Diabetic Retinopathy Treatment: A Future Therapy

Diabetic retinopathy (DR) is a common and specific microvascular complication of diabetes and one of the leading global causes of preventable blindness. The Wisconsin Epidemiologic Study of Diabetic Retinopathy (WESDR) found 3.6% of type 1 diabetes patients and 1.6% of type 2 diabetes patients were legally blind. Diabetic retinopathy is rare among children at age 10 and younger. About 10% of teens with diabetes at ages 15 to 19 have diabetic retinopathy. The proportion rises from 10% to 40% between ages 20 and 29. By age 30, about 60% of people with diabetes have diabetic retinopathy, and by age 45 the figure rises to 70%.   Diabetic retinopathy is caused by damage to blood vessels of the retina. In people with diabetes mellitus, changes in the walls of the small blood vessels in the retina are caused by blood sugar abnormalities. The temporary blurring is because the sugar in the blood can diffuse into the lens of the eye and cause it to swell, thus changing the focal point of the eye and resulting in blurring of the vision. These small blood vessels may begin to balloon forming microaneurysms, leak fluid and blood (called dot and blot hemorrhages) into the retina. As a response to decreased oxygen delivery to the retina, new blood vessels may begin to grow. Although new blood vessels may sound like a good thing considering that the old blood vessels are damaged, the new blood vessels are actually more harmful than beneficial. The new blood vessels are extremely leaky and fragile, potentially leading to bleeding inside the eye and usually resulting in severe vision loss. If not treated appropriately, this vision loss may be permanent.

Various treatments and drugs have been proposed to treat diabetic retinopathy like laser treatment, Vitrectomy or antiproliferative drugs. In laser treatment, Proxymetacaine or benoxinate drops are used to anaesthetize the cornea and bright flashes of light is introduced. But the drawback of laser therapy is it can result in diminished side and night vision, and unwanted laser burns. In Vitrectomy, blood from the middle of the eye (vitreous) as well as any scar tissue that’s tugging on the retina is removed through surgery. Vitrectomy may be followed or accompanied by laser treatment. Another therapy is to administer antiproliferative drugs (ranibizumab), but these compounds clear from the blood quickly, so high doses are needed to produce the desired effect, which increases toxicity to other tissues. These treatments helps patient to overcome the progression of diabetic retinopathy, but it’s not a cure. Because diabetes is a lifelong condition, future retinal damage and vision loss is possible. Therefore, a sustained therapeutic non-invasive device is introduced which is in developmental stage.

Mu Chiao and colleagues at the University of British Columbia have pioneered a magnetic retinal implant that can supply a regulated and on-demand release of antiproliferative drugs to treat blindness from diabetic retinopathy safer and more effective. The technology is based on a platform technology called MicroElectroMechanical Systems (MEMS). In this technology, the device consists of a drug-loaded microreservoir that is sealed with elastic PDMS (polydimethylsiloxane) magnetic membrane with a laser-drilled aperture. The circular device is improved through magnetism. When external magnetic field is applied to the device the drug is released from the aperture by deforming the magnetic membrane and therefore discharging the drug (docetaxel) solution. When the magnet is withdrawn, drug is no longer released . A single loaded device could deliver effective concentrations of drug via multiple magnetisms for weeks. It was calculated that the same device translated to the human could last for one year. This proof-of-concept is novel in that low concentrations of docetaxel were utilized plus drug can be loaded in a small device and delivered through a non-invasive procedure. This device is no larger than the head of a pin and can be implanted behind the eye.
The advantage of UBC’s device is that it requires no batteries or electricity. Moreover, the UBC device is small enough to be implanted directly into the eye, so it does not have to rely on diffusion. Early lab tests using the drug docetaxel have shown that the device consistently delivers a suitable dosage and did not break or leak after 35 days. Moreover, the docetaxel retained its pharmacological efficacy even after remaining in the device for over two months and could be targeted to the posterior region of the eye.
The next challenge is to make sure that the device is biocompatible and has the right amount of controllability. It is envisioned that biocompatibility studies along with further drug testing may provide this technology for use in proliferative diabetic retinopathy.

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