This report details the toxicology profile of victims of drug-facilitated sexual assault (DFSA) in New Zealand from 2015 to 2018. This study represents all of the toxicology results for DFSA cases in New Zealand during this time period, of which there were 161 cases. Blood and urine samples were screened for legal and illicit drugs in addition to testing for alcohol and correlating alcohol concentration with sampling delay. Our results indicate that increased delay in sampling time resulted in a corresponding decrease in alcohol concentration. In victims who had declared alcohol use but of which none was detected, the average sampling time was 14 hours for blood and 17 hours for urine, which is in excess of the average sampling delay for even the lowest alcohol-positive samples. The most frequently detected alcohol concentration was in the range of 51–80 mg/100 mL for blood and 121–200 mg/100 mL for urine with an average sampling time of 8.5 and 6.5 hours, respectively. We also examined acetone concentrations in alcohol-positive samples, and our results indicate that 82% of blood alcohol-positive samples contained acetone at concentrations between 5 and 10 mg/L and 68% of alcohol-positive urine samples contained acetone at a concentration >20 mg/L. It may be that the nature of sexual assault affects an individual’s metabolism of alcohol and results in increased acetone production. Cannabis was the most commonly detected illicit drug, followed by methamphetamine. In relation to medicinal drugs, there was a high usage of antidepressants and antipsychotics, suggesting the victims may have been people of vulnerable personality. Based on case information, it does not appear there are many cases where stupefaction by unknown administration of a drug has occurred, instead loss of consent through voluntary alcohol and drug consumption is more common and poses a greater risk than surreptitious drug administration.

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Cocaine is one of the most widely abused illicit drugs due to its euphoric and addictive properties. Cocaine‐mediated cognitive impairments are the result of dynamic cytoskeletal rearrangements involved in mediating structural and behavioural plasticity. Cytoskeletal changes initiated following cocaine abuse are regulated by the Rho family of GTPases with significant downstream activity in key actin binding proteins. Moreover, signalling via the endoplasmic reticulum chaperone protein, sigma‐1 receptor has highlighted the possibility of cocaine regulated pathology in other organ systems. However, the question of whether upstream stimulation of such a high affinity binding receptor is directly involved in cocaine‐mediated cytoskeletal changes at present remains unknown. In this review, we describe the functional role of key cytoskeletal regulators in response to cocaine‐induced signalling cues. In addition, we ascertain the extent of whether global cytoskeletal modulators involved in cocaine‐induced neurological stimulation can be used as a platform for future studies into elucidating its fibrotic potential within the hepatic microenvironment. A focus on aspects still poorly understood relating to the nonneuronal pathological impact of cocaine is discussed in the sphere of hepatic dysregulation. Lastly, we suggest that cocaine may mediate its pathological capacity via the sigma1 receptor in regulating hepatoxicity, hepatic stellate cells activity, cytoskeletal dynamics, and the transcriptional regulation of key hepato‐fibrogenic modulators.

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