| ORIGINAL ARTICLE |
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| Year : 2018 | Volume
: 8
| Issue : 2 | Page : 82-86 |
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The relationship between optic atrophy 1 polymorphism and normal tension glaucoma in Taiwan
Yan-Ting Chen1, San-Ni Chen2, Chin-San Liu3
1 Department of Ophthalmology, Changhua Christian Hospital, Changhua; Institute of Clinical Medicine, National Yang-Ming University, Taipei; Department of Optometry, Central Taiwan University of Science and Technology; Department of Medicine, Chung Shan Medical University; Department of Neurology, Changhua Christian Hospital, Changhua, Taiwan
2 Department of Ophthalmology, Changhua Christian Hospital, Changhua; Department of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
3 Department of Neurology, Changhua Christian Hospital; Vascular and Genomics Center, Changhua Christian Hospital; School of Chinese Medicine, Graduate Institute of Integrated Medicine, China Medical University, Taichung, Taiwan
Correspondence Address:
Dr. Chin-San Liu
Department of Neurology and Vascular and Genomics Center, Changhua Christian Hospital, 135 Nanhsiao Street, Changhua 500
Taiwan
 Source of Support: None, Conflict of Interest: None  | 3 |
DOI: 10.4103/tjo.tjo_92_17
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PURPOSE: The purpose of this research is to evaluate the relationship between of optic atrophy 1 (OPA1) polymorphism and normal tension glaucoma (NTG) by surveying patients from central Taiwan. This study finding could help us to understand the impact of OPA1 polymorphism on glaucoma.
METHODS: We try to identify the effect of OPA1 polymorphism by comparing the clinical presentation in three catalogs of gene polymorphism in patients with NTG. Our research team includes patients with NTG from central Taiwan and assesses the OPA1 intervening sequence 8 (IVS8) + 4 C->T and IVS8 + 32 T->C polymorphism. We divide these patients into three OPA1 IVS8 + 4 subgroups, CC, CT, TT, and three IVS8 + 32 subgroups, TT, TC, CC. By collecting their ocular clinical data, systemic background, and other possible factors related to the presentation of glaucoma, we can compare these characters of each polymorphism subgroup.
RESULTS: We find that all patients do not have OPA1 IVS8 + 4 C->T polymorphism while some of them do have IVS8 + 32 T->C polymorphism. NTG with OPA1 IVS8 + 32 T->C polymorphism inclines to have more nasal-step type visual field defect (P = 0.016) and inferior nerve fiber layer thickness loss (P = 0.098) in comparison to NTG with IVS8 + 32 wild type.
CONCLUSIONS: The OPA1 IVS8 + 32 T->C polymorphism partake to the phenotype and prognosis of NTG in central Taiwan. Even though our findings are far from clear enough to serve as guides for the differentiation of NTG etiologies, they still give us a glimpse of the impact of OPA1 in chronic optic neuropathy.
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