E. Hadasova et al., DEBRISOQUINE 4-HYDROXYLATION AND SULFAMETHAZINE N-ACETYLATION IN PATIENTS WITH SCHIZOPHRENIA AND MAJOR DEPRESSION, British journal of clinical pharmacology, 41(5), 1996, pp. 428-431
Debrisoquine 4-hydroxylation and sulphamethazine N-acetylation phenoty
pes were determined in 115 Czech drug-free in-patients with schizophre
nia (n=64) or major depressive disorder (n=51). These data were compar
ed with a control. group of 321 healthy volunteers from the North-East
German area of Greifswald. The distribution of debrisoquine hydroxyla
tor phenotypes was almost identical in patients and healthy controls.
Thus, there were 5.7% (95% CI 5.4-12.0%) of poor metabolizers (PM) amo
ng patients while 8.7% (95% CI 3.6-13.8%) PM among the control group.
The prevalences of PM amongst patients with chronic schizophrenia and
major depression were 10.9% (95% CI 4.5-21.3%) and 5.9 % (95% CI 1.24-
16.3%), respectively (chi(2) schizophrenics vs control=0.315, NS; chi(
2) depressive patients vs control=0.450, NS). However, within the grou
p of EM patients there was a significant (P<0.01) shift towards higher
debrisoquine metabolic ratios, reflecting a lower hydroxylation capac
ity in EM patients compared with EM healthy controls. The proportion o
f slow acetylators (SA) was 60.0% (95% CI 51.0-68.9%) in the entire gr
oup of psychiatric patients and 57.5% (95% CI 52.1-62.9%) in the contr
ol group (chi(2) all patients us control= 0.195, NS). Furthermore, the
re were no significant differences in the prevalence of the SA phenoty
pe between controls and schizophrenics or patients with major depressi
on. Although the results of this modest study were negative, the prese
nce of subtle differences in the metabolic capacity between psychiatri
c patients and a healthy population cannot be ruled out.