This study investigated the value of Thiol/Disulfide homeostasis and ischemia-modified albumin (IMA) levels in discriminating diabetic cases with different stages of retinopathy and without retinopathy. In total, 122 patients with type 2 diabetes mellitus (DM) were enrolled in this prospective cross-sectional study. These patients were separated into three subgroups: Group 1 included 42 patients with DM and no diabetic retinopathy (DR), Group 2 included 40 patients with DM having non-proliferative DR and the Group 3 had 40 patients with DM having proliferative DR. The native thiol, total thiol, and disulfide levels and disulfide-native thiol, disulfide-total thiol, and native thiol-total thiol ratios as well as the IMA levels were analyzed and compared among the groups. There were no statistically significant differences regarding the ages and genders of the patients between the groups. The native thiol level, the total thiol level and the native thiol-total thiol ratio showed a statistically significantly reduction, while the disulfide level, the disulfide-native thiol ratio, and the disulfide-total thiol ratio showed a statistically significantly elevation in the Group 3 compared with the Group 1 and Group 2. Additionally, the mean IMA levels were statistically significantly higher in Group 3 when compared to Group 1 and Group 2 (p = .003 and p = .014, respectively). In conclusion, both Thiol/Disulfide homeostasis parameters and IMA levels increase with the progression of DR. Thiol/Disuldife homeostasis balance and IMA levels may be used a biomarker to monitor the tissue ischemia in DM and to discriminate the different stages of DR, in the future.
There is an imbalance in the systemic thiol-disulfide homeostasis in KC patients. This metabolic imbalance may play an important role in the pathogenesis of keratoconus; thus, it can be discussed in terms of the prevention, diagnosis, and the possible treatment for keratoconus.
Purpose: The aim of this study was to evaluate thiol/disulfide homeostasis and ischemia-modified albumin levels with primary open-angle glaucoma, ocular hypertension, and control group; also to interpret the correlation between these biochemical parameters and retinal nerve fiber layer analysis. Material and methods: In a prospective cross-sectional study, 30 primary open-angle glaucoma cases, 30 ocular hypertension cases, and 30 control subjects were included in the study. Native thiol, total thiol, and disulfide measurements and disulfide/native thiol, disulfide/total thiol, and native thiol/total thiol ratios were evaluated as thiol–disulfide homeostasis. Albumin and ischemia-modified albumin parameters were also evaluated. All cases underwent detailed ophthalmologic examination including visual acuity, retinal nerve fiber layer via optical coherence tomography, intraocular pressure, and central corneal thickness measurements and visual field analysis by 24-2 Swedish Interactive Threshold Algorithm (SITA) Standard visual field test. Results: Primary open-angle glaucoma group had significantly higher ischemia-modified albumin values than ocular hypertension and control group (p < 0.001). Native thiol and total thiol values of control group were statistically higher than those of primary open-angle glaucoma and ocular hypertension groups. The correlation between the temporal retinal nerve fiber layer value and ischemia-modified albumin, disulfide/native thiol, and disulfide/total thiol values of the primary open-angle glaucoma patients included in the study was moderate correlation in negative direction (r = –0.46, r = –0.39, r = –0.39, respectively), whereas there was a statistically significant moderate correlation in positive direction between the native thiol/total thiol values (r = 0.39) (p < 0.05). Conclusion: These findings have reinforced the role of oxidative stress in the etiopathogenesis of primary open-angle glaucoma, suggesting that the thinning retinal nerve fiber layer may be associated with oxidative stress in favor of prooxidant shift.
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