Functional Vitamin B12 Deficiency in Association With Nitrous Oxide Inhalation

Abstract

There is a rise in the use and abuse of nitrous oxide (N₂O) as a recreational drug. In spite of the laws enforced internationally, it remains readily available and is an inexpensive mode of recreational drug. Commonly known as the ‘laughing gas’, its use as a euphoric agent is on the rise. Subsequently, the side effects are also coming to light, associated with medical, financial and social implications. It is not detected in routine drug testing. The key differential in an acute setting is often confused with the query for Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy and malabsorption syndromes associated with vitamin B12 and folate deficiencies. This is a case report of a 21-year-old male who presented to the hospital with concerns for weakness and tingling sensations in his extremities accompanied by an inability to bear weight, which he suggested to seem to be worsening over a period of three weeks. His blood tests suggest mild deficiencies of vitamin B12 and folate levels, and MRI revealed subacute combined degeneration of the cervical cord from C2 to C6. The radiologist advised to rule out B12 deficiency and the use of nitrous oxide as a recreational drug. This led to the discussion with the patient, during which he admitted to the use of nitrous oxide. Prompt management with B12 injections intramuscularly every two to three days a week for 11 days followed by folate supplements and monthly B12 injections were advised. He was also reviewed by the physiotherapy teams, and the patient agreed to not use nitrous oxide in the future as a recreational drug.

Severe length‐dependent peripheral polyneuropathy in a patient with subacute combined spinal cord degeneration secondary to recreational nitrous oxide abuse: A case report and literature review

“… 8 It has also been suggested that there are inhibitory effects on N‐methyl‐d‐asparate receptors in the central nervous system, stimulation of noradrenergic pathways and sympathetic actions via α‐1‐adrenergic stimulation, although these are not well understood. 8 , 9 …”

“…8 noradrenergic pathways and sympathetic actions via α-1-adrenergic stimulation, although these are not well understood. 8,9 Treatments will begin with ceasing N 2 O use and intramuscular vitamin B 12 injections. Approximately 75% of the 96 patients in the review saw either a reduction or complete resolution of neurological systems if they followed this treatment over subsequent weeks.…”

“…From a regional stand point, this seems to primarily affect the posterior columns, but also the postero‐lateral regions of the cord 8 . It has also been suggested that there are inhibitory effects on N‐methyl‐d‐asparate receptors in the central nervous system, stimulation of noradrenergic pathways and sympathetic actions via α‐1‐adrenergic stimulation, although these are not well understood 8,9 …”

Subacute combined degeneration of the spinal cord secondary to nitrous oxide-induced B12 deficiency

“…It is important to note that vitamin B12 levels are not always low in cases of N 2 O-induced SCD of the spinal cord, as evidenced in a 2016 systematic review by Garkani et al, which reported that B12 levels were only low in 46% of patients with N 2 O-induced neurological symptoms [ 2 ] . This implies that N 2 O can also cause a functional B12 deficiency rather than an absolute depletion [ 3 , 4 ] . If there is suspicion of N 2 O-induced neurological symptoms and vitamin B12 levels are normal, serum levels of methylmalonic acid and homocysteine can be measured instead, which accumulate if B12 is inactive or levels are low [ 1 ] .…”

Splenic Vein Thrombosis: A Case Series of Consequential Chronic Pancreatitis and Sequential Myeloproliferative Disorder

“…Vitamin B12 deficiency is known to be associated with increased homocysteine levels (hyperhomocysteinemia); vitamin B12 is needed as a cofactor to remethylate homocysteine to methionine. This hyperhomocysteinemia, reported to be associated with neurological symptoms arising from vitamin B12 deficiency (and with nitrous oxide abuse) [ 15 ], can increase the propensity for arterial and venous thrombosis [ 16 ] and therefore has also been reported to be associated with SVT [ 17 ].…”