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Objective
To determine whether measuring change in serum thyroid-stimulating hormone (TSH) concentration in response to thyrotropin-releasing hormone (TRH) administration can be used as a test of thyroid function in dogs suspected of having hypothyroidism.
Design
Case-cohort study.
Animals
13 healthy dogs, 20 hypothyroid dogs, and 18 euthyroid dogs with concurrent diseases.
Procedure
Blood samples were collected before and 30 minutes after TRH administration, and serum TSH concentration was measured. The 13 healthy dogs were used to establish a reference range for change in TSH concentration after TRH administration. The remaining 38 dogs were categorized as hypothyroid or euthyroid on the basis of baseline total thyroxine (T4) and TSH concentrations, T4 concentration 4 hours after TRH administration, and clinical response to administration of sodium levothyroxine.
Results
Median baseline TSH concentration was 0.25 ng/ml (range, 0.03 to 0.44 ng/ml) in healthy dogs, 0.93 ng/ml (0.21 to 3.5 ng/ml) in hypothyroid dogs, and 0.21 ng/ml (0.03 to 0.63 ng/ml) in euthyroid dogs with concurrent diseases. Median percentage change in TSH concentration after TRH administration was 207% (range, 25 to 2,200%) in healthy dogs, 24% (-21 to 134%) in hypothyroid dogs, and 167% (69 to 1,800%) in euthyroid dogs with concurrent diseases. Overall accuracy of using the TRH-induced change in TSH concentration to identify hypothyroid dogs was 90%.
Clinical Implications
Although percentage change in TSH concentration in response to TRH administration can be used to differentiate euthyroid from hypothyroid dogs, the test has little advantage over measurement of baseline TSH and total or free T4concentration. (J Am Vet Med Assoc 1998;213:1435-1438)
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
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)
Summary:
Hyperadrenocorticism caused by bilateral adrenocortical neoplasia was diagnosed in 4 dogs. Three dogs had bilateral adrenocortical adenomas, and 1 dog had bilateral adrenocortical carcinomas. The history, physical findings, clinicopathologic abnormalities, and results of acth stimulation and low-dose dexamethasone suppression tests were compatible with diagnosis of hyperadrenocorticism. Adrenocortical neoplasia was differentiated from pituitary-dependent hyperadrenocorticism on the basis of a combination of test results, including lack of suppression of plasma cortisol after being given a high dose dexamethasone (n = 4), undetectable (< 20 pg/ml) plasma endogenous acth concentration (n = 4), identification of a single mineralized adrenal mass by abdominal radiography (n = 2) and abdominal ultrasonography (n = 1), and identification of bilateral nonmineralized adrenal masses by ultrasonography (n = 1).
A left adrenal mass was excised from 1 dog. Clinical signs persisted and administration of mitotane was initiated. One dog was treated only with mitotane. Treatment with ketoconazole was attempted in 2 dogs. All dogs died or were euthanatized because of persistent hyperadrenocorticism. Necropsy and histologic evaluation of the pituitary and adrenal tissue confirmed bilateral adrenocortical neoplasia in all dogs. Bilateral adrenocortical neoplasia should be considered as an uncommon, but possible, cause of bilaterally large adrenal glands in dogs with hyperadrenocorticism.
Summary
Treatment with prostaglandin F2α (pgf 2α) was evaluated in 21 queens with open-cervix pyometra. The pgf 2α was administered (0.1 or 0.25 mg/kg of body weight, sc, q 12 to 24 h) for 3 or 5 days. Transient postinjection reactions caused by pgf 2α administration included vocalization, panting, restlessness, grooming, tenesmus, salivation, diarrhea, kneading, mydriasis, emesis, urination, and lordosis. Reactions began as quickly as 30 seconds after pgf 2α administration and lasted as long as 60 minutes. All queens improved clinically after pgf 2α treatment. One month after completion of the initial series, 1 queen required a second series of pgf 2α injections before pyometra resolved. Of 21 queens, 20 (95%) resumed normal estrous cycles without further treatment and 17 (81%) delivered normal litter(s). Use of pgf 2α is an acceptable treatment for open-cervix pyometra in queens.
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 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)
