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Hepatotoxicity of stanozolol in cats

Kenneth R. HarkinDepartments of Clinical Sciences, Kansas State University, Manhattan, KS 66506-5606.

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Laine A. CowanDepartments of Clinical Sciences, Kansas State University, Manhattan, KS 66506-5606.
Present address is Phoenix Central Laboratories, 11620 Airport Rd, Ste 100, Everett, WA 98204.

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Gordon A. AndrewsDiagnostic Medicine and Pathology, Kansas State University, Manhattan, KS 66506-5606.

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Randall J. BasarabaDiagnostic Medicine and Pathology, Kansas State University, Manhattan, KS 66506-5606.
Present address is Department of Pathology, Colorado State University, Fort Collins, CO 80523.

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Julie R. FischerDepartments of Clinical Sciences, Kansas State University, Manhattan, KS 66506-5606.

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Linda J. DeBowesDepartments of Clinical Sciences, Kansas State University, Manhattan, KS 66506-5606.

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James K. RoushDepartments of Clinical Sciences, Kansas State University, Manhattan, KS 66506-5606.

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Maria L. GuglielminoDepartments of Clinical Sciences, Kansas State University, Manhattan, KS 66506-5606.

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Claudia A. KirkDepartments of Clinical Sciences, Kansas State University, Manhattan, KS 66506-5606.

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 DVM, PhD, DACVIM, DACVN

Abstract

Objective—To determine hepatotoxicity of stanozolol in cats and to identify clinicopathologic and histopathologic abnormalities in cats with stanozololinduced hepatotoxicosis.

Design—Clinical trial and case series.

Animals—12 healthy cats, 6 cats with chronic renal failure, and 3 cats with gingivitis and stomatitis.

Procedures—Healthy cats and cats with renal failure were treated with stanozolol (25 mg, IM, on the first day, then 2 mg, PO, q 12 h) for 4 weeks. Cats with gingivitis were treated with stanozolol at a dosage of 1 mg, PO, every 24 hours.

Results—Most healthy cats and cats with renal failure developed marked inappetence, groomed less, and were less active within 7 to 10 days after initiation of stanozolol administration. Serum alanine transaminase (ALT) activity was significantly increased in 14 of 18 cats after stanozolol administration, but serum alkaline phosphatase activity was mildly increased in only 3. Four cats with serum ALT activity > 1,000 U/L after only 2 weeks of stanozolol administration had coagulopathies; administration of vitamin K resolved the coagulopathy in 3 of the 4 within 48 hours. All 18 cats survived, and hepatic enzyme activities were normal in all cats tested more than 4 weeks after stanozolol administration was discontinued. Two of the 3 cats with gingivitis developed evidence of severe hepatic failure 2 to 3 months after initiation of stanozolol treatment; both cats developed coagulopathies. Histologic evaluation of hepatic biopsy specimens from 5 cats revealed diffuse hepatic lipidosis and cholestasis without evidence of hepatocellular necrosis.

Conclusions and Clinical Relevance—Results suggest that stanozolol is hepatotoxic in cats. (J Am Vet Med Assoc 2000;217:681–684)

Abstract

Objective—To determine hepatotoxicity of stanozolol in cats and to identify clinicopathologic and histopathologic abnormalities in cats with stanozololinduced hepatotoxicosis.

Design—Clinical trial and case series.

Animals—12 healthy cats, 6 cats with chronic renal failure, and 3 cats with gingivitis and stomatitis.

Procedures—Healthy cats and cats with renal failure were treated with stanozolol (25 mg, IM, on the first day, then 2 mg, PO, q 12 h) for 4 weeks. Cats with gingivitis were treated with stanozolol at a dosage of 1 mg, PO, every 24 hours.

Results—Most healthy cats and cats with renal failure developed marked inappetence, groomed less, and were less active within 7 to 10 days after initiation of stanozolol administration. Serum alanine transaminase (ALT) activity was significantly increased in 14 of 18 cats after stanozolol administration, but serum alkaline phosphatase activity was mildly increased in only 3. Four cats with serum ALT activity > 1,000 U/L after only 2 weeks of stanozolol administration had coagulopathies; administration of vitamin K resolved the coagulopathy in 3 of the 4 within 48 hours. All 18 cats survived, and hepatic enzyme activities were normal in all cats tested more than 4 weeks after stanozolol administration was discontinued. Two of the 3 cats with gingivitis developed evidence of severe hepatic failure 2 to 3 months after initiation of stanozolol treatment; both cats developed coagulopathies. Histologic evaluation of hepatic biopsy specimens from 5 cats revealed diffuse hepatic lipidosis and cholestasis without evidence of hepatocellular necrosis.

Conclusions and Clinical Relevance—Results suggest that stanozolol is hepatotoxic in cats. (J Am Vet Med Assoc 2000;217:681–684)