Friday, November 21, 2014

DocTalk November 18

This week we Dr. Shereen and Dr. Sean are at the Abu Dhabi F1 so we take a bit of a u-turn and focus on diabetes and eye disease.

Joining me in the studio is a regular guest on Suzanne Radford's show from Moorfield Eye Hospital in Dubai, Dr. Gurbaxani.

Dr. Avinash Gurbaxani, Consultant Ophthalmologist at Moorfields Eye Hospital Dubai.

Here is the podcast of the conversation

About Diabetic Macular Edema (DME)
The treatable population for DME globally is estimated around ~ 6.2 million.1 In general, Diabetes affects 347 million people worldwide2 and all people with diabetes – both type 1 and type 2 – are at risk for developing diabetic retinopathy (DR) and diabetic macular edema (DME). 3 DME is the most frequent cause of blindness in young and mid-aged adults4 and 74 percent of people who have diabetes for 10 years or more will develop some form of DR.5
A population-based study of pooled data from general and diabetic populations in the United States, Australia, Europe and Asia estimated that there were 21.3 people million with DME globally. This is estimated to increase 32.8 million respectively in 2030.6
Approximately 70 percent of patients with the most severe form of retinopathy, proliferative retinopathy, will develop DME. 7 Approximately 55 percent are unaware that they have the disease.8
DME can cause blurred vision or, in severe cases, profound vision loss.9
·       Diabetes is a chronic disease that occurs when the body does not produce enough insulin, or because cells do not respond to the insulin that is produced.2 While diabetes patients are prescribed medication to control their blood sugar levels, there are still fluctuations that occur in their blood sugar levels. Changes in blood sugar levels can cause damage to the small blood vessels in the retina: this condition is known as DR. These damaged blood vessels can leak fluid and lipids onto the central retinal area, called the macula, causing DME.10
·       DME can occur at any stage of DR,11 although it is more likely to occur as the disease progresses.5
· As a result of the damaged blood vessels, local hypoxia (deprivation of adequate oxygen) may occur in DR and DME and lead to an increased production of growth factors such as vascular endothelial growth factor (VEGF) in the retina.12
· Release of VEGF contributes to increased vascular permeability in the eye and abnormal new vessel growth.13
DME can be broadly characterized into two main anatomic categories: Focal and Diffuse DME
· Focal DME is characterized by specific areas of separate and distinct leakage in the macula with sufficient macular blood flow14
· Diffuse DME results from leakage of the entire capillary bed surrounding the macula, resulting from a breakdown of the inner blood-retina barrier of the eye15
· In addition to Focal and Diffuse, DME is also categorized based on clinical exam findings into clinically significant macular edema (CSME), non-CSME and CSME with central involvement (CSME-CI), which involves the fovea
DME symptoms include blurred vision and vision loss
· Symptoms of DME include blurred vision, double vision, loss of contrast and floaters patches of vision loss, which may appear as small black dots or lines “floating” across the front of the eye16
Type 1 or type 2 diabetes is a risk factor for DME
· All people with type 1 or type 2 diabetes are at risk for DME16
· The risk for developing DME is closely associated with the length of time a patient has lived with diabetes and the severity of diabetic retinopathy.16,17 Poor control of blood sugar also increase the risk of developing DME.7


A diagnosis of DME is confirmed through an ocular retinal examination
·       In addition to this examination, two tests are often performed to help the clinician better treat and manage the condition:
o  Fluorescein angiogram is a picture of a special dye (injected into the patient’s arm) as it passes through the blood vessels in the retina, allowing the ophthalmologist to identify any leaking blood vessels.18
o  Optical coherence tomography (OCT) measures central retinal thickness. Increased thickness is an indicator for DME.19


It is important to treat DR and DME early to avoid significant vision loss and there are several procedures used to manage DME, with varying effects:


·       Laser treatment targets leaking blood vessels in the macula and/or is used to create a grid pattern in the macula, which can help stop the leakage. Vision improves in some patients.20 However, laser treatment causes a loss in retinal tissue which may impact vision.21
·       Vitrectomy is used if a significant amount of blood is found in the center of the eye (in the vitreous humor/gel). A small instrument is used to replace the blood-clouded vitreous gel in the eye with a salt solution. Vision improves in some patients.22 Complications of vitrectomy include infection, high intraocular pressure, bleeding in the eye, cataract and retinal detachment.23
·       Steroids are also often used as intravitreal injections or implants for the treatment of DME as  they have been shown to suppress inflammation and reduce leakage of fluid from blood vessels.24
·       Anti-VEGF treatment has been shown to help decrease vascular permeability and edema in the retina in patients with DME. Vision improves in some patients.25


VEGF Trap-Eye is under investigation for treatment of DME
·       Results from a Phase 2 study (DA VINCI) in patients with DME demonstrated significant vision gain by VEGF Trap-Eye treatment.26
·       Two Phase 3 studies (VISTA-DME27 and VIVID-DME28) are currently being conducted to determine the efficacy of VEGF Trap-Eye treatment on the best corrected visual acuity in patients with DME.

Study design
Multinational evaluation of VEGF Trap-Eye versus laser photocoagulation in DME
Dosing through
Year 3
VEGF Trap-Eye
2.0 mg q4 wks
2.0 mg q8 wks†
Laser
Photocoagulation
Macular laser photocoagulation using modified ETDRS protocol
May receive VEGF
Trap-Eye  PRN* in year 3


†After five initial monthly doses


*As needed


• Randomized, multi-center, double masked trial
Primary endpoint: mean change in BCVA and ETDRS letter score at 52 weeks (VIVID) and 100 weeks (VISTA)
Key Secondary endpoint: change in retinal thickness (OCT) at 1 year



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