Rapid decline of elevated homocysteine level in nitrous oxide use

The recreational use of nitrous oxide (N2O) has increased significantly in recent years, becoming an emerging public health concern owing to its association with severe neurological complications. Vitamin B12 is inactivated by N2O, and accumulation of homocysteine (Hcy) could be a relevant marker of N₂O toxicity. Kinetics of Hcy after cessation of exposure remain poorly understood. This retrospective study examined the Hcy levels of patients hospitalized consecutively for neurological impairment secondary to N₂O intoxication. Demographic and clinical data were collected, including clinical phenotype and motor deficit severity. Levels, dates, and hours of blood testing for vitamin B12, Hcy, and hospital entrance were collected. The statistical analysis used the Wilcoxon test or the Chi-square test. Among the 86 patients (median age 22 years; 59% woman), 92% exhibited abnormal Hcy levels, with a median Hcy concentration of 69 µmol/L [38; 106] (normal < 15 µmol/L). Vitamin B12 levels were normal in 80% of cases. Hcy levels were significantly lower in patients who had received vitamin B12 supplementation (p = 0.016). When blood testing was performed within the first 8 h after hospital admission, Hcy levels were high (median 106 µmol/L [89; 112]). A rapid decrease was observed within the following hours, reaching normal levels approximately one week after admission. The exponential decline of Hcy underscores its potential as a valuable biomarker for N₂O-induced toxicity under the condition of a very early sampling and patient reference. In current practice, Hcy values that do not increase dramatically could suggest a delay in testing rather than low N2O usage.