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      Tobacco-alcohol optic neuropathy – clinical challenges in diagnosis

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          Abstract

          Part of the large group of nutritional and toxic optic neuropathies, tobacco-alcohol optic neuropathy is a disease often underdiagnosed or detected at a stage when the full recovery of vision is not possible. This article summarizes its signs and symptoms, describes the pathophysiological processes involved and provides the necessary information for diagnosis and treatment of the entity previously known as tobacco-alcohol amblyopia, reporting in the end, a challenging case along with its findings.

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          Toxic optic neuropathy

          Pradeep Sharma, Reena Sharma (2011)
          Toxic optic neuropathy (TON) is a disease entity which is not only underdiagnosed, but also often diagnosed at a stage when recovery of vision is not possible. This article gives an overview of common causes, clinical features, and management of TON.
          Article 0 comments Cited 34 times – based on 0 reviews     Review now
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            Mitochondrial genome damage associated with cigarette smoking.

            S H Ballinger, R. Albertini, Wagner A. S. Judice … (1996)
            We have investigated the level of mitochondrial DNA (mtDNA) damage and deletions in bronchoalveolar lavage tissues from smokers and nonsmokers using quantitative, extra-long PCR and a "common" mtDNA deletion assay. Smokers had 5.6 times the level of mtDNA damage, 2.6 times the damage at a nuclear locus (beta-globin gene cluster), and almost 7 times the level of a 4.9-kb mtDNA deletion compared to nonsmokers, although the latter increase was not significant. Although both genomes (mitochondrial and nuclear) showed significantly increased levels of DNA damage in smokers (mtDNA P = 0.00072; beta-globin P = 0.0056), the relative differences were greatest in the mtDNA. Damage to the mtDNA may inhibit oxidative phosphorylation and, therefore, potentially cause or contribute to chronic lung disease and cancer. Consequently, the mtDNA may be a sensitive biomarker for environmentally induced genetic damage and mutation.
            Article 0 comments Cited 23 times – based on 0 reviews     Review now
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              Ethambutol is toxic to retinal ganglion cells via an excitotoxic pathway.

              D Zurakowski, Yujing Heng, C Vorwerk … (1998)
              Ethambutol is an essential medication in the management of tuberculosis. However, it can cause an optic neuropathy of uncertain etiology. Ethambutol toxicity was therefore studied in rodent retinal cells, and agents that might block its toxicity were considered. The toxicity of ethambutol and related agents was evaluated in rodent retinal dissociated cell preparations and whole eyes. Calcium fluxes and mitochondrial function were evaluated by fluorescent and staining techniques. For in vivo assays, adult rats were administered oral ethambutol over a 3-month period. Cell survival was assessed by stereology. Ethambutol is specifically toxic to retinal ganglion cells in vitro and in vivo. Endogenous glutamate is necessary for the full expression of ethambutol toxicity, and glutamate antagonists prevent ethambutol-mediated cell loss. Ethambutol causes a decrease in cytosolic calcium, an increase in mitochondrial calcium, and an increase in the mitochondrial membrane potential. The visual loss associated with ethambutol may be mediated through an excitotoxic pathway, inasmuch as ganglion cells are rendered sensitive to normally tolerated levels of extracellular glutamate. Ethambutol perturbs mitochondrial function. Its toxicity may depend on decreased ATPase activity and mitochondrial energy homeostasis. Glutamate antagonists may be useful in limiting the side effects seen with ethambutol.
              Article 0 comments Cited 21 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): J Med Life
                Journal ID (iso-abbrev): J Med Life
                Journal ID (publisher-id): JMedLife
                Title: Journal of Medicine and Life
                Publisher: Carol Davila University Press (Romania )
                ISSN (Print): 1844-122X
                ISSN (Electronic): 1844-3117
                Publication date (Print): Oct-Dec 2014
                Volume: 7
                Issue: 4
                Pages: 472-476
                Affiliations
                [* ]“Nicolae Malaxa” Clinical Hospital, Bucharest
                [** ]“Carol Davila” University of Medicine and Pharmacy, Bucharest
                [*** ]Clinical Ophthalmological Emergency Hospital
                Author notes
                Correspondence to:Chiotoroiu Silvia Mariana, MD, PhD Department of Ophthalmology, “Nicolae Malaxa” Clinical Hospital, 12 Vergului Street, District 2, Code: 02441, Bucharest, Romania Phone/fax: +40 21 255 5405, E-mail: chiotoroiu@yahoo.com
                Article
                Publisher ID: JMedLife-07-472
                PMC ID: 4316121
                PubMed ID: 25713605
                SO-VID: 3fe9a0e7-12b9-4a68-95b8-242fe61f4ce3
                Copyright © ©Carol Davila University Press
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 19 April 2014
                Date accepted : 18 October 2014
                Categories
                Subject: Reviews

                ScienceOpen disciplines: Medicine
                Keywords: optic neuropathy,tobacco,alcohol,toxins,visual field
                Data availability:
                ScienceOpen disciplines: Medicine
                Keywords: optic neuropathy, tobacco, alcohol, toxins, visual field

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