Efficacy of microcrystalline desoxycorticosterone pivalate for treatment of hypoadrenocorticism in dogs

Randy C. Lynn From CIBA-GEIGY Animal Health, PO Box 18300, Greensboro, NC 27419 (Lynn); the Departments of Veterinary Reproduction (Feldman) and Medicine (Nelson), School of Veterinary Medicine, University of California, Davis, CA 95616.

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Edward C. Feldman From CIBA-GEIGY Animal Health, PO Box 18300, Greensboro, NC 27419 (Lynn); the Departments of Veterinary Reproduction (Feldman) and Medicine (Nelson), School of Veterinary Medicine, University of California, Davis, CA 95616.

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Richard W. Nelson From CIBA-GEIGY Animal Health, PO Box 18300, Greensboro, NC 27419 (Lynn); the Departments of Veterinary Reproduction (Feldman) and Medicine (Nelson), School of Veterinary Medicine, University of California, Davis, CA 95616.

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the DOCP clinical study group
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the DOCP clinical study group

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Summary:

The efficacy of microcrystalline desoxycorticosterone pivalate (docp) therapy was evaluated in 60 dogs with hypoadrenocorticism. Fifty-one of the dogs were being treated with either docp or fludrocortisone acetate prior to entering the study. The disease had been recently diagnosed in 9 dogs that were not under maintenance treatment prior to entering the study. Desoxycorticosterone pivalate (2.2 mg/kg of body weight, im) was administered on days 0, 25, and 50. Physical examination was performed, and blood samples were obtained for serum biochemical analysis (Na+, K+, and bun concentrations) on days 0, 14, 25, 39, 50, 64, and 75. On day 75 of the study, a final physical examination was performed and the course of treatment was evaluated.

Sixty-eight percent (41/60) of the dogs had normal physical findings on day 0 vs 87% (52/60) on day 75. Mean (±sd) body weight increased from 24.8 ± 12.7 kg on day 0 to 26.2 ± 13.7 kg on day 75. Mean serum Na+ (137.7 ± 8.5 mEq/L) and K+ (5.6 1.0 mEq/L) concentrations and Na+-to-K+ ratio (25.4 ± 5.0:1) were outside normal reference limits on day 0. By day 75, serum Na+ (144.3 ± 4.8 mEq/L) and K+ (4.9 ± 0.8 mEq/L) concentrations and Na+-to-K+ ratio (30.4 ± 5.1:1) were normal and were significantly (P < 0.01) improved, compared with the corresponding values on day 0.

Of the 60 dogs, 58 (97%) regained the loss in body weight, appetite, and muscular strength while given docp; once achieved, these improvements were maintained. These 58 dogs did not vomit or have diarrhea, common problems in dogs with hypoadrenocorticism. The mineralocorticoid (docp) alone was not adequate to correct all clinical signs associated with endogenous mineralocorticoid and glucocorticoid deficiencies, which are typical of hypoadrenocorticism in dogs. Thus, 22 of the 58 dogs had glucocorticoid-responsive clinical signs of disease (lethargy, n = 10; anorexia, n = 8; weakness and hypoadrenal crisis, n = 2 each). These signs resolved in response to initiation of glucocorticoid therapy (prednisolone, 2.5 mg/d, po) and/or adjustments in docp dose or dosing interval. Ten dogs developed polyuria, polydipsia, or both during the study; these signs improved when the dose of prednisolone (n = 9) or docp (n = 1) was reduced. All owners but 1 chose to continue docp therapy after the trial ended, and all dogs remained free of clinical signs associated with hypoadrenocorticism for at least 1 year after the study ended.

Summary:

The efficacy of microcrystalline desoxycorticosterone pivalate (docp) therapy was evaluated in 60 dogs with hypoadrenocorticism. Fifty-one of the dogs were being treated with either docp or fludrocortisone acetate prior to entering the study. The disease had been recently diagnosed in 9 dogs that were not under maintenance treatment prior to entering the study. Desoxycorticosterone pivalate (2.2 mg/kg of body weight, im) was administered on days 0, 25, and 50. Physical examination was performed, and blood samples were obtained for serum biochemical analysis (Na+, K+, and bun concentrations) on days 0, 14, 25, 39, 50, 64, and 75. On day 75 of the study, a final physical examination was performed and the course of treatment was evaluated.

Sixty-eight percent (41/60) of the dogs had normal physical findings on day 0 vs 87% (52/60) on day 75. Mean (±sd) body weight increased from 24.8 ± 12.7 kg on day 0 to 26.2 ± 13.7 kg on day 75. Mean serum Na+ (137.7 ± 8.5 mEq/L) and K+ (5.6 1.0 mEq/L) concentrations and Na+-to-K+ ratio (25.4 ± 5.0:1) were outside normal reference limits on day 0. By day 75, serum Na+ (144.3 ± 4.8 mEq/L) and K+ (4.9 ± 0.8 mEq/L) concentrations and Na+-to-K+ ratio (30.4 ± 5.1:1) were normal and were significantly (P < 0.01) improved, compared with the corresponding values on day 0.

Of the 60 dogs, 58 (97%) regained the loss in body weight, appetite, and muscular strength while given docp; once achieved, these improvements were maintained. These 58 dogs did not vomit or have diarrhea, common problems in dogs with hypoadrenocorticism. The mineralocorticoid (docp) alone was not adequate to correct all clinical signs associated with endogenous mineralocorticoid and glucocorticoid deficiencies, which are typical of hypoadrenocorticism in dogs. Thus, 22 of the 58 dogs had glucocorticoid-responsive clinical signs of disease (lethargy, n = 10; anorexia, n = 8; weakness and hypoadrenal crisis, n = 2 each). These signs resolved in response to initiation of glucocorticoid therapy (prednisolone, 2.5 mg/d, po) and/or adjustments in docp dose or dosing interval. Ten dogs developed polyuria, polydipsia, or both during the study; these signs improved when the dose of prednisolone (n = 9) or docp (n = 1) was reduced. All owners but 1 chose to continue docp therapy after the trial ended, and all dogs remained free of clinical signs associated with hypoadrenocorticism for at least 1 year after the study ended.

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