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Haptoglobin concentrations in dogs undergoing trilostane treatment for hyperadrenocorticism
Author(s) -
McGrotty Y. L.,
Arteaga A.,
Knottenbelt C. M.,
Ramsey I. K.,
Eckersall P. D.
Publication year - 2005
Publication title -
veterinary clinical pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.537
H-Index - 51
eISSN - 1939-165X
pISSN - 0275-6382
DOI - 10.1111/j.1939-165x.2005.tb00050.x
Subject(s) - haptoglobin , medicine , hemoglobin , endocrinology , gastroenterology
Background: Increased concentrations of haptoglobin (Hp), a moderate acute phase protein, have been demonstrated in dogs with hyperadrenocorticism (HAC). Monitoring serum concentrations of Hp in hyperadrenocorticoid dogs before and after trilostane administration may provide valuable information on the response to therapy. Objective: The aim of this study was to measure Hp concentrations in dogs with spontaneously occurring HAC at the time of diagnosis and after treatment with trilostane. Methods: Serum Hp concentration was measured using an automatic biochemical assay based on Hp‐hemoglobin binding and utilizing SB‐7 reagent in 12 dogs with spontaneous HAC before and after treatment with trilostane (30 or 60 mg PO q 12–24 h). Post‐treatment Hp concentrations were measured at the time the owner reported an improvement in clinical signs. Pretreatment and post‐treatment Hp values were compared with reference values and with values from 4 healthy control dogs. Results: Two dogs with HAC had pretreatment Hp values within the reference interval; 10 dogs had moderate (n = 8) or marked (n = 2) increases in Hp concentration. After treatment with trilostane, Hp concentration remained within the reference interval (n = 2), decreased to within the reference interval (n = 3), or remained moderately increased (n = 7; 3–10 g/L). Overall, a significant decrease was observed in Hp concentration after trilostane treatment compared with pretreatment values ( P < .005). Both untreated and treated dogs with HAC had significantly higher Hp concentrations ( P < .001) when compared with control dogs. Conclusions: Clinical control of HAC did not closely relate to serum Hp concentration. Further studies are required to assess whether this is because of inadequate control of disease or because a build‐up of cortisol precursors or secondary effects of HAC affect Hp concentration.