Search

Background Maximal aldosterone secretion in healthy dogs occurs 30 minutes postadrenocorticotropin ( ACTH; 5 μg/kg IV) stimulation. The effect of trilostane and mitotane on aldosterone at that time is unknown. Objectives To assess the effect of trilostane and mitotane in dogs with pituitary-dependent hyperadrenocorticism on aldosterone secretory reserve. To determine if aldosterone concentration correlates with electrolyte concentrations. Animals Serum collected from 79 client-owned dogs and 33 stored samples. Methods Client-owned dogs had ACTH stimulation tests with cortisol concentrations measured at 0 and 60 minutes and aldosterone concentrations measured at 0, 30, and 60 minutes. Stored samples had aldosterone concentrations measured at 0 and 60 minutes. Ten historical clinically healthy controls were included. All had basal sodium and potassium concentrations measured. Results The aldosterone concentrations in the mitotane- and trilostane-treated dogs at 30 and 60 minutes post- ACTH were significantly lower than in clinically healthy dogs; no significant difference was detected in aldosterone concentration between 30 and 60 minutes in treated dogs. However, a significantly higher percentage of dogs had decreased aldosterone secretory reserve detected at 30 minutes than at 60 minutes. At 30 minutes, decreased secretory reserve was detected in 49% and 78% of trilostane- and mitotane-treated dogs, respectively. No correlation was detected between aldosterone and serum electrolyte concentrations. Conclusions and Clinical Importance Decreased aldosterone secretory reserve is common in trilostane- and mitotane-treated dogs; it cannot be predicted by measurement of serum electrolyte concentrations. Aldosterone concentration at 30 minutes post- ACTH stimulation identifies more dogs with decreased aldosterone secretory reserve than conventional testing at 60 minutes. [ABSTRACT FROM AUTHOR]

Objective– To describe a case of spontaneous pneumothorax secondary to pulmonary thromboembolism possibly associated with pituitary dependent hyperadrenocorticism. Case Summary– 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. New or Unique Information Provided– This is the first report of pulmonary thromboembolism causing spontaneous pneumothorax in the dog. [ABSTRACT FROM AUTHOR]

To evaluate the degree of pituitary exposure, completeness of hypophysectomy, and perioperative morbidity associated with an alternative paramedian surgical approach and excisional technique for the canine pituitary gland. Experimental imaging, surgical, and endocrinologic study. Nine healthy, purpose-bred Beagle dogs. Surgical landmarks for the pituitary were determined by computed tomography (CT), and then using a ventral paramedian approach medial to the rami of the mandible, the pituitary was exposed and removed en bloc by manipulation and ultrasonic aspiration. Efficacy of the procedure was evaluated using endocrinologic and pathologic observation. CT images allowed the precise location of surgical landmarks for hypophysectomy. Statistically significant decreases in secretion of all measured pituitary hormones except adrenocorticotropic hormone (ACTH) occurred after hypophysectomy. Despite the absence of gross evidence of residual pituitary tissue, immunohistochemical staining revealed residual pituitary cells in the sella turcica of most dogs. CT imaging and a paramedian approach facilitated surgical access to the pituitary gland by a transoral technique; however, use of an ultrasonic aspirator removed all visible pituitary glands but left cellular remnants capable of ACTH secretion in the sella turcica. Although this technique did not result in complete hypophysectomy, clinical use in dogs with pituitary-dependent hyperadrenocorticism is warranted because the goal is not complete hypophysectomy but removal of a pituitary tumor. [ABSTRACT FROM AUTHOR]

Background Trilostane is commonly used in the treatment of dogs with naturally occurring pituitary-dependent hyperadrenocorticism ( PDH). Dose recommendations have varied from the manufacturer and the literature. Hypothesis As body weight increases, dose/kg or dosage/day of trilostane required to control the clinical signs of PDH decreases. Animals 70 dogs with naturally occurring hyperadrenocorticism. Methods Retrospective study. Each dog must have been treated for at least 6 months and should have shown a 'good response' to trilostane, as determined by owners. Statistical comparisons of dose and dosage were made after the dogs were separated into groups weighing <15 or >15 kg; groups weighing ≤10, 10.1-20, 20.1-30, and ≥30 kg; and then groups based on body surface area versus dose/kg and total amount of trilostane required to control the condition. Results There was no significant difference in trilostane dose in mg/kg of body weight or in the total amount of trilostane required daily to control clinical signs, except when the dose for dogs weighing >30 kg was compared with that for the other groups. However, despite lack of statistical significance when comparing groups, there was a significant trend using polynomial regression analysis, suggesting that as body weight increases, the amount of trilostane (mg/kg/dose as well as mg/kg/daily dosage) required to control clinical signs decreases. Conclusions and Clinical Importance Dogs weighing >30 kg, and possibly those weighing >15 kg, might require smaller amounts of trilostane per dose or per day than those weighing less, to control PDH-associated clinical signs. [ABSTRACT FROM AUTHOR]