- •Foreword
- •Preface
- •Contents
- •Contributors
- •Acronyms
- •1.1 Introduction
- •1.2 Epidemiology
- •1.3 Risk Factors
- •1.3.1 Duration of Diabetes Mellitus
- •1.3.2 Glycemic Control
- •1.3.3 Hypertension
- •1.3.4 Ethnic Differences
- •1.3.5 Obesity
- •1.3.6 Socioeconomic Status
- •1.3.7 Other Risk Factors
- •1.4 Pathophysiology
- •Conclusion
- •References
- •2: Non-proliferative Diabetic Retinopathy
- •2.1 Clinical Overview
- •2.1.1 Clinical Findings
- •2.1.2 Classification of NPDR
- •2.1.3 Atypical Forms of NPDR
- •2.2 Diagnostic Tools
- •2.2.1 Telemedicine
- •2.2.2 Fundus Photography
- •2.2.3 Fluorescein Angiography
- •2.2.4 Ultrasonography
- •2.2.5 Optical Coherence Tomography
- •2.2.6 Adaptive Optics Scanning Laser Ophthalmoscope
- •2.2.7 Multifocal Electroretinogram
- •2.2.8 Pattern Visual Evoked Potentials
- •2.2.9 Other Diagnostic Tools
- •2.3 Present Therapies
- •2.3.1 Primary Interventions
- •2.3.1.1 Glycemic Control
- •2.3.1.2 Blood Pressure Control
- •2.3.1.3 Lipid-Lowering Therapy
- •2.3.2 Secondary Interventions
- •2.3.2.1 Protein Kinase C Inhibitors
- •2.4 Evolving Algorithms
- •2.4.1 Screening
- •2.4.2 Laser Photocoagulation
- •2.5 New Frontiers
- •References
- •3: Diabetic Macular Edema
- •3.1 Clinical Overview
- •3.1.1 Clinical Findings
- •3.1.2 Biomicroscopic Classification of DME
- •3.2 Diagnostic Tools
- •3.2.1 Fluorescein Angiography
- •3.2.2 Optical Coherence Tomography
- •3.2.3 Fundus Photography
- •3.2.4 Microperimetry
- •3.2.5 Multifocal Electroretinogram
- •3.2.6 Other Imaging Under Investigation
- •3.3 Present Therapies
- •3.3.1 Laser Photocoagulation
- •3.3.2 Intravitreal Pharmacotherapies
- •3.3.2.1 Intravitreal Steroids
- •3.3.2.2 Intravitreal Anti-VEGF
- •3.3.3 Pars Plana Vitrectomy
- •3.4 Evolving Algorithms
- •3.4.1 Therapeutic Algorithms
- •3.4.2 Factors Associated with Favorable Response to the Therapy
- •3.4.3 Treatment of DME Associated with Macular Ischemia
- •3.5 New Frontiers
- •References
- •4: Proliferative Diabetic Retinopathy
- •4.1 Clinical Overview
- •4.1.1 Clinical Findings
- •4.1.2 Classification of PDR
- •4.2 Diagnostic Tools
- •4.2.1 Fluorescein Angiography
- •4.2.2 Fundus Photography
- •4.2.3 Ultrasonography
- •4.2.4 Optical Coherence Tomography
- •4.2.5 Perimetry
- •4.2.6 Further Diagnostic Tools
- •4.3 Present Therapies
- •4.3.1 Panretinal Laser Photocoagulation
- •4.3.2 Intravitreal Injections
- •4.3.2.1 Intravitreal Steroids
- •4.3.2.2 Intravitreal Anti-VEGF Agents
- •4.4 Evolving Algorithms
- •4.5 New Frontiers
- •References
- •5.1 Introduction
- •5.2 Pathophysiology
- •5.3 Neovascular Glaucoma
- •5.4 Tractional Retinal Detachment
- •5.5 Treatment
- •5.5.1 Panretinal Laser Photocoagulation
- •5.5.2 Pars Plana Vitrectomy and Endophotocoagulation
- •5.5.4 Silicone Oil Tamponade
- •5.5.4.1 Viscodissection
- •Conclusion
- •References
2 Non-proliferative Diabetic Retinopathy |
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2.2.9Other Diagnostic Tools
Other examinations have been performed in NPDR to assess prediabetic retinopathy, including frequency doubling technology, contrast sensitivity, and dark adaption. The results showed early functional changes in eyes with NPDR, even with normal visual acuity [53].
Summary 2.3
In the recent years, telemedicine has developed worldwide a key role in the screening of DR. Color fundus photographs is still the suggested tool for monitoring the progression of NPDR. FA and OCT have a predominant role in more advanced stages and in the presence of diabetic maculopathy.
2.3Present Therapies
About 366 million people in the world are affected by diabetes mellitus (DM), a planetary health problem which incidence is growing quickly [54]. Up to 25 % of diabetic patients develop diabetic retinopathy (DR) [55]: this is a chronic, microvascular complication that can end in blindness. The patients with the highest possibility of developing diabetic retinopathy are those with long time disease and poor metabolic control. Since there are no therapies that can fight the onset of diabetic retinopathy, patients should be advised to control risk factors through lifestyle modification and optimal glycemic control. Despite this, diabetic retinopathy could go forward during entire life of patients.
Preventive treatments, useful to reduce the risk of diabetic retinopathy, include tight control of blood glucose level, blood pressure, and lipids serum level. Several clinical trials proved that incidence and progression of diabetic retinopathy could be reduced by glycemic control; visual loss and retinopathy progression are also slowed down by antihypertensive therapy. Moreover, recent investigations have reported that the risk of developing diabetic retinopathy is straightly connected with elevated serum lipids and dyslipidemias; therefore, the lipid-lowering agents represent another useful help in reducing retinopathy progression.
Today many pathways are considered implicated in the development of DR; therefore, secondary strategies have been developed focused on pathophysiologic approaches. In this chapter we will examine some of them, such as blockade of the renin-angiotensin system (RAS) and the use of protein kinase C (PKC) inhibitors.
