Elevation of beta-glucuronidase activity in medicated patients with epilepsy.

Abstract

Elevations of serum beta-glucuronidase (GRS) enzyme activity can occur under a variety of pathological conditions. Using phenolphthalein glucuronic acid as the substrate, 158 epileptic patients were randomly screened for GRS. GRS was distinctly elevated (65.9 +/- 30.0 micrograms phenolphthalein/ml serum) in patients, compared with the normal group (27.0 +/- 10.0). No difference in GRS levels were found when seizure-free (greater than 1 year) patients (n = 61; GRS, 62.6 +/- 32.7 micrograms) were compared with patients who had seizure episodes within 1 week (n = 26; GRS, 73.2 +/- 24.9 micrograms), and there were no differences when intermediate groups were examined. GRS elevations were found to be linearly and directly correlated with free phenytoin ultrafiltrate levels (n = 35, r = 0.7692, p less than 0.0001) when patients were co-medicated with valproic acid, with serum phenobarbital levels (n = 58, r = 0.5361, p less than 0.05), with serum valproic acid levels (n = 43, r = 0.3173, p less than 0.05), and with the sum of serum phenobarbital and valproic acid levels (n = 16, r = 0.8657, p less than 0.0001). The findings indicate that GRS elevations are probably due to anticonvulsant medications rather than to the frequency of seizures. There is no evidence that GRS determinations can be used for the diagnosis or prognosis of patients with epilepsy.