Purpose. To evaluate the systemic and local factors that contribute to the damage of endothelial cells in diabetic patients and to compare the endothelial structure of the cornea in diabetic and nondiabetic patients. Materials and Methods. The endothelial cell density (ECD) and central corneal thickness (CCT) were investigated in 123 eyes of type 1 diabetic patients and in 124 eyes of nondiabetic patients. The mean diabetic patients age was 15.34 ± 3.06 years versus 14.58 ± 2.01 years in the control group. The mean duration of diabetes was 8.02 ± 3.9 years. The corneal endothelium was imaged by the Topcon SP-2000P. Results. The mean ECD in diabetic eyes was 2435.55 ± 443.43？cells/mm2 and was significantly lower than in control group (2970.75 ± 270.1？cells/mm2). The mean CCT was 0.55 ± 0.03？mm in diabetic group versus 0.53 ± 0.033？mm in control group. ECD and CCT significantly correlated only with duration of diabetes. There was no correlation between ECD and CCT and patient age, sex, HbA1C level, and plasma creatinine level. Conclusions. ECD is decreased and CCT is increased in children and adolescents with diabetes mellitus. Duration of diabetes is the factor that affects ECD and CCT. 1. Introduction The corneal endothelium is a single layer of uniformly sized cells with hexagonal shape. Their amount decreases by approximately 0.5%-0.6% (100–200 cells) per year [1]. The endothelial cell dysfunction is observed in myopia and in contact lens wearers [2, 3]. The decreasing number of endothelial cells can also be a result of a surgical injury related to the opening of the anterior chamber [4]. Many studies have shown that even minor changes in the morphology of the endothelial cells may manifest in the disturbances in the tightness of the endothelial barrier. It has been demonstrated that human corneal endothelial cells have mitotic ability in vitro, but in vivo they do not exit the cell cycle but are arrested in G1 phase [5]. Loss of cells is compensated through the expanding and spreading of cells, which over time results in a lack of tightness and corneal oedema. Prevention of the corneal endothelium dysfunction, its early detection and immediate treatment are therefore crucial, especially if the problem concerns young patients. Noncontact specular microscopy, which evaluates endothelial morphology quickly and easily, can be especially useful with children. One of the conditions, which affect the cornea is diabetes. There are many reports concerning the analysis of the corneal endothelium in adults with type 1 and type 2 diabetes [6–9]; however, there
References
[1]
W. M. Bourne, L. I. L. Nelson, and D. O. Hodge, “Central corneal endothelial cell changes over a ten-year period,” Investigative Ophthalmology and Visual Science, vol. 38, no. 3, pp. 779–782, 1997.
[2]
B. Urban, A. Bakunowicz-？azarczyk, and M. Kr？towska, “Corneal endothelium in children and adolescents with myopia,” Klinika Oczna, vol. 104, no. 5-6, pp. 381–383, 2002.
[3]
S. W. Chang, F. R. Hu, and L. L. Lin, “Effects of contact lenses on corneal endothelium—a morphological and functional study,” Ophthalmologica, vol. 215, no. 3, pp. 197–203, 2001.
[4]
W. M. Bourne, L. R. Nelson, and D. O. Hodge, “Continued endothelial cell loss ten years after lens implantation,” Ophthalmology, vol. 101, no. 6, pp. 1014–1022, 1994.
[5]
N. C. Joyce and D. L. Harris, “Decreasing expression of the G1-phase inhibitors, p21Cip1 and p16ink4a, promotes division of corneal endothelial cells from older donors,” Molecular Vision, vol. 16, pp. 897–906, 2010.
[6]
T. N. Didenko, G. P. Smoliakova, E. L. Sorokin, and V. V. Egorov, “Clinical and pathogenetic features of neurotrophic corneal disorders in diabetes,” Vestnik Oftalmologii, vol. 115, no. 6, pp. 7–11, 1999.
[7]
A. Kabosova, A. A. Kramerov, A. M. Aoki, G. Murphy, J. D. Zieske, and A. V. Ljubimov, “Human diabetic corneas preserve wound healing, basement membrane, integrin and MMP-10 differences from normal corneas in organ culture,” Experimental Eye Research, vol. 77, no. 2, pp. 211–217, 2003.
[8]
G. M. Keoleian, J. M. Pach, D. O. Hodge, S. D. Trocme, and W. M. Bourne, “Structural and functional studies of the corneal endothelium in diabetes mellitus,” The American Journal of Ophthalmology, vol. 113, no. 1, pp. 64–70, 1992.
[9]
L. I. Larsson, W. M. Bourne, J. M. Pach, and R. F. Brubaker, “Structure and function of the corneal endothelium in diabetes mellitus type I and type II,” Archives of Ophthalmology, vol. 114, no. 1, pp. 9–14, 1996.
[10]
A. M. Roszkowska, C. G. Tringali, P. Colosi, C. A. Squeri, and G. Ferreri, “Corneal endothelium evaluation in type I and type II diabetes mellitus,” Ophthalmologica, vol. 213, no. 4, pp. 258–261, 1999.
[11]
M. Matsuda, N. Ohguro, I. Ishimoto, and M. Fukuda, “Relationship of corneal endothelial morphology to diabetic rentinopathy,duration of diabetes and glycemic control,” Japanese Journal of Ophthalmology, vol. 34, no. 1, pp. 53–56, 1990.
[12]
R. R. Sudhir, R. Raman, and T. Sharma, “Changes in the corneal endothelial cell density and morphology in patients with type 2 diabetes mellitus: a population-based study, Sankara Nethralaya Diabetic Retinopathy and Molecular Genetics Study (SN-DREAMS, Report 23),” Cornea, vol. 31, no. 10, pp. 1119–1122, 2013.
[13]
N. Furuse, S. Hayasaka, Y. Yamamoto, and T. Setogawa, “Corneal endothelial changes after posterior chamber intraocular lens implantation in patients with or without diabetes mellitus,” The British Journal of Ophthalmology, vol. 74, no. 5, pp. 258–260, 1990.
[14]
K. Inoue, S. Kato, Y. Inoue, S. Amano, and T. Oshika, “The corneal endothelium and thickness in type II diabetes mellitus,” Japanese Journal of Ophthalmology, vol. 46, no. 1, pp. 65–69, 2002.
[15]
J. S. Lee, B. S. Oum, H. Y. Choi, J. E. Lee, and B. M. Cho, “Differences in corneal thickness and corneal endothelium related to duration in diabetes,” Eye, vol. 20, no. 3, pp. 315–318, 2006.
[16]
S. Janiec, M. Rzendkowski, and S. Bolek, “The relation between corneal autofluorescence, endothelial cell count and severity of the diabetic retinopathy,” International Ophthalmology, vol. 18, no. 4, pp. 205–209, 1994.
[17]
J. Siribunkum, P. Kosrirukvongs, and A. Singalavanija, “Corneal abnormalities in diabetes,” Journal of the Medical Association of Thailand, vol. 84, no. 8, pp. 1075–1083, 2001.
[18]
M. Z. Ziadi, P. Moiroux, P. D'Athis, A. Bron, J. M. Brun, and C. Creuzot-Garcher, “Assessment of induced corneal hypoxia in diabetic patients,” Cornea, vol. 21, no. 5, pp. 453–457, 2002.
[19]
L. Módis Jr., E. Szalai, K. Kertész, A. Kemény-Beke, B. Kettesy, and A. Berta, “Evaluation of the corneal endothelium in patients with diabetes mellitus type I and II,” Histology and Histopathology, vol. 25, no. 12, pp. 1531–1537, 2010.
[20]
K. Zorena, E. Malinowska, D. Raczyńska, M. My？liwiec, and K. Raczyńska, “Serum concentrations of transforming growth factor-β 1 in predicting the occurrence of diabetic retinopathy in juvenile patients with type 1 diabetes mellitus,” Journal of Diabetes Research, vol. 2013, Article ID 614908, 6 pages, 2013.
[21]
J. V. Laursen, S. S. Hoffmann, A. Green, M. Nybo, A. K. Sj？lie, and J. Grauslund, “Associations between diabetic retinopathy and plasma levels of high-sensitive C-reactive protein or von Willebrand factor in long-term type 1 diabetic patients,” Current Eye Research, vol. 38, no. 1, pp. 174–179, 2013.
[22]
R. Shenoy, R. Khandekar, A. A. Bialasiewicz, and A. Al Muniri, “Corneal endothelium in patients with diabetes mellitus: a historical cohort study,” European Journal of Ophthalmology, vol. 19, no. 3, pp. 369–375, 2009.
[23]
E. K. Kim, D. H. Geroski, G. P. Holley, S. I. Urken, and H. F. Edelhauser, “Corneal endothelial cytoskeletal changes in F-actin with aging, diabetes, and after cytochalasin exposure,” The American Journal of Ophthalmology, vol. 114, no. 3, pp. 329–335, 1992.
[24]
A. Kleinzeller and F. Ziyadeh, “Cell volume regulation in epithelia with emphasis on the role of osmolytes and the cytoskeleton,” in Cell Volume Regulation, K. Beyenbach, Ed., pp. 59–86, Karger, New York, NY, USA, 1990.
[25]
H. Fujishima and K. Tsubota, “Improvement of corneal fluorescein staining in post cataract surgery of diabetic patients by an oral aldose reductase inhibitor, ONO-2235,” The British Journal of Ophthalmology, vol. 86, no. 8, pp. 860–863, 2002.
[26]
T. S. Kern and R. L. Engerman, “Distribution of aldose reductase in ocular tissues,” Experimental Eye Research, vol. 33, no. 2, pp. 175–182, 1981.
[27]
N. Ohguro, M. Matsuda, Y. Ohashi, and M. Fukuda, “Topical aldose reductase inhibitor for correcting corneal endothelial changes in diabetic patients,” The British Journal of Ophthalmology, vol. 79, no. 12, pp. 1074–1077, 1995.
[28]
Y. Kaji, S. Amano, T. Usui et al., “Advanced glycation end products in Descemet's membrane and their effect on corneal endothelial cell,” Current Eye Research, vol. 23, no. 6, pp. 469–477, 2001.
[29]
N. A. McNamara, “Effects of diabetes on anterior ocular structure and function,” International Contact Lens Clinic, vol. 24, no. 3, pp. 81–90, 1997.
[30]
C. O'Donnell, N. Efron, and A. J. M. Boulton, “A prospective study of contact lens wear in diabetes mellitus,” Ophthalmic and Physiological Optics, vol. 21, no. 2, pp. 127–138, 2001.
[31]
P. T. Mathew, S. David, and N. Thomas, “Endothelial cell loss and central corneal thickness in patients with and without diabetes after manual small incision cataract surgery,” Cornea, vol. 30, no. 4, pp. 424–428, 2011.
