title: Hyperphosphatasemia and concurrent adrenal gland dysfunction in apparently healthy Scottish Terriers.
abstract: OBJECTIVE
  To determine causes of hyperphosphatasemia (high serum alkaline phosphatase [ALP] activity) in apparently healthy Scottish Terriers.
  
  
  METHODS
  Prospective case-controlled study.
  
  
  METHODS
  34 apparently healthy adult Scottish Terriers (17 with and 17 without hyperphosphatasemia).
  
  
  METHODS
  Serum activities for 3 isoforms (bone, liver, and corticosteroid) of ALP were measured. Concentrations of cortisol, progesterone, 17-hydroxyprogesterone, androstenedione, estradiol, and aldosterone were measured before and after cosyntropin administration (ie, ACTH; 5 microg/kg [2.27 microg/lb], IM). Liver biopsy specimens from 16 dogs (11 with and 5 without hyperphosphatasemia) were evaluated histologically.
  
  
  RESULTS
  In dogs with hyperphosphatasemia, the corticosteroid ALP isoform comprised a significantly higher percentage of total ALP activity, compared with the percentage in dogs without hyperphosphatasemia (mean +/- SE, 69 +/- 5.0% and 17 +/- 3.8%, respectively). In 6 dogs with hyperphosphatasemia, but none without, serum cortisol concentrations exceeded reference intervals after ACTH stimulation. Six dogs with and 15 without hyperphosphatasemia had increased concentrations of >or = 1 noncortisol steroid hormone after ACTH stimulation. Serum ALP activity was correlated with cortisol and androstenedione concentrations (r = 0.337 and 0.496, respectively) measured after ACTH stimulation. All dogs with and most without hyperphosphatasemia had abnormal hepatocellular reticulation typical of vacuolar hepatopathy. Subjectively, hepatocellular reticulation was more severe and widespread in hyperphosphatasemic dogs, compared with that in nonhyperphosphatasemic dogs.
  
  
  CONCLUSIONS
  Hyperphosphatasemia in apparently healthy Scottish Terriers was most likely attributable to hyperadrenocorticism on the basis of exaggerated serum biochemical responses to ACTH administration and histologic hepatic changes, but none of the dogs had clinical signs of hyperadrenocorticism.
authors.affiliation: Departments of Biomedical Sciences and Pathobiology, Virginia-Maryland Regional College of Veterinary Medicine, Virginia Tech, Blacksburg, VA 24061, USA. kzimmerm@vt.edu
authors.forename: Kurt L
authors.initials: KL
authors.lastname: Zimmerman
authors.forename: David L
authors.initials: DL
authors.lastname: Panciera
authors.forename: Roger J
authors.initials: RJ
authors.lastname: Panciera
authors.forename: Jack W
authors.initials: JW
authors.lastname: Oliver
authors.forename: Walter E
authors.initials: WE
authors.lastname: Hoffmann
authors.forename: Ellen M
authors.initials: EM
authors.lastname: Binder
authors.forename: Daniel C
authors.initials: DC
authors.lastname: Randall
authors.forename: Joseph H
authors.initials: JH
authors.lastname: Kinnarney
mesh_terms: D000308:Adrenocortical Hyperfunction / Q000150:complications / Q000235:genetics / Q000662:veterinary*; D000324:Adrenocorticotropic Hormone / Q000008:administration & dosage / Q000494:pharmacology; D000818:Animals; D004283:Dog Diseases / Q000209:etiology / Q000235:genetics*; D004285:Dogs; D005260:Female; D020022:Genetic Predisposition to Disease; D054559:Hyperphosphatemia / Q000209:etiology / Q000235:genetics / Q000662:veterinary*; D008297:Male
chemical_list: D000324:Adrenocorticotropic Hormone