Important reminder: nitrous oxide (N<sub>2</sub>O) as a cause of functional vitamin B<sub>12</sub>deficiency

Mahgoub, Abdullahi; Deliwala, Smit; Bachuwa, Ghassan

doi:10.1136/bcr-2020-241414

BMJ Case Rep

2021

DOI: 10.1136/bcr-2020-241414

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Important reminder: nitrous oxide (N₂O) as a cause of functional vitamin B₁₂deficiency

Abdullahi Mahgoub

Smit Deliwala

Ghassan Bachuwa

Abstract: A 32-year-old woman who misused multiple substances, including nitrous oxide (N2O), sought medical advice after she subacutely developed bilateral lower extremity weakness without a sensory level but with ataxia—her significant other developed similar symptoms with vitamin B12 deficiency due to N2O intake. Laboratory results revealed macrocytic anaemia despite normal B12 and folate levels, with serum markers pointing towards functional cobalamin deficiency. Spinal MRIs and cerebrospinal fluid analysis were unr… Show more

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“… Abstract Background: Several causes lead to subacute combined degeneration (SACD) of the spinal cord, with nitrous oxide (N2O) inhalation rapidly emerging as the leading cause of functional Vitamin B12 deficiency [ 1 ]. Case Presentation: A 28-year-old man presented with numbness in the extremities and an unstable gait despite having a normal serum Vitamin B12 level.…”

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confidence: 99%

‘From highs to lows: a cautionary tale of nitrous oxide recreational use leading to sub-acute combined degeneration of the cord’

Osman,

Yousif,

Hickman

et al. 2024

Oxford Medical Case Reports

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Background: Several causes lead to subacute combined degeneration (SACD) of the spinal cord, with nitrous oxide (N2O) inhalation rapidly emerging as the leading cause of functional Vitamin B12 deficiency [1]. Case Presentation: A 28-year-old man presented with numbness in the extremities and an unstable gait despite having a normal serum Vitamin B12 level. He also disclosed the recreational abuse of N2O. Magnetic Resonance Imaging (MRI) of the cervical spine revealed abnormal signals consistent with SACD. The patient’s condition gradually improved after treatment with high dose Vitamin B12. Given the increasing number of N2O-induced SACD cases, the potential for drug abuse requires vigilance from clinicians. Conclusion: Healthcare providers are urged to inquire about a patient’s history of N2O inhalation to prevent the missed diagnosis of SACD.

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confidence: 99%

‘From highs to lows: a cautionary tale of nitrous oxide recreational use leading to sub-acute combined degeneration of the cord’

Osman,

Yousif,

Hickman

et al. 2024

Oxford Medical Case Reports

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The boon and bane of nitrous oxide

Kronenberg,

Schoretsanitis,

Seifritz

et al. 2024

Eur Arch Psychiatry Clin Neurosci

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Nitrous oxide (N2O) has been known since the end of the eighteenth century. Today, N2O plays a huge role as a greenhouse gas and an ozone-depleting stratospheric molecule. The main sources of anthropogenic N2O emissions are agriculture, fuel combustion, wastewater treatment, and various industrial processes. By contrast, the contribution of medical N2O to the greenhouse effect appears to be small. The recreational and medical uses of N2O gradually diverged over time. N2O has analgesic and anesthetic effects, making it widely used in modern dentistry and surgery. New research has also begun studying N2O’s antidepressant actions. N-methyl-D-aspartate (NMDA) antagonism and opioid effects are believed to be the main underlying biochemical mechanisms. At this point, numerous questions remain open and, in particular, the conduct of larger clinical trials will be essential to confirm N2O’s use as a rapid-acting antidepressant. The N2O concentration delivered, the duration of a single inhalation, as well as the number of inhalations ultimately required, deserve to be better understood. Finally, the non-medical use of N2O has gained significant attention in recent years. Sudden deaths directly attributed to N2O are primarily due to asphyxia. Heavy, chronic N2O use may result in vitamin B12 deficiency, which, among other things, may cause megaloblastic anemia, venous thrombosis, myeloneuropathy, and skin pigmentation. Helpful biochemical tests include homocysteine and methylmalonic acid. The centerpiece of treatment is complete cessation of N2O use together with parenteral administration of vitamin B12.

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Folate and Vitamin B12 Deficiency Exacerbate Inflammation during Mycobacterium avium paratuberculosis (MAP) Infection

2023

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Folate and vitamin B12 deficiency is highly prevalent among Crohn’s disease (CD) patients. Furthermore, CD pathology can be mediated by Mycobacterium avium subsp. paratuberculosis (MAP) infection. However, the direct effect of folate (B9) and cobalamin (B12) deficiency during MAP infection remains uncharacterized. This study investigates how folate and B12 deficiency impedes macrophage apoptosis and exacerbates the inflammation in macrophages infected with MAP isolated from CD patients. Accordingly, we measured folate and B12 in ex vivo plasma samples collected from CD patients with or without MAP infection (N = 35 per group). We also measured the expression of the pro-inflammatory cytokines IL-1β and TNF-α, cellular apoptosis and viability markers, and bacterial viability in MAP-infected macrophages cultured in folate and B12 deficient media. We determined that MAP-positive CD patients have significantly lower plasma folate and B12 in comparison to MAP-negative CD patients [414.48 ± 94.60 pg/mL vs. 512.86 ± 129.12 pg/mL, respectively]. We further show that pro-inflammatory cytokines IL-1β and TNF-α are significantly upregulated during folate and vitamin B12 deprivation following MAP infection by several folds, while supplementation significantly reduces their expression by several folds. Additionally, depletion of folate, B12, and folate/B12 following MAP infection, led to decreased macrophage apoptosis from 1.83 ± 0.40-fold to 1.04 ± 0.08, 0.64 ± 0.12, and 0.45 ± 0.07 in folate-low, B12-low, and folate/B12-low cells, respectively. By contrast, folate and folate/B12 supplementation resulted in 3.38 ± 0.70 and 2.58 ± 0.14-fold increases in infected macrophages. Interestingly, changes in overall macrophage viability were only observed in folate-high, folate/B12-high, and folate/B12-low media, with 0.80 ± 0.05, 0.82 ± 0.02, and 0.91 ± 0.04-fold changes, respectively. Incubation of Caco-2 intestinal epithelial monolayers with supernatant from infected macrophages revealed that folate/B12 deficiency led to increased LDH release independent of oxidative stress. Overall, our results indicate that folate and B12 are key vitamins affecting cell survival and inflammation during MAP infection.

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Important reminder: nitrous oxide (N₂O) as a cause of functional vitamin B₁₂deficiency

Cited by 3 publications

References 17 publications

‘From highs to lows: a cautionary tale of nitrous oxide recreational use leading to sub-acute combined degeneration of the cord’

‘From highs to lows: a cautionary tale of nitrous oxide recreational use leading to sub-acute combined degeneration of the cord’

The boon and bane of nitrous oxide

Folate and Vitamin B12 Deficiency Exacerbate Inflammation during Mycobacterium avium paratuberculosis (MAP) Infection

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Important reminder: nitrous oxide (N2O) as a cause of functional vitamin B12deficiency

Cited by 3 publications

References 17 publications

‘From highs to lows: a cautionary tale of nitrous oxide recreational use leading to sub-acute combined degeneration of the cord’

‘From highs to lows: a cautionary tale of nitrous oxide recreational use leading to sub-acute combined degeneration of the cord’

The boon and bane of nitrous oxide

Folate and Vitamin B12 Deficiency Exacerbate Inflammation during Mycobacterium avium paratuberculosis (MAP) Infection

Contact Info

Product

Resources

About

Important reminder: nitrous oxide (N₂O) as a cause of functional vitamin B₁₂deficiency