Case Description—A 1-year-old spayed female mixed-breed dog was evaluated because of urinary incontinence, polyuria, polydipsia, and minimally concentrated urine.
Clinical Findings—Markedly high circulating alanine transaminase activity, mildly high circulating alkaline phosphatase activity, and low urine specific gravity were detected for the dog. Results of ultrasonographic examination of the abdomen and cytologic examination of liver samples were unremarkable. Carprofen was detected in serum and plasma samples obtained from the dog. Exposure to carprofen was attributed to ingestion of feces of another dog in the household that was receiving the drug daily.
Treatment and Outcome—Access to feces of other dogs in the household was prevented; no other treatment was initiated. Urinary incontinence, polyuria, and polydipsia resolved, and urine specific gravity increased within 7 days following discontinuation of consumption of feces. Alanine transaminase activity was substantially lower than the value determined during the initial examination, and alkaline phosphatase activity was within the reference range 5 weeks after discontinuation of consumption of feces by the dog.
Clinical Relevance—Findings for the dog of this report suggested that carprofen toxicosis can be caused by consumption of feces of another dog receiving the drug. This cause of adverse effects should be a differential diagnosis for dogs with clinical signs and clinicopathologic abnormalities consistent with carprofen toxicosis.
Objective—To determine whether basal serum or plasma cortisol concentration can be used as a screening test to rule out hypoadrenocorticism in dogs.
Design—Retrospective case-control study.
Animals—110 dogs with nonadrenal gland illnesses and 13 dogs with hypoadrenocorticism.
Procedures—Sensitivity and specificity of basal serum or plasma cortisol concentrations of either ≤ 1 μg/dL or ≤ 2 μg/dL to detect dogs with hypoadrenocorticism were estimated by use of the ACTH stimulation test as the gold standard.
Results—Basal cortisol concentrations of ≤ 1 μg/dL had excellent sensitivity (100%) and specificity (98.2%) for detecting dogs with hypoadrenocorticism. For basal cortisol concentrations of ≤ 2 μg/dL, sensitivity was 100% but specificity was 78.2%.
Conclusions and Clinical Relevance—On the basis of sensitivity and specificity, basal serum or plasma cortisol concentrations had high negative predictive values over a wide range of prevalence rates and can be used to rule out a diagnosis of hypoadrenocorticism. Dogs with basal cortisol concentrations > 2 μg/dL that are not receiving corticosteroids, mitotane, or ketoconazole are highly unlikely to have hypoadrenocorticism. However, if the basal cortisol concentration is ≤ 2 μg/dL, little to no information regarding adrenal gland function can be obtained and an ACTH stimulation test should be performed.