Long-term visual damage after acute methanol poisonings: Longitudinal cross-sectional study in 50 patients

Zakharov, Sergey; Pelclová, Daniela; Diblik, Pavel; Urban, Pavel; Kuthan, Pavel; Nurieva, Olga; Kotikova, Katerina; Navrátil, Tomáš; Komarc, Martin; Běláček, Jaromír; Seidl, Zdeněk; Vaněčková, Manuela; Hubacek, Jaroslav A.; Bezdíček, Ondřej; Klempíř, Jiří; Yurchenko, Maksim; Růžička, Evžen; Miovský, Michal; Janíková, Barbara; Hovda, Knut Erik

doi:10.3109/15563650.2015.1086488

Cited by 81 publications

(70 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Methanol-induced optic neuropathy may resolve within a few weeks with complete recovery [10]. However, longterm visual sequelae may persist in up to 25-40% of patients [11][12][13].…”

Section: Importancementioning

confidence: 99%

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Zakharov

Kotikova

Nurieva

et al. 2017

Clinical Toxicology

Self Cite

View full text Add to dashboard Cite

Context: The role of neuroinflammation in methanol-induced toxic brain damage has not been studied. Objective: We studied acute concentrations and the dynamics of leukotrienes (LT) in serum in hospitalized patients with acute methanol poisoning and in survivors. Methods: Series of acute cysteinyl-LT and LTB4 concentration measurements were performed in 28/101 hospitalized patients (mean observation time: 88 ± 20 h). In 36 survivors, control LT measurements were performed 2 years after discharge. Results: The acute maximum (C max ) LT concentrations were higher than concentrations in survivors: C max for LTC4 was 80.7 ± 5.6 versus 47.9 ± 4.5 pg/mL; for LTD4, 51.0 ± 6.6 versus 23.1 ± 2.1 pg/mL; for LTE4, 64.2 ± 6.0 versus 26.2 ± 3.9 pg/mL; for LTB4, 59.8 ± 6.2 versus 27.2 ± 1.4 pg/mL (all p < 0.001). The patients who survived had higher LT concentrations than those who died (all p < 0.01). Among survivors, patients with CNS sequelae had lower LTE4 and LTB4 than did those without sequelae (both p < 0.05). The LT concentrations increased at a rate of 0.4-0.5 pg/mL/h and peaked 4-5 days after admission. The patients with better outcomes had higher cys-LTs (all p < 0.01) and LTB4 (p < 0.05). More severely poisoned patients had lower acute LT concentrations than those with minor acidemia. The follow-up LT concentrations in survivors with and without CNS sequelae did not differ (all p > 0.05). The mean decrease in LT concentration was 30.9 ± 9.0 pg/mL for LTC4, 26.3 ± 8.6 pg/mL for LTD4, 37.3 ± 6.4 pg/mL for LTE4, and 32.0 ± 8.8 pg/mL for LTB4. Conclusions: Our findings suggest that leukotriene-mediated neuroinflammation may play an important role in the mechanisms of toxic brain damage in acute methanol poisoning in humans. Acute elevation of LT concentrations was moderate, transitory, and was not followed by chronic neuroinflammation in survivors.ARTICLE HISTORY

show abstract

“…Methanol-induced optic neuropathy may resolve within a few weeks with complete recovery [10]. However, longterm visual sequelae may persist in up to 25-40% of patients [11][12][13].…”

Section: Importancementioning

confidence: 99%

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Zakharov

Kotikova

Nurieva

et al. 2017

Clinical Toxicology

Self Cite

View full text Add to dashboard Cite

show abstract

“…In 11 patients (58% of survivors), the follow-up examination was fulfilled three to six months after discharge from hospital within the prospective study of long-term visual and CNS sequelae of acute methanol poisonings 25 . The clinical examination protocol included complete ocular examination and standard ophthalmic tests (visual acuity, perimeter, color vision assessment, contrast sensibility, fundus examination), optical coherence tomography (OCT) with retinal nerve fibers layer thickness evaluation, visual evoked potentials (VEP), magnetic resonance imaging of the head, neurological and neuropsychological examinations, biochemical tests (electrolytes, glucose, glycohemoglobin, albumin, pre-albumin, renal and hepatic tests, cholesterol, lipids, thyroid-stimulating hormone (TSH), vitamin B 12 , carbohydrate deficient transferrin (CDT), complete blood count, hematocrit, ethyl glucuronide in urine), and standardized questionnaire forms (circumstances of poisoning, medical history, comorbidities, etc.…”

Section: Patients and Proceduresmentioning

confidence: 99%

Fomepizole in the treatment of acute methanol poisonings: Experience from the Czech mass methanol outbreak 2012-2013

Zakharov¹,

Navrátil²,

Pelclová³

2014

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub

Self Cite

View full text Add to dashboard Cite

Objective. During an outbreak of mass methanol poisonings in the Czech Republic in 2012-2013, fomepizole was applied as an alternative antidote to ethanol. We present the laboratory data, clinical features, adverse reactions, and treatment outcomes in all patients treated with fomepizole. Methods. Combined retrospective and prospective case series study in 25 patients, median age 50 (16-73) years, 18 males and 7 females. Results. There were 24% fatalities, 36% survivors without health impairment, and 40% survivors with sequelae. All the patients who died were comatose on admission; the mortality was 50% among patients in a coma. The median intensive care unit length of stay was six (2-22) days. The median total dose of fomepizole was 2 (1-9) g. Complications were observed in 7/25 cases: aspiration pneumonia (4), sepsis (2), bleeding (2), malignant arrhythmia (1), delirium tremens (1), and rebound of acidosis (1). The patients who survived without impairment were less acidotic than those who died or survived with sequelae (P<0.01). No difference in serum methanol and formate was found between the three groups. Conclusion. There is no evidence whether fomepizole is a more efficient antidote than ethanol with regards to the hospital mortality. The possibility of delirium tremens in the patients with a history of chronic alcohol abuse has to be taken in consideration. The benefits of fomepizole were indirect: no need to monitor serum ethanol's level during the hemodialysis in severely poisoned patients and less working overload on ICU doctors treating several poisoned patients simultaneously.

show abstract

“…Erken dönemde optik sinir normal görünebileceği gibi hiperemik de olabilir; ışık refleksinde zayıflama ya da tamamen kaybolması pupillerde dilatasyon görülebilir. Görsel semptomların çoğunluğu erken dönemde düzelmekle birlikte, görme kayıplarında kısmi düzelme ya da tam körlük gelişebilir (5,6). Düzelen görsel yakınmaların bazen geç dönemde de yeniden kötüleştiği bildirilmiştir.…”

Section: Discussionunclassified

“…Uzun dö-nemde hastalarda görme keskinliğinde azalma, görme alanında daralma, renkli görme kaybı ve optik atrofi gelişebi-lir. Geç dönemde herhangi bir görsel yakınması olmayan hastalarda bile OCT ve VEP bulgularında normal olmayan bulgular saptanabilir (6). Bizim olgumuzda geç dönemde optik diskte solukluk tespit edildiği, ayrıca hastada diskromotopsi ve fotofobi yakınması olduğu saptandı.…”

Section: Discussionunclassified

Metanol Zehirlenmesi: Olgu Sunumu

Can¹,

Kirbiyik²

2017

Bull Leg Med

View full text Add to dashboard Cite

Metil alkol endüstride yaygın olarak kullanılan bir alkoldür. Yasadışı olarak ta kaçak üretilen içkilerde kullanılmaktadır. Metil alkol zehirlenmesi yüksek oranda ölüm riski taşıyan metabolik asidoza, görme kaybına ve bazal gangliyon hasarına neden olan klinik bir durumdur. Tedavide metabolik asidozun düzeltilmesi için bikarbonat takviyesi, antidot verilmesi ve hemodiyaliz uygulanır. Bu çalışmada metil alkol zehirlenmesi olarak tedavi edilen, göz polikliniğine ani görme kaybı nedeniyle başvuran ve 48 saat önce içki içtiğini bildiren 45 yaşında bir erkek olgu sunulmuştur.Anahtar Kelimeler: Metil Alkol; Zehirlenme; Görme Kaybı. AbstractMethyl alcohol is an alcohol commonly used in the industry. It is also used in illegally produced drinks. Methyl alcohol poisoning is a clinical condition that causes vision loss, basal ganglion damage and metabolic acidosis with high risk of death. Bicarbonate supplementation, antidote administration and hemodialysis are applied to correct metabolic acidosis. We present in this study a 45-year-old male who was admitted to the Eye Polyclinic with sudden visual loss and was treated as methyl alcohol poisoning due to drinking 48 hours ago.Keywords: Methyl Alcohol; Intoxication; Visual Loss. Kliniği, Balıkesir E-mail: balikesirhumeyra@gmail.com Geliş:20.10.2017 Düzeltme:04.11.2017 Kabul:08.11.2017 GirişMetanol odunun damıtılmasıyla elde edilen bir alkoldür ve organik çözücü özelliğinden dolayı endüstride kimyasal çözücülerin çoğunda kullanılır. Oda sıcaklığın-da sıvı halde bulunan, renksiz, toksik bir maddedir. Metanol zehirlenmesi sıklıkla yasadışı yollarla üretilen içki-lerin oral alımıyla oluşmakla birlikte kazara ya da intihar amacıyla da içilebilir (1). Daha nadir olarak deri ya da inhalasyon yoluyla da metanol zehirlenmesi gelişebilir (2).Metanol kendisi çok toksik olmamakla birlikte vü-cutta alkol dehidrogenaz enzimi tarafından çok toksik metabolitlere dönüşür. Formaldehid ve Formik aside metabolize olan metanol yüksek anyon açıklı metabolik asidoza, bazal ganglion hasarına, retinal hasara ve optik sinir hasarına neden olur. Oluşan toksik formik asit mitokondrilerdeki sitokrom c oksidaz aktivitesini inhibe ederek hücresel hipoksiye neden olarak retinal ganglion hücrelerinde hasara neden olur (3,4).Metanol zehirlenmesinde bulgular sıklıkla oral alım-dan 12-24 saat sonra ortaya çıkar. Bu gecikme metanolün toksik metabolitlerine yavaş metabolize olması ile ilgilidir. Hastada erken dönemde genelde görsel problemler karın ağrısı, vertigo, bulantı, kusma ve baş ağrısı olabilir. Geç dönemde tedavi edilmediğinde ise koma, körlük, gastrointestinal kanama, putaminal kanama ve ölüm gelişebilir. Görsel problemlerin bir kısmı düzelmekle birlikte kalıcı görme hasarı da gelişebilir. OlguOlgumuz 45 yaşında erkek hastadır; her iki gözün-de görme kaybı geliştiğini belirterek göz polikliniğine başvurmuştur. Her iki gözde görme 1mps düzeyinde pupiller middilate ve fundus görüntüsü doğal bulunmuş hasta kraniyal bir patoloji şüphesi ile nöroloji kliniğine konsülte edilmiştir. Yapılan nörolojik mu...

show abstract

Long-term visual damage after acute methanol poisonings: Longitudinal cross-sectional study in 50 patients

Cited by 81 publications

References 26 publications

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Leukotriene-mediated neuroinflammation, toxic brain damage, and neurodegeneration in acute methanol poisoning

Fomepizole in the treatment of acute methanol poisonings: Experience from the Czech mass methanol outbreak 2012-2013

Metanol Zehirlenmesi: Olgu Sunumu

Contact Info

Product

Resources

About