A case of functional vitamin B12 deficiency after recreational nitrous oxide use

Abstract

The recreational use of nitrous oxide as laughing gas becomes a real public health issue among adolescents and young adults. Chronic use is deleterious and can lead to severe neurological disorders. Nitrous oxide inactivates vitamin B12, and the functional defect of vitamin B12 plays a major role in the pathogenesis of nitrous oxide-related neurological disorders. Here we report the case of a 22-year-old woman who came to the hospital after an unexplained loss of consciousness. She exhibited typical features of vitamin B12 or folate deficiency such as macrocytic anemia and hypersegmented neutrophils. However, serum concentrations of folate and vitamin B12 were normal. In contrast, circulating concentrations of total homocysteine and methylmalonic acid were significantly increased. These results clearly indicated a defect in vitamin B12 functions. The reason for this defect was clarified when she revealed that she had been consuming nitrous oxide recreationally for over a year. The present case points out the challenges in diagnosing vitamin B12 deficiency in the context of nitrous oxide abuse due to normal concentrations of total serum vitamin B12 in a significant proportion of cases. The medical community should be aware of how difficult it can be to interpret B12 status in this specific population.

Nitrous oxide abuse in a 21-year-old female: a case report and review of literature

“…However, at times, serum or active B12 levels may remain normal, suggesting that vitamin B12 deficiency may not be the sole cause of neurological damage ( 15 , 16 ). Some patients may present with macrocytic anemia, although the correlation between anemia and vitamin B12 deficiency has not been conclusively established ( 17 ). Elevated homocysteine levels are a prevalent laboratory abnormality, with around 80% of N 2 O poisoning patients exhibiting elevated homocysteine levels ( 18 ).…”