Explore the vast range of titles available.

Methanol poisoning has been a significant public health challenge for several decades in Iran. Even though alcohol use is highly criminalized, people consume illicit alcohol, which tends to be predominantly homemade and often contains methanol. Consequently, thousands of individual poisonings and hundreds of deaths annually are attributable to methanol poisoning. From February 19, 2020 through April 27, 2020, the 2019 coronavirus disease (COVID-19) epidemic rapidly expanded in Iran, and has been associated with 90,481 confirmed cases and 5710 confirmed deaths. Secondary to misinformation about the potential for alcohol to neutralize SARS-CoV-2, there has also been a significant escalation in methanol-related morbidity and mortality, with over 5000 people poisoned and over 500 confirmed deaths for the same period from February through April 2020. In some provinces, the case-fatality rate of methanol poisoning was higher than that from COVID-19. The high morbidity and mortality associated with methanol poisoning preceding and exacerbated by COVID-19 highlight the potential population level health impacts of the implementation of evidence-based education and harm reduction strategies focused on alcohol use across Iran. •Mass methanol poisoning outbreaks have become a major public health concern in Iran.•More than 5000 methanol poisonings, with more than 500 confirmed deaths, were reported amid the COVID-19 epidemic in Iran.•Policymakers should consider developing and implementing public health models to address alcohol use problems.

During an outbreak of methanol poisonings in the Czech Republic in 2012, we were able to study methanol and formate elimination half-lives during intermittent hemodialysis (IHD) and continuous veno-venous hemodialysis/hemodiafiltration (CVVHD/HDF) and the relative impact of dialysate and blood flow rates on elimination. Data were obtained from 11 IHD and 13 CVVHD/HDF patients. Serum methanol and formate concentrations were measured by gas chromatography and an enzymatic method. The groups were relatively comparable, but the CVVHD/HDF group was significantly more acidotic (mean pH 6.9 vs. 7.1 IHD). The mean elimination half-life of methanol was 3.7 and formate 1.6h with IHD, versus 8.1 and 3.6h, respectively, with CVVHD/HDF (both significant). The 54% greater reduction in methanol and 56% reduction in formate elimination half-life during IHD resulted from the higher blood and dialysate flow rates. Increased blood and dialysate flow on the CVVHD/HDF also increased elimination significantly. Thus, IHD is superior to CVVHD/HDF for more rapid methanol and formate elimination, and if CVVHD/HDF is the only treatment available then elimination is greater with greater blood and dialysate flow rates.

This manuscript describes an unusual case of a 15-year-old male who ingested alcohol fuel, resulting in severe methanol poisoning (blood concentration 175.71 mg/dL). Despite bilateral basal ganglia necrosis and hemorrhage confirmed by CT and MRI, the patient maintained normal vision. Immediate treatment with sodium bicarbonate, hemodialysis, methylprednisolone, folic acid, and vitamin B1 resulted in consciousness recovery within 24 h and normalization of metabolic parameters. Ophthalmologic examination revealed mild right optic disc edema but preserved visual acuity (20/20), normal visual fields, and color vision. At 12-week follow-up, neurological function continued to improve with no visual deterioration. This case demonstrates selective basal ganglia vulnerability in methanol toxicity with sparing of the visual system. Emergency physicians should conduct comprehensive neurological evaluations in methanol poisoning cases regardless of visual symptoms and consider investigating protective mechanisms against methanol-induced optic neuropathy. •First reported case of methanol poisoning with bilateral basal ganglia necrosis and hemorrhage without significant visual impairment.•Demonstrates selective neurotoxicity with preservation of visual function despite severe methanol poisoning (blood concentration 175.71 mg/dL).•Provides evidence for differential vulnerability of brain regions to methanol metabolites in adolescent patients.•Suggests potential protective factors against methanol-induced optic neuropathy, including patient's young age and timely medical intervention.•Challenges conventional understanding of the pathophysiology of methanol poisoning and emphasizes the importance of comprehensive neurological assessment beyond visual symptoms.

The duration of hemodialysis (HD) in methanol poisoning (MP) is dependent on the methanol concentration, the operational parameters used during HD, and the presence and severity of metabolic acidosis. However, methanol assays are not easily available, potentially leading to undue extension or premature termination of treatment. Here we provide a prediction model for the duration of high-efficiency HD in MP. In a retrospective cohort study, we identified 71 episodes of MP in 55 individuals who were treated with alcohol dehydrogenase inhibition and HD. Four patients had residual visual abnormality at discharge and only one patient died. In 46 unique episodes of MP with high-efficiency HD the mean methanol elimination half-life (T1/2) during HD was 108min in women, significantly different from the 129min in men. In a training set of 28 patients with MP, using the 90th percentile of gender-specific elimination T1/2 (147min in men and 141min in women) and a target methanol concentration of 4mmol/l allowed all cases to reach a safe methanol of under 6mmol/l. The prediction model was confirmed in a validation set of 18 patients with MP. High-efficiency HD time in hours can be estimated using 3.390 x(Ln (MCi/4)) for women and 3.534 x (Ln (MCi/4)) for men, where MCi is the initial methanol concentration in mmol/l, provided that metabolic acidosis is corrected.

Background To analyze the clinical features and prognosis of the visual loss resulted from inhalational methanol poisoning in 8 Chinese patients. Methods Eight consecutive patients seen at the Beijing Tongren Hospital of Capital Medical University, Beijing, China between January 2003 to August 2017, with complains of vision loss in both eyes, identified as inhalational methanol poisoning. Detailed medical history was extracted. All patients underwent optic nerve and brain magnetic resonance imaging (MRI) scan, laboratory tests, and visual function analysis. Treatment protocols were large dosage of methylprednisolone and B vitamins over 3 months. Patients were seen at 3-month intervals until a year. Results Eight patients with optic neuropathy caused by inhalation toxicity of methanol were under observation, whose methanol-contact time spans were form 4 days to 5 years for occupational exposure. All the patients had acute onset, transient systemic symptoms on early stage, both eyes involved with severe visual impairment (visual acuity 0.1 or even worse). Retrobulbar optic nerves (ONs) were the major sites involved. Optic nerve MRI scan showed increased signal of bilateral ONs in the orbit and the canal parts, with enhancement. After treatment, the visual function of these patients got improved in different degree in a year follow-up, but not satisfactorily. Conclusions Inhalational methanol toxicity may lead to serious damage to ON in a process of chronic intoxication with acute attack, and with poor prognosis.

During an outbreak of mass methanol poisoning in the Czech Republic in 2012–2014, we compared the total hospital costs and one-year medical costs in the patients treated with different antidotes (fomepizole versus ethanol) and modalities of hemodialysis (intermittent hemodialysis, IHD, versus continuous renal replacement therapy, CRRT). Cross-sectional study in 106 patients with confirmed diagnosis treated in 30 ICU settings. For each patient, the following data were analyzed: admission laboratory data, GCS, PSS, ICU length of stay, organ failures, treatment, outcome, and total hospital costs. Of 83 survivors, in 54 (65%) patients the follow-up examination, quality of life measurement with SF36 questionnaire two years after discharge, and one-year medical costs analysis were performed. The median total hospital costs were 7200 (IQR 1500–10,900) euros and the median one-year medical costs were 1447 (IQR 133–1163) euros in the study population. The total hospital costs were higher in the patients treated with fomepizole comparing to ethanol: 12,890 (IQR 6910–16,210) versus 5590 (IQR 1430–6940) euros (p<0.001). The hospital costs in the patients treated with IHD were 5400 (IQR 1520–6910) versus 12,410 (IQR 5380–16,960) euros in the patients with CRRT (p=0.317). The geometric mean ratio for increased hospital costs in the patients treated with fomepizole versus ethanol adjusted for the severity of poisoning was 3.30 (1.70–3.80 CI 95%), p<0.001, and in the patients treated with IHD versus CRRT - 0.70 (0.60–0.99 CI 95%), p=0.047. The patients with visual sequelae had higher total hospital costs than those without sequelae: 10,419 (IQR 2984–14,355) versus 4605 (IQR 1303–4505) euros (p=0.009). The patients with GCS≤13 on admission had higher one-year medical costs as well (p<0.001). No difference was found in physical and mental condition scores in the patients treated with different antidotes and modalities of hemodialysis two years after discharge (both p>0.05). The total hospital costs in the patients with acute methanol poisoning were more than three times higher in the patients treated with fomepizole than in the patients treated with ethanol after adjustment for the severity of poisoning. The dialysis modality did not affect the total hospital costs, but the trend to lower costs was present in IHD-group. •Total hospital costs in the patients treated with fomepizole are 3.3 times higher than that of the ethanol treated patients.•After adjustment for the severity of poisoning, the type of antidote remained significant independent variable.•No difference in the quality of life 2 years after discharge was found between the patients treated with different antidotes.•The mode of dialysis did not affect the costs in the patients treated with intermittent or continuous modalities.•The trend to the lower total hospital costs was present in the patients treated with intermittent hemodialysis.

Methanol poisoning leads to lesions in the basal ganglia and subcortical white matter, as well as to demyelination and atrophy of the optic nerve. However, information regarding cognitive deficits in a large methanol sample is lacking. The principal aim of the present study was to identify the cognitive sequelae of methanol poisoning and their morphological correlates. A sample of 50 patients (METH; age 48 ± 13 years), 3–8 months after methanol poisoning, and 57 control subjects (CS; age 49 ± 13 years) were administered a neuropsychological battery. Forty-six patients were followed in 2 years' perspective. Patients additionally underwent 1.5T magnetic resonance imaging (MRI). Three biochemical and toxicological metabolic markers and a questionnaire regarding alcohol abuse facilitated the classification of 24 patients with methanol poisoning without alcohol abuse (METHna) and 22 patients with methanol poisoning and alcohol abuse (METHa). All groups were compared to a control group of similar size, and matched for age, education, premorbid intelligence level, global cognitive performance, and level of depressive symptoms. Using hierarchical multiple regression we found significant differences between METH and CS, especially in executive and memory domains. METHa showed a similar pattern of cognitive impairment with generally more severe executive dysfunction. Moreover, all METH patients with extensive involvement on brain MRI (lesions in ≥2 anatomical regions) had a more severe cognitive impairment. From a longitudinal perspective, we did not find any changes in their cognitive functioning after 2 years' follow-up. Our findings suggest that methanol poisoning is associated with executive dysfunction and explicit memory impairment, supposedly due to basal ganglia dysfunction and disruption of frontostriatal circuitry proportional to the number of brain lesions, and that these changes are persistent after 2 years' follow-up. •Methanol poisoning leads to executive dysfunction and memory deficit, these changes are stable after two years follow-up.•Methanol patients with extensive involvement on brain MRI had more severe cognitive impairment.•The data are worldwide unique in sample size and quantity and sensitivity of methods used in the assessment.

Methanol is a widely available chemical with a range of uses including as solvent, as a fuel, in chemical synthesis and anti-freeze preparations. Most of the cases are accidental exposures to drinking beverages contaminated with methanol. In mid-September 2018, there was a single outbreak of methanol poisoning in Malaysia especially involving the state of Federal Territory Kuala Lumpur and Selangor. There were 33 reported deaths suspected due to methanol poisoning in this current outbreak where 11 of them were brought in to the Institute of Forensic Medicine (NIFM), Kuala Lumpur. The last outbreak was in the year 2013 with 29 deaths reported out of 44 cases. There were 3 cases (27.2%) died in hospital and the remaining 8 cases (72.8%) were found dead at home and were later brought in dead to the hospital. A full autopsy was carried out for each case. Autopsy findings, as well as lab results pertaining to cases that survived and directly brought in dead, were of a different spectrum. Methanol related deaths are almost always as a result of greed. The running truism is 'methanol poisoning is a result of deliberate addition/adulteration with industrial methanol'. Prevention of the illegal production of methanol and methylated spirits should be established to curb this matter in the future.

Poisonings by the toxic alcohols (methanol, ethylene glycol, isopropanol, diethylene glycol, and propylene glycol) are potentially fatal. This review summarizes the mechanisms of toxicity, methods of diagnosis, and current recommendations for treatment.

Methanol poisoning is seen in the form of isolated episodes, or intentional ingestion and epidemics. Despite its efficient treatment, methanol poisoning has high morbidity and mortality rates. So far, several studies have been performed to identify the prognostic factors in methanol poisoning. Recently, during the treatment of patients with methanol poisoning, we observed that patients’ blood glucose levels were high on presentation to the hospital, particularly in those who expired. Through a literature search, we found that no studies have been performed on blood glucose levels or hyperglycemia in methanol poisoning. Therefore, the present retrospective study was done as a preliminary investigation to understand whether there was a meaningful relationship between methanol poisoning and blood glucose level on presentation, and also if hyperglycemia could be considered as a prognostic factor for mortality. In this retrospective study, a review of the hospital charts was performed for all patients who were treated for methanol poisoning from March 2003 to March 2010 in two hospitals in Tehran, Iran. Those with definitive diagnosis of methanol poisoning, no history of diabetes mellitus, and normal or low body mass index (<25) were included. Patients’ demographic information, clinical manifestations, time elapsed between ingestion and presentation, blood glucose level on presentation (before treatment), results of arterial blood gas analysis, and the clinical outcome were recorded. Statistical analysis was done using SPSS software (version 17, Chicago, Illinois, USA) and application of Mann–Whitney U test, Pearson's chi-square test, Pearson correlation coefficient ( r ), receiver operating characteristic (ROC) curve, and logistic regression. P values less than 0.05 were considered as the statistically significant levels. Ninety-five patients with methanol poisoning met the inclusion criteria and were included in the study. Of these, 91 (96%) were male and 4 (4%) were female. Mean age was 31.61 ± 14.3 years (range, 13 to 75). Among the 95 patients, 68 survived (72%) and 27 expired (28%). Median blood glucose level was 144 mg/dL (range, 75 to 500). There was no significant statistical correlation between blood glucose level and time of treatment, age, pCO 2 , or serum bicarbonate concentration, but blood glucose level had a statistically significant correlation with pH ( r  = −0.242, P  = 0.02) and base deficit ( r  = 0.230, P  = 0.03). The mean blood glucose level was 140 ± 55 and 219 ± 99 mg/dL in the survivor and non-survivor patients, respectively ( P  < 001). Considering the cutoff level of 140 mg/dL for blood glucose and using logistic regression analysis, and adjusting according to the admission data with significant statistical difference in the two study groups, the odds ratio for hyperglycemia as a risk factor for death was 6.5 (95% confidence interval = 1.59–26.4). Our study showed that blood glucose levels were high in methanol poisoning and even higher in those who died in comparison with the survivors. Therefore, hyperglycemia might be a new prognostic factor in methanol poisoning, but further studies are needed to determine whether controlling hyperglycemia has therapeutic consequences.