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Do type 2 diabetes patients without diabetic retinopathy or subjects with impaired fasting glucose have impaired colour vision? The Okubo Color Study Report
Abstract
To investigate associations between fasting plasma glucose level and the prevalence of acquired colour vision impairment in type 2 diabetes patients without diabetic retinopathy.
Participants in this cross-sectional study of male officials aged 20-60 yr in the Japanese Self Defence Force, underwent colour vision testing, ophthalmic examination, a standardized interview and examination of venous blood samples. Ishihara plates, a Lanthony 15-hue desaturated panel and Standard Pseudoisochromatic Plates Part 2 were used to examine colour vision. The Farnsworth-Munsell 100-hue test was performed to define acquired colour vision impairment. Cardiovascular disease risk factors were determined from serum blood samples, physical records and an interview. We performed logistic regression analysis adjusted for age, diagnosed hypertension, dyslipidaemia, cataract, glaucoma, being overweight, smoking status and alcohol intake. Crude and adjusted odds ratios were calculated for three glucose levels, which included normal fasting glucose, impaired fasting glucose and diabetes.
Out of a total of 1042 men enrolled, 872 were eligible for the study, and 31 were diagnosed with acquired colour vision impairment. As compared with the subjects with normal fasting glucose (< 5.6 mmol/l), the crude odds ratio for acquired colour vision impairment was 0.93 (95% CI 0.32-2.74) for the subjects with impaired fasting glucose (5.6-6.9 mmol/l) and 8.07 (95% CI 2.48-26.22) for the patients with type 2 diabetes. The multiple-adjusted odds ratios were 0.77 (95% CI 0.25-2.34) for the subjects with impaired fasting glucose and 5.89 (95% CI 1.55-22.40) for the patients with type 2 diabetes.
Our findings suggest that there is a dramatically increased prevalence of acquired colour vision impairment in type 2 diabetes patients without diabetic retinopathy which might be attributable to another pathogenesis associated with diabetic retinopathy.
... The fact that certain visual functional alterations are common among subjects with no clinically apparent diabetic retinopathy has been published earlier. 5,8,36,37 Although in terms of quality of life the burden of functional deficits with normal vision (such as CVDs or decreased contrast sensitivity) seems to be minor, these may still be important considering their potential contribution to or prognostic value for the development of vasculopathy. Color vision tests are simple, available, non-invasive tools that can be used to screen visual function and diabetes-related damage of photoreceptors, which may be among the first manifest signs of neurodegeneration. ...
... 10,11 Discrimination of color vision may be influenced by several ophthalmological parameters (such as cataract formation of the lens and increased intraocular pressure) and metabolic factors, including dyslipidemia and elevated blood pressure. 6,8 The precise pathogenesis of CVDs in early diabetes is still not fully understood. We demonstrated earlier an increase in the number of dual cones-cones coexpressing S-and M-opsins simultaneously-in diabetic rat retinas. ...
... To the best of our knowledge, this is the first study analyzing the role of thyroid hormonal status in the development of human diabetes-related retinal alterations. In agreement with other reports, 8,36,37,57 we found a significantly larger occurrence of CVDs without manifest retinopathy in the diabetic group than in the control group. Published data suggest that, besides age and gender, metabolic factors including body mass index, blood pressure, lipid profile, duration of disease, and patient compliance (assessed by the degree of diabetic control) all affect the risk of CVDs in diabetes. ...
Purpose:
In diabetic subjects, early visual functional alterations such as color vision deficiencies (CVDs) are known to precede clinically apparent diabetic retinopathy. Prominent photoreceptor outer segment degeneration and an increase in the number of retinal dual cones (co-expressing S- and M-opsins simultaneously) have been described in diabetic rat models, suggesting a connection with the development of CVDs. As cone opsin expression is controlled by thyroid hormones, we investigated the diabetic retina in association with thyroid hormone alterations.
Methods:
In rat models of type 1 and 2 diabetes, dual cones were labeled by immunohistochemistry, and their numbers were analyzed in relation to free triiodothyronine (fT3) and free thyroxine (fT4) levels. Quantification of dual cones was also performed in human postmortem retinas. Additionally, a cross-sectional case-control study was performed where thyroid hormone levels were measured and color vision was assessed with Lanthony desaturated D15 discs.
Results:
A higher number of dual cones was detectable in diabetic rats, correlating with fT4 levels. Dual cones were also present in postmortem human retinas, with higher numbers in the three diabetic retinas. As expected, age was strongly associated with CVDs in human patients, and the presence of diabetes also increased the risk. However, the current study failed to detect any effect of thyroid hormones on the development of CVDs.
Conclusions:
Our results point toward the involvement of thyroid homeostasis in the opsin expression changes in diabetic rats and human samples. The evaluation of the possible clinical consequences warrants further research.
... [2,5] Few studies have reported risk factors for ICV among subjects with diabetes. [1,6] The aim of the present study was to report the prevalence of ICV among subjects with type 2 diabetes without any evidence of diabetic retinopathy in a population based study and to assess various associated systemic and ocular risk factors for ICV. ...
... Previous studies have found a relationship between colour vision impairment and diabetic retinopathy [1][2][3][4] and also among subjects with diabetes without retinopathy [18]. Prevalence of ICV as reported by Shoji et al [6] was 3.5% in diabetic subjects without retinopathy. The prevalence of ICV in our study (39.5%) was higher compared to those reported earlier. ...
... The prevalence of ICV in our study (39.5%) was higher compared to those reported earlier. Shoji et al [6] estimated ICV in two steps; Ishihara plates, a Lanthony 15-hue desaturated panel and Standard Pseudoisochromatic Plates Part 2 were used to examine colour vision and Farnsworth-Munsell 100-hue test was performed to define acquired colour vision impairment. Moreover, the study subjects were between 20-60 years, a predominantly younger population. ...
To assess impairment of colour vision in type 2 diabetics with no diabetic retinopathy and elucidate associated risk factors in a population-based cross-sectional study.This is part of Sankara Nethralaya Diabetic Retinopathy Epidemiology and Molecular-genetics Study (SN-DREAMS II) which was conducted between 2007-2010. FM 100 hue-test was performed in 253 subjects with no clinical evidence of diabetic retinopathy. All subjects underwent detailed ophthalmic evaluation including cataract grading using LOCS III and 45° 4-field stereoscopic fundus photography. Various ocular and systemic risk factors for impairment of colour vision (ICV) were assessed in subjects with diabetes but no retinopathy. P value of < 0.05 was considered statistically significant.The mean age of the study sample was 57.08 ± 9.21 (range: 44-86 years). Gender adjusted prevalence of ICV among subjects with diabetes with no retinopathy was 39.5% (CI: 33.5-45.5). The mean total error score in the study sample was 197.77 ± 100 (range: 19-583). The risk factors for ICV in the study were women OR: 1.79 (1.00-3.18), increased resting heart rate OR: 1.04 (1.01-1.07) and increased intraocular pressure OR: 1.12 (1.00-1.24). Significant protective factor was serum high-density lipoprotein OR: 0.96 (0.93-0.99).Acquired ICV is an early indicator of neurodegenerative changes in the retina. ICV found in diabetic subjects without retinopathy may be of non-vascular etiology.
... [2,5] Few studies have reported risk factors for ICV among subjects with diabetes. [1,6] The aim of the present study was to report the prevalence of ICV among subjects with type 2 diabetes without any evidence of diabetic retinopathy in a population based study and to assess various associated systemic and ocular risk factors for ICV. ...
... Previous studies have found a relationship between colour vision impairment and diabetic retinopathy [1][2][3][4] and also among subjects with diabetes without retinopathy [18]. Prevalence of ICV as reported by Shoji et al [6] was 3.5% in diabetic subjects without retinopathy. The prevalence of ICV in our study (39.5%) was higher compared to those reported earlier. ...
... The prevalence of ICV in our study (39.5%) was higher compared to those reported earlier. Shoji et al [6] estimated ICV in two steps; Ishihara plates, a Lanthony 15-hue desaturated panel and Standard Pseudoisochromatic Plates Part 2 were used to examine colour vision and Farnsworth-Munsell 100-hue test was performed to define acquired colour vision impairment. Moreover, the study subjects were between 20-60 years, a predominantly younger population. ...
PURPOSE:To assess impairment of colour vision in type 2 diabetics with no diabetic retinopathy and elucidate associated risk factors in a population-based cross-sectional study.
METHODS:This is part of Sankara Nethralaya Diabetic Retinopathy Epidemiology and Molecular-genetics Study (SN-DREAMS II) which was conducted between 2007-2010. FM 100 hue-test was performed in 253 subjects with no clinical evidence of diabetic retinopathy. All subjects underwent detailed ophthalmic evaluation including cataract grading using LOCS III and 45° 4-field stereoscopic fundus photography. Various ocular and systemic risk factors for impairment of colour vision (ICV) were assessed in subjects with diabetes but no retinopathy. P value of < 0.05 was considered statistically significant.
RESULTS:The mean age of the study sample was 57.08 ± 9.21 (range: 44-86 years). Gender adjusted prevalence of ICV among subjects with diabetes with no retinopathy was 39.5% (CI: 33.5-45.5). The mean total error score in the study sample was 197.77 ± 100 (range: 19-583). The risk factors for ICV in the study were women OR: 1.79 (1.00-3.18), increased resting heart rate OR: 1.04 (1.01-1.07) and increased intraocular pressure OR: 1.12 (1.00-1.24). Significant protective factor was serum high-density lipoprotein OR: 0.96 (0.93-0.99).
CONCLUSIONS:Acquired ICV is an early indicator of neurodegenerative changes in the retina. ICV found in diabetic subjects without retinopathy may be of non-vascular etiology.
... been described previously. [8][9][10] In brief, this study was a survey of the prevalence of ACVI among male officials aged 20-60 years who were on active duty in the Japanese Self Defense Force, Okubo Garrison, Kyoto, Japan. All subjects underwent annual health examinations between April 2005 and March 2006 at the Okubo Garrison. ...
... The goodness-of-fit of these models were tested using the Hosmer-Lemeshow test. In accordance with our previous reports, 8,9 the impacts of interaction between BP and LDL cholesterol and between BP and HbA1c on ACVI were also analyzed. Moreover, we performed sensitivity analysis on ACVI 15-hue patients, excluding subjects with diabetes, cataract, and glaucoma. ...
... Deterioration of color discrimination ability has long been recognized as an impairment that can precede the onset of clinically detectable neurological changes. [8][9][10][11] Previous studies have reported that Alzheimer's disease patients make significantly more errors in various color vision tests than normal control subjects. 35,36 Thus, ACVI due to middle-age hypertension may be linked to early subclinical neurological symptoms in lateonset neurodegenerative diseases such as cognitive impairment and Alzheimer's disease. ...
Background:
We sought to investigate the association between blood pressure levels and prevalence of acquired color vision impairment in middle-aged Japanese men.
Methods:
Participants underwent color vision testing, ophthalmological examination, standardized interview, physical record examination, and venous blood examination. Cardiovascular disease risk factors were determined based on blood and physical examination results and the interview. Logistic regression analysis was performed after adjusting for body mass index, systemic dyslipidemia, diabetes, cataract, glaucoma, smoking status, and drinking status.
Results:
Of 1,042 men, 872 were eligible for the study, 130 failed the Lanthony 15-hue desaturated panel (D-15 DS) diagnosed as acquired color vision impairment 15-hue, and 31 failed the Farnsworth-Munsell 100-hue test diagnosed as acquired color vision impairment 100-hue. Diastolic blood pressure was significantly correlated with both acquired color vision impairment in 100-hue patients (adjusted odds ratio (OR) for 10-mm Hg increases = 1.42; 95% confidence interval (CI) = 1.00-2.02) and acquired color vision impairment in 15-hue patients (adjusted OR for 10-mm Hg increases = 1.25; 95% CI = 1.04-1.51). The multiple-adjusted ORs for acquired color vision impairment 100-hue patients and acquired color vision impairment 15-hue patients were 7.13 (95% CI = 1.72-27.88) and 4.37 (95% CI = 1.69-11.03), respectively, for the highest blood pressure category (systolic blood pressure ≥ 160 and diastolic blood pressure ≥ 100 mm Hg) compared with those for the lowest blood pressure category (systolic blood pressure <120 and diastolic blood pressure <80 mm Hg). Tests for trends were significant (P < 0.05) in both analyses.
Conclusions:
Hypertension in middle-aged men may negatively modify vision-associated neuronal function.
... In the lens, sugar is found as polysaccharides. Meyer et al [2] showed that there are at least three different polysaccharides in the cornea stroma -keratin sulfate, chondroitin-4-sulfate, and chondroitin, and may play a role in cornea healing. ...
... Acquired dyschromatopsia has been reported to be common in people living with type 2 diabetes. The Okubo colour study, conducted among type diabetic patients showed that there is an-increased-adjusted-odds (5.89) for the development of colour vision impairment by type 2 diabetic compared with their agematched normal glycaemic peers [2]. Some studies have reported an increase in the incidence of acquired, non-sex-linked blue-yellow colour vision deficit in diabetic patients. ...
Sugar forms an integral part of the human body, and contributes to normal body function. However, sugar in high quantities can be detrimental to the body especially to the eye. In the normal concentration, sugar in the form of glucose is found in the aqueous humour, and tears, and serves to provide nourishment to the avascular cornea, and lens respectively. Sugar at this stage may also be used to determine the post mortem interval of a cadaver. However, when in excess as may be seen in patients with diabetes, sugar can cause oxidative stress to the cornea, lens, and retina resulting in cornea oedema, cataract, retinal aneurysm which can contribute significantly to the prevalence of low vision, and vision impairment.
... Exclusion criteria included previous ocular surgery or laser treatment, a postoperative CDVA worse than 20/25, previous or current use of medications known to cause colour-vision deficiency, failure to pass a colour-screening test (Ishihara plate test), intraoperative or postoperative complications and detection of macular disease in fundus examination at preoperative phase or postoperative phase. To exclude known impacts on colour vision [23], subjects with diabetes or subjects with impaired fasting glucose were excluded from the study. A control group was formed using elderly volunteers, who came to our hospital for presbyopic prescriptions. ...
... This test can be used to assess colour vision based on a total error score or the deterioration of colour perception to special hues or along single colour axes based on partial error score. The FM 100-hue test is a simple and relatively sensitive test and has been widely used in examining the effects of achromatopsia [28], optic neuropathy [29,30], diabetic retinopathy [23,31] and IOL on colour perception [32]. In the present study, colour discrimination was measured using the FM 100-hue test. ...
Background:
Cataract patients were always excluded from studies on ageing of colour vision; thus, effect of age-related cataracts on deterioration of colour perception has not been analysed. In present study, impacts of age-related cataracts on colour discrimination, postoperative recovery and related spectra were investigated.
Methods:
In this cohort study, thirty age-related cataract patients scheduled for binocular surgery and 30 elderly volunteers were enrolled. Colour discrimination under photopic (1000 lx) and mesopic (40 lx) conditions was evaluated with Farnsworth-Munsell 100-hue test. The total error score (TES) and partial error score (PES) were calculated.
Results:
Preoperatively, the TES in the patient group was 129.7 ± 59.5 at 1000 lx and 194.6 ± 74.5 at 40 lx, exhibiting worse discrimination than the volunteer group (TES1000lux = 71.5 ± 37.5 and TES40lux = 113.1 ± 38.8, p ≤ 0.001). Inferior perception were detected in the yellow to green-yellow (Y-GY), green-yellow to green (GY-G), green to blue-green (G-BG) and blue-green to blue (BG-B) colour bands (p ≤ 0.003), corresponding to the 470 nm-580 nm range of the visible light spectrum. Under mesopic conditions, the impact expanded to all colour bands except for yellow-red to yellow (YR-Y). Postoperatively, the TES in the patient group were 80.4 ± 62.4 at 1000 lx and 112.0 ± 85.2 at 40 lx, which were lower than those of the preoperative phase (p ≤ 0.001) but similar to those of the volunteer group (p ≥ 0.505). Postoperative improvement occurred in the Y-GY, GY-G and G-BG colour bands (490 nm to 580 nm) at 1000 lx (p ≤ 0.001) and shifted to the Y-GY, GY-G, G-BG and BG-B colour bands (470 nm to 580 nm) at 40 lx (p ≤ 0.001). Deterioration of hue perception for decrement of illumination was detected in the red to yellow-red (R-YR), Y-GY, G-BG, BG-B, blue to purple-blue (B-PB) and red-purple to red (RP-R) colour bands (450 nm to 500 nm) in the volunteer group (p ≤ 0.002) and the R-YR, G-BG, BG-B, B-PB, PB-P and red-purple to red (RP-R) colour bands (from the short-wavelength end to 500 nm) in the patient group preoperatively (p ≤ 0.001).
Conclusions:
Phacoemulsification could effectively rebuild colour perception in patients with age-related cataract. The postoperative benefits were most significant in colour bands corresponding with spectrum from 470 nm to 580 nm.
... Color vision impairment in diabetic subjects preceding clinical retinopathy has been established in several population-based cross-sectional studies. 24,67,74 Using the Farnsworth-Munsell 100-hue test on 872 diabetics with no DR, 37 participants were determined to have acquired color deficiency, 67 primarily tritanomaly. 74 Patients who were female, had increased intraocular pressure, were older, and had had diabetes for a longer period were more likely to be affected. ...
... Color vision impairment in diabetic subjects preceding clinical retinopathy has been established in several population-based cross-sectional studies. 24,67,74 Using the Farnsworth-Munsell 100-hue test on 872 diabetics with no DR, 37 participants were determined to have acquired color deficiency, 67 primarily tritanomaly. 74 Patients who were female, had increased intraocular pressure, were older, and had had diabetes for a longer period were more likely to be affected. ...
Diabetic retinopathy (DR) is a primary cause of visual impairment worldwide. Diabetes mellitus may be associated with ophthalmoscopically nonvisible neurovascular damage that progresses before the first clinical signs of DR appear. Reduction of the inner neuroretinal layer thickness on macular optical coherence tomography (OCT), reduced contrast sensitivity primarily at low spatial frequencies, abnormal results in color vision and microperimetry tests, and a prolonged implicit time recorded by multifocal electroretinography have been proposed for detection of early functional and nonvisible structural neuroretinal changes. Vascular abnormalities such as changes in the retinal vessels caliber, architectural indices, and blood flow have been investigated to evaluate the early stages of DR. The results of OCT angiography, retinal vessel oxygen saturation patterns, and elevated levels of circulating blood markers and cytokines have been suggested as early signs of DR. Light-based molecular imaging in rodents has been developed to demonstrate changes in protein expressions in the retinal microvessels as diagnostic biomarkers. Future clinical studies will examine the safety and efficacy of this approach in humans. We summarize all studies related to subclinical DR biomarkers.
... Acquired colour vision disorders are considered to be an early and sensitive indicator of various neurodegenerative and neurotoxic diseases. They are often found in patients with diabetes, both complicated and uncomplicated by retinopathy [5,[16][17][18]. The results of studies available in the world literature suggest that prediabetes may be a risk factor of both colour vision disturbances and impaired contrast sensitivity; although, the results of previous studies are not clear [18,19]. ...
... They are often found in patients with diabetes, both complicated and uncomplicated by retinopathy [5,[16][17][18]. The results of studies available in the world literature suggest that prediabetes may be a risk factor of both colour vision disturbances and impaired contrast sensitivity; although, the results of previous studies are not clear [18,19]. These changes are early visual dysfunction that may be present before the onset of other symptoms of retinal damage and indicate the initial stage of the disease. ...
Background. Prediabetes is the major risk factor for type 2 diabetes, but the prediabetic state itself is also associated with classical macrovascular and microvascular complications. Studies indicate that other ocular abnormalities can develop during the stage of prediabetes; however, data on the occurrence of ocular changes are limited. The aim of our study was to evaluate ocular changes in prediabetic individuals. Material and methods. Sixty subjects (40 women, 20 men) aged 37-78, with impaired fasting glucose and/or impaired glucose tolerance, were enrolled in the study and compared with 30 volunteers (20 women, 10 men) without prediabetes, aged 39-75. Both groups of patients underwent a complete physical examination, biochemical tests and ophthalmic examination: visual acuity testing, colour vision and letter contrast sensitivity tests, anterior and posterior segment evaluation, intraocular pressure measurement, fundus photographs and optical coherence tomography. Prediabetic patients underwent examinations twice: on the 1st visit and on the 2nd visit after 9-month period. Results. Ophthalmic examination revealed in prediabetic individuals as compared to healthy controls increased prevalence of cataract (31.67% vs. 6.67%; p < 0.05), corneal surface disorders (21.67% vs. 3.33%; p < 0.05), posterior vitreous detachments (76.67% vs. 55%; p < 0.05), arterial narrowing (81.67% vs. 63.33%; p < 0.05) and hypertension angiopathy (70% vs. 36.67%; p < 0.05). There were also differences between prediabetic and control groups in prevalence rate of retinopathy (8.33% vs. 3.33%; NS) and acquired colour vision impairment (8.33% vs. 0%, NS). When compared visit 1 to visit 2, statistically significant differences were observed in fasting plasma glucose level (106.9 vs. 104.1 mg/dL; p < 0.05) and HbA1c (5.80% vs. 5.99%; p < 0.05). There were no statistically significant differences in ocular changes; however, increased prevalence of retinopathy signs was noted during the examination after 9-month period (8.33% vs. 12.73%; NS). Conclusion. Prediabetic subjects present increased prevalence of ocular disorders as compared to healthy population. Results of this study indicate that prediabetic state is the independent risk factor of these complications; although, many patients with prediabetes have other features of metabolic syndrome. The regular ophthalmic monitoring seems to be essential at the stage of prediabetes in order to detect ocular abnormalities and identify individuals at risk of other diabetic complications.
... Amongst people with T2DM without diabetic retinopathy, the Okubo Color Study Report revealed that their adjusted odds ratio (AOR) for impaired color vision (ICV) was 5.89 compared with individuals with normal glucose levels [1]. It also reported the prevalence of ICV was higher among people with elevated LDL-Cholesterol (LDL-C) levels. ...
... With increasing prevalence of T2DM, the number of people with ICV is expected to expand significantly, raising their risks of poorer quality of life and reduced social functioning. In view of findings from earlier studies [1][2][3][4][5], we postulated that the local patients with diabetes mellitus were at higher risks of ICV in relation to their age, duration of disease, glycaemia and dyslipidemia control. Identifying these risk factors open up a window for intervention to mitigate the development of ICV. ...
Background
Patients with type 2 diabetes mellitus (T2DM) may develop color vision impairment. This study aimed to determine the prevalence and factors associated with impaired color vision in patients with T2DM but without diabetic retinopathy.
Methods
Enrolment criteria included multi-ethnic Asian participants, age 21 to 80 years, with known T2DM for a minimum of 2 years. Their diagnoses were affirmed from oral glucose tolerance test results and they were screened for impaired color vision using the Farnsworth D-15 instrument. Demographic characteristics were described and clinical data for the preceding 2 years were analyzed using logistic regression.
Results
Twenty-two percent of 849 eligible participants had impaired color vision with higher involvement of the right eye. Impaired blue-yellow color-vision(Tritanomaly) was the commonest impaired color vision. Participants with impaired color vision were significantly associated with age and lower education; longer duration of T2DM (median 6 years vs 4 years); higher HbA1c level and HDL-Cholesterol in 2nd year; lower mean total cholesterol, mean LDL-Cholesterol and mean triglyceride in 2nd year. They also have poorer vision beyond 6/12 in the affected eye. Logistic regression showed that impaired color vision was associated with older patients (OR=1.04), increased duration of T2DM (OR=1.07); prescription of Tolbutamide (OR=3.79) and lower mean systolic blood pressure (OR=0.98).
Conclusion
Almost one in four participants with T2DM had impaired color vision, largely with tritanomaly. Color vision screening may be considered for participants who develop T2DM for 6 years or longer, but this requires further cost-effectiveness evaluation.
... Acquired color vision impairment may occur in diabetes with a prevalence as high as 30% to 80%, 12 and diabetic patients even without vascular retinopathy have an increased risk for color vision impairment. 13 Both redgreen and yellow-blue chromatic sensitivities are reported to be affected, 7,14,15 showing a strong correlation with care of the disease. 16 Also, according to a recent study on Long Evans rats, visual deficits such as impaired visual acuity and contrast sensitivity, as well as scotopic and photopic electroretinogram abnormalities, are already present as early as 4 weeks after streptozotocin (STZ) induction of diabetes. ...
... We lack evidence on whether the functions of photoreceptors are altered or not in this experimental setup. However, it seems reasonable to assume that the degeneration of the outer segments we observed may be functional and may contribute to changes of color vision, dark adaptometry, and contrast sensitivity reported in diabetic patients 7,[12][13][14][15][16] and also in rats. 17,61 The remarkable damage of rods shown here may also go clinically unnoticed for a long time in human patients, where daylight vision depends mainly on the integrity of the cone mosaic. ...
Purpose:
Neurodegeneration as an early event of diabetic retinopathy preceding clinically detectable vascular alterations is a widely proven issue today. While there is evidence for the impairment of color vision and contrast sensitivity in early diabetes, suggesting deteriorated photoreceptor function, the underlying neuropathology of these functional alterations is still unknown. The aim of the present study was to investigate the effects of early diabetes on the outer retinal cells.
Methods:
The retinal pigment epithelium, photopigment expression, and density and morphology of photoreceptors were studied using immunocytochemistry in streptozotocin-induced diabetes in two rat strains. The fine structure of photoreceptors and pigment epithelium was also investigated with transmission electron microscopy.
Results:
Here we found that retinal thickness was unchanged in diabetic animals and that no significant increase in the number of apoptotic cells was present. Although the density of cones expressing middle (M)- and shortwave (S)-sensitive opsins was similar in diabetic and control retinas, we detected remarkable morphologic signs of degeneration in the outer segments of diabetic rods, most M-cones, and some S-cones. A decrease in thickness and RPE65 protein immunoreactivity of the pigment epithelium were evident. Furthermore, an increased number of dual cones, coexpressing both M- and S-opsins, was detected at the peripheral retina of diabetic rats.
Conclusions:
Degenerative changes of photoreceptors and pigment epithelium shown here prior to apoptotic loss of photoreceptors may contribute to functional alterations reported in diabetic human patients and different animal models, thus may serve as a potential model for testing the efficacy of neuroprotective agents in diabetes.
... More than 7 million Japanese patients have a definitive diagnosis of DM and the estimated number of patients with latent diabetes exceeds 20 million. Before the onset of the discrete clinical signs of diabetic retinopathy (DR), patients with DM have diabetic neuropathy in the retinal nerve fiber layer (RNFL) and such functional abnormalities as loss of oscillation potential on electroretinography [39,40], abnormal color sensation [41,42], contrast sensitivity [43], dark adaptation [44], and a thin, atrophic RNFL [45][46][47][48][49][50][51][52][53][54][55][56][57]. Another important clinical feature is impaired aqueous outflow facility and ocular hypertension [58][59][60][61]. ...
... With improved knowledge and treatment modalities among doctors and improved knowledge about DR among the general population, the risks of vascular problems have been decreasing in developed countries, the prevalence of diabetic neuropathy, a silent complication of DM, is, however, not decreasing. Previously known diabetic retinal nerve dysfunctions include loss of the electroretinographic oscillatory potential [39,42], abnormal color sensation [41,42], impaired contrast sensitivity [43], abnormal visually evoked cortical response [132], and dark adaptation [44]. As an organic tissue change, RNFL defects and emaciation of the RNFL appear before the signs of DR become obvious [51][52][53][54][55][56][57]. ...
Myopic deformation of the eye and metabolic alterations of the nerve tissue of patients with diabetes may modify glaucomatous optic neuropathy (GON). Blockage of axonal transport of neurotrophic factors (NTFs) is the event crucial to understanding the factors that affect GON. The primary, but not sole, blockage site is at the lamina cribrosa (LC). Other than this primary site of damage at the LC, 7 other factors may explain atypical nerve fiber layer (NFL) defects and the vulnerability of the nerve fibers in eyes with high myopia and glaucoma: a second point of blockage at the edge of the posterior scleral foramen; ectatic strain on the NFL; ectasia and distortion of the LC; association of a hypoplastic optic disc; thin and weak collagen fibers; peripapillary chorioretinal atrophy; and myopic neuropathy. Among diabetic patients, diabetic neuropathy in the retinal NFL is present initially, and increased resistance to aqueous outflow leads to ocular hypertension. Superimposition of GON on diabetic neuropathy and ocular hypertension in patients with diabetes may enhance their susceptibility to nerve damage. Results of a meta-analysis study suggested a positive association between diabetes mellitus and glaucoma whereas other reports suggested that leakage of vascular endothelial growth factor, a survival mechanism of ischemic neural tissue, and enhanced stiffness of the LC as a result of diabetic glycation may protect neurons from apoptosis. Thus, modification of GON as a result of diabetes remains controversial.
... Several studies have indicated a dramatically increased prevalence of color vision impairment in diabetic patients without diabetic retinopathy 11,29 . Some studies have found diffuse loss in color perception 11,30 , and some have shown early dominant loss in blue-yellow (tritan) discrimination 31 . ...
Effects of type 2 diabetes on achromatic and chromatic contrast sensitivity (CS) are still controversial. In this study, we aimed to investigate CS in patients without diabetic retinopathy (no-DR) and in those with non-proliferative DR (NPDR) and proliferative DR (PDR) using psychophysical methods with transient and sustained achromatic stimuli and color patches. Achromatic CS was measured with the pulsed pedestal (PP) paradigm (7, 12, and 19 cd/m²) and pedestal-△-pedestal (P-△-P) paradigm (11.4, 18, and 28.5 cd/m²). A chromatic discrimination paradigm that assesses protan, deutan, and tritan color vision was adopted. Forty-two patients (no-DR n = 24, NPDR n = 12, PDR = 6; male n = 22, mean age = 58.1 y/o) and 38 controls (male n = 18, mean age = 53.4 y/o) participated. In patients, mean thresholds were higher than in controls and linear trends were significant in most conditions. For the PP paradigm, differences were significant in the PDR and NPDR groups in the 7 and 12 cd/m² condition. For the P-△-P paradigm, differences were only significant in the PDR group in the 11 cd/m² condition. Chromatic contrast loss was significant in the PDR group along the protan, deutan and tritan axes. The results suggest independent involvements of achromatic and chromatic CS in diabetic patients.
... Res. 12,[34][35][36] ), pre-and post-surgery cataract 37 , and systemic diseases, such as diabetic retinopathy [38][39][40] or hypothyroidism 41,42 . ...
Post-COVID-19, recorded were various ophthalmological symptoms and visual impairment. We hypothesised that colour vision may be affected too. We assessed colour discrimination using the Farnsworth-Munsell 100 Hue test (FM-100) in individuals, who have had COVID-19 (N=77; 18–68 years). Total error score (TES) indicated superior colour discrimination in 34 observers. The Vingrys–King-Smith C-index (severity) exceeded the normal cutoff measure in 44 observers. In participants (N=35) with average TES, the Vingrys–King-Smith analysis revealed subtle colour deficiencies – either a mild tritan defect (‘blue’ or blue-yellow) or moderate defect with a diffuse error pattern. A minor sub-sample (N=6) manifested poor discrimination or colour vision loss (N=2), with a tritan or diffuse error pattern. √TES negatively correlated with the recovery time lapse. Partial error scores (√PES) indicated prevailing B–Y errors, regardless of the elapsed post-illness period. Overall, the results indicate that about half of those who have recovered from COVID-19 reveal predominantly mild Type III acquired colour discrimination loss, characteristic of retinal disorders and vascular disease. Conceivably, coronavirus infection caused hypoperfusion (reduced vascular supply) at the retinal and/or post-retinal stages of the visual system having affected neural mechanisms of colour discrimination. The mild impairment appears to be reversible with a favourite prognosis.
... It is reasonable to consider, therefore, whether there is a phenomena upon which such a technology could be based? Diabetes is characterized by changes of colour perception [39][40][41][42][43] and brain function. Many researchers have sought unsuccessfully to adopt these phenomena, and develop a diabetes diagnostic test, perhaps for reasons outlined in this paper. ...
... Neural dysfunction and degeneration occur early in the diabetic retina. Distorted color vision in patients with early diabetes was previously reported [14][15][16], and dysfunction of the neural retina can be detected in diabetic patients by ERG before any vascular pathologies are detected [17][18][19]. Diabetic patients without DR vascular complications usually have lower ERG amplitudes and longer implicit times than healthy subjects [20]. ...
Diabetic retinopathy (DR) is a chronic disease associated with diabetes mellitus and is a leading cause of visual impairment among the working population in the US. Clinically, DR has been diagnosed and treated as a vascular complication, but it adversely impacts both neural retina and retinal vasculature. Degeneration of retinal neurons and microvasculature manifests in the diabetic retina and early stages of DR. Retinal photoreceptors undergo apoptosis shortly after the onset of diabetes, which contributes to the retinal dysfunction and microvascular complications leading to vision impairment. Chronic inflammation is a hallmark of diabetes and a contributor to cell apoptosis, and retinal photoreceptors are a major source of intraocular inflammation that contributes to vascular abnormalities in diabetes. As the levels of microRNAs (miRs) are changed in the plasma and vitreous of diabetic patients, miRs have been suggested as biomarkers to determine the progression of diabetic ocular diseases, including DR. However, few miRs have been thoroughly investigated as contributors to the pathogenesis of DR. Among these miRs, miR-150 is downregulated in diabetic patients and is an endogenous suppressor of inflammation, apoptosis, and pathological angiogenesis. In this review, how miR-150 and its downstream targets contribute to diabetes-associated retinal degeneration and pathological angiogenesis in DR are discussed. Currently, there is no effective treatment to stop or reverse diabetes-caused neural and vascular degeneration in the retina. Understanding the molecular mechanism of the pathogenesis of DR may shed light for the future development of more effective treatments for DR and other diabetes-associated ocular diseases.
... including neural apoptosis, loss and thinned retinal ganglion cell (RGC) and retinal nerve fiber layer (RNFL) [4][5][6]. Moreover, reduced contrast sensitivity, abnormal color vision, and a prolonged implicit time recorded by electroretinogram (ERG) have been suggested to indicate early functional neural changes in diabetic patients [7][8][9]. Therefore, although the pathogenesis of DR is thought to be mostly vascular, retinal neurodegeneration is also considered to be an important part of the pathogenesis of DR. ...
PurposeTo investigate whether abnormal retinal microcirculation correlates with retinal neuronal changes in untreated diabetic eyes without macular edema.Methods
This study enrolled 29 diabetic patients without diabetic retinopathy (DR), 18 patients with mild non-proliferative diabetic retinopathy (NPDR), 15 patients with moderate NPDR, 14 patients with severe NPDR, 27 patients with proliferative diabetic retinopathy (PDR), and 25 healthy control subjects. Pattern electroretinography (PERG) and optical coherence tomography angiography (OCT-A) tests were performed.ResultsDifferences in the mean values for the area, acircularity index, and perimeter of foveal avascular zone were statistically significant between the healthy control group and the diabetic patients (P < 0.05 for all). P50 and N95 amplitudes were statistically significantly lower in the PDR group compared to diabetic patients without DR, control, and moderate NPDR groups (P < 0.05 for all). The whole retina vessel densities in superficial and deep capillary plexus were lower in the PDR group compared to the diabetic patients without DR and control group (P < 0.05 for all). There were statistically significant positive correlations between the amplitudes of the P50 and N95 waves with the vessel densities.Conclusion
The existence of significant correlations between PERG and OCT-A parameters in diabetic patients has shown that vascular and neuronal changes in the macula affect each other in diabetic patients.
... Results of this study showed higher association of blue color defect in type 2 diabetics. [18]. ...
Purpose: To determine blue color vision defect in type II diabetics and to compare it with the duration of diabetes.
Methodology: Cross-sectional study was conducted at Abdullah Memorial Hospital on 120 eyes of type-II diabetics in duration of 5 months from August 2018 to January 2019. Sample was collected through non-probability convenient sampling technique. Subjects with minimum 6/12 vision with or without correction were included and age group 35 to 65 years of both genders. Eye of diabetic type 2 without any sign of retinopathy were included. Any individual with congenital color vision defect, retinal, optic nerve or choroidal lesion was excluded. Ishihara plates were used initially to screen out congenital defects. Later, D-15 test was performed for evaluation of color vision for acquired changes due to diabetes. Data was entered using latest version 20 of SPSS and chi-square was used to assess association between color anomaly and type-II diabetes.
Results: In a sample of 120 eyes, 60% of population is Trichromate, 30% of population is tritanomalous, 1.7% population is deuteranomalous and 8.3% population is both deuteranomalous and tritanamolous. Comparison of blue color sensitivity in diabetic patients before onset of retinopathy was evaluated using Chi square with p value .000 at the level of 5% of confidence interval that shows highly significant results. Results conclude that there is strong association between blue color vision defects in diabetics. This defect was observed more with increase in duration of diabetes.
Conclusion: Study concluded that diabetic type 2 patients have impaired color vision specifically triatanomaly. Color vision must be evaluated and assessed in every diabetic patient and should be made an early assessment and screening tool. Timely assessment of color vision may detect tritanomaly earlier in type 3 diabetics.
... Capillary non-perfusion, on the other hand, did not contribute independently to the risk prediction model [120]. Reported prevalence [121,122] of impaired color vision in subjects with DM but no retinopathy has varied from 3.5% [123] to as high as 39.5% [124]. Color vision impairment is known to worsen with increasing retinopathy severity [121] and with macular edema [125]. ...
Purpose of Review
Diabetic retinopathy (DR) is a major cause of visual impairment and blindness throughout the world. Microvascular changes have long been regarded central to disease pathogenesis. In recent years, however, retinal neurodegeneration is increasingly being hypothesized to occur prior to the vascular changes classically associated with DR and contribute to disease pathogenesis.
Recent Findings
There is growing structural and functional evidence from human and animal studies that suggests retinal neurodegeneration to be an early component of DR. Identification of new therapeutic targets is an ongoing area of research with several different molecules undergoing testing in animal models for their neuroprotective properties and for possible use in humans.
Summary
Retinal neurodegeneration may play a central role in DR pathogenesis. As new therapies are developed, it will be important to develop criteria for clinically defining retinal neurodegeneration. A standardization of the methods for monitoring neurodegeneration along with more sensitive means of detecting preclinical damage is also needed.
... In our present study, we also found similar signs of degeneration in the rod pathway, like rod outer segment degeneration, rod arrestin mislocalization and changes in the morphology and number of AII amacrine cells that -in theory -may all contribute to the alteration of scotopic ERG reported in diabetic patients 59,60 and in animal models 45,60 . Colour vision defects 61,62 and photopic ERG changes 63 can be related to changes in cone opsin expression pattern and M-cone outer segment degeneration. Changes in oscillatory potentials 45 may be the ERG manifestations of amacrine cell dysfunctions -from which AII amacrine cells, dopaminergic amacrine cells and PKC-α positive amacrine cells certainly show alterations in ZDF rats, as well as STZ induced diabetic rats. ...
In diabetes, retinal dysfunctions exist prior to clinically detectable vasculopathy, however the pathology behind these functional deficits is still not fully established. Previously, our group published a detailed study on the retinal histopathology of type 1 diabetic (T1D) rat model, where specific alterations were detected. Although the majority of human diabetic patients have type 2 diabetes (T2D), similar studies on T2D models are practically absent. To fill this gap, we examined Zucker Diabetic Fatty (ZDF) rats - a model for T2D - by immunohistochemistry at the age of 32 weeks. Glial reactivity was observed in all diabetic specimens, accompanied by an increase in the number of microglia cells. Prominent outer segment degeneration was detectable with changes in cone opsin expression pattern, without a decrease in the number of labelled elements. The immunoreactivity of AII amacrine cells was markedly decreased and changes were detectable in the number and staining of some other amacrine cell subtypes, while most other cells examined did not show any major alterations. Overall, the retinal histology of ZDF rats shows a surprising similarity to T1D rats indicating that despite the different evolution of the disease, the neuroretinal cells affected are the same in both subtypes of diabetes.
... Although ffERG does not capture ganglion cell function, it is interesting to note that retinal ganglion cells primarily synapse with bipolar cells within the cone system. Retinal ganglion cells have been identified as the retinal cells most affected by ER stress due to diabetes (Yang et al. 2013) and glaucoma (Zode et al. 2014), and color vision defects have been documented in both acquired disease states (Lin and Yang 2010;Shoji et al. 2011). The unique retinal staining pattern of ATF6 with strongest localization to ganglion cells might imply that the ATF6 pathway within the retinal ganglion cells plays a major role in color vision. ...
Achromatopsia (ACHM) is an early-onset retinal dystrophy characterized by photophobia, nystagmus, color blindness and severely reduced visual acuity. Currently mutations in five genes CNGA3, CNGB3, GNAT2, PDE6C and PDE6H have been implicated in ACHM. We performed homozygosity mapping and linkage analysis in a consanguineous Pakistani ACHM family and mapped the locus to a 15.12-Mb region on chromosome 1q23.1–q24.3 with a maximum LOD score of 3.6. A DNA sample from an affected family member underwent exome sequencing. Within the ATF6 gene, a single-base insertion variant c.355_356dupG (p.Glu119Glyfs*8) was identified, which completely segregates with the ACHM phenotype within the family. The frameshift variant was absent in public variant databases, in 130 exomes from unrelated Pakistani individuals, and in 235 ethnically matched controls. The variant is predicted to result in a truncated protein that lacks the DNA binding and transmembrane domains and therefore affects the function of ATF6 as a transcription factor that initiates the unfolded protein response during endoplasmic reticulum (ER) stress. Immunolabeling with anti-ATF6 antibodies showed localization throughout the mouse neuronal retina, including retinal pigment epithelium, photoreceptor cells, inner nuclear layer, inner and outer plexiform layers, with a more prominent signal in retinal ganglion cells. In contrast to cytoplasmic expression of wild-type protein, in heterologous cells ATF6 protein with the p.Glu119Glyfs*8 variant is mainly confined to the nucleus. Our results imply that response to ER stress as mediated by the ATF6 pathway is essential for color vision in humans.
Electronic supplementary material
The online version of this article (doi:10.1007/s00439-015-1571-4) contains supplementary material, which is available to authorized users.
Background:
Home foot temperature monitoring (HFTM) is recommended for those at moderate to high ulcer risk. Where a >2.2°c difference in temperature between feet (hotspot) is detected, it is suggested that individuals (1) notify a healthcare professional (HCP); and (2) reduce daily steps by 50%. We assess adherence to this and HFTM upon detecting a recurrent hotspot.
Methods:
PubMed and Google Scholar were searched to 9 June 2023 for English-language peer-reviewed HFTM studies which reported adherence to HFTM, daily step reduction or HCP hotspot notification. The search returned 1,030 results excluding duplicates of which 28 were shortlisted and 11 included.
Results:
Typical adherence among HFTM study participants for >3 days per week was 61-93% or >80% of study duration was 55.6-83.1%. Monitoring foot temperatures >50% of study duration was associated with decreased ulcer risk (Odds Ratio: 0.50, p<0.001) in one study (n=173), but no additional risk reduction was found for >80% adherence. Voluntary drop-out was 5.2% (Smart mats); 8.1% (sock sensor) and 4.8%-35.8% (infrared thermometers). Only 16.9-52.5% of participants notified an HCP upon hotspot detection. Objective evidence of adherence to 50% reduction in daily steps upon hotspot detection was limited to one study where average step reduction was a pedometer-measured 51.2%.
Conclusions:
Ulcer risk reduction through HFTM is poorly understood given only half of participants notify HCPs of recurrent hotspots and the number reducing daily steps is largely unknown. HFTM adherence and drop-out are variable and more research needed to determine factors affecting adherence and those likely to adhere.
Introduction: The visible spectrum (about 400 to 700 nm) with a mosaic of three classes of photoreceptors compose the human visual system. They are sensitive to different wavelength ranges with overlapping. The receivers have high sensitivities at short wavelengths (~440 nm), medium (~535 nm), or longer (~565 nm), which are S, M, and L cones, respectively. The study aimed to determine blue color vision defects in diabetes mellitus. Methods: A cross-sectional study was done at an ophthalmology clinic on 200 eyes (right and left) of patients with DM for a period of 5 one years (2021). Ishihara plates were used initially for screening. The D-15 test was performed for the evaluation of color vision. Results: The mean age of the sample was 45.66±15.65 years. The most frequent disorder visualized was tritanomaly in 63%, followed by trichromate in 27%, and the least disorder was deuteranomaly in 2%. In addition, mixed disorder is seen in 8% of cases. In relation to laterality, right eye tritanomaly was found in 34%, while the left eye was recorded in 29%. The right eye trichromate was observed in 12%, whereas the left eye was reported in 15%. The left eye deuteranomaly was reported more than the right (1.5% vs. 0.5%). Conclusion: Color vision evaluation with good screening color vision test can be detected even before clinically visible diabetic retinopathy. Early detection was helpful in the prevention of vascular changes in the retina. All diabetic patients should be given proper awareness and health education regarding color vision deficiency. Timely assessment of color vision may detect tritanomaly earlier in diabetics.
Objective
In a world where digital media is deeply engrained into our everyday lives, there lies an opportunity to leverage interactions with technology for health and wellness. The Vision Performance Index (VPI) leverages natural human–technology interaction to evaluate visual function using visual, cognitive, and motor psychometric data over 5 domains: field of view, accuracy, multitracking, endurance, and detection. The purpose of this study was to describe a novel method of evaluating holistic visual function through video game-derived VPI score data in patients with specific ocular pathology.
Design
Prospective comparative analysis.
Participants
Patients with dry eye, glaucoma, cataract, diabetic retinopathy (DR), age-related macular degeneration, and healthy individuals.
Methods
The Vizzario Inc software development kit was integrated into 2 video game applications, Balloon Pop and Picture Perfect, which allowed for generation of VPI scores. Study participants were instructed to play rounds of each video game, from which a VPI score was compiled.
Main Outcome Measures
The primary outcome was VPI overall score in each comparison group. Vision Performance Index component, subcomponent scores, and psychophysical inputs were also compared.
Results
Vision Performance Index scores were generated from 93 patients with macular degeneration (n = 10), cataract (n = 10), DR (n = 15), dry eye (n = 15), glaucoma (n = 16), and no ocular disease (n = 27). The VPI overall score was not significantly different across comparison groups. The VPI subcomponent “reaction accuracy” score was significantly greater in DR patients (106 ± 13.2) versus controls (96.9 ± 11.5), P = 0.0220. The VPI subcomponent “color detection” score was significantly lower in patients with DR (96.8 ± 2.5; p=0.0217) and glaucoma (98.5 ± 6.3; P = 0.0093) compared with controls (101 ± 11). Psychophysical measures were statistically significantly different from controls: proportion correct (lower in DR, age-related macular degeneration), contrast errors (higher in cataract, DR), and saturation errors (higher in dry eye).
Conclusions
Vision Performance Index scores can be generated from interactions of an ocular disease population with video games. The VPI may offer utility in monitoring select ocular diseases through evaluation of subcomponent and psychophysical input scores; however, future larger-scale studies must evaluate the validity of this tool.
Financial Disclosure(s)
Proprietary or commercial disclosure may be found after the references.
Purpose:
To assess early retinal microvascular and functional changes in diabetic patients without clinical evidence of diabetic retinopathy with optical coherence tomography angiography and central visual analyzer.
Methods:
This was an observational case-control study of diabetic patients without diabetic retinopathy and nondiabetic controls. Patients underwent optical coherence tomography angiography imaging and visual acuity testing using the central visual analyzer. The foveal avascular zone area and the capillary density in the superficial and deep capillary plexuses were measured manually by a masked grader.
Results:
Sixty eyes from 35 diabetic patients were included in the study group, and 45 eyes from 31 nondiabetic patients were included in the control group. The foveal avascular zone area was not significantly different between the diabetic group and controls (both P > 0.05). The mean capillary density in the deep capillary plexus was significantly lower in diabetic eyes compared with control eyes (P = 0.04). The mean visual acuity in all central visual analyzer modules was significantly decreased in diabetic patients compared with controls (all P < 0.05).
Conclusion:
Optical coherence tomography angiography was able to detect retinal microvascular changes in the deep capillary plexus, and the central visual analyzer showed signs of decreased visual acuity under conditions simulating suboptimal contrast and glare in diabetic patients without diabetic retinopathy.
Background: Conventional studies showed that the primary pathological change of diabetic retinopathy (DR) is retinal microangiopathy. However, recent studies found that the disorder of visual function appears prior to retinal microangiopathy in diabetic patients. Thereby, this findings can not be explained by conventional view.
The retina is the association of the neurosensory tissue and the retinal pigment epithelium (RPE). Despite the presence of the blood retinal barrier, the retina is submitted to changes of the external milieu, including dietary modulation and environmental stresses. With advanced age, the exchanges of nutrients and elimination of cellular and metabolic wastes via the RPE become limited. Age-related Macular Degeneration (AMD) and Diabetic Retinopathy (DR) are the most prevalent retinal pathologies in Western adult populations before and after the age of 50 years, respectively. Geographic atrophy and neovascular AMD are advanced stages of age-related maculopathies. DR afflicts 60% of type 2 diabetic (T2D) patients in the first 15 years of the disease. Dietary factors interfere in the development of both AMD and T2D. Accounting the worldwide epidemics of T2D in the one hand, and the improvement of life expectancy in the other hand, medical care to the patients is expected to worsen the socioeconomic burden of both T2D and AMD. Metabolic syndrome (MetS) is one of the major risk factor for T2D. Lowering the development of MetS would potentially lessen the incidence of T2D, and its complications. The daily intake of omega 3 long chain polyunsaturated fatty acids (LC-PUFA) is now recommended by health agencies for the prevention of MetS. Meanwhile dietary omega 3 LC-PUFA are associated with reduced risk of AMD. The association between T2D, DR, and AMD remains controversial, although large-scale population-based studies have reported increased prevalence of AMD in patients with diabetes or DR. Our objectives were first to evaluate whether MetS would represent a favorable environment for the development of neovascular complications in the retina, and second to test the efficacy of omega 3 LC-PUFA to reduce the consequences of MetS in the retina. For that purpose, a pro-diabetogenic high fructose diet was fed to rats to induce MetS and choroidal neovascularization was triggered by laser impacts in the eye fundus. We focused first on short term diet periods, and showed impairment on cone photoreceptor sensitivity after 8 days, as well as changes in gene expression in relation to crystallin sub-families. A long term - up to 6 months - fructose diet period triggered MetS as illustrated by body fat increase, hyperinsulinemia, hyperleptinemia and liver steatosis. Rats exhibited exacerbated laser-induced choroidal neovascularization after 1 and 3 months of feeding, that was associated with up-regulation of genes coding pro-angiogenic factors such as VEGF and leptin, as well as infiltration of macrophages and/or activation of retinal microglia. Electroretinographic data showed decreased sensitivity of rod photoreceptors and inner retinal cell functionality at 6 months of feeding. In a second time, the efficacy of dietary omega 3 LC-PUFA (EPA plus DHA) to reduce the consequences of MetS in the retina was tested. Our data showed that a high dose of EPA+DHA in rats did not improve MetS. Furthermore, side effects were generated as illustrated by localized atrophy in the retina submitted to the combination of laser-impacts, and normal light exposure. These works allowed us to suggest that MetS generated a favorable environment in the retina for the development of neovascular complications. Meanwhile, the sensitivity of cones and rods was impaired by MetS. Accounting the deleterious long term effects of omega 3 LC-PUFA in the retina, caution may be taken while recommending massive supplementation with omega 3 LC-PUFA in the context of MetS.
To elucidate changes in the neurosensory retina in the macular area, using spectral domain OCT and correlate with functional loss on fundus-related microperimetry, in patients with diabetes and no diabetic retinopathy compared with age-matched healthy volunteers.
This was a prospective study enrolling 39 patients in each group. All patients underwent comprehensive dilated eye examination. The foveal thickness and the photoreceptor layer thickness at the foveal centre were measured using spectral domain OCT, and the mean retinal sensitivity of central 20 degrees was measured using microperimetry.
The mean age of the patients with diabetes was 50.92+/-4.75 years, and of controls, 49.87+/-5.50 years. SD-OCT measured photoreceptor layer thickness (PLT) to be 61.62+/-4.48 microm in cases, and 68.79+/-7.84 microm in controls (P<0.0001); foveal thickness (FT) was 168.64+/-16.46 microm in cases and 177.74+/-14.58 microm in controls (P=0.012). The mean retinal sensitivity (MRS) of the central 20 degrees, measured on microperimetry was 15.74+/-3.74 db in cases and 17.70+/-1.5 db in controls (P<0.003). In cases compared with controls (aged under 50 years) statistically significant differences were noted in all the three outcome variables: FT, P=0.030; PLT, P=0.015; and MRS, P=0.020. The duration of diabetes influenced only the PLT (P=0.017). Statistical analysis was performed with Student's t-test and chi2 test.
Neuronal damage was observed in those eyes that did not have clinical evidence of diabetic retinopathy.
To better understand the reference values and adequate discrimination values of colour vision function with described quantitative systems for the Lanthony desaturated D-15 panel (D-15DS).
A total of 1042 Japanese male officials were interviewed and underwent testing using Ishihara pseudoisochromatic plates, standard pseudoisochromatic plates part 2, and the D-15DS. The Farnsworth-Munsell (F-M) 100-hue test and the criteria of Verriest et al were used as definitive tests. Outcomes of the D-15DS were calculated using Bowman's Colour Confusion Index (CCI). The study design included two criteria. In criterion A, subjects with current or past ocular disease and a best-corrected visual acuity less than 0.7 on a decimal visual acuity chart were excluded. In criterion B, among subjects who satisfied criterion A, those who had a congenital colour sense anomaly were excluded.
Overall, the 90th percentile (95th percentile) CCI values for criteria A and B in the worse eye were 1.70 (1.95) and 1.59 (1.73), respectively. In subjects satisfying criterion B, the area under the receiver operating characteristic curve was 0.951 (95% confidence interval, 0.931-0.971). The CCI discrimination values of 1.52 or 1.63 showed 90.3% sensitivity and 90% specificity, or 71.5% sensitivity and 95% specificity, respectively, for discriminating acquired colour vision impairment (ACVI).
We provided the 90th and 95th percentiles in a young to middle-aged healthy population. The CCI is in good agreement with the diagnosis of ACVI. Our results could be helpful for using D-15DS for screening purposes.
Color vision was assessed in 103 insulin-dependent diabetic patients using the Farnsworth-Münsell 100-Hue Test. All showed color vision impairment. Thirty-four had true dyschromatopsia while 22 suffered from tritanopia or other axial defects. We evaluated how accurately diabetic patients could monitor their own blood glucose by asking them to read a series of 30 precalibrated BM Test Glycemic Strips (Chemstrip, Boehringer, Mannheim, West Germany) without a meter. Patients with axial defects performed least well regardless of 100-Hue scores. Reading accuracy of patients with no axial defects was strongly correlated to 100-Hue scores, although patients having dyschromatopsia were consistently hesitant about their readings. Our results suggest that self-monitoring of blood glucose without a meter is indicated only after color vision has been examined by the 100-Hue Test. Self-monitoring should be voided with patients suffering from axial defects or having unsatisfactory 100-Hue scores.
In 102 insulin-dependent diabetic patients without retinopathy and with visual acuity 20/20, the Farnsworth-Munsell 100-Hue test was performed, and glycosylated hemoglobin (GlHb) levels were determined. In 70% of the patients, a dyschromatopsia in the yellow-blue axis (tritanopia) was found. No correlation existed between duration of diabetes and tritanopia. On the other hand, the degree of this visual defect was positively correlated with GlHb levels. Thus, dyschromatopsia might be associated with poor metabolic control. It is suggested that dyschromatopsia is a consequence of hypoxia at the neuroepithelial level. The high levels of GlHb could be a contributory cause of hypoxia by reduction of both oxygen release capacity and erythrocyte deformability.
To develop the Lens Opacities Classification System III (LOCS III) to overcome the limitations inherent in lens classification using LOCS II. These limitations include unequal intervals between standards, only one standard for color grading, use of integer grading, and wide 95% tolerance limits.
The LOCS III contains an expanded set of standards that were selected from the Longitudinal Study of Cataract slide library at the Center for Clinical Cataract Research, Boston, Mass. It consists of six slit-lamp images for grading nuclear color (NC) and nuclear opalescence (NO), five retroillumination images for grading cortical cataract (C), and five retroillumination images for grading posterior subcapsular (P) cataract. Cataract severity is graded on a decimal scale, and the standards have regularly spaced intervals on a decimal scale. The 95% tolerance limits are reduced from 2.0 for each class with LOCS II to 0.7 for nuclear opalescence, 0.7 for nuclear color, 0.5 for cortical cataract, and 1.0 for posterior subcapsular cataract with the LOCS III, with excellent interobserver agreement.
The LOCS III is an improved LOCS system for grading slit-lamp and retroillumination images of age-related cataract.
Contrast sensitivity testing, in common with color vision (another test of psychophysical function), demonstrates significant changes in diabetic subjects compared with nondiabetic controls, and there is some evidence for a relationship with grade of retinopathy. Changes in contrast sensitivity have been demonstrated in children and adults with diabetes of short duration, and some evidence exists for a correlation with poor glycemic control, although prospective studies are required to assess this relationship over a longer time period. Although both color vision and contrast sensitivity demonstrate similar patterns, studies that directly compare the two tests suggest that measurement of contrast sensitivity is the more sensitive and specific.
PURPOSE: To describe the causes of and risk factors for persistent severe visual loss occurring in the Early Treatment Diabetic Retinopathy Study (ETDRS).METHODS: The ETDRS was a randomized clinical trial investigating photocoagulation and aspirin in 3,711 persons with mild to severe nonproliferative or early proliferative diabetic retinopathy. Severe visual loss, defined as best-corrected visual acuity of less than 5/200 on at least two consecutive 4-month follow-up visits, developed in 257 eyes (219 persons). Of these 257 eyes, 149 (127 persons) did not recover to 5/200 or better at any visit (persistent severe visual loss). Ocular characteristics of these eyes were compared with those of eyes with severe visual loss that improved to 5/200 or better at any subsequent visit. Characteristics of patients with severe visual loss that did and did not improve and those without severe visual loss were also compared.RESULTS: Severe visual loss that persisted developed in 149 eyes of 127 persons. In order of decreasing frequency, reasons recorded for persistent visual loss included vitreous or preretinal hemorrhage, macular edema or macular pigmentary changes related to macular edema, macular or retinal detachment, and neovascular glaucoma. Compared with all patients without persistent severe visual loss, patients with persistent severe visual loss had higher mean levels of hemoglobin A1c (10.4% vs 9.7%; P = .001) and higher levels of cholesterol (244.1 vs 228.5 mg/dl; P = .0081) at baseline. Otherwise, patients with persistent severe visual loss were similar to patients with severe visual loss that improved and to those without severe visual loss.CONCLUSIONS: Persistent severe visual loss was an infrequent occurrence in the ETDRS. Its leading cause was vitreous or preretinal hemorrhage, followed by macular edema or macular pigmentary changes related to macular edema and retinal detachment. The low frequency of persistent severe visual loss in the ETDRS is most likely related to the nearly universal intervention with scatter photocoagulation (either before or soon after high-risk proliferative diabetic retinopathy developed) and the intervention with vitreous surgery when clinically indicated.
LR: 20061115; JID: 7501160; 0 (Antilipemic Agents); 0 (Cholesterol, HDL); 0 (Cholesterol, LDL); 57-88-5 (Cholesterol); CIN: JAMA. 2001 Nov 21;286(19):2401; author reply 2401-2. PMID: 11712930; CIN: JAMA. 2001 Nov 21;286(19):2400-1; author reply 2401-2. PMID: 11712929; CIN: JAMA. 2001 Nov 21;286(19):2400; author reply 2401-2. PMID: 11712928; CIN: JAMA. 2001 Nov 21;286(19):2400; author reply 2401-2. PMID: 11712927; CIN: JAMA. 2001 May 16;285(19):2508-9. PMID: 11368705; CIN: JAMA. 2003 Apr 16;289(15):1928; author reply 1929. PMID: 12697793; CIN: JAMA. 2001 Aug 1;286(5):533-5. PMID: 11476650; CIN: JAMA. 2001 Nov 21;286(19):2401-2. PMID: 11712931; ppublish
The science of color vision testing has evolved since its inception in the late 1700s. Since then, the rudimentary technique of comparing color names has been replaced by more sophisticated methods. Commonly used tests in clinical practice today include isochromatic plates, arrangement tests, anomaloscopes, and lantern tests. Each category has unique attributes that make it suitable for a particular clinical situation. The clinician should be aware of the requirements for administering and grading each test type. Factors such as the quality of the illuminant and the size of the field of view are important elements in setting up a proper color vision laboratory. Currently, no treatment exists for congenital color vision defects. However, studies show that diagnosis of these defects early in life may help children adjust better to tasks at school and may help adults understand their limitations at work. Acquired color vision defects are often used as markers of ocular pathology in the clinical setting. Different color vision tests are appropriate for diagnosing the different categories of defects. Sometimes, a battery of tests may be appropriate. This paper is a review of the current knowledge in the field of color vision testing.
To investigate associations between blood low-density lipoprotein cholesterol (LDL-C) levels and the prevalence of acquired color vision impairment (ACVI) in middle-aged Japanese men.
Participants in this cross-sectional study underwent color vision testing, ophthalmic examination, a standardized interview and examination of venous blood samples. Ishihara plates, a Lanthony 15-hue desaturated panel, and Standard pseudoisochromatic Plates part 2 were used to examine color vision ability. The Farnsworth-Munsell 100-hue test was performed to define ACVI. Smoking status and alcohol intake were recorded during the interview. We performed logistic regression analysis adjusted for age, LDL-C level, systemic hypertension, diabetes, cataract, glaucoma, overweight, smoking status, and alcohol intake. Adjusted odds ratios for four LDL-C levels were calculated.
A total of 1042 men were enrolled, 872 participants were eligible for the study, and 31 subjects were diagnosed with ACVI. As compared to the lowest LDL-C category level (<100 mg/dl), the crude OR of ACVI was 3.85 (95% confidence interval [CI], 1.24-11.00) for the 2nd highest category (130-159 mg/dl), and 4.84 (95% CI, 1.42-16.43) for the highest level (>or=160 mg/dl). The multiple-adjusted ORs were 2.91 (95% CI, 0.87-9.70) for the 2nd highest category and 3.81 (95% CI, 1.03-14.05) for the highest level. Tests for trend were significant (P<0.05) in both analyses.
These findings suggested that the prevalence of ACVI is higher among middle-aged Japanese men with elevated LDL-C levels. These changes might be related to deteriorated neurologic function associated with lipid metabolite abnormalities.
To compare retinal nerve fibre layer thickness (RNFLT) obtained by optical coherence tomography (OCT) between patients with preclinical diabetic retinopathy (DR) and healthy subjects.
Cross-sectional study.
Ninety-nine type I or II diabetic patients with no visible funduscopic retinal alteration and 77 healthy subjects were included in this study.
All participants were evaluated for peripapillary RNFLT by Stratus OCT. In diabetic patients, levels of blood sugar and glycosylated hemoglobin were examined.
The mean RNFLT in diabetic patients and healthy subjects was significantly different (104.2 [SD 10.4] and 108.6 [SD 9.2] microm, respectively; p = 0.004). Compared with the healthy group, the RNFLT in the diabetic group was also significantly less in the superior quadrant and at the 5, 11, and 12 o'clock sectors (p = 0.04, 0.002, and 0.001, respectively). The average RNFLT in diabetic patients with preclinical DR showed a low correlation with fasting blood sugar level (p = 0.03).
The mean and superior quadrant peripapillary RNFLT was slightly less in diabetic patients without abnormal vascular manifestations than in healthy subjects. Furthermore, lower RNFLT values in patients with preclinical DR appears to be weakly associated with high levels of fasting blood sugar.
A simple system has been developed for the clinical grading of the presence and severity of lens opacities. The density of nuclear opacities as seen on clinical slit-lamp examination are graded in comparison with a set of standard photographs. The extent of cortical opacities seen on retroillumination is estimated in terms of segments involved. The dimensions of posterior subcapsular opacities are measured using slit beam. It should prove to be of considerable use in clinical and epidemiologic studies of cataract.
In an attempt to elucidate more fully the pathophysiologic basis of early visual dysfunction in patients with diabetes mellitus, color vision (hue discrimination) and spatial resolution (contrast sensitivity) were tested in diabetic patients with little or no retinopathy (n = 57) and age-matched visual normals (n = 35). Some evidence of visual dysfunction was observed in 37.8% of the diabetics with no retinopathy and 60.0% of the diabetics with background retinopathy. Although significant hue discrimination and contrast sensitivity deficits were observed in both groups of diabetic patients, contrast sensitivity was abnormal more frequently than hue discrimination. However, only 5.4% of the diabetics with no retinopathy and 10.0% of the diabetics with background retinopathy exhibited both abnormal hue discrimination and abnormal contrast sensitivity. Contrary to previous reports, blue-yellow (B-Y) and red-green (R-G) hue discrimination deficits were observed with approximately equal frequency. In the diabetic group, contrast sensitivity was reduced at all spatial frequencies tested, but for individual diabetic patients, significant deficits were only evident for the mid-range spatial frequencies. Among diabetic patients, the hue discrimination deficits, but not the contrast sensitivity abnormalities, were correlated with the patients' hemoglobin A1 level. A negative correlation between contrast sensitivity at 6.0 cpd and the duration of diabetes also was observed.
Four color vision tests were used to assess color vision in 51 insulin-dependent diabetic patients and 41 normal controls. Right and left eyes of diabetic patients, selected because they had minimal retinopathy, had significantly more color vision defects than controls on Lanthony desaturated D-15, Farnsworth-Munsell 100-Hue, and chromagraph tests. The 100-Hue scores were significantly higher in both right and left eyes of diabetic patients than in controls. There were no significant associations between presence or absence of a color vision defect and age, sex, age at onset, duration of diabetes, or its metabolic control.
The Farnsworth-Munsell 100-hue test has been assessed as a screening test for the detection of diabetic retinopathy likely to benefit from laser photocoagulation therapy. Two hundred and thirty-two diabetic eyes of 126 patients were tested. The results were assessed both for total error score relative to age and for the presence of polarity. Although the incidence of abnormal colour discrimination was found to correlate with the severity of retinopathy, the test was not sufficiently selective to be of value as a screening test in the detection of retinopathy requiring treatment.
We gave the Farnsworth-Munsell 100-hue color vision test to 232 normal subjects between 10 and 80 years of age. One half the subjects underwent binocular testing followed by monocular testing. In the other half monocular testing preceded binocular testing. Performance was better with both eyes than with either eye alone. The worst performance occurred on monocular tests in subjects without previous experience with the task (that is, those for whom this was the first test). The well-known age trend was apparent (children and elderly have the worst color vision). New data are provided for judging the point at which the total error score may be considered pathologic.
An incidence of and risk factors for retinal nerve fiber layer defect were investigated in patients with type II diabetes mellitus and compared with that of age-matched control subjects.
The authors photographed the retinal nerve fiber layer of the right eye in each of 137 patients with diabetes and 144 healthy control subjects. The level of diabetic retinopathy ranged from levels 1 (no microaneurysm) to 4 (eyes with localized intra-retinal microvascular abnormalities or venous beading). Risk factors for the nerve fiber layer defect analyzed were age of patients, visual acuity, axial length, optic disc size, glycosylated hemoglobin, systolic blood pressure, and level of diabetic retinopathy.
Defects of the retinal nerve fiber layer were found in 6/30 (20%) eyes with level 1 retinopathy, 8/14 (57%) eyes with level 2 retinopathy, 24/47 (51%) eyes with level 3 retinopathy, and 36/46 (78%) eyes with level 4 retinopathy. These defect incidences were significantly higher than that of the control group, which had 5/144 (3.5%) defects (P < or = 0.001). Risk factors for this nerve defect were level of diabetic retinopathy (P = 0.002), high systolic blood pressure (P = 0.0232), and patient's age (P = 0.0478). Not correlated with the incidence of the retinal nerve fiber layer defect were visual acuity, disc size, axial length, and glycosylated hemoglobin level at the time of examination.
These findings suggest that the retinal nerve fiber layer defect is common in patients with early diabetic retinopathy. Risk factors for this defect were higher level of diabetic retinopathy, systemic hypertension, and advanced age.
People with impaired glucose tolerance are considered to be prone to diabetes. To evaluate their visual function we investigated colour vision with the Farnsworth-Munsell 100 Hue test and contrast sensitivity with Arden's grating cards in people with imparied glucose tolerance (IGT), people with normal glucose tolerance (NGT) and others with type II diabetes (NIDDM). Eyes with low vision or any anterior or posterior segment abnormalities were excluded. Contrast sensitivity and color vision differed significantly between the groups (p < 0.01). It thus appears that patients with IGT but without clinical diabetes could be followed up to see whether these alterations have any predictive value for the development of diabetes and diabetic retinopathy.
The short wavelength-sensitive (S-) cone electroretinogram (ERG) is selectively reduced in diabetic patients both with and without retinopathy, but the exact mechanism of the vulnerability of the S-cone system is still unclear. This study examined relationships of the S-cone ERG to systemic factors in diabetes. Cone ERGs to different color flash stimuli were examined in the presence of bright white background illumination in 17 diabetic patients without retinopathy and in 17 diabetics with background retinopathy. Relationships of the amplitude and implicit time of the S-cone ERG to the following systemic factors were statistically analyzed: patients' age, hemoglobin A1 level, method of diabetic control, presence of retinopathy, and presence of nephropathy. The amplitude of the S-cone ERG b-wave was significantly reduced in diabetics treated with insulin and in those associated with nephropathy. No significant correlation was found between the S-cone ERG and patient's age, hemoglobin A1 level and presence or absence of retinopathy. A selective reduction of the S-cone ERG is observed in patients whose metabolic control has been poor for a longer period, suggesting that microvascular changes may play a role in the S-cone ERG impairment.
To describe the causes of and risk factors for persistent severe visual loss occurring in the Early Treatment Diabetic Retinopathy Study (ETDRS).
The ETDRS was a randomized clinical trial investigating photocoagulation and aspirin in 3,711 persons with mild to severe nonproliferative or early proliferative diabetic retinopathy. Severe visual loss, defined as best-corrected visual acuity of less than 5/200 on at least two consecutive 4-month follow-up visits, developed in 257 eyes (219 persons). Of these 257 eyes, 149 (127 persons) did not recover to 5/200 or better at any visit (persistent severe visual loss). Ocular characteristics of these eyes were compared with those of eyes with severe visual loss that improved to 5/200 or better at any subsequent visit. Characteristics of patients with severe visual loss that did and did not improve and those without severe visual loss were also compared.
Severe visual loss that persisted developed in 149 eyes of 127 persons. In order of decreasing frequency, reasons recorded for persistent visual loss included vitreous or preretinal hemorrhage, macular edema or macular pigmentary changes related to macular edema, macular or retinal detachment, and neovascular glaucoma. Compared with all patients without persistent severe visual loss, patients with persistent severe visual loss had higher mean levels of hemoglobin A1c (10.4% vs 9.7%; P = .001) and higher levels of cholesterol (244.1 vs 228.5 mg/dl; P = .0081) at baseline. Otherwise, patients with persistent severe visual loss were similar to patients with severe visual loss that improved and to those without severe visual loss.
Persistent severe visual loss was an infrequent occurrence in the ETDRS. Its leading cause was vitreous or preretinal hemorrhage, followed by macular edema or macular pigmentary changes related to macular edema and retinal detachment. The low frequency of persistent severe visual loss in the ETDRS is most likely related to the nearly universal intervention with scatter photocoagulation (either before or soon after high-risk proliferative diabetic retinopathy developed) and the intervention with vitreous surgery when clinically indicated.
In the last 15 years an increasing number of studies have investigated color discrimination in workers exposed to various neurotoxins. Color vision was generally evaluated using the Lanthony D-15 desaturated panel (D-15 d), a test suited to identify mild acquired impairments, that can be easily performed at the workplace. In most studies, results were quantitatively expressed using the method of Bowman or that of Vingrys and King-Smith: the former is the most widely reported, while the latter gives information on the type of color defect. Applying D-15 d, or other color perception tests, impairment in color vision was observed among workers exposed to several solvents (styrene, perchloroethylene, toluene, n-hexane, and carbon disulfide), or to solvent mixtures, and also to metals like mercury. Chemical related color vision loss is a sub-clinical early effect, and in most studies proved dose-related. For styrene and perchloroethylene, and also for solvent mixtures, an impairment was observed at exposure levels lower than the current occupational limits, suggesting that these limits may be inadequate for a proper protection of visual function of workers.
To evaluate the natural course of age-related maculopathy (ARM) and to assess the incidence and absolute risk of its final stage, age-related macular degeneration (AMD).
In a population-based prospective cohort study of 6418 persons 55 years and older, we studied the incidence and natural course of ARM. Subjects underwent identical examinations, including stereoscopic fundus photography, at baseline and at 2.0 and 6(1/2) years' follow-up. Age-related maculopathy was graded according to the International Classification and Grading System for ARM and AMD, and stratified into 5 exclusive stages. Incidence was expressed in rates and 5-year absolute risks.
At follow-up, 47 new cases of AMD were identified, with a ratio of neovascular-atrophic AMD of 1.4:1. The 5-year risk of AMD increased with more severe stages to 28.0% for subjects 55 years and older with indistinct drusen and pigmentary irregularities (stage 3). Age, but not sex, independently increased this risk to a maximum of 42.0% for subjects with stage 3 ARM who were 80 years and older. Individual ARM fundus signs that predicted best the development of AMD were 10 or more large drusen (> or =125 microm) and 10% or more of the grid area covered by drusen. Subjects who developed atrophic AMD showed no significant (P =.25) differences in baseline fundus signs and natural course compared with subjects who developed neovascular AMD.
We provided the absolute risk of AMD as a function of age and early ARM fundus signs, and showed that both are prominent independent risk factors. The progression of ARM stages follows, after the appearance of the first soft drusen, a distinct course at a gradual pace that accelerates with increasing age.
Type 2 diabetes is now epidemic. In the U.S., there has been a 61% increase in incidence between 1990 and 2001 (1). There are currently 1.5 million new cases per year, and the prevalence in 2005 was almost 21 million (2). The epidemic has affected developed and developing countries alike, and the worldwide prevalence of diabetes is projected to increase dramatically by 2025 (3). The increase in type 2 diabetes is related to lifestyle changes that have resulted in overweight, obesity, and decreased physical activity levels. These environmental changes, superimposed on genetic predisposition, increase insulin resistance, which, in concert with progressive β-cell failure, results in rising glycemia in the nondiabetic range. In addition to the risk for diabetes, insulin resistance and impaired insulin secretion are accompanied by a host of major cardiovascular disease (CVD) risk factors including hypertension and dyslipidemia. Further reduction in insulin secretion over time results in increasing glycemia and the development of diabetes, which in turn is associated with the development of microvascular and cardiovascular complications.
The transition from the early metabolic abnormalities that precede diabetes, impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), to diabetes may take many years; however, current estimates indicate that most individuals (perhaps up to 70%) with these pre-diabetic states eventually develop diabetes (4–10). During the pre-diabetic state, the risk of a CVD event is modestly increased (11–22). With the development of diabetes, however, there is a large increase in risk for CVD, as well as for long-term complications affecting the eyes, kidneys, and nervous system. The complications of diabetes, which are the cause of major morbidity and mortality, are related to its duration, chronic level of glycemia, and other risk factors.
Although clinical trials have demonstrated the effectiveness of intensive glycemic and blood pressure control to …
Recent research shows that occupational exposure to several solvents, metals and other industrial chemicals can impair color vision in exposed workers. Occupation-related color vision impairment usually results in blue-yellow color discrimination loss or, less frequently, a combination of blue-yellow and red-green loss. The eyes may be unequally involved, and the course is variable depending on exposure and other factors. The pathogenesis of occupational color vision loss has not been elucidated; it may be due to, e.g. a direct action of neurotoxins on receptors, possibly on the cone's membrane metabolism, and/or to an interference with neurotransmitters within the retina. Other possible pathogenetic mechanisms, such as a direct effect to the optic nerve, have also been suggested. Occupational color vision loss is usually sub-clinical, and workers are unaware of any deficit. It can be assessed using sensitive tests, such as the Farnsworth-Munsell 100 Hue (FM-100) or the Lanthony D-15 desaturated panel (D-15 d). The latter is the most widely used for studies in groups of exposed workers, and offers the possibility of a quantitative evaluation of the results by calculation of the Bowman's Color Confusion Index (CCI), or of the Vingrys' and King Smith's Confusion Index (CI). Other advantages of D-15 d are the possibility to perform the test directly at the workplace, and the reproducibility when performed in standardized conditions. In most cases, occupation-related color vision impairment is correlated to exposure levels, and has often been observed in workers exposed to environmental concentrations below the current occupational limit proposed by the ACGIH. Progression with increasing cumulative exposure has been reported, while reversibility is still discussed. Acquired color vision impairment related to occupational exposure to styrene, perchloroethylene (PCE), toluene, carbon disulfide, n-hexane, solvent mixtures, mercury and some other chemicals are discussed. Results show that color vision testing should be included in the evaluation of early neurotoxicity of chemicals in exposed workers. The D-15 d would be useful in the surveillance of workers exposed to solvents and other chemicals toxic to the visual system.
Epidemiological studies have shown that the incidence of coronary artery disease increases as the LDL- C, TC1-9), and TG10, 11) levels rise and the HDL-C level lowers5, 8, 12) both in Japan and in Western countries (Fig.1). At present, prevalence of coronary artery disease in Japan is much lower than that in Western countries13-16). However, recent increases in the LDL-C and TC levels in Japanese associated with so-called Westernization of diet implies future increases in coronary artery disease. In this guideline, therefore, criteria for the diagnosis of dyslipidemia were defined as in Table 1, with a greater emphasis on the prevention of coronary artery disease.
The first step in this diagnostic procedure is to measure TC, TG, and HDL-C levels after overnight fasting. LDL-C level is then calculated by use of the Friedewald equation (LDL-C=TC – HDL-C – TG/5). The LDL-C level may be measured by a homogenous method especially in the case of postprandial examination or when the TG level is 400 mg/dL or higher.
The WHO and American Diabetes Association criteria for diagnosing diabetes mellitus assume the presence of a glycaemic threshold with high sensitivity for identifying retinopathy. However, this assumption is based on data from three previous studies that had important limitations in detecting retinopathy. We aimed to provide updated data for the relation between fasting plasma glucose (FPG) and retinopathy, and to assess the diagnostic accuracy of current FPG thresholds in identifying both prevalent and incident retinopathy.
We examined the data from three cross-sectional adult populations: those in the Blue Mountains Eye Study (BMES, Australia, n=3162), the Australian Diabetes, Obesity and Lifestyle Study (AusDiab, Australia, n=2182), and the Multi-Ethnic Study of Atherosclerosis (MESA, USA, n=6079). Retinopathy was diagnosed from multiple retinal photographs of each eye, and graded according to the modified Airlie House Classification system. Plasma glucose concentrations were measured from fasting venous blood samples.
The overall prevalence of retinopathy was 11.5% in BMES (95% CI 10.4-12.6%), 9.6% in AusDiab (8.4-10.9), and 15.8% in MESA (14.9-16.7). However, we found inconsistent evidence of a uniform glycaemic threshold for prevalent and incident retinopathy, with analyses suggesting a continuous relation. The widely used diabetes FPG cutoff of 7.0 mmol/L or higher had sensitivity less than 40% (range 14.8-39.1) for detecting retinopathy, with specificity between 80.8% and 95.8%. The area under receiver operating characteristic curves for FPG and retinopathy was low and ranged from 0.56 to 0.61.
We saw no evidence of a clear and consistent glycaemic threshold for the presence or incidence of retinopathy across different populations. The current FPG cutoff of 7.0 mmol/L used to diagnose diabetes did not accurately identify people with and without retinopathy. These findings suggest that the criteria for diagnosing diabetes could need reassessment.
Diabetic retinopathy has long been recognized as a vascular disease that develops in most patients, and it was believed that the visual dysfunction that develops in some diabetics was due to the vascular lesions used to characterize the disease. It is becoming increasingly clear that neuronal cells of the retina also are affected by diabetes, resulting in dysfunction and even degeneration of some neuronal cells. Retinal ganglion cells (RGCs) are the best studied of the retinal neurons with respect to the effect of diabetes. Although investigations are providing new information about RGCs in diabetes, including therapies to inhibit the neurodegeneration, critical information about the function, anatomy and response properties of these cells is yet needed to understand the relationship between RGC changes and visual dysfunction in diabetes.
JAS) guideline for diagnosis and prevention of atherosclerotic cardiovascular diseases for Japanese
- T Teramoto
- J Sasaki
- H Ueshima
- G Egusa
- M Kinoshita
- K Shimamoto
Teramoto T, Sasaki J, Ueshima H, Egusa G, Kinoshita M,
Shimamoto K et al. Diagnostic criteria for dyslipidemia. Executive
summary of Japan Atherosclerosis Society (JAS) guideline for
diagnosis and prevention of atherosclerotic cardiovascular diseases
for Japanese. J Atheroscler Thromb 2007; 14: 155-158.
Report of the expert committee on the diagnosis and classification of diabetes mellitus
- Expert Committee on the Diagnosis and Classification of Diabetes Mellitus