Démence postopératoire : toxicité du protoxyde d’azote

Otmani, Hicham El; Moutawakil, Bouchra El; Moutaouakil, F.; Gam, I.; Rafai, M.A.

doi:10.1016/s0013-7006(07)91563-8

Cited by 14 publications

(4 citation statements)

References 8 publications

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“…Neuropathy associated with PA classically involves disease progression, beginning in the cervicothoracic region of the spine,202,441 with upper extremity findings classically occurring before lower extremity findings, followed by peripheral nerve involvement, and lastly, if at all, brain involvement 23,200,203. Dementia is believed to be a late and rare finding of neuropathy associated with PA 19,25,48,203,290. Alternatively, dementia with B12 deficiency often occurs independently from PA 13,25,146,290,427,432,433…”

Section: Discussionmentioning

confidence: 99%

“…B12-deficient dementia without PA is relatively common,25,146,290,427,432,433 but B12-deficient dementia with PA is considered rare,14,19,25,30,32,48,93,203,290,427,432 where it causes only a small fraction of B12 deficiency in demented individuals 14,25,30,32,93,290,427,432. PA incidence peaks late in midlife,181,429 while dementia incidence increases with age 233.…”

Section: Discussionmentioning

confidence: 99%

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Cobalamin deficiency, hyperhomocysteinemia, and dementia

Werder¹

2010

NDT

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IntroductionAlthough consensus guidelines recommend checking serum B12 in patients with dementia, clinicians are often faced with various questions: (1) Which patients should be tested? (2) What test should be ordered? (3) How are inferences made from such testing? (4) In addition to serum B12, should other tests be ordered? (5) Is B12 deficiency compatible with dementia of the Alzheimer’s type? (6) What is to be expected from treatment? (7) How is B12 deficiency treated?MethodsOn January 31st, 2009, a Medline search was performed revealing 1,627 citations related to cobalamin deficiency, hyperhomocysteinemia, and dementia. After limiting the search terms, all abstracts and/or articles and other references were categorized into six major groups (general, biochemistry, manifestations, associations and risks, evaluation, and treatment) and then reviewed in answering the above questions.ResultsThe six major groups above are described in detail. Seventy-five key studies, series, and clinical trials were identified. Evidence-based suggestions for patient management were developed.DiscussionEvidence is convincing that hyperhomocysteinemia, with or without hypovitaminosis B12, is a risk factor for dementia. In the absence of hyperhomocysteinemia, evidence is less convincing that hypovitaminosis B12 is a risk factor for dementia. B12 deficiency manifestations are variable and include abnormal psychiatric, neurological, gastrointestinal, and hematological findings. Radiological images of individuals with hyperhomocysteinemia frequently demonstrate leukoaraiosis. Assessing serum B12 and treatment of B12 deficiency is crucial for those cases in which pernicious anemia is suspected and may be useful for mild cognitive impairment and mild to moderate dementia. The serum B12 level is the standard initial test: 200 picograms per milliliter or less is low, and 201 to 350 picograms per milliliter is borderline low. Other tests may be indicated, including plasma homocysteine, serum methylmalonic acid, antiparietal cell and anti-intrinsic factor antibodies, and serum gastrin level. In B12 deficiency dementia with versus without pernicious anemia, there appear to be different manifestations, need for further workup, and responses to treatment. Dementia of the Alzheimer’s type is a compatible diagnosis when B12 deficiency is found, unless it is caused by pernicious anemia. Patients with pernicious anemia generally respond favorably to supplemental B12 treatment, especially if pernicious anemia is diagnosed early in the course of the disease. Some patients without pernicious anemia, but with B12 deficiency and either mild cognitive impairment or mild to moderate dementia, might show some degree of cognitive improvement with supplemental B12 treatment. Evidence that supplemental B12 treatment is beneficial for patients without pernicious anemia, but with B12 deficiency and moderately-severe to severe dementia is scarce. Oral cyanocobalamin is generally favored over intramuscular cyanocobalamin.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Werder¹

2010

NDT

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“…A ~4 days exposure resulted in agranulocytosis and a 7 days exposure resulted in death of two patients (171). With short exposure periods (~2 to 3 hours), patients with vitamin B12 deficiency can develop severe neurologic symptoms (172)(173)(174)(175)(176), permanent neurological damage (177), or even death (178).…”

Section: Metabolic Effects Of Nitrous Oxidementioning

confidence: 99%

Effect of Nitrous Oxide Exposure During Surgery on the Homocysteine Concentrations of Children

Pichardo¹,

Luginbuehl²,

Shakur³

et al. 2013

Survey of Anesthesiology

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In this study we determined the effect of nitrous oxide (N 2 O) on homocysteine concentrations in children and whether blood levels of folate, vitamin B12, B6, methylmalonic acid (MMA) and methylenetetrahydrofolate reductase C6777T genotype affected this relationship. Homocysteine was measured before and after N 2 O. Vitamin levels, MMA and genotype were determined preoperatively. Median age of the 32 participants was 11 months (3-126 months). All children had folate and B6 levels above deficiency values (7.4, 20nmol/L respectively). Five children had MMA levels indicating deficiency (≥0.21µmol/L). Postexposure homocysteine concentrations increased by 25% (P= <0.001). Duration of exposure and initial homocysteine concentrations were predictors of the increase (r 2 = 0.821, P= <0.001).Vitamin B12 and initial homocysteine concentrations were inversely associated (r 2 = 0.277, P= 0.004). Folate, vitamin B6 and genotype showed no effect. In conclusion, N 2 O exposure leads to increased homocysteine in children. Studies investigating benefit of pre-surgical vitamin B12 supplementation may prove worthwhile.iii ACKNOWLEDGMENTS

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“…Regarding the cognitive aspect, vitamin B12 deficiency is a known etiology of dementia-like clinical presentation that can improve after supplementation [ 26 ]. A French study conducted in rats concluded with a diminished exploration ratio when the animals had been exposed to N 2 O in a dose-dependent manner.…”

Section: Clinical Manifestationsmentioning

confidence: 99%

Nitrous Oxide Abuse: Clinical Outcomes, Pharmacology, Pharmacokinetics, Toxicity and Impact on Metabolism

Gernez,

Lee,

Niguet

et al. 2023

Toxics

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The recreational use of nitrous oxide (N2O), also called laughing gas, has increased significantly in recent years. In 2022, the European Monitoring Centre for Drugs and Drug Addiction (EMCDDA) recognized it as one of the most prevalent psychoactive substances used in Europe. Chronic nitrous oxide (N2O) exposure can lead to various clinical manifestations. The most frequent symptoms are neurological (sensitive or motor disorders), but there are also other manifestations like psychiatric manifestations or cardiovascular disorders (thrombosis events). N2O also affects various neurotransmitter systems, leading to its anesthetic, analgesic, anxiolytic and antidepressant properties. N2O is very challenging to measure in biological matrices. Thus, in cases of N2O intoxication, indirect biomarkers such as vitamin B12, plasma homocysteine and plasma MMA should be explored for diagnosis and assessment. Others markers, like oxidative stress markers, could be promising but need to be further investigated.

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Démence postopératoire : toxicité du protoxyde d’azote

Cited by 14 publications

References 8 publications

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Cobalamin deficiency, hyperhomocysteinemia, and dementia

Effect of Nitrous Oxide Exposure During Surgery on the Homocysteine Concentrations of Children

Nitrous Oxide Abuse: Clinical Outcomes, Pharmacology, Pharmacokinetics, Toxicity and Impact on Metabolism

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