Medullar toxicity after prolonged nitrous oxide exposure: an unexpected cause of bone marrow failure post allogeneic transplant

Vozy, Aurore; Cohen, Milton; Mt, Rubio; Rostaing-Rigattieri, S.; Mohty, Mohamad; Ac, Mamez

doi:10.1038/bmt.2015.314

Cited by 4 publications

(2 citation statements)

References 11 publications

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“…Vozy et al reported a 16-year-old girl who presented with secondary bone marrow failure following an allogeneic haploidentical stem cell transplant. This was mainly because of the heavy use of N 2 O (analgesia) over a prolonged period [7].…”

Section: Discussionmentioning

confidence: 99%

Pancytopenia Caused by Nitrous Oxide Toxicity: Two Cases Report

Jiang,

Xia

2024

Asp Biomed Clin Case Rep

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Recreational nitrous oxide (N2O) is increasingly common among young people, leading to attendant health disadvantages. Related complications primarily involve the hematological and neurological systems. We report two relatively uncommon cases of pancytopenia due to substantial N2O inhalation. One possible cause is that N2O toxicity results in vitamin B12 inactivation and an insufficient intake of nutrients. The patient’s symptoms partially improved after cessation of N2O inhalation and supplementation with vitamin B12. In conclusion, if the patients presented with unexplained bone marrow failure, a history of prolonged N2O exposure should be considered, which would greatly help in early diagnosis, therapy, and the reduction of unnecessary costs.

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Section: Discussionmentioning

confidence: 99%

Pancytopenia Caused by Nitrous Oxide Toxicity: Two Cases Report

Jiang,

Xia

2024

Asp Biomed Clin Case Rep

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“…Recent case reports have also provided anecdotal evidence associating chronic N 2 O use with subacute combined degeneration and limb weakness [12], myeloneuropathy [13], pernicious anemia [14], hematologic changes and risk of thrombosis [15,16], myocardial infarction [17], pneumomediastinum [18], vitamin B12 deficiency with lower motor neuronal degeneration [19,20], and stroke [21], and many conditions that are considered significant risk factors for AD onset, including headache [22], anemia [23], gait imbalance/ataxia [24], thrombosis [25], stroke [26], and myocardial infarction [27]. Moreover, clinical evidence suggests that trace N 2 O exposure induces impairments in the Digit Span Test [28], a test that has predictive power in identifying cognitive decline in participants with mild cognitive impairment (MCI)—a condition often prodromal to AD [29].…”

Section: Environmental Nitrous Oxide (N2o) Exposure and Ad Pathologymentioning

confidence: 99%

A model of lipid dysregulation and altered nutrient status in Alzheimer's disease

Fluegge

2019

A&D Transl Res & Clin Interv

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Introduction Dysregulated lipid metabolism and nutrient status are thought to play a role in the pathophysiology of Alzheimer's disease (AD). However, the precise involvement is not well understood, and it remains unclear exactly how such dysregulated lipid metabolism and altered nutrient status, especially changes in phosphatidylcholine, B12, and folate, are connected to the hallmark pathology in AD (i.e., amyloidogenesis). Methods We have postulated that genetic susceptibility (i.e., APOE ε4/ε4) to environmental exposure to emissions of nitrous oxide (N 2 O) could underlie the onset of AD and its early neuropsychiatric correlates Results and Discussion The current theoretical editorial describes, using clinical, preclinical, and in vitro evidences, how this model contributes not only to amyloidogenesis but also other nonopioid effects, specifically altered lipid metabolism, depletion of vitamin B12, and disruption of the folate-mediated one carbon metabolic pathway.

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