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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.

Full access
in Journal of the American Veterinary Medical Association

Objective

To evaluate low- and high-dose dexamethasone suppression tests for differentiating pituitary dependent hyperadrenocorticism (PDH) from adrenal tumor hyperadrenocorticism (ATH) in dogs.

Design

Prospective study.

Animals

181 dogs with PDH and 35 dogs with ATH.

Procedure

Plasma Cortisol concentrations from dogs with naturally developing hyperadrenocorticism were evaluated before, and 4 and 8 hours after administration of standard low- and high-doses of dexamethasone (0.01 mg/kg of body weight, IV, and 0.1 mg/kg, IV; respectively).

Results

In response to the low-dose test, all but 3 dogs had an 8-hour post-dexamethasone plasma Cortisol concentration that was consistent with a diagnosis of hyperadrenocorticism, that is, ≥ 1.4 μg/dl. Criteria used to distinguish PDH from ATH in response to low-dose dexamethasone included a 4-hour post-dexamethasone plasma Cortisol concentration < 50% of the basal value or < 1.4 μg/dl, or an 8-hour post-dexamethasone plasma Cortisol concentration < 50% of the basal concentration. Criteria used to distinguish PDH from ATH in response to high-dose dexamethasone included 4- or 8-hour post-dexamethasone plasma Cortisol concentrations < 50% of the basal concentration or < 1.4 μg/dl. In response to the low-dose test, 111 dogs met criteria for suppression (each had PDH). In response to the high-dose test, 137 dogs met criteria for suppression (2 had ATH, 135 had PDH). Twenty-six dogs with PDH (12%) had indications of adrenal suppression in response to high-dose but not low-dose testing.

Clinical Implications

Low-dose dexamethasone test has value as a discrimination test to distinguish dogs with PDH from those with ATH. The high-dose test need only be considered in dogs with hyperadrenocorticism that do not have adrenal suppression in response to the low-dose test. (J Am Vet Med Assoc 1996;209:772–775)

Free access
in Journal of the American Veterinary Medical Association

Objective

To evaluate use of the oral hypoglycemic drug glipizide in diabetic cats.

Design

Prospective study.

Animals

50 cats with recently diagnosed but untreated diabetes mellitus.

Procedure

Each cat received glipizide (5 mg, q 12 h) for 16 weeks. Medication was not given during the subsequent 16 weeks; then glipizide treatment was repeated. Each cat was evaluated prior to treatment and at 2, 4, 8, 12, and 16 weeks during each of the 3 phases: blood samples for serum glucose and insulin determinations were obtained every 2 hours, from 8 AM to 6 PM. A preprandial blood glycosylated hemoglobin percentage was determined for the first sample obtained at each visit.

Results

During the first 22 weeks of the study, diabetes worsened in 28 of the 50 cats, which then were disqualified from the study and treated with insulin. Of the remaining 22 cats that improved clinically, 7 had corresponding metabolic improvement in each diabetes-related parameter assessed and did not become hypoglycemic. Six of the 22 cats became hypoglycemic. Glipizide was discontinued, and diabetes did not recur. Serum glucose concentration did not improve in 6. Three cats had metabolic and clinical improvement during initial glipizide treatment, but had recurrence of the disease during repeated treatment; glipizide was discontinued and insulin was administered. None of the 50 treated cats died, and observed morbidity was mild and transient. Transient anorexia and vomiting were observed in 8 cats, and 4 became transiently icteric with abnormal liver enzyme activities.

Clinical Implications

Trial use of glipizide is feasible in diabetic cats of owners who are unable or unwilling to administer insulin. (J Am Vet Med Assoc 1997;210:772–777

Free access
in Journal of the American Veterinary Medical Association

Objective

To assess the efficacy and determine prognostic factors of megavoltage irradiation for pituitary macrotumors in dogs with neurologic signs.

Design

Prospective clinical trial.

Animals

24 dogs with pituitary macrotumor syndrome; 19 ACTH-secreting and 5 clinically endocrine-inactive tumors.

Procedure

Dogs were treated with 48 Gy of radiation during 4 weeks on an alternate-day schedule of 4 Gy/fraction. Three (12.5%) dogs did not complete the planned treatment because of progression of neurologic signs.

Results

A significant correlation was found between relative tumor size (ie, size of tumor relative to calvarium size) and severity of neurologic signs and between relative tumor size and remission of neurologic signs after irradiation. In dogs with pituitary dependent hyperadrenocorticism, a significant correlation was found between relative tumor size and plasma endogenous ACTH concentrations. Prognostic factors that independently affected duration of remission of neurologic signs were relative tumor size and endocrine activity. The prognostic factor that independently affected overall survival time was severity of neurologic signs. Prognostic factors of duration of eucortisolism were not found. Use of a large field of irradiation was associated with substantial damage to brain tissue.

Clinical Implications

Because radiation therapy was effective for treatment of tumors of small relative size in dogs, early treatment of pituitary tumors should improve prognosis. Further improvements may be obtained, using protocols in which higher total radiation doses and smaller radiation dose fractions are given. Irradiation was effective for long-term control of functional pituitary macrotumors and resulted in acceptably low complication rates when small fields of radiation were used. (J Am Vet Med Assoc 1998;213:225-231)

Free access
in Journal of the American Veterinary Medical Association

Summary

A urine cortisol:creatinine (c:c) ratio, determined from a free-catch morning sample, was evaluated in each of 83 dogs as a screening test for hyperadrenocorticism. The dogs evaluated were allotted to 3 groups, including 20 healthy dogs, 40 dogs with confirmed hyperadrenocorticism (hac), and 23 dogs with polyuria and polydipsia not attributable to hac (polyuria/polydipsia group; pu/pd). Overlap in the urine c:c ratios (mean ± sem), comparing results from the healthy dogs (5.7 × 10-6 ± 0.9) with those from the hac dogs (337.7 × 10-6 ± 72.0) was not found. However, 11 (64%) of the 18 values from the pu/pd dogs (42.6 × 10-6 ± 9.4) were above the lowest ratio in the hac group and 50% of the hac group had a urine c:c ratio below the highest value in the pu/pd group. When the mean urine c:c ratio (± 2 sd) for the group of healthy dogs was used as a reference range, 100% of the hac dogs and 18 (77%) of 23 dogs in the pu/pd group had abnormal urine c:c ratios. The sensitivity of the urine c:c ratio to discriminate dogs with hac was 100%. The specificity of the urine c:c ratio was 22% and its diagnostic accuracy was 76%.

On the basis of our findings, a urine c:c ratio within the reference range provides strong evidence to rule out hac. However, abnormal urine c:c ratios are obtained from dogs with clinical diseases other than hac. Therefore, measurement of a urine c:c ratio should not be used as the sole screening test to confirm a diagnosis of hac.

Free access
in Journal of the American Veterinary Medical Association

Summary

Two low-dose dexamethasone suppression test protocols were evaluated in 18 dogs with hyperadrenocorticism (14 dogs with pituitary-dependent hyperadrenocorticism [pdh) and 4 dogs with adrenocortical tumor) and in 5 healthy control dogs. Blood was obtained immediately before and 2, 4, 6, and 8 hours after iv administration of either 0.01 mg of dexamethasone sodium phosphate/kg of body weight or 0.015 mg of dexamethasone polyethylene glycol/kg.

At 8 hours after dexamethasone administration, 18 of 18 (100%) dogs with hyperadrenocorticism given the sodium phosphate preparation and 16 of 18 (89%) affected dogs given the polyethylene glycol preparation failed to have suppression of plasma cortisol concentration (< 1.4 μg/dl). Plasma cortisol concentration was suppressed to < 1.4 μg/dl at 2, 4, and/or 6 hours after administration of either dexamethasone preparation in 5 of 14 dogs with pdh and to < 50% of baseline cortisol concentration in 10 of 14 dogs with pdh. Suppression, as identified by these 2 criteria, was not observed at 2, 4, 6, or 8 hours after administration of either dexamethasone preparation in dogs with adrenocortical tumor. For both protocols, the 8-hour plasma cortisol concentration was suppressed to < 1.4 μg/dl and to < 50% of baseline in the 5 control dogs.

Both protocols were comparable for use as screening tests in establishing a diagnosis of hyperadrenocorticism. Suppression of plasma cortisol concentration to < 50% of baseline (or < 1.4 μg/dl) during the test was consistent with diagnosis of pdh. Failure to have such suppression, however, was observed in dogs with pdh as well as in those with adrenocortical tumor.

Free access
in Journal of the American Veterinary Medical Association

Objective

To evaluate use of urine cortisol-to-creatinine ratio (UC:C) as a means of monitoring response to long-term mitotane treatment in dogs with pituitary-dependent hyperadrenocorticism.

Design

Prospective uncontrolled study.

Animals

101 dogs with pituitary-dependent hyperadrenocorticism.

Procedure

Urine samples were obtained from dogs on the morning an ACTH stimulation test was performed, and owners were asked their opinion on the health of their dog to monitor response to mitotane treatment. Urine was assayed for cortisol and creatinine concentrations, and UC:C was calculated. The UC:C was compared with post-ACTH plasma cortisol concentration.

Results

Post-ACTH plasma cortisol concentration was used to categorize each dog's response to mitotane treatment. The UC:C did not correlate satisfactorily with results of ACTH stimulation testing. Twenty-seven of 85 (32%) dogs would have been incorrectly considered as having received appropriate doses using UC:C. In addition, 16 dogs that received overdoses could not be distinguished from 29 dogs that received appropriate doses.

Clinical Implications

UC:C does not provide a consistent, correct assessment of mitotane-induced adrenocortical destruction. The ACTH stimulation test, although more time-consuming and expensive, is recommended for monitoring response to mitotane treatment. (J Am Vet Med Assoc 1997;211:1002–1004)

Free access
in Journal of the American Veterinary Medical Association

Summary

The purpose of this study was to determine the sensitivity of dogs with hyperadrenocorticism to treatment with the adrenocorticolytic agent mitotane. Specifically, we looked for differences in response to treatment using this drug in dogs with adrenocortical tumors (adrenal tumor hyperadrenocorticism, ath) vs those with pituitary-dependent hyperadrenocorticism (pdh). For inclusion in this study, each dog must have had clinical signs, data base laboratory abnormalities, and endocrine screening test results consistent with the diagnosis of hyperadrenocorticism. Further, each dog had to have been treated for at least 6 months with mitotane and have histologic evidence for adrenocortical or pituitary neoplasia (all dogs were necropsied). Thirteen dogs with ath (8 carcinomas, 5 adenomas) were identified. The ages and body weights of these 13 dogs were computer-matched to 13 dogs with pdh. All dogs were initially treated with approximately 50 mg of mitotane/kg/d of body weight. Reexaminations were performed after 7, 30, 90, and 180 days of treatment.

Individual dosages varied widely after the initial 5 to 12 days of treatment. The mean (± sd) dose of mitotane (mg/kg/d) for the first 7 days of treatment was 47.5 ± 9.4 for dogs with ath vs 45.7 ± 11.9 for dogs with pdh. The mean plasma cortisol concentrations 1 hour after acth administration at the 7-day recheck were significantly higher in dogs with ath (502 ± 386 nmol/L) than in dogs with pdh (88 ± 94 nmol/L). At 30 days, the mean daily dose of mitotane and post-acth cortisol concentration were significantly greater in dogs with ath (28.8 ± 15.4 mg/kg/d; 392 ± 356 nmol/L, respectively) than in dogs with pdh (10.5 ± 7.5 mg/kg/d; 99 ± 72 nmol/L, respectively). After 90 days of treatment, these values were larger (25.3 ± 16.8 mg/kg/d; 340 ±193 nmol/L in dogs with ath vs those in dogs with pdh (5.4 ± 2.5 mg/kg/d, 110 ± 94 nmol/L) and again after 180 days (26.0 ± 22.1 mg/kg/d, 268 ± 152 nmol/L in dogs with ath vs 6.3 ± 3.4 mg/kg/d, 80 ± 116 nmol/L in dogs with pdh). Clinical signs were consistent with laboratory values, that is, cortisol control was not as good in dogs with ath as in the dogs with pdh. On the basis of these findings, we suggest that dogs with hyperadrenocorticism caused by ath are more resistant to mitotane than are dogs with pdh.

Free access
in Journal of the American Veterinary Medical Association

Objective—

To determine what effects long-term phenobarbital administration to dogs with epilepsy would have on serum biochemical factors and adrenocortical function.

Design—

Prospective, uncontrolled study.

Animals—

Five dogs with idiopathic epilepsy.

Procedure—

Serum total protein, albumin, total bilirubin, and cholesterol concentrations and serum alkaline phosphatase and alanine aminotransferase activities were measured before and 2 weeks, 6 months, and 12 months after initiation of phenobarbital administration. Endogenous ACTH concentration was measured, and ACTH stimulation and low-dose dexamethasone suppression tests were performed at the same time.

Results—

Serum albumin concentration decreased in 4 of 5 dogs, and serum cholesterol concentrations decreased in all 5 dogs over the course of the study. Serum alkaline phosphatase concentration and alanine aminotransferase activities increased over time, and were greater than the upper reference limits in 4 of the 5 dogs by the end of the study. Endogenous ACTH concentration increased in all dogs but remained within reference limits. Plasma ACTH-stimulated aldosterone concentration increased over the course of the study. Plasma cortisol concentration did not suppress, after administration of dexamethasone, in 1 dog after 6 and 12 months of phenobarbital administration.

Clinical Implications—

Although endogenous acthconcentration should be normal in dogs receiving phenobarbital, results of ACTH stimulation and dexamethasone suppression tests may be altered. Serum albumin and cholesterol concentrations, and serum alkaline phosphatase and alanine aminotransferase activities may also be abnormal.

Free access
in Journal of the American Veterinary Medical Association

Abstract

Objective—

To determine normal adrenal gland size by means of ultrasonography in dogs and to determine the value of ultrasonography in the diagnosis of pituitary-de-pendent hyperadrenocorticism (PDH) in dogs.

Design—

Prospective observational study.

Animals—

62 dogs: 20 healthy dogs, 20 dogs with non-endocrine disease, and 22 dogs with untreated PDH.

Procedure—

Length and maximum and minimum diameter of the adrenal glands were measured ultrasonographically. Multiple regression and correlation analyses were used to determine whether body weight, kidney length, aortic diameter, or age was related to adrenal gland size. Two-tailed t-tests and multiple linear regression analysis were used to compare values between groups. Sensitivity and specificity of using ultrasonographic measurement of adrenal gland size as a diagnostic test for PDH were determined.

Results—

There was a significant linear relationship between adrenal gland length, but not maximum and minimum diameters, and body weight, aortic diameter, and kidney length in healthy dogs and in dogs with nonenocrine diseases. Length, maximum diameter, and minimum diameter of the right adrenal gland and maximum and minimum diameters of the left adrenal gland were significantly greater in dogs with PDH than in healthy dogs and dogs with nonendocrine diseases. As a diagnostic test for pdh, ultrasonographic measurement of maximum or minimum diameter of the left adrenal gland gave the best combination of sensitivity and specificity. For maximum diameter of the left adrenal gland, sensitivity was 77% and specificity was 80%. For minimum diameter of the left adrenal gland, sensitivity was 73% and specificity was 85%.

Clinical Implication—

Ultrasonography of the adrenal glands is a valuable diagnostic procedure in dogs suspected of having pituitary-dependent hyperadrenocorticism.

Free access
in Journal of the American Veterinary Medical Association