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Recent eLetters

Displaying 1-10 letters out of 514 published

  1. Increased expression of connective tissue growth factor play a role in the pathogenesis of thyroid eye disease

    We read with great interest the article entitled "Pathogenesis of thyroid eye disease: review and update on molecular mechanisms" by Khong et al [1]. We would like to contribute to the article with our novel findings.

    In our previous study, we first demonstrated the up-regulation of mRNA and protein expression of fibrosis-related genes including fibronectin, apolipoprotein J and connective tissue growth factor (CTGF), in the orbital fibroblasts from patients with TED, as compared with those of normal controls [2]. In addition, the expression of CTGF in orbital fibroblasts can be modulated by oxidative stress. Recently, we further revealed that the enhanced expression of CTGF in TED orbital fibroblasts correlated with the clinical activity score and ophthalmopathy index, suggesting that increased levels of CTGF are pathologically significant [unpublished data].

    CTGF, a cysteine-rich matricellular protein of the CCN family, has been implicated in mediating various cellular processes, including adhesion, proliferation, differentiation, and migration, and extracellular matrix production, all of which are common features of tissue remodelling and fibrosis. Evidence has been increased suggesting that over-expression of CTGF has been noted in numerous fibrotic disorders, including pulmonary, renal, hepatic, skin, cardiac, and ocular fibrosis.

    Inflammation often dominates the early course of TED, followed by remodeling of orbital connective tissue, including accumulation of extracellular matrix and fibrosis. Fibrosis process represents a relative quiescent stage in the disease course of TED; however, it may cause much of the substantial morbidity of the patients including severe lid retraction, restrictive strabismus, proptosis, exposure keratopathy, and compressive optic neuropathy. Current knowledge about the inflammatory process of TED has been rapidly expanding, however, only limited studies have addressed the fibrosis process of this disease. Elucidation of the molecular mechanisms that initiate and regulate the process of fibrosis, especially the role of CTGF in TED, is crucial for the development of novel treatments.

    References

    1. Khong JJ, McNab AA, Ebeling PR, Craig JE, Selva D. Pathogenesis of thyroid eye disease: review and update on molecular mechanisms. Br J Ophthalmol 2016;100:142-50.

    2. Tsai CC, Wu SB, Chang PC, Wei YH. Alteration of Connective Tissue Growth Factor (CTGF) Expression in Orbital Fibroblasts from Patients with Graves' Ophthalmopathy. PLoS One 2015;10:e0143514.

    Conflict of Interest:

    None declared

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  2. Optic disc edema in astronauts following long-duration space flight

    Optic disc edema in astronauts following long-duration space flight

    We commend Morgan and colleagues for their discussion of optic disc changes during and after long-duration space flight (LDSF). 1 They note that astronauts after LDSF have developed clinical features (disc edema, globe flattening) similar to those of idiopathic intracranial hypertension (IIH) that may persist for many months post flight and suggest that these changes result from increased intracranial pressure (ICP) "which persists for months and years after their return to Earth."1

    Cephalad microgravity fluid shifts may increase head and neck venous pressure, thus inhibiting cerebrospinal fluid (CSF) drainage into the venous system, increasing CSF pressure and leading to changes similar to those seen in patients with IIH. However, lumbar puncture opening pressure (LPOP) has been only moderately elevated (21 to 28.5 cm H20) in the 4 astronauts examined from 12 to 60 days post-mission.2 Although LPOP may have been higher during the mission, we doubt these post-flight pressures are sufficiently high to sustain disc edema for months post-mission.

    As Morgan et al. note, microgravity exposure may disrupt flow within the orbital optic nerve subarachnoid space (ONSAS), causing accumulation of toxic metabolites and creating a ball-valve like effect that allows CSF to enter the ONSAS but inhibits outflow, thus increasing pressure within that compartment.3 In theory, either one or both ON sheaths may be affected in a given astronaut, with or without increased ICP. Of seven astronauts with disc edema, four have displayed disc asymmetry. One of these had unilateral disc edema associated with an LPOP of 18 cmH20 1 week after space flight.4 We also have observed persistent asymmetric disc edema 6 months following LDSF in an astronaut with LPOP's of 22 and 16 cm H20 performed 7 days and 1 year post mission respectively, again suggesting ON sheath compartmentalization (manuscript in preparation). We thus believe that increased ICP may not be the sole, or even primary, cause of persistent optic disc changes post LDSF.

    Thomas H. Mader MD C. Robert Gibson OD Andrew G. Lee MD Prem S. Subramanian, MD, PhD Neil R. Miller MD

    References

    1. Morgan WH, Balaratnasingam C, Lind CRP, Colley S, Kang MH, House PH, Yu D. Cerebrospinal fluid pressure and the eye. Br J Ophthalmol 2015; 0:1-7.

    2. Mader TH, Gibson CR, Pass AF, et al. Optic disc edema, globe flattening, choroidal folds, and hyperopic shifts observed in astronauts after long-duration space flight. Ophthalmology 2011;118:2058-69.

    3. Killer HE, Subramanian PS. Compartmentalized cerebrospinal fluid. Internat Ophthalmol Clin 2014;54(1):95-102.

    4. Mader TH, Gibson CR, Pass AF, et al. Optic disc edema in an astronaut after repeat long-duration space flight. J Neuroophthalmol 2013;33:249-55.

    Conflict of Interest:

    None declared

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  3. RE: Global variations and time trends in the prevalence of primary open angle glaucoma (POAG): a systematic review and meta-analysis. Kapetanakis, et al. 100:1 86-93 doi:10.1136/bjophthalmol-2015-307223

    Dear Editor,

    We thank Cheng and Tham for their interest in our systematic review of global variations and time trends in primary open angle glaucoma (POAG).[1] The comments raise some important issues relating to the assimilation of evidence from observational studies, particularly in summarising estimates of chronic disease prevalence.

    Cheng and Tham have questioned our inclusive approach, which resulted in us having a greater number of studies, number of POAG cases and population denominator, and led to more precise estimates of POAG prevalence compared to their earlier review.[2] The purpose of our more complex approach was to explicitly model and quantify the heterogeneity between population surveys, which used different survey methods and case definitions of POAG. By quantifying these differences we are able to provide estimates of POAG prevalence standardised to studies which use optimal methods, i.e., that did not rely on intraocular pressure and routinely performed visual field assessments on all participants, while allowing studies with suboptimal methods to contribute to overall estimates by accounting for the differences in study methods. This is particularly important when attempting to appreciate time trends in POAG, given changes in study methods over time. Moreover it allows greater global representation of studies, allowing more recent studies, particularly from less developed countries often with suboptimal methods, to contribute. This would not have been the case if a more exclusive approach had been adopted.

    Cheng and Tham also raise the issue of examining response rates. However, we examined differences in response rates in our earlier review,[3] and found that these had little effect on our prevalence estimates. We acknowledge in the paper the difficulty of extracting response rates, as these are not routinely reported, and sometimes confused with participation rates, i.e., the number who took part and completed an examination out of those who agreed to take part. In general, our experience is that assessment of study quality of observational studies is complex, compared to established methods in experimental studies. Attempts were made to judge the quality of studies on criteria such as response rates and methods used. However, it is difficult to extract measures of study quality in a meaningful way; for example well- designed studies may have low response rates. Our experience suggests that subjective assessments of study quality can sometimes be arbitrary and may not capture characteristics which may influence the outcome of interest. Hence, we have chosen an approach which seeks to understand variability by explicitly modelling differences in study methods. We believe that this makes for a fuller assessment, providing evidence based guidance for the conduct of future studies. For instance, our work suggests that a recent shift away from routine visual field testing, perhaps as an inadvertent consequence of recent ISGEO guidelines,[4] may have artefactually influenced prevalence estimates; such an effect would not have been identified and quantified by a more exclusive approach.

    Cheng and Tham also question whether our more inclusive strategy may have led to lower global estimates of POAG prevalence; 2.2% (95% CrI 1.8% to 2.8%) in our study [1] versus 3.1% (1.7% to 5.3%) in their earlier review.[2] However, we would like to point out that these estimates are not dissimilar, with our more precise estimate being encapsulated within the much wider confidence interval of their earlier estimate.[2] That our estimate is marginally lower may in part be attributable to our different ethnic/regional categorization of studies, particularly amongst Asians. The earlier review simply treated Asians as one population.[2] However, we found evidence suggesting that the age specific prevalence differed across Asian populations,[1] which needs to be accounted for when deriving global estimates, especially given the large population size of Asia. Moreover, our review includes more recent studies from Asian populations, where POAG numbers are high given the large population, but age-specific prevalence is actually lower compared to other ethnic groups. We feel that our modelling approach is justified and provides an important corrective to earlier work. For example, the earlier review suggested urban-rural differences in disease prevalence,[2] where we showed no effect as urban- rural associations were inextricably linked to ethnicity and the ethnic specific associations with age.[1]

    We hope that these estimates provide greater certainty and transparency so we understand how the global and regional estimates of POAG prevalence are derived. Greater precision allows for more accurate and appropriate planning of health care service needed to care for those with the condition. We also believe that our work will assist with the design of future population based studies, which seek to describe the population prevalence of glaucoma.

    Authors: Dr Alicja R Rudnicka,* Dr Venediktos V Kapetanakis,* Miss Michelle P Y Chan,# Professor Paul J Foster,#** Professor Derek G Cook,* Professor Christopher G Owen

    *Population Health Research Institute, St George's, University of London, Cranmer Terrace, London, SW17 0RE, UK

    #Division of Genetics and Epidemiology, UCL Institute of Ophthalmology, 11-43 Bath Street, London EC1V 9EL, UK

    **NIHR Biomedical Research Centre Moorfields Eye Hospital NHS Foundation Trust, 162 City Road, London EC1V 2PD, UK.

    References:

    1. Kapetanakis VV, Chan MP, Foster PJ, Cook DG, Owen CG, Rudnicka AR. Global variations and time trends in the prevalence of primary open angle glaucoma (POAG): a systematic review and meta-analysis. Br J Ophthalmol 2015.

    2. Tham YC, Li X, Wong TY, Quigley HA, Aung T, Cheng CY. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta-analysis. Ophthalmology 2014; 121(11):2081- 2090.

    3. Rudnicka AR, Mt-Isa S, Owen CG, Cook DG, Ashby D. Variations in primary open-angle glaucoma prevalence by age, gender, and race: a Bayesian meta-analysis. Invest Ophthalmol Vis Sci 2006; 47(10):4254-4261.

    4. Foster PJ, Buhrmann R, Quigley HA, Johnson GJ. The definition and classification of glaucoma in prevalence surveys. Br J Ophthalmol 2002; 86(2):238-242.

    Conflict of Interest:

    None declared

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  4. Re: Global variations and time trends in the prevalence of primary open-angle glaucoma: a systemic review and meta-analysis

    Dear Editor,

    We read with interest the article by Kapetanakis et al.[1] The authors presented a systemic review of published population-based surveys to provide estimates of global and regional prevalence of primary open- angle glaucoma (POAG). The authors claimed that this review provided the most precise estimates of POAG prevalence thus far, as they adopted a more "inclusive" approach, compared to previous review.[2] As a result of this inclusive approach, more publications were included in this review with greater total number of cases and participants, and thus the authors believed that these estimates provided greater certainty compared to previous reviews.[2 3]

    Nevertheless, while an 'inclusive' approach adopted in this review generated a 'seemingly' more precise estimate (slightly narrower credible intervals), it may not necessarily provide estimates which 'accurately' reflect the trends of POAG prevalence. This is mainly because, the review also included older studies with improper definition/ diagnosis of POAG which used raised IOP (i.e. greater than 21mmHg) as a key diagnostic criterion for POAG. It has been widely recognized that using IOP as a diagnostic criterion is not appropriate and may miss POAG cases with lower levels of IOP.[4] This point has also been reiterated and acknowledged by the authors themselves in the manuscript. Furthermore, in Table 2, the authors showed that reliance on IOP in POAG diagnosis was associated with lower POAG prevalence. This finding befittingly concurs with the point that studies which used IOP as a diagnostic criterion would indeed underestimate the prevalence of POAG. Thus, inclusion of older studies with improper POAG definition in the meta-analysis would naturally result in an underestimated overall pooled estimate despite having a seemingly narrower range of credible intervals (mainly due to higher number of POAG cases). This is evident when comparing the global POAG prevalence in this review (2.2%) with the prevalence estimated in our group's recent meta- analysis project (3.05%).[2]

    The idea to include more studies in order to have 'greater power' but at the expense of compromised study quality inclusion criteria, is fundamentally flawed in the context of conducting a reliable meta- analysis. Estimation errors caused by inclusion of poor quality studies may not be sufficiently accounted for by using modeling method to adjust for study design factor. Thus, the authors' claim that 'more precise and accurate estimates were produced in this review' appears to be unconvincing and overly stated.

    Secondly, response rate was not taken into account when identifying studies to be included in this meta-analysis. It was noticed that studies of low response rates (i.e. less than 60% or 70%) were also included in the analysis. It should be noted that population-based studies with suboptimal response rate can give rise to sampling bias even though random sampling method was adopted. Thus, estimates from these studies may not be accurately representative of their respective underlying populations. Inclusion of such studies may further introduce error to the overall pooled estimate. Furthermore, if greater weights were attributed by studies which relied on IOP diagnostic criterion or by studies with poor response rate in this meta-analysis, the impact on the overall pooled estimate would be even greater. With regards to this, a forest plot ought to be included in this meta-analysis to illustrate the effect size and the weight rendered by each study. Such illustration with additional sensitivity analyses (stratified by study design factors or response rate) may help to further validate or refute the approach adopted in this analysis.

    Taken together, we humbly opine that a more 'inclusive' approach but without adequate screening of study quality, may not necessarily yield more accurate estimates. The seemingly more precise estimate (i.e. slightly narrower credible intervals) was simply due to increase in sheer number of POAG cases from studies of inadequate quality. Robust and comprehensive assessments of study quality are central to a valid, high quality meta-analysis.

    Thank you.

    References:

    1. Kapetanakis VV, Chan MP, Foster PJ, et al. Global variations and time trends in the prevalence of primary open angle glaucoma (POAG): a systematic review and meta-analysis. Br J Ophthalmol 2015.

    2. Tham YC, Li X, Wong TY, et al. Global prevalence of glaucoma and projections of glaucoma burden through 2040: a systematic review and meta- analysis. Ophthalmology 2014;121(11):2081-90.

    3. Quigley HA, Broman AT. The number of people with glaucoma worldwide in 2010 and 2020. Br J Ophthalmol 2006;90(3):262-7.

    4. Quigley HA. Glaucoma. Lancet (London, England) 2011;377(9774):1367 -77.

    Conflict of Interest:

    None declared

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  5. Real life visual improvements with anti vascular endothelial growth factor treatment for wet age-related macular degeneration - Absolute or relative?

    Dear Editor

    We congratulate Holz et al.1 on their most important contribution to anti-vascular endothelial growth factor therapy in neovascular age-related macular degeneration (n-AMD). We think it is important to note that their main finding "visual acuity improved until about day 120; thereafter visual acuity changes were not maintained" does not contradict the findings of the MARINA2 [Ranibizumab Vs sham injection] clinical trial. We have previously re-evaluated3 the published results of the MARINA study to assess the absolute risk reduction (The absolute difference of outcome between experimental - i.e. ranibizumab treated - and control participants in the MARINA trial). This being the approach specified in The ABPI Code of Practice4 Clause 7; Information, Claims and Comparisons "Referring only to relative risk, especially with regard to risk reduction, can make a medicine appear more effective than it actually is. In order to assess the clinical impact of an outcome, the reader also needs to know the absolute risk involved. In that regard relative risk should never be referred to without also referring to the absolute risk. Absolute risk can be referred to in isolation." We set out in the graph below our evaluation of mean letter change from baseline (visual acuity change) derived from MARINA Figure 2 A results page 14262. The published change in letter score is at 3 month intervals rather than for each monthly injection as our efforts to acquire the raw data from the authors of the MARINA study2 have been unsuccessful. The best we can do is to show the letter change for the ranibizumab treated patients (we have confined our analysis to 0.5 mg group) letter score is in green, sham injection is in blue and the difference between the groups is in pink - this being the absolute risk reduction at every time we have data for. Our re-analysis seemingly confirms Holtz's findings1; ranibizumab is apparently most beneficial in the initial stages of treatment of n-AMD and visual gains cease between 3 - 6 months.

    Figure 1 - Green line - Ranibizumab treated patients (0.5mg) - change in letters read since last injection. Blue line - Sham-injection treated patients - change in letters read since last injection. Pink line - Absolute risk reduction (The arithmetic difference between the Ranibizumab and sham groups for each 3-monthly time point.)

    We note that Holtz and colleagues presented the mean change in visual acuity score after start of anti-VEGF as their primary endpoints. Our graph demonstrates the change in visual acuity score since previous visit and we note the striking resemblance in that both the analysis plots a very similar graph. While the patient demographics include the various subsets of n-AMD, we could not find any mention of visual acuity outcomes for these subset groups of patients. As MARINA showed visual benefits (stabilization or improvement of letters read) due to Ranibizumab treatment was achieved in only 27.6% of patients, we ask the authors if they are able to predict likely responders based on any base-line characteristics that would distinguish them from non-responders. Also would the authors be able to share if available their analysis of change in visual acuity from the previous visit. This could help in the early identification of those patients unlikely to benefit either prior to treatment or as the treatment progresses and avoid exposing patients unlikely to benefit to the risks of treatment.

    References

    1. Frank G Holz, Ramin Tadayoni, Stephen Beatty et al. Multi-country real-life experience of anti-vascular endothelial growth factor therapy for wet age-related macular degeneration.Br J Ophthalmol doi:10.1136/bjophthalmol-2014-305327

    2. Philip J. Rosenfeld, M.D., Ph.D., David M. Brown, M.D., Jeffrey S. Heier, M.D. et al. for the MARINA Study Group. N Engl J Med 2006; 355:1419-1431.

    3. B. Ramasamy, S Tiew, J Wason, L Clearkin . Absolute Risk Reduction and Natural Frequencies of Ranibizumab treatment in neovascular Age-Related Macular Degeneration (nvAMD). Poster and rapid fire presentation, Oxford Ophthalmological Congress ( 7/7/2015)

    4. ABPI Code of Practice for The Pharmaceutical Industry https://www.bsped.org.uk/resources/docs/ABPIguidelines

    Conflict of Interest:

    None declared

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  6. Amniotic membrane graft to conjunctival flap in treatment of non-viral resistant infectious keratitis: a randomised clinical study

    Dear Editor; We have read the article entitled "Amniotic membrane graft to conjunctival flap in treatment of non-viral resistant infectious keratitis: a randomised clinical study" by Abdulhalim et al. with interest.1 The authors compare the results of bipedicle conjunctival flap and cryopreserved amniotic membrane graft in the treatment of non-viral infectious keratitis resistant to medical treatment. We want to express our reservation about using amniotic membrane in the acute stage of fungal keratitis. The main immune mechanism against fungal keratitis depends on neutrophils.2 Karthikeyan et al. revealed that neutrophils constitute the vast majority (90%) of cellular infiltrates in fungus-infected human corneas.3 In the course of the anti-fungal immune activity reactive oxygen species secreted through the infected tissues play very critical roles. Furthermore, the balance between the host oxidant and the fungal anti- oxidant substances has been studied in order to decrease hyphal survival. Besides that; the balance between the host oxidant and the fungal anti- oxidant substances has lately been discussed to be targeted for diminishing hyphal survival.2 On the other hand, Lockington et al. recently reported that amniotic membrane can scavenge reactive oxygen species because of abundant hyaluronic acid.4 Besides, amniotic membrane may suppress immune defense by absorbing live inflammatory cells into its stroma and force them to apoptosis.5 Therefore, we suppose that antioxidant and anti-inflammatory properties of amniotic membrane could be objectionable during the acute phase of fungal keratitis in which fungicidal activity is essential. We propose that amniotic membrane transplantation should be delayed until the infection is limited to a certain location.

    Conflict of Interest:

    None declared

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  7. Response to " Recovery of photoreceptor inner and outer segment layer thickness after reattachment of rhegmatogenous retinal detachment"

    We read with great interest the study" Recovery of photoreceptor inner and outer segment layer thickness after reattachment of rhegmatogenous retinal detachment" by Terauchi G, et al.[1] Authors concluded that thickness of inner segment layer (20.4 +/- 5.0 microns) at one month after surgery was significantly less than fellow eye (28.9 =/- 2.9 microns). However, we know that the axial resolution of Spectral Domain(SD)-OCT is approximately 5 microns i.e. one pixel on the scan image would represent for 5 microns. This would lead to a difference between the outer segment measurements in operated eye and fellow eye in the range of 1-2 pixels, leaving very little room for error. Although, coefficient of repeatability for total macular thickness in Diabetic Macular Edema was found as high as 9 micron.[2] The measurement error and coefficient of repeatability of outer segment and inner segment measurements using SD-OCT is still not known. Keeping this in account, would the results still remain statistically significant? Hence, if measurements were taken by Adaptive optics-OCT with axial resolution of 3micron[3]there would be greater reliability of measurements and results compared to SD-OCT especially considering smaller measurements like outer and inner segment layer thickness.

    We keenly wait authors' reply.

    References

    1. Terauchi, G., et al., Recovery of photoreceptor inner and outer segment layer thickness after reattachment of rhegmatogenous retinal detachment. Br J Ophthalmol, 2015. 99(10): p. 1323-7. 2. Sohn, E.H., et al., Reproducibility of diabetic macular edema estimates from SD-OCT is affected by the choice of image analysis algorithm. Invest Ophthalmol Vis Sci, 2013. 54(6): p. 4184-8. 3. Miller, D.T., et al., Adaptive optics and the eye (super resolution OCT). Eye (Lond), 2011. 25(3): p. 321-30.

    Conflict of Interest:

    None declared

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  8. Genetic Testing for Chromosomal Aberration in Choroidal Melanoma

    The authors have investigated the and compared the chromosome 3 aberrations of Choroidal melanoma (CM) as determined by multiplex ligation probe amplification (MLPA) or microsatellite analysis (MSA)in intra ocular tumor biopsies with those results obtained from subsequent endoresection/enucleation of the same Choroidal melanoma. However few points need clarification from the authors: 1. Since the investigators used few markers on chromosome 3, technically speaking the use of the word "Monosomy" is not appropriate to describe the generic findings. This is at best can be called "Partial monosomy" or even better, just describe the chromosome 3 locations of the deletions or chromosome 8 duplications. 2. There are better genetic techniques currently available to detect chromosomal deletions(s) and/or duplication(s) than multiplex ligation probe amplification (MLPA) or micro-satellite markers. For example, array comparative genomic hybridization (arrayCGH) high definition can be used to screen the full genomic for chromosomal abnormalities and even detect deletion(s) and/or duplication(s) as small as 10 Kb in size. The 100 ng of DNA which was used by the investigators for MLPA can be easily used for arrayCGH with small alterations to the protocol. This would make the results more comprehensive and may able to detect other alterations on other chromosomes. 3. The use of microsatellite markers to measure chromosomal abnormalities (duplication or deletion) is not appropriate. Microsatellite markers, if informative, can give you whether the tested individual is homozygous or heterozygous for a particular allele. They are not design to give you a quantitative answer and the peak height cannot be used for quantitative measure. 4. It will be great if the authors can elaborate on the genes encompassed in the deleted areas of chromosome-3 and how those genes may contribute to the development and/or metastatic effect on the melanoma. For example, are those genes involved in suppressing the tumor? or do they play some other role ? 5. In Table-2, the authors list 13 patients with Chr3 loss vs. 12 patients with no chr3 loss, can we actually use the deletion(s) on chr3 as a genetic marker for choroidal melanoma?

    Conflict of Interest:

    None declared

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  9. response to: 3D printed reproductions of orbital dissections: a novel mode of visualising anatomy for trainees in ophthalmology or optometry

    Dear Editor,

    We read the article '3D printed reproductions of orbital dissections: a novel mode of visualising anatomy for trainees in ophthalmology or optometry' by Adams JW. et al with great interest. The authors have successfully identified the need for experience handling and navigating through anatomical material to understand clinical ophthalmology. Furthermore, they have brilliantly created a means for this teaching to occur due to the difficulties obtaining cadaveric specimens, and the similar issues and expense of using plastinated models.

    We were particularly interested in the preparation of the orbital dissections, and the choice of views to optimise the teaching value of the prosections. In the paper, it is stated quite rightly that 'it is essential to optimise the number of features displayed' (1). Given the authors' expertise in recreating the best from the cadaveric specimens to generate models, we would like the authors' opinion on how best to conduct an ophthalmic anatomy teaching session for students using approximately ten cadaveric heads which we will be running next year. What do the authors think would be the most important teaching aims, and how do the authors recommend specimens should be approached to maximise educational effectiveness? Furthermore, other than using techniques outlined in their paper to create the best views for models, are there any other ways in which we should take advantage of this privileged access to cadaveric tissue?

    We would very much appreciate some advice and guidance with regards to this, and once again we commend the authors for this innovative method of teaching dissection.

    References: 1. Adams JW, Paxton L, Dawes K, Burlak K, Quayle M, McMenamin PG, 3D printed reproductions of orbital dissections: a novel mode of visualising anatomy for trainees in ophthalmology or optometry, Br J Ophthalmol, 2015; 99(9): 1162-7

    Conflict of Interest:

    None declared

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  10. Re:Significance of hyper auto fluorescent (HAF) ring in choroidal neovascularization (CNV) in Age related Macular Degeneration (AMD)

    Dear Editor,

    Dr. Sagar and colleagues made reference to our paper "Significance of the Hyperautofluorescent Ring Associated with Choroidal Neovascularization in Eyes Undergoing Anti-VEGF therapy for Wet Age-Related Macular Degeneration", and pointed out the fact that they did not find a statistically significant difference in subretinal fluid (SRF) between eyes with and without a hyperautofluorescent ring (HAF) in their studied population.

    We would first like to thank Dr Sagar et al. for their interest in our publication and in this newly reported autoflourescence phenomenon, which as was mentioned, is quite common among eyes diagnosed with neovascular AMD. Our rigorous data collection, measurements (including vertical and horizontal SRF extend, as well as SRF area) and analysis led to our results showing that the HAF ring had a positive correlation with baseline subretinal fluid and outer retinal disruption. Similar to their findings, our study did not show a statistically significant association with visual acuity.

    Despite our thorough research on this topic, we agree that more work is indicated on this subject to fully understand the meaning and importance of the HAF ring.

    Sincerely,

    William R. Freeman, MD Distinguished Professor and Director UCSD Jacobs Retina Center Vice Chairman Department of Ophthalmology, UCSD Shiley Eye Center 9415 Campus Point Drive La Jolla, CA 92093-0946

    Tel: 858 534 3513 Fax: 858 534 7985

    Conflict of Interest:

    None declared

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