Nitrous oxide-induced vitamin B(12) deficiency
M Jameson1, S Roberts, N E Anderson
1Departments of Clinical Oncology, Auckland Hospital, Auckland, New Zealand.
Summary
Nitrous oxide exposure can trigger peripheral neuropathy in patients with vitamin B12 deficiency. Cyclophosphamide treatment may exacerbate these neurological symptoms by reducing available vitamin B12 stores.
Area of Science:
- Neurology
- Hematology
- Anesthesiology
Background:
- Vitamin B12 deficiency can lead to peripheral neuropathy.
- Nitrous oxide is known to inactivate vitamin B12.
- Cyclophosphamide is a chemotherapy agent with potential hematologic side effects.
Purpose of the Study:
- To report two cases of peripheral neuropathy in patients with asymptomatic vitamin B12 deficiency.
- To investigate the potential role of nitrous oxide exposure and cyclophosphamide treatment in triggering neurological symptoms.
- To highlight the temporal relationship between these exposures and symptom onset.
Main Methods:
- Case report of two patients.
- Clinical observation of neurological symptoms development.
- Biochemical analysis of serum vitamin B12 levels.
- Assessment of symptom resolution following vitamin B12 replacement therapy.
Main Results:
- Both patients presented with peripheral neuropathy 6-7 weeks after nitrous oxide exposure and shortly after cyclophosphamide treatment.
- Serum vitamin B12 levels were critically low (<20 pmol/l).
- Neurological symptoms resolved completely after vitamin B12 supplementation.
Conclusions:
- Nitrous oxide exposure is a likely trigger for peripheral neuropathy in individuals with underlying vitamin B12 deficiency.
- Cyclophosphamide treatment may have contributed to the onset or severity of symptoms by further depleting vitamin B12.
- This case series suggests a potential interaction between nitrous oxide, cyclophosphamide, and vitamin B12 metabolism.
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