N-acetylation and debrisoquine hydroxylation polymorphisms in patients with Gilbert's syndrome.
1. N-acetylation and debrisoquine hydroxylation phenotypes were determined in 54 patients with Gilbert's syndrome and in 247 (sulphamethazine) and 76 (debrisoquine) non-related healthy volunteers. 2. Forty (74.1%) of the patients and 135 (54.7%) of the healthy volunteers were slow acetylators (chi 2 = 6.87). In the patients, the cumulative urinary excretion of sulphamethazine up to 6 h (Ae(0,6)) was significantly lower. No differences in the frequency of debrisoquine poor metabolizers were observed: Gilbert's syndrome 5/54 (9.3%), healthy volunteers 5/76 (6.6%). The metabolic ratios were similar in both groups as well as the urinary recoveries of debrisoquine and its 4-hydroxy metabolite. 3. Gilbert's syndrome seems to be related in some way to N-acetylation but not to the debrisoquine hydroxylation polymorphism.
Siegmund
W
W
Department of Clinical Pharmacology, University of Greifswald, Germany.
Fengler
J D
JD
Franke
G
G
Zschiesche
M
M
Eike
O
O
Eike
E
E
Meisel
P
P
Wulkow
R
R
D000107:Acetylation; D000293:Adolescent; D000328:Adult; D000368:Aged; D003647:Debrisoquin / Q000378:metabolism*; D005260:Female; D005878:Gilbert Disease / Q000378:metabolism*; D006801:Humans; D006900:Hydroxylation; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D011110:Polymorphism, Genetic
D003647:Debrisoquin