DEBRISOQUINE 4-HYDROXYLATION AND SULFAMETHAZINE N-ACETYLATION IN PATIENTS WITH SCHIZOPHRENIA AND MAJOR DEPRESSION

Citation
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
Citations number
34
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
03065251
Volume
41
Issue
5
Year of publication
1996
Pages
428 - 431
Database
ISI
SICI code
0306-5251(1996)41:5<428:D4ASNI>2.0.ZU;2-E
Abstract
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.