Clinically important differences between diet groups were observed regarding pharmacokinetics of phenobarbital, changes in CBC and serum biochemical variables, and body composition. Drug dosage must be reevaluated if a dog's diet, body weight, or body composition changes during treatment. Changes in blood variables that may indicate liver toxicosis caused by phenobarbital may be amplified by diet-drug interactions. (J Am Vet Med Assoc 2000;217:847–852)
Objective—To evaluate changes in resting energy expenditure (REE) as well as protein and carbohydrate metabolism in dogs with osteosarcoma (OSA).
Animals—15 weight-stable dogs with OSA that did not have other concurrent metabolic or endocrine illness and twelve 1-year-old sexually intact female Beagles (control dogs).
Procedures—Indirect calorimetry was performed on all dogs to determine REE and respiratory quotient (RQ). Stable isotope tracers (15N-glycine, 4.5 mg/kg of body weight, IV; 6,6-deuterium-glucose, 4.5 mg/kg, IV as a bolus, followed by continuous-rate infusion at 1.5 mg/kg/h for 3 hours) were used to determine rate of protein synthesis and glucose flux in all dogs. Dualenergy x-ray absorptiometry (DEXA) scans were performed to determine total body composition.
Results—Accounting for metabolic body size, REE in dogs with OSA was significantly higher before and after surgery, compared with REE of healthy control dogs. The RQ values did not differ significantly between groups. Dogs with OSA also had decreased rates of protein synthesis, increased urinary nitrogen loss, and increased glucose flux during the postoperative period.
Conclusions and Clinical Relevance—Alterations in energy expenditure, protein synthesis, urinary nitrogen loss, and carbohydrate flux were evident in dogs with OSA, similar to results documented in humans with neoplasia. Changes were documented in REE as well as protein and carbohydrate metabolism in dogs with OSA. These changes were evident even in dogs that did not have clinical signs of cachexia. (Am J Vet Res 2001;62:1234–1239)
Objective—To determine outcome for dogs with grade-II mast cell tumors treated with surgery alone.
Procedures—Medical records were examined, and signalment; location and size of tumor; staging status; dates of local recurrence, metastasis, death, or last follow-up examination; status of surgical margins; previous surgery; postoperative complications; and cause of death were recorded. Follow-up information was obtained via reexamination or telephone conversations with owners or referring veterinarians. Univariate analysis was performed to identify prognostic factors.
Results—60 tumors in 55 dogs were included. Median follow-up time was 540 days. Three (5%) mast cell tumors recurred locally; median time to local recurrence was 62 days. Six (11%) dogs developed another mast cell tumor at a different cutaneous location; median time to a different location was 240 days. Three (5%) dogs developed metastases; median time to metastasis was 158 days. Fourteen dogs died; 3 deaths were related to mast cell tumor, and 7 were unrelated. The relationship with mast cell tumor was not known for 4. Median survival times were 151, 841, and 827 days, respectively, for these 3 groups. Forty-six (84%) dogs were free of mast cell tumors during the study period. A reliable prognostic factor could not be identified.
Conclusions and Clinical Relevance—Results suggest that additional local treatment may not be required after complete excision of grade-II mast cell tumors and that most dogs do not require systemic treatment. (J Am Vet Med Assoc 2001;218:1120–1123)
Objective—To determine the effect of dietary n-3 fatty acids on the pharmacokinetics of doxorubicin in dogs with lymphoma.
Animals—23 dogs with lymphoma in stages IIIa, IVa, and Va.
Procedure—Dogs receiving doxorubicin chemotherapy were randomly allocated to receive food with a high (test group) or low (control group) content of n-3 fatty acids. Serum doxorubicin and doxorubicinol concentrations were measured via high-performance liquid chromatography before and 6 to 9 weeks after initiation of the diets. Lymph node concentrations of doxorubicin were assessed 6 hours after the initial treatment. Dogs' body composition was assessed by means of dual-energy x-ray absorptiometry scans.
Results—No significant differences in doxorubicin pharmacokinetics were detected between treatment groups. Significant differences existed between the first and second sampling times among all dogs for area under the curve, maximum serum concentration, and clearance. Differences in body composition did not affect measured pharmacokinetic variables. The terminal elimination half-life was longer in dogs in which a long-term remission was achieved than in dogs that did not have remission.
Conclusions and Clinical Relevance—Dietary supplementation of n-3 fatty acids is common in veterinary patients with neoplasia, but supplementation did not affect doxorubicin pharmacokinetics in this population of dogs. Explanations for the beneficial effects of n-3 fatty acids other than alterations in the pharmacokinetics of chemotherapy drugs should be investigated. Dogs may metabolize drugs differently prior to remission of lymphoma than when in remission. The pharmacokinetics of doxorubicin at the time of the first administration may predict response to treatment.