The results of this study demonstrated that choroidal thickness decreases in patients with systemic arterial hypertension. This may be caused by arteriolar sclerosis and vascular contraction caused by high intravascular pressure in the choroid.
Purpose: This study explores retinal structural changes in type 1 diabetes without clinically diagnosed diabetic retinopathy (DR). Methods: Peripapillary retinal nerve fiber layer (RNFL) thickness, macular ganglion cell complex (GCC) thickness, and macular thickness (MT) were measured in 90 type 1 diabetic patients by using spectral domain optical coherence tomography. The values were compared with 100 sex- and age-matched healthy controls. The independent t test was used to assess differences in the mean age, mean diabetic and ocular parameters, and the thickness values between the diabetic and control groups. Multiple linear regression analysis was performed to investigate the correlation between the thickness values and diabetic and ocular parameters. Results: Whole-RNFL, the superior and inferior quadrants, and the superior half of the peripapillary RNFL thicknesses were significantly thinner in diabetic patients compared with controls (p < 0.05). GCC thicknesses in the average macular, outer temporal superior and outer temporal inferior sectors were significantly thinner in diabetic patients (p < 0.05). Central and average MTs were similar in both groups (p > 0.05). There were significant negative correlations of the duration of type 1 diabetes with the inner nasal MT, inner temporal superior GCC thickness, inner nasal inferior GCC thickness, and outer nasal superior GCC thickness (p < 0.05). Similarly, there were significant negative correlations of the level of HbA1c with the whole-RNFL thickness, superior-half-RNFL thickness, and superior-quadrant-RNFL thickness (p < 0.05). Conclusions: Type 1 diabetic patients without clinically diagnosed DR had neurodegeneration in the inner retinal layers compared with healthy controls.
Background/aims: Intraocular bone is seen in a wide spectrum of ocular disorders. The pathogenetic mechanisms of bone formation in the eye are unclear. Growth differentiation factor-5 (GDF-5), bone morphogenic protein-7 (BMP-7), and transforming growth factor beta-1 (TGF b1) are multifunctional cytokines that have important roles in bone formation. Immunohistochemistry was used to localise GDF-5, BMP-7, and TGF b1 in the human eye to determine their role in intraocular bone formation. Methods: Paraffin embedded sections from human eyes included fetal eyes (n = 5), normal adult eyes (n = 4), eyes with osseous metaplasia (n = 8), and eyes with focal fibrous metaplasia of the retinal pigment epithelium (RPE) without osseous metaplasia (n = 2). Immunohistochemistry was performed using indirect immunofluorescence with antibodies to GDF-5, BMP-7, and TGF b1. The staining intensity was evaluated semiquantitatively in the RPE, retina, ciliary epithelium, and cornea; and analysed statistically. Results: When compared with normal adult eyes, which showed no RPE immunoreactivity, the RPE metaplasia surrounding areas of osseous metaplasia showed mild GDF-5 and moderate BMP-7 (p = 0.004) intracytoplasmic immunoreactivity. In contrast, trace GDF-5 and mild BMP-7 staining was seen in zones of RPE fibrous metaplasia in areas not associated with osseous metaplasia. Mild intracytoplasmic TGF b1 expression was seen in the RPE metaplasia surrounding the bone when compared with adult eyes. Both fetal and adult eyes showed trace to mild GDF-5 and BMP-7 labelling of the non-pigmented ciliary epithelium which was increased in the eyes with osseous metaplasia. In eyes with osseous metaplasia, a significant decrease in GDF-5 and BMP-7 labelling was noted in fetal keratocytes (p = 0.0159 for both antibodies) when compared to adult eyes. Also, a significant decrease in BMP-7 labelling was seen in keratocytes in eyes with osseous metaplasia (p = 0.0162). Conclusions: The increase in GDF-5, BMP-7, and TGF b1 immunoreactivity in zones of RPE metaplasia in eyes with osseous metaplasia suggests that these proteins have an important role in intraocular ectopic bone formation.
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