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Nitrous Oxide-Induced Vitamin B12 Deficiency and Myelopathy in Whippets Abusers: A Report of Two Cases
Fahim Barmak1, Jamil Numan1, Mariam Shabih1
1Neurology, Marshall University Joan C. Edwards School of Medicine, Huntington, USA.
Abstract:
Whippets abuse, prevalent among recreational drug users, poses significant health risks, particularly through the inactivation of vitamin B12 by nitrous oxide (N2O). This deficiency can lead to myelopathy, resulting in serious neurological complications. We present two female patients, aged 22 and 35, with a history of regular whippet use over the past three years, who exhibited clinical symptoms of myelopathy, including motor weakness, rigidity, sensory changes, and gait abnormalities. The 35-year-old patient showed weakness and swelling in her legs; magnetic resonance imaging (MRI) revealed no acute findings, but lab results indicated a critically low serum vitamin B12 level (102 pg/mL), elevated homocysteine (44 µmol/L), and high methylmalonic acid (29,054 nmol/L). She improved with vitamin B12, vitamin D supplementation, and physical and occupational therapy. The 22-year-old patient reported progressive stiffness and tingling, with MRI revealing T2 hyperintensities in the brain and longitudinal T2 hyperintensities in the posterior spinal cord; her vitamin B12 level was 180 pg/mL, and she responded positively to supplementation and physical therapy. These cases underscore the risk of nitrous oxide-induced myelopathy associated with vitamin B12 deficiency among whippet users. Early recognition and intervention are essential to prevent irreversible neurological damage, and routine screening for vitamin B12 deficiency in this population is recommended. Further research is needed to explore the long-term implications of N2O abuse.
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