Serum alkaline phosphatase isoenzyme profiles in phenobarbital-treated epileptic dogs.
BACKGROUND
Serum total alkaline phosphatase (AP) activity commonly is high in dogs receiving phenobarbital. Specific isoenzymes responsible for this increase are not well documented.


OBJECTIVE
The purposes of this study were 1) to qualitatively and quantitatively describe serum AP isoenzymes in phenobarbital-treated dogs and 2) to monitor changes in serum AP isoenzyme activities associated with phenobarbital treatment over time.


METHODS
Serum AP isoenzyme activities were determined in a cross-sectional study of 29 dogs receiving phenobarbital (duration of treatment 2 months to 6.5 years). Additionally, in a prospective study of 23 dogs, serum AP isoenzyme activities were determined before and 3 weeks, 6 months, and 12 months after the start of phenobarbital treatment. Isoenzyme activities were quantitatively determined using wheat germ lectin precipitation and levamisole inhibition, and qualitatively (ie, present or absent) evaluated using cellulose acetate affinity electrophoresis.


RESULTS
In phenobarbital-treated dogs with high serum total AP activity in the cross-sectional study, the increase was due predominantly to increased activities of the corticosteroid-induced (C-AP) and liver (L-AP) isoenzymes. Prospectively, serum total AP and L-AP activities were significantly higher at 3 weeks, 6 months, and 12 months after the start of phenobarbital treatment compared with pretreatment values. Serum C-AP and bone isoenzyme (B-AP) activities were significantly higher after 6 and 12 months of treatment. B-AP accounted for only a small amount of the total AP activity. No unusual or previously unidentified AP isoenzymes were identified.


CONCLUSIONS
Phenobarbital treatment was associated with increased C-AP and L-AP isoenzyme activities and with a minor increase in B-AP activity. No unique "phenobarbital-induced" isoenzyme was identified. Isoenzyme analysis does not appear to be useful for differentiating between high serum total AP due to phenobarbital therapy and other causes.
Gaskill
Cynthia L
CL
Department of Biomedical Sciences, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Prince Edward Island, Canada. cgaskill@upei.ca
Hoffmann
Walter E
WE
Cribb
Alastair E
AE
D000469:Alkaline Phosphatase / Q000097:blood*; D000818:Animals; D000927:Anticonvulsants / Q000009:adverse effects*; D003430:Cross-Sectional Studies; D004283:Dog Diseases / Q000188:drug therapy* / Q000201:enzymology; D004285:Dogs; D004827:Epilepsy / Q000188:drug therapy / Q000201:enzymology / Q000662:veterinary*; D007527:Isoenzymes / Q000097:blood; D010634:Phenobarbital / Q000009:adverse effects*; D011446:Prospective Studies
D000927:Anticonvulsants; D007527:Isoenzymes; D000469:Alkaline Phosphatase; D010634:Phenobarbital