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- Author or Editor: Edward C. Feldman x
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Abstract
Objective—To evaluate effectiveness and incidence of adverse reactions to twice-daily lower-dose oral administration of trilostane in the treatment of dogs with naturally occurring hyperadrenocorticism (NOH).
Design—Clinical trial.
Animals—47 dogs with NOH.
Procedures—47 dogs were treated orally with trilostane (0.21 to 1.1 mg/kg [0.1 to 0.5 mg/lb], q 12 h). All dogs were reevaluated at 2 weeks and 2 months, 38 dogs at 6 months, and 28 dogs at 1 year of treatment.
Results—9 of 47 dogs had an adrenocortical tumor causing NOH, and all had good responses after 2 months (mean trilostane dosage, 0.89 mg/kg [0.40 mg/lb], q 12 h). All successfully underwent surgical adrenal tumor extirpation. Thirty-eight dogs had pituitary-dependent hyperadrenocorticism (PDH); 15 dogs did not require a dose increase during the study, and at each of 4 reevaluations, 10 of 15, 13 of 15, 14 of 15, and 11 of 11 had a good response. Twenty-three dogs with PDH had their dose or frequency of trilostane administration increased during the study. Mean trilostane dosage at 1-year reevaluation in dogs with a good response was 1.7 mg/kg (0.8 mg/lb), twice daily, or 1.1 mg/kg, 3 times daily. At each of 4 reevaluations, 17 of 23, 14 of 23, 17 of 23, and 13 of 17 dogs with PDH had a good response. Five dogs became ill because of trilostane-induced adverse effects, but only 1 required hospitalization.
Conclusions and Clinical Relevance—Administration of initial lower doses of trilostane to dogs with NOH is effective.
Abstract
Objective—To compare imaging findings in dogs with pituitary-dependent hyperadrenocorticism (PDH) that did or did not have neurologic abnormalities.
Design—Retrospective case series.
Animals—157 dogs with PDH that did (n = 73) or did not (84) have neurologic abnormalities.
Procedures—Medical records were reviewed for the presence and nature of clinical signs of CNS disease, and computed tomographic and magnetic resonance images were reviewed for evidence of a pituitary tumor.
Results—60 of the 84 (71%) dogs without neurologic abnormalities and 48 of the 73 (66%) dogs with neurologic abnormalities had a detectable pituitary tumor. However, 17 of the 84 (20%) dogs without neurologic abnormalities had a pituitary macrotumor (ie, a tumor ≥ 10 mm in height), and 41 of the 73 (56%) dogs with neurologic abnormalities did not have a detectable pituitary tumor or had a pituitary microtumor. Vague signs of CNS dysfunction (ie, lethargy, inappetence, and mental dullness) were more specific for detection of pituitary macrotumors than were CNS-specific signs (ie, seizure or blindness).
Conclusions and Clinical Relevance—Results suggested that there was no apparent relationship between a pituitary tumor and development of neurologic abnormalities in dogs with PDH. In addition, neurologic abnormalities in dogs with pituitary macrotumors were often vague (ie, lethargy, inappetence, and mental dullness).
Abstract
Objective—To evaluate the effects of twice-daily oral administration of a low-dose of trilostane treatment and assess the duration of effects after once-daily trilostane administration in dogs with naturally occurring hyperadrenocorticism (NOH).
Design—Prospective study.
Animals—28 dogs with NOH.
Procedures—22 dogs received 0.5 to 2.5 mg of trilostane/kg (0.23 to 1.14 mg/lb) orally every 12 hours initially. At intervals, dogs were reevaluated; owner assessment of treatment response was recorded. To assess drug effect duration, 16 of the 22 dogs and 6 additional dogs underwent 2 ACTH stimulation tests 3 to 4 hours and 8 to 9 hours after once-daily trilostane administration.
Results—After 1 to 2 weeks, mean trilostane dosage was 1.4 mg/kg (0.64 mg/lb) every 12 hours (n = 22 dogs; good response [resolution of signs], 8; poor response, 14). Four to 8 weeks later, mean dosage was 1.8 mg/kg (0.82 mg/lb) every 12 or 8 hours (n = 21 and 1 dogs, respectively; good response, 15; poor response, 5; 2 dogs were ill). Eight to 16 weeks after the second reevaluation, remaining dogs had good responses (mean dosages, 1.9 mg/kg [0.86 mg/lb], q 12 h [n = 13 dogs] and 1.3 mg/kg [0.59 mg/lb], q 8 h [3]). At 3 to 4 hours and 8 to 9 hours after once-daily dosing, mean post-ACTH stimulation serum cortisol concentrations were 2.60 and 8.09 μg/dL, respectively.
Conclusions and Clinical Relevance—In dogs with NOH, administration of trilostane at low doses every 12 hours was effective, although 2 dogs became ill during treatment. Drug effects diminished within 8 to 9 hours. Because of potential adverse effects, lower doses should be evaluated.
Abstract
Objective—To evaluate effect of acarbose on control of glycemia in dogs with diabetes mellitus.
Design—Prospective randomized crossover controlled trial.
Animals—5 dogs with naturally acquired diabetes mellitus.
Procedure—Dogs were treated with acarbose and placebo for 2 months each: in 1 of 2 randomly assigned treatment sequences. Dogs that weighed ≤ 10 kg (22 lb; n = 3) or > 10 kg (2) were given 25 or 50 mg of acarbose, respectively, at each meal for 2 weeks, then 50 or 100 mg of acarbose, respectively, at each meal for 6 weeks, with a 1-month interval between treatments. Caloric intake, type of insulin, and frequency of insulin administration were kept constant, and insulin dosage was adjusted as needed to maintain control of glycemia. Serum glucose concentrations, blood glycosylated hemoglobin concentration, and serum fructosamine concentration were determined.
Results—Significant differences in mean body weight and daily insulin dosage among dogs treated with acarbose and placebo were not found. Mean preprandial serum glucose concentration, 8-hour mean serum glucose concentration, and blood glycosylated hemoglobin concentration were significantly lower in dogs treated with insulin and acarbose, compared with insulin and placebo. Semisoft to watery feces developed in 3 dogs treated with acarbose.
Conclusions and Clinical Relevance—Acarbose may be useful as an adjunctive treatment in diabetic dogs in which cause for poor glycemic control cannot be identified, and insulin treatment alone is ineffective. (J Am Vet Med Assoc 2000;216:1265–1269)
Abstract
Objective—To evaluate pretreatment clinical and laboratory findings in dogs with naturally occurring primary hyperparathyroidism.
Design—Retrospective study.
Animals—210 dogs with primary hyperparathyroidism and 200 randomly selected, age-matched control dogs that did not have primary hyperparathyroidism.
Procedure—Medical records for dogs with primary hyperparathyroidism were reviewed for signalment; clinical features; and results of clinicopathologic testing, serum parathyroid hormone assays, and diagnostic imaging.
Results—Mean age of the dogs with primary hyperparathyroidism was 11.2 years (range, 6 to 17 years). The most common clinical signs were attributable to urolithiasis or urinary tract infection (ie, straining to urinate, increased frequency of urination, and hematuria). Most dogs (149 [71%]) did not have any observable abnormalities on physical examination. All dogs had hypercalcemia, and most (136 [65%]) had hypophosphatemia. Overall, 200 of the 210 (95%) dogs had BUN and serum creatinine concentrations within or less than the reference range, and serum parathyroid hormone concentration was within reference limits in 135 of 185 (73%) dogs in which it was measured. Urolithiasis was identified in 65 (31%) dogs, and urinary tract infection was diagnosed in 61 (29%). Mean serum total calcium concentration for the control dogs was significantly lower than mean concentration for the dogs with primary hyperparathyroidism, but mean BUN and serum creatinine concentrations for the control dogs were both significantly higher than concentrations for the dogs with primary hyperparathyroidism.
Conclusions and Clinical Relevance—Results suggest that urolithiasis and urinary tract infection may be associated with hypercalcemia in dogs with primary hyperparathyroidism, but that development of renal insufficiency is uncommon. (J Am Vet Med Assoc 2005;227: 756–761)
Abstract
Objective—To evaluate serum 17-hydroxyprogesterone (17-OHP) concentration measurement after administration of ACTH for use in the diagnosis of hyperadrenocorticism in dogs.
Design—Prospective study.
Animals—110 dogs.
Procedure—Serum 17-OHP concentrations were measured before and after ACTH stimulation in 53 healthy dogs to establish reference values for this study. Affected dogs had pituitary-dependent (n = 40) or adrenal tumor–associated (12) hyperadrenocorticism or potentially had atypical hyperadrenocorticism (5; diagnosis confirmed in 1 dog). In affected dogs, frequency interval and borderline and abnormal serum 17-OHP concentrations after ACTH stimulation were determined. Serum cortisol concentrations were assessed via low-dose dexamethasone suppression and ACTH stimulation tests.
Results—In healthy dogs, serum 17-OHP concentration frequency intervals were grouped by sex and reproductive status (defined as < 95th percentile). Frequency intervals of serum 17-OHP concentrations after ACTH stimulation were < 7.7, < 2.0, < 3.2, and < 3.4 ng/mL (< 23.3, < 6.1, < 9.7, and < 10.3 nmol/L) for sexually intact and neutered females and sexually intact and neutered males, respectively. In 53 dogs with confirmed hyperadrenocorticism, serum cortisol concentrations after ACTH stimulation and 8 hours after administration of dexamethasone and serum 17- OHP concentrations after ACTH stimulation were considered borderline or abnormal in 79%, 93%, and 69% of dogs, respectively. Two of 5 dogs considered to have atypical hyperadrenocorticism had abnormal serum 17-OHP concentrations after ACTH stimulation.
Conclusions and Clinical Relevance—Serum 17-OHP concentration measurement after ACTH stimulation may be useful in the diagnosis of hyperadrenocorticism in dogs when other test results are equivocal. (J Am Vet Med Assoc 2005;227:1095–1101)
Abstract
Objective—To evaluate accuracy of 6 portable blood glucose meters (PBGMs) by comparing results of these meters with results obtained with a reference chemistry analyzer.
Design—Evaluation study.
Animals—49 dogs (158 blood samples).
Procedures—Venous blood samples were tested with the 6 PBGMs, and results were compared with results of a commercially available analyzer that used a reference method based on the hexokinase reaction.
Results—Plasma glucose concentrations obtained with the reference analyzer ranged from 41 to 639 mg/dL. There were significant correlations between blood glucose concentrations obtained with the 6 PBGMs and plasma glucose concentrations obtained with the reference analyzer (r ≥ 0.96). However, for all 6 PBGMs, results differed from results for the reference analyzer, with the difference increasing as plasma glucose concentration increased. Significant differences in bias were found among meters. For 142 samples classified as hypoglycemic, euglycemic, or hyperglycemic on the basis of results of the reference analyzer, the percentage of samples that were misclassified on the basis of results of the PBGMs ranged from 2.1% to 38.7%.
Conclusions and Clinical Relevance—Results of the present study suggested that there were substantial differences in the accuracy of currently available PBGMs when used to determine blood glucose concentration in dogs.
Abstract
Objective—To evaluate the efficacy and safety of ultrasonographically guided radiofrequency heat ablation of parathyroid masses in dogs with primary hyperparathyroidism.
Design—Clinical trial.
Animals—11 dogs.
Procedure—In all dogs, either 1 or 2 parathyroid masses were evident ultrasonographically. Dogs were anesthetized, and a 20-gauge over-the-needle catheter was directed into the parathyroid mass via ultrasonographic guidance. Radiofrequency heat was applied to the stylet of the catheter until there was sonographically apparent change to the entire parenchyma of the mass. Serum total and ionized calcium and parathyroid hormone concentrations were monitored daily for 5 days after the ablation procedure and again at 1, 2, and 3-month intervals, if possible. Dogs were monitored for adverse effects.
Results—One treatment was required in 6 dogs, 2 treatments were required in 2 dogs, and treatment was unsuccessful in 3 dogs. Serum total and ionized calcium concentrations were within reference ranges within 2 days of the last procedure in all 8 successfully treated dogs. Serum parathyroid hormone concentration was decreased 24 hours after treatment in all 8 dogs. Hypocalcemia developed in 5 of the 8 successfully treated dogs, all of which required treatment. One dog had a transient voice change. Other adverse effects were not reported.
Conclusions and Clinical Relevance—Ultrasonographically guided radiofrequency heat ablation of parathyroid masses is a safe and effective alternative to surgery in dogs with primary hyperparathyroidism. (J Am Vet Med Assoc 2001;218:1106–1110)
Abstract
Objective—To evaluate the reliability of history and physical examination findings for assessing control of glycemia in insulin-treated diabetic dogs.
Design—Retrospective study.
Animals—53 insulin-treated dogs with diabetes mellitus.
Procedure—Medical records of insulin-treated diabetic dogs from June 1995 to June 1998 were reviewed, and information on owner perception of their dog's response to insulin treatment, physical examination findings, body weight, insulin dosage, and concentrations of food-withheld (ie, fasting) blood glucose (FBG), mean blood glucose (MBG) during an 8-hour period, blood glycosylated hemoglobin (GHb), and serum fructosamine was obtained. Owner's perception of their dog's response to insulin treatment, physical examination findings, and changes in body weight were used to classify control of glycemia as good or poor for each dog. The FBG, MBG/8 h, blood GHb, and serum fructosamine concentrations were compared between well-controlled and poorly controlled insulin-treated diabetic dogs.
Results—Presence or absence of polyuria, polydipsia, polyphagia, lethargy, and weakness were most helpful in classifying control of glycemia. Mean FBG and MBG/8 h concentrations, blood GHb concentrations, and serum fructosamine concentrations were significantly decreased in 25 well-controlled diabetic dogs, compared with 28 poorly controlled diabetic dogs. Most well-controlled diabetic dogs had concentrations of FBG between 100 and 300 mg/dl, MBG/8 h ≤ 250 mg/dl, blood GHb ≤ 7.5%, and serum fructosamine ≤ 525 µmol/L, whereas most poorly controlled diabetic dogs had results that were greater than these values.
Conclusion and Clinical Relevance—Reliance on history, physical examination findings, and changes in body weight are effective for initially assessing control of glycemia in insulin-treated diabetic dogs. (J Am Vet Med Assoc 2000;217:48–53)
