Diagnosis Of Pituitary-dependent Hyperadrenocorticism Research Articles

The interpretive contribution of the baseline serum cortisol concentration of the ACTH stimulation test in the diagnosis of pituitary dependent hyperadrenocorticism in dogs.

BackgroundCurrent recommendation for performing the ACTH stimulation test (ACTHST) for diagnosis of hyperadrenocorticism (HAC) advocates the collection of baseline serum cortisol concentration (BC), but no references for interpretation of its results exist.ObjectiveEvaluate the contribution of BC of the ACTHST to the diagnosis of HAC.AnimalsFifty‐four dogs were evaluated for suspected HAC at a referral hospital.MethodsRecords of dogs that had been evaluated by ACTHST for suspected HAC were reviewed. Receiver operator characteristics (ROC) analyses were used to assess the performance of BC, post‐stimulation serum cortisol concentrations (PC), post‐to‐baseline cortisol concentration difference (DeltaC) and quotient (RatioC) for the diagnosis of HAC by comparing the area under the ROC curve (AUC) of PC to each of the other tests.ResultsThe AUC of PC (95% confidence interval [CI]: 0.92; 95% CI, 0.81‐0.98) was significantly higher than AUCs of BC (0.70; 95% CI, 0.56‐0.82; P = .01) and RatioC (0.55; 95% CI, 0.41‐0.69; P < .001), and was not significantly different from AUC of DeltaC (0.86; 95% CI, 0.74‐0.94; P = .09). An optimal cutoff value of 683 nmol/L (24.8 μg/dL) for PC yielded a sensitivity of 86% and a specificity of 94%, respectively, and a cutoff value of 718 nmol/L (26.0 μg/dL) yielded a specificity of 100% with of 81% sensitivity for the diagnosis of pituitary‐dependent HAC.Conclusion and Clinical ImportanceThe PC had good discriminatory ability for the diagnosis of HAC. It was comparable to DeltaC, whereas BC and RatioC were ineffective. Current recommendations to collect samples for BC appear redundant.

Comparison of Survival Times for Dogs with Pituitary-Dependent Hyperadrenocorticism in a Primary-Care Hospital: Treated with Trilostane versus Untreated.

BackgroundAlthough pituitary‐dependent hyperadrenocorticism (PDH) is one of the most common endocrinopathies in dogs, the effects of withholding treatment on survival time in dogs with PDH remain unclear.Hypothesis/ObjectivesThe purpose of this study was to clarify the effects of treatment in dogs with PDH by comparing survival times between dogs treated with trilostane and untreated dogs.AnimalsForty‐three dogs diagnosed with PDH at a primary‐care hospital in Japan between June 2009 and January 2014.MethodsRetrospective cohort study. The medical records of dogs with PDH treated with trilostane (n = 17) or left untreated (n = 26) were reviewed retrospectively. Survival analysis at 2 years after diagnosis of PDH was performed.ResultsMedian survival time for the trilostane group was not reached (95% confidence interval [CI], 443 days–not applicable) and was significantly longer than the 506 days (95% CI, 292–564 days; P = .016) for the untreated group. Multivariate Cox proportional hazards analysis (including age at diagnosis, basal cortisol concentration at diagnosis, and treatment group) only identified assignment to the untreated group (hazard ratio, 5.01; 95% CI, 1.63–15.44) as associated with increased mortality.Conclusions and Clinical ImportanceThe results of this retrospective cohort study suggest that withholding treatment for dogs with PDH might be associated with a higher risk of death. This represents the largest study to date to report survival times of untreated dogs with PDH.

Pituitary-dependent hyperadrenocorticism in a terrier dog: A case report

We report a case of pituitary-dependent hyperadrenocorticism in a 10-year-old, female, terrier dog. The animal was admitted due to polyphagia, weight gain, polyuria, polydipsia, hair loss, exercise intolerance and panting at rest. On physical examination, abdominal distention, truncal and bilaterally symmetric alopecia, thin hypotonic skin, comedones, bruising, hyperpigmentation and calcinosis cutis on the dorsal midline were observed. Hematologic investigations showed stress leukogram, high serum alkaline phosphatase activity, mild to moderate alanine aminotransferase activity, hypercholesterolemia, hypertriglyceridemia and hyperglycemia. Mild generalized interstitial lung patterns and hepatomegaly were detected in the radiographs. Bilaterally symmetric normal-sized adrenal glands were also diagnosed in ultrasonography. Diagnosis of pituitary-dependent hyperadrenocorticism was confirmed with low-dose dexamethasone suppression test. The dog was successfully treated with mitotane.

High-resolution fluorodeoxyglucose positron emission tomography and magnetic resonance imaging findings of a pituitary microtumor in a dog.

A 16-year-old, castrated, male English cocker spaniel dog was presented due to generalized alopecia. Routine clinical pathology, endocrine and abdominal ultrasonography results were consistent with a diagnosis of pituitary-dependent hyperadrenocorticism. The adenohypophyseal lesion was clearly visualized on both 3 T and 7 T magnetic resonance imaging (MRI) of the pituitary gland. Although biochemical and MRI findings were consistent with a functional pituitary microtumor, a pituitary lesion was not detected using 18F-fluorodeoxyglucose positron emission tomography (FDG-PET). This report firstly describes the application of high-resolution FDG-PET to a spontaneous pituitary microtumor in a dog.

Suspected pituitary gland double adenoma in a cat with insulin-resistant diabetes mellitus

A 10-year-old castrated male Korean shorthair cat weighing 4 kg was referred with signs of insulin-resistant diabetes mellitus based on clinical signs of polyuria, polydipsia, and polyphagia. Diagnosis of pituitary-dependent hyperadrenocorticism (PDH) was made based on results of an adrenocorticotropic hormone stimulation test and a dexamethasone screening test. In addition, plasma concentrations of insulin-like growth factor 1 (IGF-1) increased. Radiography, ultrasonography, and computed tomography (CT) revealed hepatomegaly, renomegaly, and adrenomegaly affecting both adrenal glands as well as multiple cysts in a generally enlarged pancreas. Magnetic resonance imaging (MRI) showed that the cat’s pituitary gland was enlarged. The pituitary gland had a predominantly unilateral extension to the left. The signal intensity of the pituitary gland on precontrast T1 weighted images was hypointense compared to that of soft tissue and hyperintense compared to that of cerebrospinal fluid. On T2 weighted images, the pituitary gland was predominantly hypointense with a hyperintense rim. Contrast enhancement of the pituitary gland was not evident, and a mild degree of ring-like enhancement was seen. In addition, mild peritumoral edema was present. This is the first report of a cat with suspected double adenoma of the pituitary gland on the basis of compatible clinical signs, increased serum IGF-1 concentration, PDH, CT images, and MRI findings in diabetic cats with insulin resistance.

PlasmaACTHPrecursors in Cats with Pituitary‐Dependent Hyperadrenocorticism

Diagnosis of pituitary-dependent hyperadrenocorticism (PDH) in cats is challenging because there is no specific diagnostic test. The determination of plasma ACTH precursor (POMC and pro-ACTH) concentration might facilitate the diagnosis of PDH in cats. The aim of the study was to evaluate prospectively the plasma concentrations of ACTH precursors in a small cohort of cats with PDH and to estimate the value of this approach for diagnosis. Four groups of cats were included: group 1 (cats with PDH), group 2 (cats with diabetes mellitus but not hyperadrenocorticism (HAC)), group 3 (cats with diabetes mellitus and confirmed acromegaly but not HAC), and group 4 (healthy cats). PDH diagnosis was based on clinical data, low-dose dexamethasone suppression test (LDDST), and adrenal and pituitary gland computed tomography (CT) scan. For groups 2, 3, and 4, hyperadrenocorticism was excluded by LDDST or urine cortisol:creatinine ratio (UCCR). An immunoluminometric assay was used to determine plasma concentrations of ACTH precursors in the 4 groups of cats. Group 1 contained 9 cats (enlarged pituitary gland in 7/9). Plasma ACTH precursor concentrations ranged from <53 to >1010 pmol/L with 8/9 concentrations ≥ 229 pmol/L. Groups 2, 3, and 4 included 13, 7, and 13 cats, respectively. Plasma ACTH precursor concentrations ranged from <53 to 96 pmol/L in group 2, <53 to 72 pmol/L in group 3, and <53 to 99 pmol/L in group 4. High plasma concentration of ACTH precursors in cats (>100 pmol/L) is highly suggestive of PDH.

Pneumothorax secondary to pulmonary thromboembolism in a dog

To describe a case of spontaneous pneumothorax secondary to pulmonary thromboembolism possibly associated with pituitary dependent hyperadrenocorticism. A 7-year-old spayed female Collie weighing 26 kg was referred for evaluation of spontaneous pneumothorax. An exploratory thoracotomy was performed and revealed 2 lung lobes to be diffusely hemorrhagic and they were resected. Histologic examination of multiple sections documented diffuse thromboembolism. A 2-3 cm thrombus was visualized distal to the bifurcation of the pulmonary artery during an echocardiographic examination postoperatively. The dog was discharged to the owner after recovery from surgery. The thrombus had resolved at the 4-week recheck examination. Diagnosis of pituitary dependent hyperadrenocorticism was confirmed based on follow-up endocrine testing. This is the first report of pulmonary thromboembolism causing spontaneous pneumothorax in the dog.

One-year follow-up evaluation of magnetic resonance imaging of the brain in dogs with pituitary-dependent hyperadrenocorticism

Objective To evaluate magnetic resonance imaging (MRI) brain scans of dogs with pituitary-dependent hyperadrenocorticism (PDH) and no signs of CNS dysfunction 1 year after diagnosis and initial MRI. Design Prospective study of surviving dogs from a previous study. Animals 13 dogs underwent MRI of the brain at the time that PDH was diagnosed and prior to treatment. At that time, none of the dogs had clinical signs suggestive of an intracranial mass. Approximately 1 year after diagnosis and MRI, the brain was again evaluated by MRI. Results On the initial MRI scan, 5 of the 13 dogs had normal findings, and 8 had evidence of a mass (tumor) in the area of the pituitary gland. Of the 5 dogs that had no visible pituitary mass on the initial MRI scan, 3 had a normal MRI brain scan 1 year later. Of the 5 dogs that had no visible pituitary mass on initial MRI scan, 2 had a visible pituitary mass at 1 year. The 8 dogs that had a visible mass on the initial MRI brain scan had easily identified pituitary masses on the second MRI scan. Of these 8 dogs, 4 had no apparent change in pituitary mass size, and 4 had obvious increase in vertical height of the pituitary mass. Of the 4 dogs, 2 developed signs of neurologic dysfunction within 1 year after diagnosis of PDH, presumably attributable to that mass. Of the 13 dogs, 12 were treated with mitotane soon after completion of the initial MRI scan. Sensitivity to mitotane and initial pituitary mass size or growth were not correlated. Of the 13 dogs evaluated initially and 1 year after diagnosis, 10 had pituitary masses identified on MRI brain scans. Clinical Implications The incidence of visible pituitary masses among dogs with PDH at the time of or within a year of diagnosis was &gt; 75%. In 2 dogs, signs of CNS dysfunction developed within 1 year of PDH diagnosis when pituitary masses were ≥ 10 mm. (J Am Vet Med Assoc 1996;208: 1268–1273)