In crimes facilitated by γ-hydroxybutyric
acid (GHB) administration, the frequent occurrence of
anterograde amnesia of the victims as well as the short detection window and variations of endogenous GHB concentrations complicate obtaining analytical proof of GHB administration. Because elevated endogenous organic
acid concentrations have been found in the urine of patients with
succinic semialdehyde deficiency (leading to accumulation of GHB in human specimens) and after GHB ingestion, we searched for an alternative way to prove GHB administration via detection of elevated organic
acid concentrations in blood plasma and urine. We collected blood and urine samples from
narcolepsy patients (n = 5) treated with pharmaceuticals containing GHB
sodium salt (1.86-3.72 g GHB as free
acid per dose). Although GHB was detectable only up to 4 h in concentrations greater than the commonly used cutoff levels in blood plasma, 3,4-dihydroxybutyric
acid (3,4-DHB) could be detected up to 12 h in blood plasma in concentrations exceeding initial concentrations of the same patient before GHB ingestion. Furthermore, four of the five patients showed an increase above endogenous levels described in the scientific literature. In urine, GHB concentrations above commonly used cutoff levels could be observed 4.5-9.5 h after GHB intake.
Creatinine standardized initial concentrations were reached again for
glycolic acid (GA), 3,4-DHB, and 2,4-dihydroxybutyric (2,4-DHB)
acid at 6.5-22, 11.5-22, and 8.5-70 h after GHB intake, respectively. Therefore,
2,4-DHB, 3,4-DHB, and GA are promising and should be further investigated as potential
biomarkers to prolong the detection window of GHB intake.