A drinking experiment with participants suffering from
Gilbert's syndrome was performed to study the possible influence of this glucuronidation disorder on the formation of
ethyl glucuronide (EtG).
Gilbert's syndrome is a rather common and, in most cases, asymptomatic congenital metabolic aberration with a prevalence of about 5 %. It is characterized by a reduction of the
enzyme activity of the
uridine diphosphate glucuronosyltransferase (UGT)
isoform 1A1 up to 80 %. One of the glucuronidation products is EtG, which is formed in the organism following exposure to
ethanol. EtG is used as a short-term marker for
ethyl alcohol consumption to prove abstinence in various settings. After 2 days of abstinence from ethanol and giving a void urine sample, 30 study participants drank 0.1 L of sparkling wine (9 g
ethanol). 3, 6, 12, and 24 h after drinking, urine samples were collected. 3 hours after drinking, an additional blood sample was taken, in which liver
enzyme activities,
ethanol, hematological parameters, and
bilirubin were measured. EtG and
ethyl sulfate (EtS), another short-term marker of
ethanol consumption, were determined in the urine samples using liquid chromatography-tandem mass spectrometry (LC-MS/MS);
creatinine was measured photometrically. In all participants, EtG and EtS were detected in concentrations showing a wide range (EtG: 3 h sample 0.5-18.43 mg/L and 6 h sample 0.67-13.8 mg/L; EtS: 3 h sample 0.87-6.87 mg/L and 6 h sample 0.29-4.48 mg/L). No evidence of impaired EtG formation was found. Thus, EtG seems to be a suitable marker for
ethanol consumption even in individuals with
Gilbert's syndrome.