Central Diabetes Insipidus and Hyperglycemic Hyperosmolar State Following Accidental Carbon Monoxide Poisoning.
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ABSTRACT:
SUBMITTER: Ul Abideen Z
PROVIDER: S-EPMC5493463 | biostudies-other | 2017 Jun
REPOSITORIES: biostudies-other
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Project description:ObjectivesCarbon monoxide (CO) poisoning from coal briquette combustion has been a major public health problem in Korea. In this study, we estimated the time trends of the consumption of anthracite coal and the number of CO poisoning victims over the past 7 decades, in the context of changes in heating facilities.MethodsUsing Population and Housing Census data and energy statistics, we estimated the number of houses using briquettes as heating fuel between 1951 and 2018. After estimating the incidence of CO poisoning in housing units by heating facility type, we determined the ratio of the number of household members who experienced CO poisoning to the overall number of household members. Finally, we estimated the distribution of the victims according to poisoning severity, excluding victims of intentional exposure.ResultsWe estimated that, overall, over 26 million people experienced CO poisoning between 1951 and 2018 in Korea. The household consumption of anthracite peaked in 1986, but the number of victims of CO poisoning peaked at approximately 1 million people in 1980. From 1951 to 2018, the cumulative number of CO poisoning victims comprised approximately 22,830,000 mild cases, 3,570,000 severe cases, and 65,000 deaths.ConclusionsThe peak in the number of CO poisoning victims occurred 6 years earlier than the peak in the number of people using briquettes for heating. This gap resulted from improvements in briquette heating systems. This finding provides a quantitative basis for epidemiological studies on the health outcomes of CO poisoning in the Korean population.
| S-EPMC7871165 | biostudies-literature
Project description: Not available
| S-EPMC4016057 | biostudies-literature
Project description:Carbon monoxide (CO) is the leading cause of poisoning deaths in many countries, including Japan. Annually, CO poisoning claims about 2000-5000 lives in Japan, which is over half of the total number of poisoning deaths. This paper discusses the physicochemical properties of CO and the toxicological evaluation of CO poisoning.
| S-EPMC6992844 | biostudies-literature
Project description:Carbon monoxide (CO) poisoning causes brain damage, which is attenuated by treatment with hydrogen [1], [2], a scavenger selective to hydroxyl radical (•OH) [3]. This suggests a role of •OH in brain damage due to CO poisoning. Studies have shown strong enhancement of •OH production in rat striatum by severe CO poisoning with a blood carboxyhemoglobin (COHb) level > 70% due to 3000 ppm CO, but not less severe CO poisoning with a blood COHb level at approximately 50% due to 1000 ppm CO [4]. Interestingly, 5% O2 causes hypoxia comparable with that by 3000 ppm CO and produces much less •OH than 3000 ppm CO does [4]. In addition, cAMP production in parallel with •OH production [5] might contribute to •OH production [6]. It is likely that mechanisms other than hypoxia contribute to brain damage due to CO poisoning [7]. To search for the mechanisms, we examined the effects of 1000 ppm CO, 3000 ppm CO and 5% O2 on gene expression in rat striatum. All array data have been deposited in the Gene Expression Omnibus (GEO) database under accession number GSE94780.
| S-EPMC5374847 | biostudies-literature
Project description:We have proposed the existence of a threshold for brain damage, in terms of hydroxyl radical production in rat striatum, between poisoning of carbon monoxide (CO) at 1000 ppm and 3000 ppm, where blood CO-hemoglobin levels reach approximately 50% and over 70%, respectively. To search for factors involved in brain damage, we examined the effects of air, 1000 ppm CO, 3000 ppm CO and 5% O2 (hypoxic conditions comparable with those by 3000 ppm CO) on gene expression in rat striatum, using microarray analysis.
2017-04-03 | GSE94780 | GEO
Project description:Carbon monoxide poisoning (COP) causes hypoxic injury and inflammatory and immunological reactions in the brain and local organs including the pancreas. Therefore, it is plausible that COP may increase the risk for developing diabetes mellitus (DM), but studies on this possible association are limited. We conducted a nationwide study in Taiwan to fill the data gap. We used the Nationwide Poisoning Database and the Longitudinal Health Insurance Database 2000 to identify all COP patients diagnosed between 1999 and 2012 (the study cohort) and then construct a comparison cohort of patients without COP through matching at 1:3 by the index date and age. The risk for DM between the two cohorts was compared by following up until 2013. We also investigated the independent predictors for DM in all the patients. During the study period, 22,308 COP patients were identified, and 66,924 non-COP patients were included in the comparison cohort accordingly. Patients with COP had an increased risk for DM with an adjusted hazard ratio (AHR) of 1.92 (95% confidence interval [CI]: 1.79-2.06) after adjusting for age, sex, comorbidities, and monthly income, especially in the subgroups of age <35 years, age ≥ 65 years, female sex, and comorbidities with congestive heart failure, hyperthyroidism, and polycystic ovary syndrome. Cox proportional hazard regression analysis showed that the increased risk for DM was highest in the first month after COP (AHR= 3.38; 95% CI: 2.29-4.99) and lasted even after 4 years (AHR= 1.82; 95% CI: 1.62-2.04). We found that COP, older age, male sex, hypertension, hyperlipidemia, hyperuricemia, and low monthly income were independent predictors for DM. Intervention studies are needed to validate the results and delineate the detailed mechanisms.
| S-EPMC5609952 | biostudies-literature
Project description:BackgroundPoisoning with carbon monoxide (CO) remains an important cause of accidental and intentional injury worldwide. Several unblinded non-randomized trials have suggested that the use of hyperbaric oxygen (HBO) prevents the development of neurological sequelae. This has led to the widespread use of HBO in the management of patients with carbon monoxide poisoning.ObjectivesTo examine randomised trials of the efficacy of hyperbaric oxygen (HBO) compared to normobaric oxygen (NBO) for the prevention of neurologic sequelae in patients with acute carbon monoxide poisoning.Search strategyWe searched the following electronic databases; Cochrane Injuries Group Specialised Register (searched June 2010), Cochrane Central Register of Controlled Trials (The Cochrane Library 2010, Issue 2), MEDLINE (Ovid SP) 1950 to June 2010, EMBASE (Ovid SP) 1980 to June 2010, ISI Web of Science: Science Citation Index Expanded (SCI-EXPANDED) 1970 to June 2010, ISI Web of Science: Conference Proceedings Citation Index-Science (CPCI-S) 1990 to June 2010.Selection criteriaAll randomised controlled trials of HBO compared to NBO, involving non-pregnant adults who are acutely poisoned with carbon monoxide (regardless of severity).Data collection and analysisTwo authors independently extracted from each trial information on: the number of randomised patients, types of participants, the dose and duration of the intervention, and the prevalence of neurologic symptoms at follow-up.Main resultsSeven randomised controlled trials of varying quality were identified; one was excluded because it did not evaluate clinical outcomes. Of the six remaining trials involving 1361 participants, two found a beneficial effect of HBO for the reduction of neurologic sequelae at one month, while four others did not. One of these is an incomplete publication (an abstract of an interim analysis). Although pooled random effects meta-analysis does not suggest a significant benefit from HBOT (OR for neurological deficits 0.78, 95%CI 0.54 to 1.12), significant methodologic and statistical heterogeneity was apparent among the trials, and this result should be interpreted cautiously. Moreover, design or analysis flaws were evident in all trials. Importantly, the conclusions of one positive trial may have been influenced by failure to adjust for multiple hypothesis testing, while interpretation of the other positive trial is hampered by a high risk of bias introduced during the analysis including an apparent change in the primary outcome. Both were also stopped early 'for benefit', which is likely to have inflated the observed effect. In contrast three negative trials had low power to detect a benefit of HBO due to exclusion of severely poisoned patients in two and very poor follow-up in the other. One trial that was said to be finished around eight years ago has not reported the final analysis in any forum.Authors' conclusionsExisting randomised trials do not establish whether the administration of HBO to patients with carbon monoxide poisoning reduces the incidence of adverse neurologic outcomes. Additional research is needed to better define the role, if any, of HBO in the treatment of patients with carbon monoxide poisoning. This research question is ideally suited to a multi-center randomised controlled trial.
| S-EPMC7066484 | biostudies-literature
Project description:The severity of acute carbon monoxide (CO) poisoning is often based on non-specific clinical criteria because there are no reliable laboratory markers. We hypothesized that a pattern of plasma protein values might objectively discern CO poisoning severity. This was a pilot study to evaluate protein profiles in plasma samples collected from patients at the time of initial hospital evaluation. The goal was to assess whether any values differed from age- and sex-matched controls using a commercially available plasma screening package.Frozen samples from 63 suspected CO poisoning patients categorized based on clinical signs, symptoms, and blood carboxyhemoglobin level were analyzed along with 42 age- and sex-matched controls using Luminex-based technology to determine the concentration of 180 proteins.Significant differences from control values were found for 99 proteins in at least one of five CO poisoning groups. A complex pattern of elevations in acute phase reactants and proteins associated with inflammatory responses including chemokines/cytokines and interleukins, growth factors, hormones, and an array of auto-antibodies was found. Fourteen protein values were significantly different from control in all CO groups, including patients with nominal carboxyhemoglobin elevations and relatively brief intervals of exposure.The data demonstrate the complexity of CO pathophysiology and support a view that exposure causes acute inflammatory events in humans. This pilot study has insufficient power to discern reliable differences among patients who develop neurological sequelae but future trials are warranted to determine whether plasma profiles predict mortality and morbidity risks of CO poisoning.
| S-EPMC3941305 | biostudies-literature
Project description:BackgroundAccidental non-fire-related (ANFR) carbon monoxide (CO) poisoning is a cause of fatalities and hospital admissions. This is the first study that describes the characteristics of ANFR CO hospital admissions in England.MethodsHospital Episode Statistics (HES) inpatient data for England between 2001 and 2010 were used. ANFR CO poisoning admissions were defined as any mention of ICD-10 code T58: toxic effect of CO and X47: accidental poisoning by gases or vapours, excluding ICD-10 codes potentially related to fires (X00-X09, T20-T32 and Y26).ResultsThere were 2463 ANFR CO admissions over the 10-year period (annual rate: 0.49/100 000); these comprised just under half (48.7%) of all non-fire-related (accidental and non-accidental) CO admissions. There was seasonal variability, with more admissions in colder winter months. Higher admission rates were observed in the north of England. Just over half (53%) of ANFR admissions were male, and the highest rates of ANFR admissions were in those aged >80 years.ConclusionThe burden of ANFR CO poisoning is preventable. The results of this study suggest an appreciable burden of CO and highlight differences that may aid targeting of public health interventions.
| S-EPMC4750524 | biostudies-literature
Project description:The purpose of this study was to evaluate the effects of hyperbaric oxygen therapy (HBOT) on reducing neurological sequelae (NS) in patients with carbon monoxide poisoning (COP). Using a nationwide database of insurance claims in Taiwan, we conducted a population-based cohort study to identify 24,046 patients with COP diagnosed between 1999 and 2012, including 6793 (28.2%) patients who received HBOT and 17,253 (71.8%) patients who did not. We followed the two cohorts of patients and compared the occurrence of NS. The two cohorts had similar sex ratios, but patients who received HBOT were younger (34.8 ± 14.8 vs. 36.1 ± 17.2 years, p < 0.001). Patients who received HBOT had a higher risk for NS (adjusted hazard ratio [AHR]: 1.4; 95% confidence interval [CI]: 1.4⁻1.5), after adjusting for age, sex, underlying comorbidities (hypertension, diabetes, chronic obstructive pulmonary disease, hyperlipidemia, malignancy, coronary artery disease, congestive heart failure, liver disease, renal disease, connective tissue disease, human immunodeficiency virus [HIV] infection, and alcoholism), monthly income, suicide, drug poisoning, and acute respiratory failure. We observed similar findings when we stratified the patients by age, sex, underlying comorbidities, and monthly income. The increased risk was most prominent in the first 2 weeks (AHR: 2.4; 95% CI: 2.1⁻2.7) and remained significant up to 6 months later (AHR: 1.6; 95% CI: 1.4⁻1.7). The risk for NS was higher in patients with COP who received HBOT than in those who did not, even after considering the possible impact of longer observation periods on survivors. Further studies that included the potential confounding factors we did not measure are needed to confirm findings in this study.
| S-EPMC6211110 | biostudies-literature