title: Vacuolar hepatopathy in dogs: 336 cases (1993-2005).
abstract: OBJECTIVE
  To determine disorders associated with vacuolar hepatopathy (VH), morphologic hepatic and clinicopathologic abnormalities, and affiliation with steroidogenic hormone excess in dogs.
  
  
  METHODS
  Retrospective case series. Animals-336 dogs with histologically confirmed moderate or severe VH.
  
  
  METHODS
  Information on signalment, results of diagnostic testing, definitive diagnoses, and exposure to glucocorticoids (ie, exogenous glucocorticoid administration or high endogenous concentrations of steroidogenic hormones) was obtained from medical records. Dogs were grouped by underlying disorder, glucocorticoid exposure, acinar zonal distribution of lesions, and histologic severity.
  
  
  RESULTS
  12 disease groups (neoplastic, acquired hepatobiliary, neurologic, immune-mediated, gastrointestinal tract, renal, infectious, cardiac disease, diabetes mellitus, portosystemic vascular anomaly, adrenal gland dysfunction, and miscellaneous disorders) were identified. There were 186 (55%) dogs with and 150 (45%) dogs without evidence of glucocorticoid exposure. Acinar zonal distribution of hepatic vacuolation and clinicopathologic values did not differ between dogs with and without evidence of glucocorticoid exposure. However, a 3-fold increased likelihood of severe VH was associated with steroidogenic hormone exposure. Of 226 dogs with high serum alkaline phosphatase activity, 102 (45%) had no evidence of glucocorticoid exposure.
  
  
  CONCLUSIONS
  Results suggest that neoplasia and congenital or acquired hepatobiliary disease are common in dogs with VH and provide support for the suggestion that VH, high alkaline phosphatase activity, and illness-invoked physiologic stress may be associated. Histologic confirmation of VH should initiate a diagnostic search for a primary disease if glucocorticoid treatment and hyperadrenocorticism are ruled out.
authors.affiliation: Department of Clinical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, NY 14853, USA.
authors.forename: Lisa M
authors.initials: LM
authors.lastname: Sepesy
authors.forename: Sharon A
authors.initials: SA
authors.lastname: Center
authors.forename: John F
authors.initials: JF
authors.lastname: Randolph
authors.forename: Karen L
authors.initials: KL
authors.lastname: Warner
authors.forename: Hollis N
authors.initials: HN
authors.lastname: Erb
mesh_terms: D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D001660:Biliary Tract Diseases / Q000150:complications / Q000175:diagnosis / Q000473:pathology / Q000662:veterinary*; D003937:Diagnosis, Differential; D004283:Dog Diseases / Q000175:diagnosis* / Q000201:enzymology / Q000209:etiology / Q000473:pathology; D004285:Dogs; D005260:Female; D005938:Glucocorticoids / Q000009:adverse effects*; D008099:Liver / Q000201:enzymology* / Q000473:pathology; D008107:Liver Diseases / Q000175:diagnosis / Q000209:etiology / Q000473:pathology / Q000662:veterinary*; D008297:Male; D012189:Retrospective Studies; D012720:Severity of Illness Index
chemical_list: D005938:Glucocorticoids; D000469:Alkaline Phosphatase