Increased Risk of Parkinson Disease in Patients With Carbon Monoxide Intoxication

Lai, Chun-Ting; Chou, Mei-Chun; Lin, Cheng‐Li; Kao, Chia‐Hung

doi:10.1097/md.0000000000000869

Cited by 24 publications

(9 citation statements)

References 45 publications

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“… 39 A recent retrospective cohort study showed that victims of CO poisoning exhibited a 9.08-fold increased risk for Parkinsonism. 40 Other studies also found patients with CO poisoning are at a higher risk of developing cardiovascular complications. 33 , 41 However, there are conflicting findings about the risk of cardiovascular deaths after CO poisoning.…”

Section: Discussionmentioning

confidence: 99%

Patients With Carbon Monoxide Poisoning and Subsequent Dementia

et al. 2016

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The present study evaluated the dementia risk after carbon monoxide poisoning (CO poisoning).Using the National Health Insurance Research Database of Taiwan, a total of 9041 adults newly diagnosed with CO poisoning from 2000 to 2011 were identified as the CO poisoning cohort. Four-fold (N = 36,160) of non-CO poisoning insured people were randomly selected as controls, frequency-matched by age, sex, and hospitalization year. Incidence and hazard ratio (HR) of dementia were measured by the end 2011.The dementia incidence was 1.6-fold higher in the CO exposed cohort than in the non-exposed cohort (15.2 vs 9.76 per 10,000 person-years; n = 62 vs 174) with an adjusted HR of 1.50 (95% CI = 1.11–2.04). The sex- and age-specific hazards were higher in male patients (adjusted HR = 1.74, 95% CI = 1.20–2.54), and those aged <=49 years (adjusted HR = 2.62, 95% CI = 1.38–4.99). CO exposed patients with 7-day or longer hospital stay had an adjusted HR of 2.18 (95% CI = 1.42, 3.36). The CO poisoning patients on hyperbaric oxygen (HBO2) therapy had an adjusted HR of 1.80 (95% CI = 0.96–3.37).This study suggests that CO poisoning may have association with the risk of developing dementia, which is significant for severe cases. The effectiveness of HBO2 therapy remains unclear in preventing dementia. Patients with CO poisoning are more prevalent with depression.

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Section: Discussionmentioning

confidence: 99%

Patients With Carbon Monoxide Poisoning and Subsequent Dementia

et al. 2016

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“…Mutations in genes, such as ubiquitin C-terminal hydrolase L1 ( UCHL1 ) [ 71 ], α-synuclein ( SNCA ) [ 72 ], leucine-rich repeat kinase 2 ( LRRK2 ) [ 73 ], Parkin RBR E3 ubiquitin-protein ligase ( Parkin ) [ 74 ], PTEN-induced kinase 1 ( PINK1 ) [ 74 ], protein deglycase ( DJ-1 ) [ 75 ], and glucocerebrosidase ( GBA ) [ 76 ] can result in the development of PD. Several environmental factors, like exposure to pesticides (rotenone, and paraquat) [ 77 ], methanol (CH 3 OH) [ 78 ], injury to the head [ 79 ], and poisoning of carbon monoxide (CO) [ 80 ] are thought to be associated with the development of PD.…”

Section: Parkinson’s Diseasementioning

confidence: 99%

Elucidating the Neuroprotective Role of PPARs in Parkinson’s Disease: A Neoteric and Prospective Target

Behl

Madaan

Sehgal

et al. 2021

IJMS

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One of the utmost frequently emerging neurodegenerative diseases, Parkinson’s disease (PD) must be comprehended through the forfeit of dopamine (DA)-generating nerve cells in the substantia nigra pars compacta (SN-PC). The etiology and pathogenesis underlying the emergence of PD is still obscure. However, expanding corroboration encourages the involvement of genetic and environmental factors in the etiology of PD. The destruction of numerous cellular components, namely oxidative stress, ubiquitin-proteasome system (UPS) dysfunction, autophagy-lysosome system dysfunction, neuroinflammation and programmed cell death, and mitochondrial dysfunction partake in the pathogenesis of PD. Present-day pharmacotherapy can alleviate the manifestations, but no therapy has been demonstrated to cease disease progression. Peroxisome proliferator-activated receptors (PPARs) are ligand-directed transcription factors pertaining to the class of nuclear hormone receptors (NHR), and are implicated in the modulation of mitochondrial operation, inflammation, wound healing, redox equilibrium, and metabolism of blood sugar and lipids. Numerous PPAR agonists have been recognized to safeguard nerve cells from oxidative destruction, inflammation, and programmed cell death in PD and other neurodegenerative diseases. Additionally, various investigations suggest that regular administration of PPAR-activating non-steroidal anti-inflammatory drugs (NSAIDs) (ibuprofen, indomethacin), and leukotriene receptor antagonists (montelukast) were related to the de-escalated evolution of neurodegenerative diseases. The present review elucidates the emerging evidence enlightening the neuroprotective outcomes of PPAR agonists in in vivo and in vitro models experiencing PD. Existing articles up to the present were procured through PubMed, MEDLINE, etc., utilizing specific keywords spotlighted in this review. Furthermore, the authors aim to provide insight into the neuroprotective actions of PPAR agonists by outlining the pharmacological mechanism. As a conclusion, PPAR agonists exhibit neuroprotection through modulating the expression of a group of genes implicated in cellular survival pathways, and may be a propitious target in the therapy of incapacitating neurodegenerative diseases like PD.

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“…The patient was initially treated with 100% normobaricoxygen, and then intubated and mechanically ventilated, the most common treatment for CO toxicity [24]. Neurological injury is well documented after CO toxicity, with reports of patients that range from transient neurologic deficits to chronic debilitating diseases such as Parkinson's disease and multiple sclerosis after exposure to CO. [17,18,27]. The patient presented here suffered from neurological outcomes, where we were able to, for the first time ever, uncover potential mechanisms for neurological outcomes using a multi-time point, multi-omics strategy.…”

Section: Introductionmentioning

confidence: 93%

Multi-Omic integration after carbon monoxide toxicity in a child reveals gene transcripts related to Parkinson and Multiple Sclerosis

Leimanis-Laurens

Prokop

Nedveck

et al. 2020

Preprint

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Background This report highlights the unique transcriptomic and lipidomic changes noted in a 4-year-old African American female patient exposed to a house fire. She required admission to the pediatric Intensive care unit due to organ failure that resulted from CO and cyanide toxicity. Patient was neurologically intact initially but later developed neurological symptoms consistent with Parkinsonism, a transient state resembling Parkinson’s Disease. Results An integrative omics-based approach was used to examine both gene expression and the lipidome of the patient which was then compared to 4 control patients. Total blood RNA from a PaxGene®collection system was correlated to plasma-based metabolomics measured over three time points and correlated with the clinical condition of the patient. We see significant elevation of the Parkinson’s associated gene ( SELENOT ) on day one. This gene plays a crucial role in the protection of dopaminergic neurons against oxidative stress in Parkinson's disease. The Multiple Sclerosis linked gene DDX39B which mediates ATP hydrolysis during pre-mRNA splicing was increased on day 8. We noted increased UGCG gene expression which correlated with increased ceramide lipids on lipidome analysis. The elevated ratio of hexosylceramide to its ceramide precursor is indicative of an elevated UGCG mediated ceramide glucosyltransferase activity. This correlation of clinical symptoms with both increased gene activity and lipid dyshomeostasis is unique, highlighting the potential of personalized omics. ConclusionsIn clinical practice, the ability to predict and quantify neurological injury using gene expression has the potential to make meaningful changes to management. This report shows the potential for real time transcriptomics and metabolomics to modify not only initial therapy, but the eventual physical rehabilitation of patients exposed to neurotoxins.

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Increased Risk of Parkinson Disease in Patients With Carbon Monoxide Intoxication

Cited by 24 publications

References 45 publications

Patients With Carbon Monoxide Poisoning and Subsequent Dementia

Patients With Carbon Monoxide Poisoning and Subsequent Dementia

Elucidating the Neuroprotective Role of PPARs in Parkinson’s Disease: A Neoteric and Prospective Target

Multi-Omic integration after carbon monoxide toxicity in a child reveals gene transcripts related to Parkinson and Multiple Sclerosis

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