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- Author or Editor: David S. Bruyette x
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Summary
Hypothyroidism is 2 possible predisposing factor in a number of disorders of companion psittacine birds. We developed and validated a thyroid-stimulating hormone (tsh) response testing protocol for cockatiels (Nymphicus hollandicus), using 0.1 IU of tsh/bird given IM, with blood sample collection at 0 and 6 hours after tsh, and a commercial radioimmunoassay for thyroxine (T4). This protocol was used to document a seasonal sex difference in stimulated T4 values— females responded with higher T4 values than those in males in summer—and a stress-induced depression of baseline T4 values was detected in a group of cockatiels with normal tsh response. An experimental model for mature-onset hypothyroidism in cockatiels was created by radiothyroidectomizing cockatiels with 3.7 MBq (100 μCi) of 131I/bird given IV. Induction of the hypothyroid state was confirmed by baseline T4 concentration, tsh response test results, thyroid pertechnetate scintigraphy, and gross and microscopic examinations. Classical signs of hypothyroidism (eg, hypercholesterolemia, obesity, poor feathering) were lacking or mild at 48 days after thyroid ablation.
Abstract
Objective—To evaluate thyroid function in healthy Greyhounds, compared with healthy non-Greyhound pet dogs, and to establish appropriate reference range values for Greyhounds.
Animals—98 clinically normal Greyhounds and 19 clinically normal non-Greyhounds.
Procedures—Greyhounds were in 2 groups as follows: those receiving testosterone for estrus suppression (T-group Greyhounds) and those not receiving estrus suppressive medication (NT-group Greyhounds). Serum thyroxine (T4) and free thyroxine (fT4) concentrations were determined before and after administration of thyroid-stimulating hormone (TSH) and thyroid-releasing hormone (TRH). Basal serum canine thyroid stimulating hormone (cTSH) concentrations were determined on available stored sera.
Results—Basal serum T4 and fT4 concentrations were significantly lower in Greyhounds than in non- Greyhounds. Serum T4 concentrations after TSH and TRH administration were significantly lower in Greyhounds than in non-Greyhounds. Serum fT4 concentrations after TSH and TRH administration were significantly lower in NT-group than T-group Greyhounds and non-Greyhounds. Mean cTSH concentrations were not different between Greyhounds and non-Greyhounds.
Conclusions and Clinical Relevance—Previously established canine reference range values for basal serum T4 and fT4 may not be appropriate for use in Greyhounds. Greyhound-specific reference range values for basal serum T4 and fT4 concentrations should be applied when evaluating thyroid function in Greyhounds. Basal cTSH concentrations in Greyhounds are similar to non-Greyhound pet dogs. (Am J Vet Res 2001;62:1130–1133)
Abstract
Objective—To compare adrenal gland stimulation achieved following administration of cosyntropin (5 μg/kg [2.3 μg/lb]) IM versus IV in healthy dogs and dogs with hyperadrenocorticism.
Design—Clinical trial.
Animals—9 healthy dogs and 9 dogs with hyperadrenocorticism.
Procedures—In both groups, ACTH stimulation was performed twice. Healthy dogs were randomly assigned to receive cosyntropin IM or IV first, but all dogs with hyperadrenocorticism received cosyntropin IV first. In healthy dogs, serum cortisol concentration was measured before (baseline) and 30, 60, 90, and 120 minutes after cosyntropin administration. In dogs with hyperadrenocorticism, serum cortisol concentration was measured before and 60 minutes after cosyntropin administration.
Results—In the healthy dogs, serum cortisol concentration increased significantly after administration of cosyntropin, regardless of route of administration, and serum cortisol concentrations after IM administration were not significantly different from concentrations after IV administration. For both routes of administration, serum cortisol concentration peaked 60 or 90 minutes after cosyntropin administration. In dogs with hyperadrenocorticism, serum cortisol concentration was significantly increased 60 minutes after cosyntropin administration, compared with baseline concentration, and concentrations after IM administration were not significantly different from concentrations after IV administration.
Conclusions and Clinical Relevance—Results suggest that in healthy dogs and dogs with hyperadrenocorticism, administration of cosyntropin at a dose of 5 μg/kg, IV or IM, resulted in equivalent adrenal gland stimulation.
Abstract
OBJECTIVE To evaluate clinical signs, endocrine test results, and pituitary tumor size for dogs with medically managed pituitary-dependent hyperadrenocorticism (PDH) and macroadenoma following 6 months of concurrent treatment with pasireotide.
DESIGN Prospective case series.
ANIMALS 9 client-owned dogs with PDH and macroadenoma in which PDH had been successfully managed with adrenal-directed treatment (trilostane or mitotane).
PROCEDURES Dogs were given pasireotide (0.03 mg/kg [0.014 mg/lb], SC, q 12 h) for 6 months, while adrenal-directed treatment was continued. Physical examination, basic clinicopathologic testing, ACTH stimulation testing, and plasma ACTH concentration measurement were performed before (baseline) and 3 and 6 months after treatment began. Measurements of pituitary gland volume and pituitary gland-to-brain ratio were performed via MRI at baseline and 6 months after treatment began.
RESULTS No dog developed neurologic abnormalities or signs of adverse effects during the study period. No differences from baseline were identified in clinicopathologic values, ACTH stimulation test results, or plasma ACTH concentration at the 3- or 6-month assessment points. After 6 months of pasireotide treatment, 6 dogs had decreases in MRI-measured values, and 3 had increases.
CONCLUSIONS AND CLINICAL RELEVANCE Pasireotide as administered in this study had no noted adverse effects on dogs with PDH and macroadenoma successfully managed with standard treatment. Placebo-controlled, randomized studies are needed to determine whether pasireotide protects from the development of neurologic signs or improves outcome in dogs with pituitary macroadenomas.
Summary
The effect of orally administered ketoconazole on plasma cortisol concentration in dogs with hyperadrenocorticism was evaluated. Every 30 minutes from 0800 hours through 1600 hours and again at 1800 hours, 2000 hours, and 0800 hours the following morning, 15 clinically normal dogs and 49 dogs with hyperadrenocorticism had plasma samples obtained and analyzed for cortisol concentration. The mean (± sd) plasma cortisol concentration for the initial 8-hour testing period was highest in 18 dogs with adrenocortical tumor (5.3 ±1.6 µg/dl), lowest in 15 control dogs (1.3 ± 0.5 µg/dl), and intermediate in 31 dogs with pituitary-dependent hyperadrenocorticism (pdh; 3.4 ± 1.2 µg/dl). Results in each of the 2 groups of dogs with hyperadrenocorticism were significantly (P < 0.05) different from results in control dogs, but not from each other. The same cortisol secretory experiment was performed, using 8 dogs with hyperadrenocorticism (5 with pdh; 3 with adrenocortical tumor) before and after administration at 0800 hours of 15 mg of ketoconazole/kg of body weight. Significant (P < 0.05) decrease in the 8-hour mean plasma cortisol concentration (0.9 ± 0.2 µg/dl) was observed, with return to baseline plasma cortisol concentration 24 hours later.
Twenty dogs with hyperadrenocorticism (11 with pdh, 9 with adrenocortical tumor) were treated with ketoconazole at a dosage of 15 mg/kg given every 12 hours for a half month to 12 months. The disease in 2 dogs with pdh failed to respond to treatment, but 18 dogs had complete resolution of clinical signs of hyperadrenocorticism and significant (P < 0.05) reduction in plasma cortisol responsiveness to exogenous adrenocorticotropin (acth). The healthy control dogs had a mean baseline plasma cortisol concentration of 1.4 ± 0.4 µg/dl and a post-acth cortisol concentration of 10.6 ± 3.1 µg/dl. Before ketoconazole administration, all 11 dogs with pdh had a mean baseline plasma cortisol concentration of 4.4 ± l.9 µg/dl and a post-acth cortisol concentration of 33.6 ± 17.6 µg/dl. The 9 dogs with adrenocortical tumor had a mean baseline plasma cortisol concentration of 4.4 ± 1.3 µg/dl and post-acth cortisol concentration of 28.1 ± 14.1 µg/dl. After 5 days of ketoconazole administration, the post-acth plasma cortisol concentration for dogs with pdh or adrenocortical tumor was 4.0 ± 5.4 µg/dl and 6.0 ± 3.3 µg/dl, respectively. Similar responses were observed after 60, 180, and 360 days of ketoconazole treatment.
Abstract
OBJECTIVE
To determine whether serum total thyroxine (TT4) concentration at admission to an intensive care unit (ICU) was associated with mortality rate and duration of hospitalization for critically ill dogs.
ANIMALS
166 client-owned dogs that were hospitalized in the ICU of a private veterinary practice from January 2013 through December 2016 and for which serum TT4 concentration had been measured at admission.
PROCEDURES
Medical records were reviewed to collect data regarding patient signalment, concurrent illnesses, medications, reason for hospitalization, outcome (death, euthanasia, or survival to hospital discharge), duration of hospitalization, and initial serum TT4 concentration.
RESULTS
Mean age of the 166 dogs was 8.6 years (range, 1 to 16 years). Overall mortality rate was 15.7%, with 26 dogs failing to survive to hospital discharge. Of these 26 dogs, 7 died and 19 were euthanized. No significant association was identified between serum TT4 concentration at admission and survival to discharge (yes or no) or duration of hospitalization. Age was significantly associated with survival to discharge, with older dogs less likely to survive than younger dogs. Duration of hospitalization was also associated with survival to discharge, with longer hospital stays associated with a lower likelihood of survival to discharge.
CONCLUSIONS AND CLINICAL RELEVANCE
Findings suggested that serum TT4 concentration at admission to an ICU had no prognostic value in this population of critically ill dogs.
Abstract
Objective—To evaluate response rate and duration of malignant melanomas in dogs treated with carboplatin.
Design—Retrospective study.
Animals—27 client-owned dogs with spontaneously occurring measurable malignant melanomas.
Procedure—Records of dogs with melanomas treated with carboplatin from October 1989 to June 2000 were reviewed. Carboplatin was administered IV at doses of 300 or 350 mg/m2 of body surface area. Response to treatment and evidence of drug toxicity were determined.
Result—Response to treatment could be evaluated in 25 dogs. Of those, overall response rate was 28%. One dog had a complete response, 6 (24%) dogs had a partial response (> 50% reduction in tumor burden). Median duration of partial response was 165 days. Eighteen dogs had stable disease (n = 9; 36%) or progressive disease (9; 36%). Response to treatment was significantly associated with carboplatin dose on a milligram per kilogram basis (15.1 mg/kg [6.9 mg/lb] of body weight vs 12.6 mg/kg [5.7 mg/lb]). Evidence of gastrointestinal toxicosis could be assessed in 27 dogs. Mean body weight of 5 dogs that developed gastrointestinal toxicosis was significantly less than that of 22 dogs without gastrointestinal toxicosis (9.9 kg [21.8 lb] vs 19.3 kg [42.5 lb]).
Conclusions and Clinical Relevance—Carboplatin had activity against macroscopic spontaneously occurring malignant melanomas in dogs and should be considered as an adjunctive treatment for microscopic local or metastatic tumors. Gastrointestinal toxicosis was associated with body weight. Because small dogs are more likely to have adverse gastrointestinal effects, gastrointestinal protectants should be considered for these patients. (J Am Vet Med Assoc 2001;218:1444–1448)