Questions & answers from AMD Masterclasses presented by Ingebret Mojord
- Q1 How sensitive is the visual field testing for detecting AMD at an early stage if you don’t have an OCT? And which test and strategy would you recommend in general?
- Q2 What is your opinion about the vitamins/pills that are supposed to slow down AMD development or decrease the chance of developing AMD?
- Q3 Which is most common, type 1 or type 2 neovascularisation? Do they respond equally to treatment?
- Q4 What is the best optometric practice for follow-up in the different AMD situations, in your opinion? Especially dry AMD - how often do you see the patient?
- Q5 What are the risk factors of diet low in Omega 3 & 6, vitamins and minerals?
- Q6 Is there any evidence for the use of filter glasses preventing harmful light for young people (who show early signs of drusen in the macula)?
- Q7 I have some younger patients, 30-40 years old, who have a pigment dispersion close to macula, but no development over the years. What is the cause of this condition at an early age?
- Q8 At what stage of AMD do you see the first changes on an Amsler test?
- Q9 Where do I find a calculator that can predict the risk for AMD?
- Q10 Are the Valeda treatment tried in other macular diseases than AMD (i.e. Histoplasmosis)?
- Q11 What's the difference between macuShield and ocuvite?
- Q12 How do drusen outside the macula impact the risk of developing AMD? Should the conversation start there?
- Q13 How many potential customers will you have in your hometown? You only mentioned 42 persons?
- Q14 Could optometrists acquire the Valeda system and treat AMD without starting a war between the professions and the optometrists?
- Q15 Would treating (supplements and PBM) on the basis of dark adaption loss alone be indicated? Would it be accepted among ophthalmologists?
- Q16 Is Valeda only used in Norway? And do you know how many clinics in Norway offer this now?
How sensitive is the visual field testing for detecting AMD at an early stage if you don’t have an OCT? And which test and strategy would you recommend in general?
In Goldstein’s study, the modified Amsler grid was used (white lines on black background), having observed positivity in 53 % of the patients with choroidal neovascularisation, while in the present study, 70 % of positivity was found when the original grid was used (black lines on white background). The preferential hyperacuity perimeter has greater sensitivity than the Amsler grid in the detection of choroidal neovascularisation among patients over 50 years. It is a promising method for monitoring patients with age-related macular degeneration.
Goldstein M et al.; Preferential Hyperacuity Perimeter Research Group. Results of a multicenter clinical trial to evaluate the preferential hyperacuity perimeter for detection of age-related macular degeneration. Retina. 2005;25(3):296-303.
Isac et al. Comparison of the original Amsler grid with the preferential hyperacuity perimeter for detecting choroidal neovascularization in age-related macular degeneration. Arq Bras Oftalmol. 2007;70(5):771-6.
According to Albert et al., the original Amsler grid for the overall study population provided significantly better results than the modified version. The evaluation of data from the different subgroups showed no significant difference between patients with visual acuity ranging from 0.1 to 0.3. For patients with visual acuity of 0.5 or better, the original Amsler grid was significantly more informative and reliable than the modified version. The conclusion we can make from this study is that for patients with macular diseases, using the original Amsler grid (white lines on a black background) should be recommended. This is particularly important for patients with visual acuity of 0.5 or better.
Finally, Faes et al. concluded that results from small preliminary studies show promising test performance characteristics for the Amsler grid and the preferential hyperacuity perimeter in the diagnostic work-up of wet AMD. Based on test performance, the Amsler grid showed some advantages in ruling in wet AMD and could thereby be more helpful in monitoring the disease, but data were very heterogeneous. The preferential hyperacuity perimeter, in return, had small advantages over the Amsler grid in ruling out wet AMD and could thereby be more useful in the screening context.
Faes et al. Diagnostic accuracy of the Amsler grid and the preferential hyperacuity perimetry in the screening of patients with age-related macular degeneration: systematic review and meta-analysis. Eye (2014) 28, 788–796.
Yet, to what extent our findings can be transferred to a real clinic or practice still needs to be established. In addition to that, we’re seeing some new promising technologies emerging with theoretical advantages over the Amsler grid and the preferential hyperacuity perimeter, which need a careful clinical examination to confirm their usefulness in a screening and monitoring context. If confirmed, further studies assessing their impact on patient management still need to be quantified.
What is your opinion about the vitamins/pills that are supposed to slow down AMD development or decrease the chance of developing AMD?
There is no recommendation of taking any supplement before the intermediate level of risk factors is reached. See the guidelines from The College of Optometrists (UK) below.
Also, see instructions from the Danish Ophthalmology Association (Dansk Oftalmologisk Selskab) here.
Which is most common, type 1 or type 2 neovascularisation? Do they respond equally to treatment? Or is one of them worse than the other?
There are different neovascular subtypes, and it’s different from culture to culture. As evidenced by FA (Fluorescein Angio), occult lesions accounted for 49.6% of cases, whereas type 1 lesions were estimated to represent 39.9% by OCT. Classic lesions were found in 12.0% of cases, whereas type 2 lesions by OCT were estimated to represent 9.0%. And finally, RAP lesions were identified by FA in 28.6% of cases and in 34.2% of cases by OCT. Mixed lesions represented 9.8%, and 16.9% of the FA and OCT analysed images.
As a result, the use of OCT enhances the capacity of clinicians to detect type 3 lesions, which might be missed when performing an FA-based approach.
In an observational retrospective series of 154 eyes in 138 patients with neovascular AMD managed with treatment and extended regimen (TER), those patients with type 1 neovascularisation were significantly more likely to maintain good vision than other neovascular subtypes. It was also evidenced that vision achieved at three months following the initial intravitreal treatment was the best predictor for favourable long-term vision. The positive visual outcome was considered to be 20/60 or better.
The presence of type 1 lesions evidenced a robust and statistically significant association with a positive visual outcome at two, three and four years of follow-up into a TER. On the other hand, type 3 lesions were predictive of a positive visual outcome at two and three years, but the significance was lost by the fourth year. Finally, the presence of type 2 lesions was a negative predictor to achieve positive visual outcomes throughout the entire follow-up.
What is the best optometric practice for follow-up in the different AMD situations, in your opinion? Especially dry AMD - how often do you see the patient?
For people aged 50-60, I see them every second year. After the age of 60, I see them once a year.
Suppose there’s a high risk for developing choroidal neovascularisation. In that case, I see the patients more often – depending on their motivation and understanding of the risk factors and home testing possibilities.
What are the risk factors of diet low in Omega 3 & 6, vitamins and minerals?
There is no good evidence from randomized controlled trials that the general population should be taking antioxidant vitamin supplements to reduce their risk of developing AMD later on in life. Although observational studies have shown that the consumption of dietary omega 3 long-chain polyunsaturated fatty acids may reduce the risk of progression to advanced AMD, two randomized controlled trials failed to show any benefit of omega 3 supplements on AMD progression.
If you search in the Cochrane library on ‘antioxidant vitamin and mineral supplements for preventing age-related macular degeneration’, this is what you’ll find:
The Cochrane researchers found five relevant studies. The studies were large and included a total of 76,756 people. They took place in Australia, Finland, and the USA. The studies compared vitamin C, vitamin E, beta-carotene, and multivitamin supplements with placebo.
The review showed that, compared with taking a placebo:
- Taking vitamin E supplements made little or no difference to the chances of developing AMD (high-certainty evidence)
- Taking vitamin E supplements made little difference, or slightly increased, the chances of developing late AMD (moderate-certainty evidence)
- Taking beta-carotene made little or no difference to the chances of developing any AMD (high-certainty evidence) or late AMD (moderate-certainty evidence)
- Taking vitamin C made little or no difference to the chances of developing any AMD (high-certainty evidence) or late AMD (moderate-certainty evidence)
- Taking multivitamin tablets may slightly increase the chances of developing any AMD or late AMD (moderate-certainty evidence)
- Adverse effects were not consistently reported in these eye studies. Still, there is evidence from other large studies that beta-carotene increases the risk of lung cancer in people who smoke or who have been exposed to asbestos.
None of the studies reported quality of life or resource use and costs.
In conclusion, research has proved that older people with poor diets, especially with low antioxidants and Omega 3 fatty acid micronutrients intake and subsequently having low plasmatic levels, are more prone to develop AMD. Micronutrient supplementation enhances antioxidant defence and healthy eyes and might prevent/retard/modify AMD.
Is there any evidence for the use of filter glasses (511/527 wavelength) preventing harmful light for young people (who show early signs of drusen in the macula)?
People above 50 years old do not have the Dx of AMD. There is no evidence of using yellow lenses for AMD.
I have some younger patients, 30-40 years old, who have a pigment dispersion close to macula, but no development over the years. What is the cause of this condition at an early age?
Maybe some form of dystrophy or an earlier accident? There are many diseases that have to be excluded from the AMD diagnoses.
At what stage of AMD do you see the first changes on an Amsler test?
When the risk of neovascular development is realistic. For example, when patients are in the position to use the Amsler in a system and turns up at least at intermediate or high risk for developing late AMD.
Where do I find a calculator that can predict the risk for AMD?
Are the Valeda treatment tried in other macular diseases than AMD (i.e. Histoplasmosis)?
The indicated use is for treatment of ocular damage and disease using photobiomodulation, including inhibition of inflammatory mediators, edema or drusen deposition; improvement of wound healing following ocular trauma or surgery, an increase in visual acuity, and contrast sensitivity in patients with degenerative diseases such as dry age-related macular degeneration.
But the key focus at this moment is the Treatment of Dry Aged Macular Degeneration. The first pilot studies in the US & EU have started treating DR & DME patients.
Possible next steps in the future will be to explore the treatment of Glaucoma, Methanol intoxication, Retinitis Pigmentosa, retinopathy of prematurity, Leber’s hereditary optic neuropathy, amblyopia, and possibly others.
What's the difference between macuShield and ocuvite?
Ocuvite 2 tabl: Vitamin C 180 mg, Vitamin E 30 mg, Zinc 15 mg, Lutein 10 mg, Zeaxanthin 2 mg, Omega 3
MacuShield: Meso-Zeaxanthin 10 mg, Lutein 10 mg, Zeaxanthin 2 mg ++
The AREDS2 formula is the recommended formula in; PreservVision: vitamin C 500 mg, Zinc 80 mg, Copper 2 mg, Vitamin E (400 iu), Lutein 10 mg, Zeaxanthin 2 mg.
The AREDS mixture is the absolute recommended nutritional supplement.
What about drusen outside the macula. How do they impact the risk of developing AMD? Should the conversation start there?
There is no consensus about the connection between peripheral drusen and drusen associated with the AMD.
How many potential customers will you have in your hometown? You only mentioned 42 persons?
In the masterclass, I first mentioned the prevalence:
- 60-69 years old: 16% of the population
- 70-79 years old: 25% of the population
- 80-84 years old: 33% of the population.
The following slides from my masterclass then touched upon incidence (how many new cases per year) of late AMD per year (neovascular or geographic AMD):
- < 70 years old 0.5/1000 inhabitants
- > 70 years old 6.7/1000 inhabitants.
2/3 of those have neovascular AMD. So you can calculate from this information how many new wet patients there should be in your area.
Could optometrists acquire the Valeda system and treat AMD without starting a war between the professions and the optometrists?
Optometrists use photobiomodulation in the treatment of MGD for dry eyes already. Fundamentally it is the same process and to apply the treatment is not the same as doing surgery. One thing is to deliver the treatment; another thing is to decide when that treatment is the best decision. The legal question is then if optometrists will be allowed to treat a posterior eye disease independently.
Would treating (supplements and PBM) on the basis of dark adaption loss alone be indicated? Would it be accepted among ophthalmologists?
I don’t think dark adaption reduction itself should be an indicator for nutritional supplement or PBM. You should have at least intermediate drusen or intermediate risk factor for progression to late AMD.
About Valeda, you said that it is only in Norway? Is that correct, and do you know how many clinics in Norway offer this now?
Øyehelseklinikken Oslo and St. Olav Eye Clinic Tønsberg/Oslo do the Valeda treatment today.
I would expect this treatment to become more common in all markets.