Macular Degeneration Treatment

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Macular degeneration is one of the leading causes of vision loss among those over 50. It involves degeneration of the central part of the retina known as macula and can result in blurry central vision. There are two types of macular degeneration – dry and wet.

The wet form is distinguished by a proliferation of abnormal blood vessels beneath the retina – this condition is also referred to as choroidal neovascularisation.

What is macular degeneration?

Macular degeneration refers to the breakdown or deterioration of your retina (back of eyeball) known as the macula, the area which allows for fine detail vision like threading needles, driving safely or reading books; as well as recognising faces and colors. Macular degeneration can result in blurriness, dark areas or distortion in straight-ahead vision; side and peripheral vision typically remain clear.

Macular degeneration occurs when light-sensitive cells in the macula begin to break down and cease working effectively as we age, becoming one of the leading causes of blindness among adults aged 50 years or over.

Macular degeneration most frequently takes the form of dry macular degeneration, which is marked by yellow deposits beneath the retina called drusen that do not damage sight but indicate that your macula may begin to thin over time. Unfortunately, dry macular degeneration can progress into wet macular degeneration and become even more serious over time.

Wet macular degeneration occurs when abnormal blood vessels form and leak fluid beneath the retina, scarring the macula and leading to rapid loss of vision. Symptoms may include sudden central vision loss, dark or empty areas in your visual field, distortion of straight lines and faded or muted colors. Wet macular degeneration should be addressed promptly by medical practitioners using an Amsler grid chart as well as possibly performing an ophthalmologic exam using dye.

Diabetic macular oedema

Diabetic macular oedema (DME) is caused by changes to small blood vessels in the retina – the light-sensitive layer at the back of your eye – leaking fluid, leading to macula swelling and blurred vision over time. Over time this condition may progress into permanent loss of central vision unless properly managed with care by diabetic patients managing blood sugar, blood pressure and cholesterol to avoid further retina damage.

Diabetics have an increased risk of diabetic macular oedema (DME), the primary cause of vision loss among those living with the disease. DME occurs when retinal blood vessels leak fluid and thicken, creating pools of liquid in the center of retina known as the macula; this fluid deposits itself on its way towards providing sharp central vision used for reading or driving; its loss results in difficulty seeing faces, reading or driving.

Fluid accumulates due to disruption of the blood-retinal barrier which separates blood vessels from retina. This complication of diabetes needs urgent treatment to avoid visual loss.

Your physician may suggest laser photo-coagulation to reduce fluid retention in the macula, using noninvasive laser photo-coagulation procedures and eye drops with anti-inflammatory properties, to inject drugs directly into vitreous gel (the gel-like substance inside of eyes). Alternately, surgery such as vitrectomy may be recommended; this procedure removes vitreous gel to release any pooled blood that’s been trapped inside, typically only recommended if other methods fail.

Aflibercept (Eylea)

Aflibercept is a recombinant human fusion protein designed to act as a decoy receptor for vascular endothelial growth factor (VEGF) family ligands such as VEGF-A and VEGF-B. By binding tightly with these molecules, Aflibercept inhibits their downstream signalling pathways while protecting normal tissue functions.

Eylea was approved for treating wet age-related macular degeneration (wet AMD), commonly referred to as wet age-related macular degeneration, in November 2011. Additionally, Eylea can help manage macular oedema caused by central retinal vein occlusion (CRVO) or diabetic macular oedema (DME).

Clinical trials conducted with intravitreal administration of Aflibercept were generally well tolerated, with minimal potential for systemic drug accumulation. Within two weeks of injection, plasma concentrations of free Aflibercept had declined below the lower limit of quantification while adjusted bound VEGF binding concentrations remained at or above its LLOQ.

Renal Impairment

A subgroup of patients with renal impairment was evaluated in one wet AMD study and one RVO/DME trial; no dose modifications based on renal impairment status were implemented; there were also no significant variations between mean plasma concentrations of free aflibercept between these groups of individuals.

Studies of pediatric ROP found aflibercept superior to standard laser treatment in two phase 3 clinical trials: VGFTe-ROP-1920 and 20090/20275, where its primary efficacy endpoint was defined as proportion of participants without both active ROP and unfavorable structural outcomes at 52 weeks chronological age per investigator assessment; noninferiority could not be demonstrated between them, therefore not recommended for use among children with ROP.

Ranibizumab (Lucentis)

ranibizumab (Lucentis) and its biosimilar SB11 have both been shown to be comparable in their ability to reduce macular edema caused by neovascular age-related macular degeneration, according to findings published by Clinical Ophthalmology. Both drugs were shown effective for treating this form of AMD while possessing similar safety profiles, making biosimilar drugs an attractive way of cutting costs while still providing comparable patient care.

On August 7, 2014, an sBLA for this medicine was submitted to the FDA, with an action date confirmed as February 6, 2015. Priority Review designation was awarded for diabetic retinopathy treatment by the FDA as well as Breakthrough Therapy Designation designation from this agency in 2012.

Ranibizumab differs from Aflibercept in that it blocks both receptors for Vascular Endothelial Growth Factor (VEGF), thus preventing VEGF-induced macular edema by decreasing activity of vasotonic acid molecules related to VEGF. As such, it has been approved by the FDA as the only anti-VEGF therapy that treats wet macular degeneration, neovascular age-related macular edema, diabetic macular edema, and myopic choroidal neovascularization.

MINERVA was designed as a clinical trial comparing monthly intravitreal injections of ranibizumab with best supportive care (BSC). The primary endpoint was one year gain in best corrected visual acuity as measured using ETDRS letters at six month and annual visits. Results indicated that, despite a minor difference in mean ETDRS letter gains, ranibizumab’s benefit persisted over one year. The authors concluded that a monthly dose of 0.5 mg ranibizumab is superior to BSC in patients with advanced neovascular AMD with central retinal thickness exceeding 250 microns. Furthermore, those requiring treatment of their DME in RIDE/RISE’s open-label extension phase showed less advanced centre-involving DME at extension baseline compared with those who did not require therapy.

Verteporfin (Avastin)

Before the advent of anti-VEGF medications, photodynamic therapy (PDT) was the standard of care for many forms of wet age-related macular degeneration. PDT involves injecting verteporfin, a photosensitising drug, into an arm vein before shining a special light to activate it; laser beams then targeted any new blood vessels forming within the macula and destroyed them without harming its surrounding retina.

PDT uses verteporfin, a drug which binds to proteins present in abnormal blood vessels, to kill them off using special light exposure from an optometrist and stop vision loss as well as improve sight in some cases. Unfortunately, this treatment option has an extremely limited success rate and therefore may not be appropriate for everyone suffering from neovascular AMD.

Current treatments for wet-ARMD include bevacizumab (Lucentis and Avastin). Both drugs must be injected directly into the eye, with bevacizumab being particularly successful; approximately nine out of ten patients taking these medicines experience their vision improving after taking these injections; they must be repeated every few weeks to remain effective.

Other treatments are currently under study for wet ARMD, such as radiation treatment, surgical techniques and drugs that inhibit blood vessel growth in the eye. Furthermore, research is underway into methods of transplanting peripheral retinal cells onto dead macular areas to restore some lost vision – but this technology still remains too far-off from being widely available.

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