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- Author or Editor: Linda J. DeBowes x
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SUMMARY
The effect of systemic administration of glucocorticoids was evaluated on 3 populations of macrophages obtained from healthy dogs. Phagocytic and Fc-receptor activities were determined for mononuclear phagocytes from blood and pulmonary and peritoneal lavage fluids. Samples were collected from 12 dogs before treatment and again on the same dogs after glucocorticoid administration. Thirty or more days were allowed between treatment periods.
Twelve hours after combined prednisolone sodium succinate and dexamethasone sodium phosphate administration, the percentage of phagocytosing cells decreased for blood monocytes and increased for pulmonary macrophages. The percentage of pulmonary macrophages positive for erythrocyte antibody-rosette formation (Fcreceptor activity) increased. After 7 days of oral administration of prednisone, the percentage of phagocytosing peritoneal macrophages increased, whereas the percentage of blood monocytes with Fc-receptor activity increased.
Results indicate that significant (P < 0.05) changes in macrophage function occur after systemic administration of the glucocorticoid doses used in this study. Also, the effect of systemic administration of glucocorticoids on mononuclear phagocytes varies, depending on the specific cell location.
Summary:
Gastrostomy tubes were placed percutaneously in 28 cats by use of an endoscope. French-pezzar mushroom-tip catheters were used for 14 of the procedures, and Malecot catheters were used for the remainder. Inner flanges were not used in gastrostomy tube placement. The french-pezzar catheters remained in place and functional for 2 weeks in all 14 cats. The Malecot catheters remained in place and functional for 2 weeks in 4 cats. Malecot catheters pulled out in 10 cats, and 2 of these cats died or were euthanatized because of complications. The gastrostomy tubes were removed in 18 cats 2 weeks after placement by applying gentle, steady traction and removing the entire catheter or by cutting the tube flush with the skin and leaving the catheter tip in the cat's stomach. Neither method of removal was associated with problems.
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)