AEMV-Lafeber Case Report: Pituitary-Dependent Hyperadrenocorticism and Cholangiohepatitis in a Guinea Pig

Key Points

  • This case report earned first place in the 2018 AEMV Lafeber Company Student Case Report Contest.
  • A 3-year old intact male guinea pig (Cavia porcellus) was presented on emergency for suspected bloat and with a history of chronic hair loss.
  • Clinical examination revealed non-pruritic symmetric truncal alopecia, thin skin, severe cachexia, and an abdominal fluid wave.
  • Alkaline phosphatase, alanine transaminase, aspartate aminotransferase, gamma-glutamyl transferase, leukocytes (neutrophils), bilirubin, and serum cortisol were markedly elevated.
  • Abdominal ultrasonography revealed peritoneal effusion, cholestasis, and cholelithiasis.
  • Hyperadrenocorticism was diagnosed based on adrenocorticotropic stimulation testing. The patient’s initial serum cortisol was 6125 nmol/L, which increased to 7063 nmol/L 4 hours post-injection with cosyntropin (20 IU IM).
  • Cholangiohepatitis was treated with enrofloxacin, metronidazole, fluid therapy, metoclopramide, ursodeoxycholic acid, buprenorphine, and nutritional and liver health support; however, the patient further declined over eight days of hospitalization. Surgical correction of cholelithiasis was not elected, as this patient did not appear to be fully obstructed nor stable for general anesthesia. Due to a rapid decline in condition, the patient was humanely euthanized before treatment of hyperadrenocorticism commenced.
  • Post-mortem examination was consistent with pituitary-dependent hyperadrenocorticism of suspected neoplastic origin, necrotizing cholangiohepatitis, and sepsis.
  • Reports of hyperadrenocorticism and cholangiohepatits in guinea pig are rare. A connection between hyperadrenocorticism and cholestatic disease has been proposed in other species but is poorly understood.

A 3-year old intact male guinea pig was presented on emergency for suspected bloat and with a history of chronic hair loss. Clinical examination revealed non-pruritic symmetric truncal alopecia, thin skin, severe cachexia, and an abdominal fluid wave. Alkaline phosphatase, alanine transaminase, aspartate aminotransferase, gamma-glutamyl transferase, leukocytes (neutrophils), bilirubin, and serum cortisol were markedly elevated. Abdominal ultrasonography revealed peritoneal effusion, cholestasis, and cholelithiasis. Hyperadrenocorticism was diagnosed based on . . .


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