Ophthalmology (Eye & Ear Hospital) - Theses
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ItemOptimising the management of diabetic retinopathy in pregnant women with pre-existing diabetes in Australia( 2021)Background: Diabetic Retinopathy (DR) is a leading cause of blindness among people of reproductive age and is thought to be worsened by pregnancy. Findings from prior studies have been conflicting, many are outdated, and the majority only studied women with type 1 diabetes (T1DM). It is crucial to identify those within this population who are most at risk of developing DR progression towards sight-threatening disease, so that appropriate management can be planned. Clinical decisions regarding DR management in pregnancy can be fraught, due to the need to give timely sight-saving treatment while also minimising adverse effects to the foetus. Despite these concerns, DR management guidelines have been inconsistent across the globe due to disparate findings. Purpose: This thesis aimed to 1) report the prevalence of DR, sight-threatening DR (STDR), and its progression rate during pregnancy in Metropolitan Melbourne; 2) assess the use of optical coherence tomography angiography (OCTA) in evaluating retinal changes in diabetic patients during different stages of pregnancy; and 3) determine the adherence rate and the barriers to the recommended eye screening guidelines in pregnant women with pre-existing diabetes. Research Design and Methods: This doctoral research project was a prospective longitudinal cohort study of women with T1DM or type 2 diabetes who were pregnant or planning to get pregnant from two tertiary maternity hospitals in Melbourne, Australia. Eye examinations were scheduled in each trimester and at 3-months postpartum. DR severity was graded for each eye from 2-field retinal photographs. Progression was defined as worsening by >= 1-step on the Airlie House classification, development of diabetic macular oedema (DMO), or the need for laser treatment during pregnancy. Sight-threatening (ST) progression was defined as development of proliferative DR or DMO. Additionally, 3x3-mm OCTA scans (macula-centred) were taken from participants who attended Melbourne Eyecare Clinic using swept-source OCT (Triton, Topcon Corp). Foveal avascular zone (FAZ) area and vessel density (VD) from the superficial capillary plexus were measured. Barriers to attending eye screening were assessed with the modified Compliance with Annual Diabetic Eye Exams Survey. Results: Aim 1: A total of 147 from 191 eligible women (77%) were recruited, with at least one eye exam performed in 130 (88.4%). Sixty-two women (47.7%) had T1DM. DR and STDR prevalence were 20.8 (95% confidence interval [CI] 16.3-26.1) and 6.6 (CI 4.1 - 10.4) per 100 eyes, respectively. Among the 144 eyes (72 women) with more than one eye exam, 9.7% (CI 5.8 - 15.8) had DR progression and 4.5% (CI 1.9 - 9.6) had ST progression. Elevated systolic blood pressure (risk ratio [RR] 10.36, CI 3.14 - 34.12) and pre-existing DR (RR 5.07, CI 1.90 - 13.49) in early pregnancy significantly increased the risk of progression. Aim 2: A total of 125 eyes from 64 women were imaged. The majority of women were in the pregnant group (77%) with 38 (59%) having T1DM. The majority of eyes had no DR (81.6%) or DMO (97.6%). The VD in the pericentral region and superior, temporal, and nasal subfields were significantly lower in eyes with DR than eyes without in the non-pregnant and pregnant groups (p-values <=0.039). The nasal VD in eyes with no DR in the pregnant group was significantly higher than that of the postpartum group (p=0.010). Although not reaching statistical significance, a trend towards higher VD in the pregnant group than the non-pregnant group was observed in all subfields, except in the temporal subfield. The temporal VD was lower in the pregnant group than the non-pregnant group and was especially marked in eyes with DR. No significant difference was found in the mean FAZ area between various pregnancy statuses and DR severities. Aim 3: There were 125 pregnant women who completed the survey. The median age was 34 years (range 19-47). Sixty-four respondents (51.2%) had T1DM. A retinal assessment was performed at least once in the first trimester in 56 (44.8%) and 33 (26.4%) had the ideal number of examinations. Competing priorities (p=0.012) and the belief of having reasonable diabetes control (p=0.007) were the main reasons given for non-attendance. Interestingly, the presence of multiple eye care providers in the neighbourhood was also associated with non-adherence (p=0.003). Conclusion: This PhD study has provided updated data on the prevalence of DR and its rate of progression in the Australian pregnant population with pre-existing diabetes, illustrated the use of OCTA in this population, and reported the adherence rate and barriers to the recommended eye screening guidelines. The DR prevalence in pregnant women was similar to the non-pregnant diabetic population in Australia. However, nearly 1 in 10 eyes had DR progression during pregnancy, with almost half of these developing STDR. DR presence could be reflected by a decrease in the VD in the OCTA scan, which is in concordance with the findings from previous studies in non-pregnant populations, suggesting a potential role for OCTA in the evaluation of DR during pregnancy in a non-invasive manner. Worryingly, more than half of our cohort did not adhere to the recommended eye screening schedule in pregnancy, and about 70% did not receive frequent exams as recommended, highlighting the need to address barriers to eye screening attendance given the significant risk of vision loss from DR in this population. This study benefits society by providing findings that may help inform the future development of evidence-based guidelines for DR screening and management in this unique and growing population. Based on this study’s findings, it is recommended that pregnant women with pre-existing diabetes should have an eye examination in the first trimester or as soon as pregnancy is recognised. If no DR is found, an additional exam during pregnancy is advised only for women with T1DM. However, if DR is present, an eye exam in each trimester is recommended irrespective of diabetes type.
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ItemBiomarkers in diabetic retinopathy: genetic and proteomic profiling( 2014)Diabetic retinopathy (DR) is a common complication of diabetes mellitus and currently threatens the vision of over 100 million people worldwide. Blindness in diabetes is mostly preventable if sight threatening DR (STDR) is detected and treated early. However, the ophthalmic course in people diagnosed with diabetes can be difficult to predict, as risk indicators are not DR specific. This study adopted a multifactorial approach, assessing systemic circulating biomarkers and genetic markers, to investigate risk of blinding disease. The overriding aim of this thesis was to identify protein and genetic blood-based biomarkers that are consistently associated with severe STDR. METHOD: Samples were obtained from the Diabetes Management Project (DMP). The proteomic fraction of the thesis comprised 190 plasma samples from Type 2 diabetic patients, (n=60) STDR (proliferative DR (PDR) or severe non PDR (NPDR), (n=60) minimal or moderate NPDR, patients without DR (n=60) and (n=10) reference sample. Protein levels were analysed using iTRAQ conducted using mass spectrometry. To replicate this work a total of 70 samples with Type 2 diabetes was analysed for the candidate proteins using liquid chromatography/tandem mass spectrometry (LC/MS/MS) by high resolution multiple reaction monitoring (MRM- HR). The genetic aspects of the thesis utilised DNA extracted from the whole blood of patients from the DMP. Cases had STDR, and control participants had either no evidence of DR or only mild DR. Twenty-four single nucleotide polymorphisms (SNPs) were selected from previous genome-wide association studies (GWAS), eight VEGF and three EPO SNPs were selected from previous DR association studies, and rs4636297 has been implicated in-vivo to be associated with microvascular dysfunction. Samples were genotyped using the Sequenom iPLEX Gold chemistry on an Autoflex mass spectrometer. Association was tested using logistic regression analysis, adjusting for potential confounding variables. RESULTS: The most significant STDR protein biomarker candidates (p<0.0003) were; APOB100 (p<1.0 x 10-27), fibronectin (p<1.0 x 10-27), ceruloplasmin (p=5.34 x 10-12), gelsolin (p=9.51 x 10-12), C5 (p=4.71 x 10-8), ZAG (p=5.35 x 10-7), CD5L (p=6.57 x 10-6), protein AMBP (p=2.04 x 10-6) and ITIH1 (p=1.53 x 104) when compared to those without DR. These candidates were unable to be replicated by MRM-HR for STDR compared to without DR. Two loci from the GWAS replication were nominally associated with STDR: rs1073203 (OR=0.31, 95% CI 0.13-0.74, p=0.01 at the G allele and OR=0.24, 95% CI 0.09-0.63, p=0.003 in a dominate genotypic model), and rs4838605 (OR=1.64, 95% CI 1.02-2.65, p=0.04 in a co-dominant genotypic model). No statistically significant associations were found for VEGF and EPO polymorphisms with STDR to control participants. The miR-126-24A SNP variant was significantly associated with STDR: rs4636297 (OR=2.02, 95% CI 1.22-3.35, p=0.006 at the A allele after co-variable adjustment, and OR=2.00, 95% CI 1.19-3.38, p=0.009 in a co-dominant genotypic model). CONCLUSION: This thesis has shortlisted eight novel proteomic biomarkers, as well as one novel and two previously investigated genetic markers associated with STDR. Once replicated, we propose these biomarkers could help appropriate risk stratification of DR which would, in time allow for early diagnosis and rationalise screening programs.
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ItemLuminance flicker-induced retinal vasodilation in humans with and without type 1 diabetes( 2014)PURPOSE Luminance flicker-induced retinal vasodilation is reduced in people with type 1 diabetes compared with non-diabetic controls. However, the mechanisms of this response and causes for its reduction are not well understood. I therefore investigated potential acute causes of reduced luminance flicker-induced retinal vasodilation in people with and without type 1 diabetes. My doctoral project had four specific aims: 1) To investigate the effect of repeated testing on luminance flicker-induced retinal vasodilation in healthy people; 2) To study the effect of ambient lighting on luminance flicker-induced retinal vasodilation in healthy people; 3) To determine the importance of epoxyeicosatrienoic acids (EETs) and prostaglandins (PGs) in luminance flicker-induced retinal vasodilation in healthy people; and 4) To study the effect of glucose levels and antioxidant treatment on retinal flicker responses, ganglion cell function and systemic arterial elasticity in people with type 1 diabetes. METHODS My doctoral project involved a total of 72 participants (60 non-diabetic and 12 with type 1 diabetes). I first assessed the impact of repeated testing with five or 30 minutes between tests on luminance flicker-induced retinal vasodilation in 20 healthy people. Next, I used a balanced crossover study investigated the effect of reduced and normal ambient lighting on these responses in another 20 healthy people. In my third study, I used oral fluconazole 400 mg and dispersible aspirin 600 mg to investigate the role of EETs and PGs, respectively, in healthy luminance flicker-induced retinal vasodilation. Twelve healthy people participated in a balanced crossover study with three treatments (no drug, fluconazole and aspirin). In addition, six healthy people, each for fluconazole and aspirin, were followed at 30-minute intervals for two hours after drug ingestions. My final study involved 12 otherwise healthy people with type 1 diabetes. I investigated luminance flicker-induced retinal vasodilation, retinal ganglion cell function and systemic arterial elasticity at baseline, euglycaemia (plasma glucose = 6 mmol/l) and hyperglycaemia (plasma glucose = 15 mmol/l). Participants were seen twice: once with vitamin C (2 g intravenous) and once with placebo immediately prior to the initiation of hyperglycaemia. Retinal vasodilation in response to 20 seconds of 12.5 Hz luminance flicker with green light was assessed with the Dynamic Vessel Analyzer (DVA) after pupil dilation with tropicamide 1%. Ganglion cell activity was measured from the pattern electroretinogram (PERG) transient (1 Hz stimulus) and steady-state (8.33 Hz) responses to black and white check reversals without pupil dilation. Systemic arterial elasticity was also assessed by radial artery pulsewave tonometry with the HD/Pulsewave CR-2000. Participant characteristics were compared by analysis of variance (ANOVA) for continuous variables or Fisher’s exact test for categorical variables. Within-subject changes in group means were assessed by ANOVA. Significant differences identified by ANOVA were explored by post-hoc Student’s t-tests with corrections for multiple comparisons where necessary. Within-subjects Pearson’s correlation coefficients were assessed in my final study for luminance flicker-induced retinal vasodilation, ganglion cell function and systemic arterial elasticity. Two-tailed P < 0.05 was considered statistically significant. All statistical analyses were performed in STATA version 12.1. RESULTS Aim 1 Twenty healthy people aged (mean [standard deviation [SD]]) 33.1 (5.7) years were studied. Maximum luminance flicker-induced arteriolar dilations were 3.2 (2.1) % initially, 2.4 (1.6) % after five minutes of rest and 3.4 (2.1) % after 30 minutes of rest (P < 0.001 by ANOVA). Compared with the first test, arteriolar dilations were reduced after five minutes (P = 0.02 after Bonferroni’s adjustment), but not after 30 minutes of rest (P > 0.05). Maximum venular dilations were 4.3 (1.3) % initially, 3.8 (1.6) % after five minutes of rest and 4.4 (1.7) % after 30 minutes of rest (P > 0.05 by ANOVA). Pre-flicker vessel diameters were unchanged between tests (P > 0.05 for arterioles and venules). Aim 2 Twenty healthy people aged 32.8 (6.5) years were studied. Maximum luminance flicker-induced retinal arteriolar dilations were 4.8 (2.3) % and 4.1 (1.9) % under reduced and normal ambient lighting, respectively (P = 0.02 by ANOVA). Corresponding maximum venular dilations were 5.4 (1.8) % and 5.1 (2.1) % under reduced and normal ambient lighting, respectively (P > 0.05). Pre-flicker arteriole and venules diameters were unchanged between tests (P > 0.05 for both). Aim 3 Twenty healthy people aged 25.6 (4.6) were studied. In 12 crossover study participants, maximum luminance flicker-induced retinal arteriolar and venular dilations without drug administration were 4.4 (2.0) % and 4.6 (1.7) %, respectively. Neither fluconazole nor aspirin affected these responses (P > 0.05 for both by ANOVA). Pre-flicker arteriole and venule diameters without drug administration were 120 (11) measurement units (MU) and 146 (17) MU, respectively. Fluconazole reduced pre-flicker venule diameters by (mean ± 95% confidence interval [CI]) 5 ± 4 MU (P = 0.02 after Dunnett’s adjustment). In six participants, fluconazole did not affect arteriolar or venular dilations or pre-flicker arteriole diameters (P > 0.05 for all) but did reduce pre-flicker venule diameters over two hours (P < 0.001 by ANOVA). Aspirin did not affect arteriolar or venular dilations or pre-flicker diameters in six participants over two hours (P > 0.05 for all). Aim 4 Twelve otherwise healthy people with type 1 diabetes aged (median [interquartile range [IQR]]) 24 (20.5 – 30) years with 10.5 (3.8 – 17) years of diabetes were studied. Plasma glucose levels decreased from (mean [SD]) 8.4 (3.6) mmol/l at baseline to 6.1 (0.8) mmol/l at euglycaemia (P < 0.01). Plasma glucose levels then increased during hyperglycaemia to 15.0 (1.9) mmol/l with vitamin C and 14.4 (0.8) mmol/l with placebo (both P < 0.001 vs. euglycaemia). Insulin levels increased from 65 (24) pmol/l at baseline to 334 (63) pmol/l at euglycaemia (P < 0.001) and were stable thereafter. Euglycaemic clamp increased retinal venule maximum dilation by 1.7 (2.0) % and area under the curve (AUC) during flicker by 28.7 (28.9) % x sec. compared to baseline (both P < 0.01). No change in flicker responses was observed between euglycaemia and either hyperglycaemia arm or between vitamin C and placebo hyperglycaemia arms. Ganglion cell function and systemic arterial elasticity were unaffected across glucose conditions (P > 0.05 for all). The one exception was the ratio of the second harmonic frequency (2F) amplitude with 0.8° check sizes to the amplitude with 7° check sizes from the PERG steady-state response. The ratio increased from 1.1 (0.3) at baseline to 1.4 (0.6) after hyperglycaemia with vitamin C (P < 0.05). In within-subjects correlation analyses, the arteriole AUC during flicker was positively correlated with plasma glucose levels (r = 0.27, P = 0.04), although this correlation became non-significant when data from hyperglycaemia with vitamin C were excluded. Arteriole and venule maximum dilations and AUC during flicker were positively correlated with free insulin levels, although only venule dilation responses remained significant after data from hyperglycaemia with vitamin C were excluded. Large artery elasticity (LAE) was positively correlated with arteriole maximum dilations (r = 0.26, P = 0.04) and AUC during flicker (r = 0.26, P = 0.04) and these correlations remained significant after the exclusion of data obtained after vitamin C treatment. Both LAE (r = -0.32, P = 0.01) and small artery elasticity (SAE) (r = -0.35, P = 0.01) were negatively correlated with systolic blood pressure. These correlations were unchanged by the exclusion of vitamin C data. In PERG tests, the N95 amplitude was positively correlated with diastolic blood pressure, the 0.8° 2F amplitude was negatively correlated with systolic blood pressure and the 7° 2F amplitude was negatively correlated with insulin levels. After the exclusion of vitamin C data, the correlation between the 0.8° 2F amplitude and systolic blood pressure was not statistically significant. CONCLUSIONS Several factors may impact on luminance flicker-induced retinal vasodilation in humans. Arteriolar responses, in particular, are reduced with repeated stimulation and higher ambient lighting. This may reflect light adaptation in photoreceptors and lower modulation depths during luminance flicker, respectively, with secondary reductions in ganglion cell activation. My data do not support a major role for EETs and PGs in luminance flicker-induced retinal vasodilation. Nitric oxide remains the most likely signalling molecule and dysfunction in its signalling pathways may contribute to reduced responses in type 1 diabetes. Increased venule dilations during euglycaemic clamp suggest that glucose normalisation with insulin improves retinal microvascular function. Furthermore, antioxidants such as vitamin C may improve retinal neurovascular function in adults with type 1 diabetes. This finding indirectly implicates oxidative stress as a contributor to impaired retinal neurovascular function in type 1 diabetes. My doctoral project highlights several important factors that may reduce luminance flicker-induced retinal vasodilation and may lead to its use as a clinical marker of neurovascular function in retinal diseases.
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ItemThe relationship between myopia and diabetic retinopathy: potential protective effects and underlying mechanisms( 2013)There is controversy over observations that myopia is protective of diabetic retinopathy (DR) due to the uncertainty over the contributory roles of ocular biometric parameters (i.e. axial length [AL], corneal curvature [CC], and anterior chamber depth [ACD]) all of which are closely associated with myopia. Moreover, theories on the mechanisms underpinning the supposed protective myopia-DR relationship are educated guesses inferred from observations of reduced retinal blood flow and/or oxygen (O2) consumption in myopic eyes. Therefore, this thesis has three main aims. The first is to investigate the associations of myopia and myopia-related ocular biometric parameters with DR (and diabetic macular edema [DME]). The second and third aims are to assess the respective roles of a reduction in retinal capillary blood flow (RCF) and O2 consumption as potential mechanisms underlying this protective myopia-DR relationship. Aim one included 609 patients with diabetes aged 18+ years. After multivariable adjustments, eyes with longer AL were less likely to have mild (odds ratio [OR]: 0.58, 95% confidence interval [CI]: 0.41- 0.83 per mm increase), moderate (OR: 0.73, 95% CI: 0.60-0.88), and severe DR (OR: 0.67, 95% CI: 0.53-0.85), and also had a lower risk of mild (OR: 0.70, 95% CI: 0.56- 0.86); and moderate DME (OR: 0.72, 95% CI: 0.56- 0.93). No associations were found for refractive error, CC or ACD with DR, suggesting that the myopia-DR association is likely due to a longer AL in myopic eyes. For aim two, I utilized 85 persons with diabetes aged 18+ years, independent of the sample used in aim one. Evaluating the relationship between AL, RCF and DR, I found no association between AL and RCF (per mm increase in AL, regression coefficient [β] -1.80, 95% CI: -13.50-9.50) or between RCF and the risk of DR (per unit increase in RCF, OR 1.00, 95% CI 0.99-1.00) after multivariable adjustments. These findings suggest that diminished RCF may not be a major mechanism underlying the protective association between axial elongation and DR. In aim three, I utilized the arterio-venous (A-V) difference in O2 saturation (SO2), as a surrogate marker of relative O2 consumption. A reliability and reproducibility study in 20 healthy individuals aged 18+ years found extremely high intra-class correlation coefficient (ICC) values for intra-observer reliability (0.99 for both arteriolar and venular SO2), inter-observer reliability (ICC of 0.94 for arteriolar SO2 and 0.96 for venular SO2) and intra-subject reproducibility (ICC of 0.98 for both arteriolar and venular SO2) for the retinal oximeter utilized in this doctoral thesis. Finally I explored the role of O2 consumption as one of the mechanisms underpinning the protective association between AL and DR. Due to the potential confounding effects of diabetes on retinal function, the relationship between AL, retinal function (assessed using multifocal electroretinogram [mfERG] P1 amplitude) and the A-V difference was conducted in 50 healthy subjects aged 18+ years. Path analysis models including AL (study factor), retinal function (intermediate variable) and A-V difference (outcome variable) showed that AL had little direct association with A-V difference (βp = -0.002), while the indirect effect of AL on A-V difference via changes in retinal function were substantial (βp = -0.51). These findings suggest that longer eyes have decreased retinal function and O2 consumption, and thus are relatively less hypoxic in the presence of diabetes, which may partly explain the reduced risk of DR in these eyes. In conclusion, I have demonstrated that a longer AL is the main factor contributing to the protective association of myopia with risk of DR. Furthermore, I have established that the protective myopia-DR relationship may be partially due to the alleviation of hypoxia in diabetes, due to a reduction in retinal function as the eye elongates.
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ItemDevelopment of an “item bank” to assess the impact of diabetic retinopathy on quality of life: the RetBank project( 2012)Diabetic retinopathy and diabetic macular oedema are common ocular complications of diabetes that can lead to significant vision impairment and have a devastating impact on quality of life. However, our understanding of the impact of diabetic retinopathy on quality of life is limited by the lack of an appropriate patient reported outcome measure. Most instruments tend to focus primarily on activity limitation rather than the holistic concept of quality of life. Moreover, most outcome measures have undergone minimal validation using classical test theory rather than modern psychometric theory such as Rasch analysis. With the emergence of new treatment modalities for diabetic retinopathy and diabetic macular oedema such as anti-vascular endothelial growth factor intraocular injections, the time is propitious for an instrument that can accurately yet quickly quantify the quality of life impact of diabetic retinopathy. This doctoral work developed an item bank – Retbank – to comprehensively assess the impact of diabetic retinopathy, diabetic macular oedema and associated vision impairment on all relevant quality of life parameters. The domains and items for Retbank were developed following a thorough literature review including a survey of extant functioning and quality of life questionnaires, and qualitative interviews with diabetic retinopathy patients and retinal and diabetes specialists. The large initial item pool was reduced to 314 items across nine quality of life domains, namely visual symptoms; ocular surface symptoms; activity limitation; mobility; emotional; health concerns; social; convenience; and economic via the systematic processes of binning and winnowing based on key criteria and expert panel consensus and cognitive interviewing. The pilot instrument was tested in a large sample of patients (n=466) with diabetic retinopathy and diabetic macular oedema using face to face and telephone interviews. The psychometric properties of the nine domains were explored using Rasch analysis according to key parameters, including rating scales performance, measurement precision, item fit, unidimensionality, differential item functioning and scale targeting. For most domains, precision was excellent and multidimensionality and differential item functioning were negligible. However, targeting and measurement range were frequently suboptimal, and the rating scales of some of the domains demonstrated disordered or bunched thresholds. These trends are most likely due to the large proportion of the pilot sample with no or unilateral vision impairment and/or those with non-vision threatening stages of diabetic retinopathy and diabetic macular oedema. As the performance of these parameters should improve in a more visually impaired sample, a lenient approach to category collapse and other major modifications was applied throughout the analysis. Finally, the impact of diabetic retinopathy, diabetic macular oedema and associated vision impairment on patients’ quality of life was explored using preliminary Retbank data. The findings indicated a strong association between worsening bilateral vision impairment and reduced quality of life outcomes. Vision-threatening diabetic retinopathy (i.e. severe non-proliferative diabetic retinopathy, proliferative diabetic retinopathy and severe diabetic macular oedema) was also associated with poorer quality of life outcomes overall. Retbank demonstrates a promising capacity to provide accurate and precise measurement of the impact of diabetic retinopathy and diabetic macular oedema on a range of important quality of life parameters. Ultimately, Retbank will allow researchers to assess the outcomes of traditional and novel treatment therapies for diabetic retinopathy from the patient’s perspective. It may also benefit policy planners in the design and evaluation of interventions and allocation of funding and resources. Finally, as it can be easily implemented into clinical settings via a computerised system which produces quick results with few items, clinicians will be able to track ongoing patient progress and assess the longitudinal effectiveness of treatments.
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ItemAssociation of serum lipids with diabetic retinopathy, macular edema and macular thickness in adults with diabetes: the Diabetes Management Project (DMP)( 2011)PURPOSE: To assess the association of serum lipids with diabetic retinopathy (DR), diabetic macular edema (DME), and macular thickness in adults with diabetes. RESEARCH DESIGN AND METHODS: Diabetic patients aged 18 years or older were prospectively recruited from eye clinics at the Royal Victorian Eye and Ear Hospital, Melbourne, Australia. Fasting total-C [cholesterol], HDL-C, non-HDL-C, triglyceride and LDL-C were assessed. DR was graded from fundus photographs (dilated) as mild, moderate and severe non-proliferative and proliferative; and separately graded for presence of DME, including clinically significant macular edema (CSME). Macular thickness was assessed using optical coherence tomography (OCT). RESULTS: A total of 500 participants (median age = 65 years) were examined. DR, DME and CSME were present in 321 (66.2%), 149 (33.0%), and 68 (15.0%) patients, respectively. In multivariate models adjusting for traditional risk factors and lipid medications, persons with higher total-, LDL-, and non-HDL-C were more likely to have CSME (odds ratio of 1.54, 1.49, and 1.63 per 1 SD increase, respectively; all P<0.05). Serum lipid levels were not related to DR, DME or macular thickness. CONCLUSION: Serum lipids are independently associated with the CSME, but not with DR, mild or moderate DME or macular thickness. These data reflect the impact of hyperlipidaemia in the pathogenesis of severe macular edema and suggest that differential dyslipidemia therapies targeting DR and CSME may be needed.
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ItemBarriers to regular eye examinations for people with diabetes( 2000)It was hypothesised that barriers exist for people with diabetes that prevent them from accessing eye care services regularly. Thus, the aim of this study was to identify barriers to regular eye examinations reported by people with diabetes in order to improve compliance with screening recommendations for diabetic retinopathy. Patients were recruited from the Retina and Primary Care Clinics of the Royal Victorian Eye and Ear Hospital during the study period. They were eligible if they were 18 years of age or older, had diabetes for at least 2 years duration and were new to the clinic. A researcher-administered questionnaire was used to elicit information on patient demographics, diabetes status, previous eye care and reasons for not having had regular eye examinations for those who had not. Medical examinations included visual acuity, dilated fundus examinations and a haemoglobin Al c test for control of diabetes. A total of 203 patients participated in this study. Less than half had regular screening for diabetic retinopathy. Of those that did not have regular eye exams, more than half had vision loss less than 6/12 due to diabetic retinopathy. Almost everyone that did not have regular exam1S identified reasons for not having done so. The majority mentioned knowledge barriers such as not being aware of screening recommendations for diabetic retinopathy. However, for some having knowledge did not prompt eye examinations. Other barriers such as access, language, medical problems and beliefs were reported. This study highlights the problems faced by people with diabetes in having regular eye examinations. With the increase in prevalence of diabetes more people will be at risk of vision loss fron1 diabetic retinopathy. However, prevention or progression to sight-threatening retinopathy can be achieved by having regular eye examinations beginning at diagnosis of diabetes. Eye health promotion programmes need to target all people with diabetes with a special emphasis on older people, those from non-English speaking backgrounds and those that medical problems. These people had knowledge of screening recommendations but were not compliant.