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).
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.
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).
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).
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 ). 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.
Animals—5 dogs with naturally acquired diabetes
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)
Objective—To evaluate pretreatment clinical and laboratory
findings in dogs with naturally occurring primary
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
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
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:
Objective—To evaluate serum 17-hydroxyprogesterone
(17-OHP) concentration measurement after
administration of ACTH for use in the diagnosis of
hyperadrenocorticism in 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)
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.
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.
Objective—To evaluate the efficacy and safety of
ultrasonographically guided radiofrequency heat ablation
of parathyroid masses in dogs with primary
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
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)
Objective—To evaluate the reliability of history and
physical examination findings for assessing control of
glycemia in insulin-treated diabetic dogs.
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)