Clinical and genetic determinants of chronic visual pathway changes after methanol - induced optic neuropathy: four-year follow-up study

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61388955%3A_____%2F19%3A00497105" target="_blank" >RIV/61388955:_____/19:00497105 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/00216208:11110/19:10394883 RIV/00216208:11510/19:10394883 RIV/00023001:_____/19:00078006 RIV/75010330:_____/19:00012587 RIV/00064165:_____/19:10394883

Výsledek na webu

<a href="http://hdl.handle.net/11104/0290804" target="_blank" >http://hdl.handle.net/11104/0290804</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1080/15563650.2018.1532083" target="_blank" >10.1080/15563650.2018.1532083</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Clinical and genetic determinants of chronic visual pathway changes after methanol - induced optic neuropathy: four-year follow-up study

Popis výsledku v původním jazyce

Context: Methanol poisoning induces acute optic neuropathy with possible long-term visual damage.nObjective: To study the dynamics and key determinants of visual pathway functional changes during 4 years after acute methanol poisoning.nMethods: A total of 42 patients with confirmed methanol poisoning (mean age 45.7 ± 4.4 years) were examined 4.9 ± 0.6, 25.0 ± 0.6, and 49.9 ± 0.5 months after discharge. The following tests were performed: visual evoked potential (VEP), retinal nerve fiber layer (RNFL) measurement, brain magnetic resonance imaging (MRI), complete ocular examination, biochemical tests, and apolipoprotein E (ApoE) genotyping.nResults: Abnormal VEP P1 latency was registered in 18/42 right eyes (OD) and 21/42 left eyes (OS), abnormal N1P1 amplitude in 10/42 OD and OS. Mean P1 latency shortening during the follow-up was 15.0 ± 2.0 ms for 36/42 (86%) OD and 14.9 ± 2.4 ms for 35/42 (83%) OS, with maximum shortening up to 35.0 ms. No significant change of mean N1P1 amplitude was registered during follow-up.nA further decrease in N1P1 amplitude ≥1.0 mcV in at least one eye was observed in 17 of 36 patients (47%) with measurable amplitude (mean decrease −1.11 ± 0.83 (OD)/−2.37 ± 0.66 (OS) mcV versus −0.06 ± 0.56 (OD)/−0.83 ± 0.64 (OS) mcV in the study population, both p < .001).nApoE4 allele carriers had lower global and temporal RNFL thickness and longer initial P1 latency compared to the non-carriers (all p < .05). The odds ratio for abnormal visual function was 8.92 (3.00–36.50, 95%CI) for ApoE4 allele carriers (p < .001). The presence of ApoE4 allele was further associated with brain necrotic lesions (r = 0.384, p = .013) and brain hemorrhages (r = 0.395, p = .011).nConclusions: Improvement of optic nerve conductivity occurred in more than 80% of patients, but evoked potential amplitude tended to decrease during the 4 years of observation. ApoE4 allele carriers demonstrated lower RNFL thickness, longer P1 latency, and more frequent methanol-induced brain damage compared to non-carriers.

Název v anglickém jazyce

Clinical and genetic determinants of chronic visual pathway changes after methanol - induced optic neuropathy: four-year follow-up study

Popis výsledku anglicky

Context: Methanol poisoning induces acute optic neuropathy with possible long-term visual damage.nObjective: To study the dynamics and key determinants of visual pathway functional changes during 4 years after acute methanol poisoning.nMethods: A total of 42 patients with confirmed methanol poisoning (mean age 45.7 ± 4.4 years) were examined 4.9 ± 0.6, 25.0 ± 0.6, and 49.9 ± 0.5 months after discharge. The following tests were performed: visual evoked potential (VEP), retinal nerve fiber layer (RNFL) measurement, brain magnetic resonance imaging (MRI), complete ocular examination, biochemical tests, and apolipoprotein E (ApoE) genotyping.nResults: Abnormal VEP P1 latency was registered in 18/42 right eyes (OD) and 21/42 left eyes (OS), abnormal N1P1 amplitude in 10/42 OD and OS. Mean P1 latency shortening during the follow-up was 15.0 ± 2.0 ms for 36/42 (86%) OD and 14.9 ± 2.4 ms for 35/42 (83%) OS, with maximum shortening up to 35.0 ms. No significant change of mean N1P1 amplitude was registered during follow-up.nA further decrease in N1P1 amplitude ≥1.0 mcV in at least one eye was observed in 17 of 36 patients (47%) with measurable amplitude (mean decrease −1.11 ± 0.83 (OD)/−2.37 ± 0.66 (OS) mcV versus −0.06 ± 0.56 (OD)/−0.83 ± 0.64 (OS) mcV in the study population, both p < .001).nApoE4 allele carriers had lower global and temporal RNFL thickness and longer initial P1 latency compared to the non-carriers (all p < .05). The odds ratio for abnormal visual function was 8.92 (3.00–36.50, 95%CI) for ApoE4 allele carriers (p < .001). The presence of ApoE4 allele was further associated with brain necrotic lesions (r = 0.384, p = .013) and brain hemorrhages (r = 0.395, p = .011).nConclusions: Improvement of optic nerve conductivity occurred in more than 80% of patients, but evoked potential amplitude tended to decrease during the 4 years of observation. ApoE4 allele carriers demonstrated lower RNFL thickness, longer P1 latency, and more frequent methanol-induced brain damage compared to non-carriers.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10403 - Physical chemistry

Projekt

<a href="/cs/project/NV16-27075A" target="_blank" >NV16-27075A: NEURODEGENERATIVNÍ PROCESY U PACIENTŮ EXPONOVANÝCH METANOLU: PROSPEKTIVNÍ STUDIE PO HROMADNÉ OTRAVĚ METANOLEM V ČESKÉ REPUBLICE V ROCE 2012</a><br>

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2019

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Clinical Toxicology

ISSN

1556-3650

e-ISSN

—

Svazek periodika

57

Číslo periodika v rámci svazku

6

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

11

Strana od-do

387-397

Kód UT WoS článku

000467843900003

EID výsledku v databázi Scopus

2-s2.0-85057571190