Abstract

Nitrous oxide (N2O) toxicity is a well-known entity. It is capable of inactivating vitamin B12, producing a relative B12 deficiency. Vitamin B12 is needed for neurologic development and is necessary for the body to complete vital biologic functions. We look at a case of a 28 year old patient who abused N2O, then went on to develop neurologic symptoms of ataxia, numbness and subacute combined degeneration of the dorsal columns as seen on MRI. Her symptoms were consistent with vitamin B12 deficiency despite having normal vitamin B12 levels by conventional lab measurements. Her methylmalonic acid (MMA) levels however were elevated. After administering daily B12 injections for 2 weeks and complete abstinence from N2O, her neurologic deficits have nearly resolved.

Highlights

  • Mean corpuscular volume (MCV) is a lab measurement used to determine the different etiologies of anemia

  • Low MCV values are seen with anemia of chronic disease, thalassemias, and most commonly iron deficiency anemia [6]

  • Our patient presented with neurologic deficits consistent with a B12 deficiency in spite of having normal B12 levels

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Summary

Introduction

The family history only revealed cancer of unknown etiology on the father’s side Her laboratory investigation reports were grossly normal, with the following being of note: MCV of 105.3 fL (normal range 84.5-101.5), WBC of 13.7 K/uL (normal range 4.2-11.1), UDS was positive for opiates, benzodiazepines, and marijuana. In the weeks after discharge, she followed up with a primary care physician Her B12 measurements were within normal levels and she was started on oral B12 supplementation. A phone interview with the patient revealed complete resolution of the ataxia by week 3 She had minimal sensation abnormalities, but they continued to improve daily.

Discussion
Findings
B12 For the conversion of Methylmalonyl CoA into
Conclusion
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