Transcript Macular Degeneration Foundation - Welcome

Macular Degeneration
A Journey through the Eye
Dr Dianne Sharp
Ophthalmologist
Retina Specialists, Auckland
What is the Macula?
optic
nerve
retina
macula
Normal Retina
What is Macular Degeneration (AMD)?
•
Progressive, chronic
disease of central
retina
• Loss of central vision
• Peripheral vision not
affected
• Not black blind
Macular Degeneration in New Zealand
Leading cause of severe vision loss
Other
Cataract
Glaucoma
Macular
Degeneration
Macular Degeneration
Facts and Figures
• Deloitte Access Economics
2011 and Macular
Degeneration Foundation
Australia
www.mdfoundation.com.au
Macular Degeneration in NZ
Australian pop 22 million: NZ pop 4.4million = approx. 1/5th
 Macular Degeneration (MD) is a chronic disease with no cure1
 Cause of up to 50% of all blindness
 Affects 1 in 7 people over 50 in some way:1
o 170,000 have early MD in NZ
o 33,400 have late MD in NZ. 7,000 are legally blind.
 1 in 4 people over 80 have vision loss from MD1
 The number of people with MD will increase by 70% by 20301
¹ Deloitte Access Economics
Prevalence of chronic diseases
Australia 2010 – ref Deloitte
The Impact of Macular Degeneration*
2x Risk of falls
4 to Risk of hip fracture
8x
3x Risk of depression
2x Rate of social
dependence
3yr Nursing home
Employment
admission
• Access Economics & AMDAI 2010.
The impact of MD on quality of life is
equivalent to cancer or coronary heart
disease.
Cost of vision loss from
Macular Degeneration
$AU2.55 billion in 2010 in Australia
$NZ 0.64 billion in NZ
(Adjusted for population and currency)
Deloitte Access Economics & Macular Degeneration Foundation 2011,
Optimal integrated model of care
for Macular Degeneration (AMD)
1. Primary prevention
2. Early detection & timely diagnosis
3. Early & regular treatment with on-going
monitoring for wet AMD
4. Rehabilitation & emotional support
Macular Degeneration symptoms
How does MD Develop?
Normal Retina
Macula
Retina
RPE
Choroid
Healthy retina
RETINA
RPE
Bruch’s membrane
CHOROID
Early AMD -“Drusen”
Early AMD
Drusen
Normal Retina
Early AMD
Drusen
Early Stages of MD
• Normally no symptoms but at risk of
progression
• Lipid deposits (drusen)
• No treatment but progression slowed by
diet and lifestyle modifications
Dry AMD
Drusen
Atrophy 7rs later
Dry AMD
Late Stages of AMD
Dry AMD:
• Atrophy of retinal tissue.
• Gradual loss of central vision over years
end stage has significant vision loss
Wet AMD:
• Formation leaky blood vessels under
retina
• Rapid loss central vision
Wet AMD
Advanced Wet AMD
Wet AMD
Late Stages of MD
Dry MD:
• Atrophy of retinal tissue.
• Gradual loss of central vision over years
end stage has significant vision loss
Wet MD:
• Formation leaky blood vessels under
retina
• Rapid loss central vision over weeks or
months
Visual impairment by severity of
vision loss
Optimal integrated model of care
for Macular Degeneration (AMD)
1. Primary prevention
2. Early detection & timely diagnosis
3. Early & regular treatment with on-going
monitoring for wet AMD
4. Rehabilitation & emotional support
Risk Factors for MD
Age
Prevalence AMD (%)
Blue Mountains Eye Study
Age
Early
group
AMD
50-59 yr
6%
60-69 yr
11%
70-79 yr
20%
80-89 yr
25%
90+ yr
35%
All 50 yr+
13%
Dry Late
AMD
<0.5%
<0.5%
1%
3%
18%
0.7%
Wet Late All Late
AMD
AMD
<0.5%
<0.5%
0.5%
0.5%
2%
3%
7%
10%
13%
31%
1.5%
% Prevalence AMD by age
Risk Factors for MD
Genetics
• 50 -70% cases have
a genetic link
• 50% risk of MD if a
direct family history
AMD Principal genes CFH & ARMS2
Rotterdam Eye Study
• Early AMD 75% had one
risk allele
• Late AMD 93% had one
risk allele
• Risk of developing AMD
by 85yrs increases with
number of alleles
Genetics: Risk Alleles
CFH
• Mainly dry AMD
• Inhibitory effect on
complement pathway
• ? Less effective
inhibition of
inflammatory pathway
ARMS2
• Mainly wet MD
• Gene located in
mitochondria
• ? Interferes with normal
oxidation
Rotterdam Eye Study
Modifying Genetic Risk Factors
Smoking
Diet
With 1 CFH allele
Risk of AMD:
Non smokers risk 12x
Smokers risk 34x
1 CFH &/or ARMS2 allele
High dose Zn, omega 3,
lutein rate close to no
genetic risk
Risk Factors for MD
Smoking
 Smoking increases risk 3 to 4 times
 Smokers get MD 10 years earlier, on average
 BUT 20 years after quitting, a smoker’s risk is
the same as a non-smoker
Reduce Your Risk of MD
• Eye test every 2 years or earlier
if any new symptoms
• Recommend family members
have eye test.
• Protect eyes from sun
• Healthy lifestyle:
o Control weight
o Exercise
o Eat eye health foods
o Consider a supplement
Eating for Eye Health
Lutein
Dark green and naturally
yellow vegetables and fruit
every day
Eating for Eye Health
Omega 3
Fish 2-3 times per week
(salmon, sardines, mackerel, anchovies, tuna)
Eating for Eye Health
Handful of nuts per week
(brazil nuts, almonds, walnuts, pine nuts)
Limit fat intake
Low Glycaemic Index foods
Low GI Foods
• Break down more
slowly
• Prolong energy
release
• Leave less waste
products in the eye
What supplements?
3 key supplements to consider:
• AREDS formulation
• Lutein
• Omega 3 (fish oil)
AREDS Formula
Age Related Eye Disease Study
Per day
• Zinc 80mg
• Vitamin C 500mg
• Vitamin E 400IU
• Copper 2mg
• ß-carotene 15mg
Macu-Vision
Daily dose = 2 tablets
People who smoke, suffer from lung cancer or
asbestosis should not take a supplement with betacarotene. This is the reason it is removed from most
AREDS supplement products.
Diet supplements
AREDS Formulation: for intermediate or late AMD
in one eye, reduces risk of progression by 20-25%
AREDS 2: trial in progress. Reducing Zn,
removing beta-carotene, addition Lutein
Optimal integrated model of care
for Macular Degeneration (AMD)
1. Primary prevention
2. Early detection & timely diagnosis
3. Early & regular treatment with on-going
monitoring for wet AMD
4. Rehabilitation & emotional support
Symptoms of Macular Degeneration
Early stages
o Early MD may be asymptomatic.
Eye tests are the key.
Late stages
o Difficulty distinguishing faces
o Difficulty reading & fine vision
o Distortion (straight lines appear
wavy or bent)
o Dark / blank patches in central
vision
Use an Amsler grid
(one eye at a time)
Normal
Lines distorted
Dark patches or
empty spaces
Treatments for AMD
Chronic disease
• Dry AMD: diet and lifestyle important
• Wet AMD: treatment available
•diet and lifestyle also important
Treatment for Wet MD
• Injection Lucentis or
Avastin into the eye
• Average every 4–6
weeks
• Early treatment
saves sight! Aim to
stabilise vision and
prevent further
vision loss.
AMD Treatment Trials (Anchor & Marina)
Lucentis treatment: Mean gain in vision over 2yr
ANCHOR +2
2
MARINA +1.5
Lines on vision chart
1
0
2
4
6
8
10
12
14
16
18
20
22
24
-1
PDT -2
-2
-3
***p<0.0001 vs. sham
sham -3
Month
Current drug treatments
• Lucentis or Avastin
o Normally given as monthly injections
o Highly effective.
• CATT study: Comparing Lucentis and Avastin
o Similar effect at 24 months
o Still some unanswered questions re adverse
events with Avastin
Optimal integrated model of care
for Macular Degeneration (AMD)
1. Primary prevention
2. Early detection & timely diagnosis
3. Early & regular treatment with on-going
monitoring for wet AMD
4. Rehabilitation & emotional support
AMD treatment trials (PIER)
Subset analysis highlights need for individualised
dosing
Mean (SE) change in BCVA from baseline (letters)
15
10
Maintained initial gain
(>0 at month 3)
(n=16, 26% total & 40%
initial gainers)
Initial gain not maintained
(n=24, 40% total & 60%
initial gainers)
5
0
-5
No initial gain
(no gain at month 3)
(n=21, 34% total)
-10
-15
0
1
2
3
4
5 6 7
Month
BCVA, best corrected visual acuity
8
9
10 11 12
New Therapies on horizon
• Treatments that allow decreased Rx frequency
• Improved drug delivery methods (drops, oral)
• Therapies allowing self monitoring rather than
doctor visits
• Combined drug therapies →improve efficacy
& decreasing Rx burden
• Drugs that reverse disease process
Wet AMD: New treatments
• VEGF Trap-Eye
o Similar effect to Lucentis / Avastin
o lasts two months
o Available later this year in NZ
• Pazopanib (Eye drop)
o Used with anti-VEGF injections to help
spread number of injections
o In phase 3 trials
Dry AMD: New treatments
• Fenretinide
A tablet, derived from Vitamin A
• Slows development of drusen
• Reduces risk of wet AMD by 2 fold
• In phase 3 trials
• Brimonidine
An implant inside eye
• May protect against late dry AMD
• In phase 2 trials
Laser for early (dry) AMD
• Ellex 2RT (Laser)
o Ultra-short duration, non-thermal laser
o Appears to reduce formation of drusen
o May improve waste transport in retina
o Trials ongoing
Gene therapy for wet AMD
• Gene therapy inserts a ‘normal’ gene into
cells to replace disease-causing genes.
• RetinoStat – gene-therapy to stop new
blood vessel formation.
Early clinical trials.
When retinal cells die
• Treatments that could directly replace lost
retinal cells
•
•
RPE cell transplantation from donor
Stem Cell treatment
• Artificial (‘bionic’) vision
– Only useful if total vision loss
Retinal cell transplantation
• Many animal studies,
some human studies
• Only limited efficacy
reported
• Very difficult surgery
Stem cells
• Stem cells have the ability to develop into
different types of adult cells such as
photoreceptor cells or RPE cells
• Possible sources: Embryonic stem cells
(Most adaptable), Adult stem cells (more
restricted)
Please note: MDNZ recognises and respects different points of
view concerning stem cell research. Our role is to simply report on
all research occurring for your information.
Stem cell treatment
Artificial vision “Bionic eyes”
An electronic prosthesis to replace the function of
dead retinal cells.
NOTE:
Current ‘bionic eyes’ provide MUCH LESS vision
than most people with end stage AMD already
possess.
Pathogenesis of AMD for future
treatments
Early AMD: Drusen
OCT
Infra red
Auto fluorescence
Normal
Anti-inflammatory
AMD
Pro-inflammatory
Drusen
Complement inflammation
pathways
Membrane Attack Complex
Complement mediated inflammation in AMD
C5 cleavage products
beneath RPE.
Drusen contain almost
all alternative complement
pathway proteins
Anti-C5b-9 Membrane
Attack Complex
Rattner and Nathans 7, 860–872 (November 2006) | doi:10.1038/ nrn2007
Complement inflammation
pathways
Exercise
CFB
CFH
Complement inflammation
pathways
Exercise
Tobacco
CFH
CFB
CFH
Complement inflammation
pathways
Exercise
Tobacco
CFH
High fat intake
CFB
CFH
Complement inflammation
pathways
Exercise
Tobacco
CFB
CFH
CFH
High fat intake
HDL
Membrane Attack Complex
INTERACTION OF ENVIRONMENTAL AND
GENETIC RISK FACTORS IN AMD
Risk of AMD
• Genetic and environmental risk factors are not
merely additive
• Resultant risk in some cases is greater than
that conferred by each risk factor individually.
Potential Targets for AMD Therapy
Membrane Attack Complex
AMD is a complex disease
• Medical research takes time and vast amounts
of money.
o New drug: 12 years and $500m - $1.2 billion
o Other research:
 New mechanisms
 Identify risk and protective factors
• More research is needed!
Optimal integrated model of care
for Macular Degeneration (AMD)
1. Primary prevention
2. Early detection & timely diagnosis
3. Early & regular treatment with on-going
monitoring for wet AMD
4. Rehabilitation & emotional support
Optimal integrated model of care
for Macular Degeneration (AMD)
1. Primary prevention
2. Early detection & timely diagnosis
3. Early & regular treatment with on-going
monitoring for wet AMD
4. Rehabilitation & emotional support
Our Vision:
To reduce the
incidence and impact
of
Macular Degeneration
in New Zealand
Our Objectives
•
Education
•
Awareness
•
Representation
•
Research
•
Support Services
For more information
0800 MACULA
Free call, NZ-wide
Web: www.mdnz.co.nz
The Ageing Eye: Integrated Care
GP
Optometrist
Ophthalmologist
The Ageing Eye: Integrated Care
GP
Optometrist
Ophthalmologist