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      Evaluation of Iron Deficiency Anemia Frequency as a Risk Factor in Glaucoma

      research-article
      1 , , 2 , 3 , 4 , 5
      Anemia
      Hindawi

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          Abstract

          Purpose

          Iron deficiency anemia is an important public health problem. Also it is considered to be a risk factor for many diseases. The study demonstrates the iron deficiency anemia frequency in glaucoma patients and compares with the normal subjects. We aimed to determine the iron deficiency anemia frequency in glaucoma patients.

          Methods

          Prospective, controlled study in a single university hospital setting. A total of 130 normal subjects (Group 1) and 131 glaucoma patients (Group 2) were included. The erythrocytes parameters, hemoglobin, red blood cell, hematocrit, mean corpuscular volume, mean corpuscular hemoglobin concentration, mean corpuscular hemoglobin, and red blood cell distribution width, and iron status indicators, Fe (iron), total iron binding capacity, and ferritin of the cases, in normal subjects and glaucoma patients were compared.

          Results

          There was no statistically significant difference for the erythrocyte parameters between the groups (p≥0.05). The number of the patients with iron deficiency anemia in both groups was similar. No statistically significant difference was found in the comparison of erythrocyte parameters and iron status indicators values according to the number of antiglaucomatous agents and visual field changes according to the presence of anemia in Group 2 (p≥0.05). A statistically significant difference was found only in MCH when the erythrocyte parameters and iron status indicators values of the cases in glaucoma patients were compared with the glaucoma duration (p<0.05).

          Conclusion

          The iron deficiency anemia frequency was like the normal population in glaucoma patients.

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          Most cited references14

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          The role of oxidative stress in glaucoma.

          DNA damage is related to a variety of degenerative diseases such as cancer, atherosclerosis and neurodegenerative diseases, depending on the tissue affected. Increasing evidence indicates that reactive oxygen species (ROS) play a key role in the pathogenesis of primary open angle glaucoma (POAG), the main cause of irreversible blindness worldwide. Oxidative DNA damage is significantly increased in the ocular epithelium regulating aqueous humor outflow, i.e., the trabecular meshwork (TM), of glaucomatous patients compared to controls. The pathogenic role of ROS in glaucoma is supported by various experimental findings, including (a) resistance to aqueous humor outflow is increased by hydrogen peroxide by inducing TM degeneration; (b) TM possesses remarkable antioxidant activities, mainly related to superoxide dismutase-catalase and glutathione pathways that are altered in glaucoma patients; and (c) intraocular-pressure increase and severity of visual-field defects in glaucoma patients parallel the amount of oxidative DNA damage affecting TM. Vascular alterations, which are often associated with glaucoma, could contribute to the generation of oxidative damage. Oxidative stress, occurring not only in TM but also in retinal cells, appears to be involved in the neuronal cell death affecting the optic nerve in POAG. The highlighting of the pathogenic role of ROS in POAG has implications for the prevention of this disease as indicated by the growing number of studies using genetic analyses to identify susceptible individuals and of clinical trials testing the efficacy of antioxidant drugs for POAG management.
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            Redox metals and neurodegenerative disease.

            Multiple lines of evidence implicate redox-active transition metals as mediators of oxidative stress in neurodegenerative diseases. Among the recent research discoveries is the finding that transition metals bind to proteins associated with neurodegeneration, including the prion protein. Whereas binding in the latter case may serve an antioxidant function, adventitious binding of metals to other proteins appears to preserve their catalytic redox activity in a manner that disturbs free radical homeostasis. Alterations in the levels of copper- and iron-containing metalloenzymes, involved in processing partially reduced oxygen species, are also likely to contribute to altered redox balance in neurodegenerative diseases. Nonetheless, even in familial forms of amyotrophic lateral sclerosis linked to mutations in superoxide dismutase, it is unclear whether an altered enzyme activity or, indirectly, a disturbance in transition-metal homeostasis is involved in the disease pathogenesis.
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              Differential susceptibility of retinal ganglion cells to reactive oxygen species.

              Retinal light exposure is a source of oxidative stress, and retinal cells contain molecules that scavenge or inactivate reactive oxygen species (ROS). Yet, ROS also play a role in signal transduction, and some retinal cells (e.g., neurotrophin-dependent retinal ganglion cells, RGCs) may use ROS as part of the signaling process for cell death. RGCs might therefore have specialized mechanisms for regulating ROS levels. The hypothesis that RGCs might regulate ROS differently from other retinal cells was tested by studying their differential response to oxidative stress in vitro. RGCs were retrogradely labeled by injecting the fluorescent tracer DiI into the superior colliculi of postnatal day 2 through 4 Long-Evans rats. At postnatal days 7 through 9 the retinas were dissociated with papain and cultured with and without specific ROS-generating systems and/or scavengers. RGCs were identified by their DiI positivity using rhodamine filters. Living cells, determined by metabolism of calcein-AM viewed with fluorescein filters, were counted in triplicate. Degenerate reverse transcription-polymerase chain reaction (RT-PCR) using primers specific to peroxidase homology regions was used to survey for novel peroxidases expressed within normal retinas. Compared with other retinal cells, RGCs were remarkably resistant to cell death induced by superoxide anion, hydrogen peroxide, or hydroxyl radical. Catalase counteracted the effect of each ROS-generating system on retinal cells, consistent with damage occurring via a hydrogen peroxide intermediate. Aminotriazole, L-buthionine sulfoximine, and sodium azide partly abrogated the RGC resistance to oxidative stress, suggesting that this resistance may be mediated by catalase and/or glutathione peroxidase. A limited expression survey within the retina using degenerate RT-PCR did not demonstrate novel peroxidases. These data suggest a role for one or more endogenous peroxidases within RGCs, which could possibly be protective under conditions of axonal damage. Exploration of the unique characteristics of RGC resistance and susceptibility to injury may help in better understanding the pathophysiology of diseases associated with primary axonal damage.
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                Author and article information

                Contributors
                Journal
                Anemia
                Anemia
                ANEMIA
                Anemia
                Hindawi
                2090-1267
                2090-1275
                2018
                1 August 2018
                : 2018
                : 1456323
                Affiliations
                1Associate Professor, Inonu University School of Medicine, Department of Ophthalmology, Malatya, Turkey
                2MD, Sarkısla State Hospital, Department of Ophthalmology, Sivas, Turkey
                3Assistant Professor, Inonu University School of Medicine, Department of Ophthalmology, Malatya, Turkey
                4Professor, Inonu University School of Medicine, Department of Hematology, Malatya, Turkey
                5MD, Mujde Hospital, Department of Ophthalmology, Malatya, Turkey
                Author notes

                Academic Editor: Duran Canatan

                Author information
                http://orcid.org/0000-0002-9427-3610
                http://orcid.org/0000-0003-2062-3515
                Article
                10.1155/2018/1456323
                6093034
                30155291
                290826e9-bed7-4e0b-abfd-04aa59757592
                Copyright © 2018 Penpe Gul Firat et al.

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

                History
                : 18 May 2018
                : 11 July 2018
                Categories
                Research Article

                Hematology
                Hematology

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