Corneal alteration and pathogenesis in diabetes mellitus

The incidence of diabetes mellitus (DM) and its complications have increased considerably worldwide. Diabetic keratopathy is the major complication of the cornea characterized by delayed corneal wound healing, decreasing corneal epithelial sensitivity, and recurrent corneal ulcers. There is accumulating evidence that diabetic keratopathy is correlated with the hyperglycemic state. Different corneal components may produce different alterations under hyperglycemia. In addition, diabetic nerve alteration may become a novel biomarker of early-stage DM. Abnormalities of the corneal nerve plexus have been associated with diabetic inflammatory states. There is rapidly growing evidence based on investigations of diabetic corneal nerves through in vivo confocal microscopy. Understanding the molecular pathogenesis caused by hyperglycemia may assist in the identification of novel biomarkers, as well as therapeutic targets for early treatment. This review mainly summarizes recent findings on corneal alteration and pathogenesis in DM.     

Corneal sensitivity and vibratory perception in diabetes mellitus

36 patients suffering from diabetes mellitus and 45 controls were subjected to blind studies for corneal sensitivity using Cochet & Bonnet's aesthesiometer and of vibratory perception of the left index finger and great toe by biothesiometer. 83% of the diabetics had a corneal sensitivity below 60 mm against 38% of the controls. Likewise a significantly reduced vibratory perception was noticed among the diabetics. Further, the reductions of corneal senstivity and vibratory perception were correlated in the diabetics. In both groups falling corneal sensitivity and vibratory perception were found with increasing age over and above 50 years. There is evidence to suggest that a reduced corneal sensitivity in relation to diabetes mellitus forms part of a polyneuropathy.     

Corneal hydration control in contact lens wearers with diabetes mellitus.

PURPOSE: The purpose of this study was to assess the acute swelling and recovery response to contact lens-induced corneal hypoxia in diabetic patients who wear contact lenses. METHODS: A thick, low water content, soft contact lens was fitted under a light patch to one eye of 23 diabetic patients and one eye of 23 nondiabetic control subjects in a single-masked, controlled clinical study. After 2.5 hours an ultrasonic pachymeter was used to measure the induced corneal edema and the rate at which the cornea recovered to baseline thickness. RESULTS: The induced corneal edema was significantly less for the diabetic patients compared with the nondiabetic control subjects (p = 0.004). The corneas of the diabetic patients were found to recover from the induced edema at a similar rate to the corneas of the nondiabetic control subjects (p = 0.28). CONCLUSIONS: Diabetes mellitus alters aspects of corneal hydration control.     

Corneal changes in type II diabetes mellitus in Malaysia

AIM: To compare corneal endothelial structure and central corneal thickness (CCT) between type II diabetics and non-diabetic control patients. To look for correlations between diabetic status and corneal findings. METHODS: Hospital-based, observational study. 200 eyes (from 100 type II diabetic patients and 100 controls) were included. Specular microscopy and pachymetry were used to measure endothelial cell density, size, coefficient of variation in cell area, hexagonality as well as corneal thickness. Independent t-tests were used to compare variables between diabetics and controls. Pearson correlation tests were used to evaluate correlations between corneal findings and diabetic status such as duration of diabetes, haemoglobin A1c (HbA1c) level and severity of diabetic retinopathy. RESULTS: Endothelial cell density in the diabetic group (2541.6±516.4 cells/mm2) was significantly lower than that in the control group (2660.1±515.5 cells/mm2, P <0.05). The average size of endothelial cells, standard deviation (SD) of cell size and coefficient of variation (CV) of cell area were all significantly higher in diabetics. Hexagonality was significantly lower in diabetics (41.1%±19.6%) compared to non- diabetics (45.2%±20.6%). CCT was higher in diabetics but not significant (P >0.05). Duration of diabetes, HbA1c level and severity of diabetic retinopathy were not significantly correlated with corneal endothelial findings. CONCLUSION: Type II diabetes causes a significant alteration in the state of the cornea including reduction in endothelial cell density and increased pleomorphism and polymegathism. Central corneal thickness is unaffected.     

Corneal structure and sensitivity in type 1 diabetes mellitus

PURPOSE: Corneal wound healing is impaired in diabetic cornea. The purpose of this study was to examine patients with type 1 diabetes mellitus for changes in corneal morphology and to correlate corneal sensitivity, subbasal nerve morphology, and degree of polyneuropathy with each other. METHODS: Forty-four eyes of 23 patients with diabetes and nine control eyes were included. Corneal sensitivity was tested with a Cochet-Bonnet esthesiometer (Luneau, Paris, France), and corneal morphology and epithelial and corneal thickness were determined by in vivo confocal microscopy. The density of subbasal nerves was evaluated by calculating the number of long subbasal nerve fiber bundles per confocal microscopic field. The degree of polyneuropathy was evaluated using the clinical part of the Michigan Neuropathy Screening Instrument (MNSI) classification, and retinopathy was evaluated using fundus photographs. RESULTS: A reduction of long nerve fiber bundles per image was noted to have occurred already in patients with mild to moderate neuropathy, but corneal mechanical sensitivity was reduced only in patients with severe neuropathy. Compared with control subjects the corneal thickness was increased in patients with diabetes without neuropathy. The epithelium of patients with diabetes with severe neuropathy was significantly thinner than that of patients with diabetes without neuropathy. CONCLUSIONS: Confocal microscopy appears to allow early detection of beginning neuropathy, because decreases in nerve fiber bundle counts precede impairment of corneal sensitivity. Apparently, the cornea becomes thicker in a relatively early stage of diabetes but does not further change with the degree of neuropathy. A reduction in neurotrophic stimuli in severe neuropathy may induce a thin epithelium that may lead to recurrent erosions.     

Corneal endothelial morphology and central thickness in patients with type II diabetes mellitus

Purpose: To investigate corneal endothelial cell density and morphology in type II diabetic and non‐diabetic patients and to relate potential differences to the glycaemic status. Methods: A prospective clinical study including 107 patients with type II diabetes and 128 non‐diabetic patients. Sample size was based on a power calculation (power = 0.90; p = 0.05). The diabetic patients had on average more than four HbA1c tests performed (mean 4.1; range 2–14) with intervals of at least 3 months as a reflection of the long‐term glycaemic status. The controls had no diabetes confirmed by two causal blood tests. The endothelial cell density, the variation in endothelial cell size (CV), the percentage of hexagonal cells, and the central corneal thickness (CCT) were recorded. Results: Type II diabetic subjects did not differ from the non‐diabetic control subjects with regards to endothelial cell density, hexagonality or variation in CV, but showed a significant increase in CCT (538 versus 546 μm, p < 0.05). In the diabetic group, lower cell counts were associated with higher HbA1_c values (p < 0.05). The HbA1c did not, however, have any impact on the CCT. Conclusion: Type II diabetes has no impact on corneal cell density or morphology in subjects with good glycaemic status. However, higher HbA1c was associated with lower endothelial cell density. CCT was significantly increased in the diabetic group_.     

Corneal endothelium evaluation in type I and type II diabetes mellitus.

BACKGROUND: The purpose of this study is to evaluate the corneal endothelium in type I and type II diabetic patients. METHODS: Seventy-five diabetics divided into type I and type II groups and 62 healthy volunteers took part in the study. The mean endothelial cell density and morphology, and the central corneal thickness were evaluated and statistical analysis was done. RESULTS: All evaluated parameters were found to be significantly different in both diabetic groups with reduction of the mean cell density of 5% in type II and of 11% in type I diabetes with respect to the normal age-matched control group. Important alterations of endothelial morphology were observed. The central corneal pachymetry was significantly higher in diabetics, with p < 0.01 in the type I group and p < 0.05 in the type II group. CONCLUSION: It is concluded that corneal endothelium in diabetics should still be considered as a tissue under continuous metabolic stress with consequent high vulnerability, especially in case of any external insult such as a surgical procedure.     

近视人群中角膜生物力学特性的分布

目的：分析伊朗近视眼及散光人群中角膜生物力学参数的分布特征。

方法：对接受激光矫正手术的近视眼及散光患者180眼进行前后节、显然验光等效球镜度、Orbscan II和Zywave全面的术前检查。用眼反应分析仪测量角膜滞后量,角膜阻力因子,模拟Goldmann眼压值及角膜补偿后眼压值。分析所有角膜生物力学的分布特性及其与显然验光等效球镜度、性别和年龄的相关性。数据采用SPSS 17软件进行统计学分析,以P<0.05为有显著性差异。

结果：平均年龄为28.20±6.78岁。平均显然验光等效球镜为-4.21±1.19D。平均角膜滞后量,角膜阻力因子,模拟Goldmann眼压值和角膜补偿后眼压值分别为10.00±1.28mmHg,10.17±1.45mmHg,15.71±2.67mmHg和 16.68±2.41mmHg。近视人群中,28.4%角膜滞后量约为10mmHg,71%从9mmHg增长到11mmHg。25.9%的近视人群的角膜阻力因子为10mmHg,48.7%为9mmHg增长到11mmHg。显然验光等效球镜与角膜滞后量(Rs=0.001,P=0.71)和显然验光等效球镜与角膜阻力因子(Rs=0.01,P=0.18)之间正相关性不明显。

结论：研究显示了伊朗近视眼人群中角膜生物力学的分布特征(角膜滞后量,角膜阻力因子,模拟Goldmann眼压值及角膜补偿后眼压值),并证实了角膜生物力学特性参数和显然验光等效球镜,年龄及性别之间没有统计学相关性。     

Corneal biomechanical properties and their correlates with refractive error

Purpose: The aim was to study the link between refractive error and corneal biomechanical properties. Methods: Corneal hysteresis and corneal resistance factor were measured using the Ocular Response Analyser in 117 participants. The spherical equivalent refractive error of the participants ranged between ‐9.00 and +3.00 D. Results: Corneal hysteresis and corneal resistance factor showed a considerable degree of variability between individuals. Corneal hysteresis was not found to correlate significantly with refractive error (p = 0.82). Corneal resistance factor showed a weak but significant correlation with spherical equivalent refractive error (r²= 0.04; p = 0.03), with myopic participants exhibiting a higher corneal resistance factor compared with non‐myopes. Conclusions: Refractive error accounted for four per cent of the variance in corneal resistance factor measurements, indicating that patients with mild to moderate myopia have higher corneal resistance compared with non‐myopes.