Blood tests find no clear cannabinoid signature for cannabis vomiting

The underlying pathophysiology of cannabinoid hyperemesis syndrome remains poorly understood. Proposed mechanisms include "hyperintoxication" with delta-9-tetrahydrocannabinol, accumulation of delta-9-tetrahydrocannabinol metabolites, and differential exposure to non-psychotropic phytocannabinoids. This study sought to examine quantitative differences in serum concentrations of delta-9-tetrahydrocannabinol, delta-9-tetrahydrocannabinol metabolites, delta-8-tetrahydrocannabinol, and common non-psychotropic phytocannabinoids between patients presenting to the emergency department with either acute, symptomatic cannabinoid hyperemesis syndrome or acute cannabis intoxication. This was a retrospective cohort study performed in the emergency department of a single academic medical center. Subjects were screened based on discharge diagnosis consistent with either cannabinoid hyperemesis syndrome or acute cannabis intoxication and on availability of remnant blood samples. Chart data including emergency department length of stay, disposition, treatment, and labs were abstracted, and blood samples were analyzed via liquid chromatography-triple quadrupole tandem mass spectrometry for serum concentrations of delta-9-tetrahydrocannabinol, delta-8-tetrahydrocannabinol, 11-nor-9-carboxy-delta-9-tetrahydrocannabinol, 11-hydroxy-delta-9-tetrahydrocannabinol, delta-8-carboxy-tetrahydrocannabinol, cannabidiol, cannabigerol, and cannabinol. Fifty subjects were enrolled; thirty-five presented with cannabinoid hyperemesis syndrome and 15 with acute cannabis intoxication. Groups were well matched with regard to baseline demographics, emergency department disposition, and emergency department length of stay. No significant differences were noted in serum concentrations of delta-9-tetrahydrocannabinol, delta-9-tetrahydrocannabinol metabolites, non-psychotropic phytocannabinoids, or their respective ratios. While limited by uncontrolled host factors, the results of this study further existing literature arguing against the differential accumulation of psychoactive cannabinoids, non-psychoactive cannabinoids, or their metabolites as causative factors in the development of acute symptomatic episodes of cannabinoid hyperemesis syndrome. There does not appear to be a significant difference in concentrations of psychoactive and non-psychoactive cannabinoids between emergency department patients with symptomatic cannabinoid hyperemesis syndrome and those with acute cannabis intoxication.