In a reply to my editorial in the November issue, Dr Lempert raises several valid concerns regarding vision screening for amblyopia. I would like to thank Dr Lempert for his reply and this possibility for a discussion on a difficult and important topic!
I was, however, slightly surprised to find that the reply is written as a rebuttal of my arguments, while I am of the same opinion as Dr Lempert, and have...
In a reply to my editorial in the November issue, Dr Lempert raises several valid concerns regarding vision screening for amblyopia. I would like to thank Dr Lempert for his reply and this possibility for a discussion on a difficult and important topic!
I was, however, slightly surprised to find that the reply is written as a rebuttal of my arguments, while I am of the same opinion as Dr Lempert, and have tried to express this in the editorial!
In the first paragraph Dr Lempert cautions against assuming that treatment for amblyopia normalizes visual function. I absolutely agree, and in my editorial I explicitly state:
“There is a clear need for objective studies on the possible relationship between unilateral amblyopia and functional disabilities. In such studies, comparisons should be made between three groups: (1) normal controls, (2) non-treated amblyopes, and (3) amblyopes after successful treatment.”
Dr Lempert claims that my editorial “implies that lack of screening and treatment of amblyopia cause a lifelong handicap.”
I have never intended to say this, and even find it slightly amusing, since I have countless times been accused of being “anti-screening” when pointing out that we currently do not have evidence to be able say that untreated unilateral amblyopia is disabling! I write “In discussing the rationale for preschool vision screening programmes, more results on possible associations between amblyopia and increased lifetime risk of visual impairment, as well as quality of life/utility measures for unilateral amblyopia, are required.”
Dr Lempert also claims my editorial implies that “treatment offers a significant cost / benefit gain.” I do report on results from previously published papers 1, 2, however, results showing that treatment for spontaneously presenting amblyopia (which these two papers deal with) is cost-efficient must not be confused with evidence for vision screening being cost-efficient!
In the final paragraph Dr Lempert points to the need for effective allocation of medical resources. I, again, agree, and have written in my editorial: “In a world with limited economic resources and ever-growing expenses for medical services, we will most likely see an increasing demand for evaluation, evidence of benefit and proof of cost-effectiveness for government-financed screening programmes.”
I still do believe that van Leeuwen’s paper3 is a very important contribution, and as I conclude my editorial: “As of today, we do not have all of the information required, but van Leewen et al’s work has provided us with very valuable data, moving us closer to determining whether preschool vision screening can be justified.”
References
1. Membreno JH, Brown MM, Brown GC, Sharma S, Beauchamp GR. A cost-utility analysis of therapy for amblyopia. Ophthalmology 2002;109:2265-71.
2. König HH, Barry JC. Cost effectiveness of treatment for amblyopia: an analysis based on a probabilistic Markov model. Br J Ophthalmol 2004;88:606-12.
3. van Leewen R, Eijkemans M, Vingerling JR, Hofman A, de Jong P, Simonsz HJ. Risk of bilateral visual impairment in persons with amblyopia: The Rotterdam Study. Br J Ophthalmol 2007;91:1450-1.
We read with interest the editorial by Miller which comments on the
paper, ‘Epidemiology of giant-cell arteritis in an Arab population: a 22-year study’[1]. The author of the editorial comments on geographical
variation in the incidence of giant cell arteritis and cites evidence
supporting both genetic and environmental aetiologies.
We re-examined the data from our 5 year study[2] looking at...
We read with interest the editorial by Miller which comments on the
paper, ‘Epidemiology of giant-cell arteritis in an Arab population: a 22-year study’[1]. The author of the editorial comments on geographical
variation in the incidence of giant cell arteritis and cites evidence
supporting both genetic and environmental aetiologies.
We re-examined the data from our 5 year study[2] looking at biopsy
proven giant cell arteritis at Leicester Royal Infirmary and identified
the ethnicity of the patients. This unit is the only tertiary ophthalmic
referral centre for the county of Leicestershire, United Kingdom. Census
data from 2001 indicates that ethnic Asians in Leicestershire make up 30%
of the population. Out of a total of 42 biopsies, only 3 cases (7.1%) were
from patients of Asian ethnicity. Whilst our study was not a prospective
population based study, the data lends weight to the idea that GCA is
relatively rare in ethnic Asians.
Interestingly our findings differ from those of Lam et al[3] who found
the prevalence of GCA to be similar in Hispanic and non-Hispanic patients.
Inferences can be made about the aetiology of a disease by examining the
incidence of a disease in migrant populations when the direction of
migration is from an area of low incidence to an area of high incidence.
For example, the incidence of multiple sclerosis in Indian and Pakistani
migrants to the UK has been studied[4] and it has been found that migration
prior to the age of 15 years confers an increased risk of developing
multiple sclerosis, a finding which implicates environmental agents.
Similar prospective studies looking at the relationship between age at
migration and risk of developing GCA may yield more information about the
interplay between genetic and environmental factors.
References
1. Miller NR. Epidemiology of giant cell arteritis in an Arab
population: a 22-year study. Br J Ophthalmol. 2007 Jun;91(6):705-6.
2. Jain S, Shah A, Deane J. Giant cell arteritis. (letter).
Ophthalmology. 2007 Jun;114(6):1235
3. Lam BL, Wirthlin RS, Gonzalez A, Dubovy SR, Feuer WJ. Giant cell
arteritis among Hispanic Americans. Am J Ophthalmol. 2007 Jan;143(1):161-3
4. Dean G, Elian M. Age at immigration to England of Asian and
Caribbean immigrants and the risk of developing multiple sclerosis. J
Neurol. Neurosurg. Psychiatry 1997;63:565-568
We read with great interest the recent commentary by Stewart et al [1] describing the evidence of the blood flow disturbances in the pathogenesis of the glaucomatous damage.
Although I agree with some of the findings of this excellent review, there are some important points that should be addressed:
1.After reading this article, one may think that there is not evidence that ocular bl...
We read with great interest the recent commentary by Stewart et al [1] describing the evidence of the blood flow disturbances in the pathogenesis of the glaucomatous damage.
Although I agree with some of the findings of this excellent review, there are some important points that should be addressed:
1.After reading this article, one may think that there is not evidence that ocular blood flow abnormalities are involved in the pathogenesis of the glaucomatous damage. Different studies, using different devices, point in the same general direction indicating that on average blood flow is decreased in some glaucoma patients, especially in primary open-angle glaucoma (POAG) patients and in patients that progress despite normalized intraocular pressure (IOP) [2]. Furthermore this decrease in blood flow is not confined to the eye alone [3].
2. Many different methods are being used to measure directly or calculate
indirectly in vivo ocular blood flow. Although there is not still a single method that can provide all the relevant information in one reading, the development of newer techniques and their corrected use provides the potential for assessing blood flow in humans.
3. On the other hand, the Authors reveal the lack of evidence of a pathogenic link between glaucoma and impaired ocular blood flow. They asked for a long-term prospective study, that includes carefully selected patient groups, with similar baseline demographic and clinical characteristics, but with dissimilar baseline ocular hemodynamics. We published a paper that prospectively investigated the value of color Doppler imaging of the ophthalmic artery and short posterior ciliary arteries in the prognosis of disease progression in patients with POAG.
[4] When baseline demographic and clinical characteristics were stratified according to whether the eyes progressed during the 3-year follow-up period, the only parameters to show significant differences were the resistivity index of the ophthalmic artery and the resistivity index of the short posterior ciliary arteries.
Our study concluded that poor blood flow in the retrobulbar vessels is closely linked to visual field deterioration in POAG patients.
In conclusion, we think that the understanding of the role of ocular blood flow disturbances in the pathogenesis of glaucoma has improved greatly. We have evidence that ocular blood flow is altered independently from IOP or level of damage in patients with progressive glaucoma, which could represent a primary risk factor for disease progression. In looking forward, we need long-term prospective multicenter studies to evaluate both the impact of ocular blood flow in glaucoma and the benefit of improving ocular blood flow.
References
1. Stewart WC, Feldman R, Mychaskiw MA. Ocular blood flow in
glaucoma: the need for further clinical evidence and patient outcomes research. Br J Ophthalmol. 2007; 91: 1263-1264.
2. Flammer J., Orgül S., Costa VP., et al. The impact of ocular blood flow in glaucoma. Prog Retin Eye Res 2002; 21: 359-393.
3. Gasser P, Flammer J. Blood-cell velocity in the nailfold capillaries of patients with normal-tension and high-tension glaucoma. Am J Ophthalmol. 1991; 111: 585-588.
4. Martinez A, Sanchez M. Predictive Value of Color Doppler Imaging in a Prospective Study of Visual Field Progression in Primary Open-Angle Glaucoma. Acta Ophthalmol Scand 2005; 83: 716-723.
In their article Doctors Agrawal and McKibbin evaluate the one-year
frequency and the clinical outcome data of Putscher’s retinopathy through
the British Ophthalmological Surveillance Unit. [1] All their 15 cases
were visually symptomatic. Twelve cases were associated with trauma and 3
cases with acute pancreatitis. The authors conclude that the incidence of
Purtsher’s retinopathy is low (0.24 case...
In their article Doctors Agrawal and McKibbin evaluate the one-year
frequency and the clinical outcome data of Putscher’s retinopathy through
the British Ophthalmological Surveillance Unit. [1] All their 15 cases
were visually symptomatic. Twelve cases were associated with trauma and 3
cases with acute pancreatitis. The authors conclude that the incidence of
Purtsher’s retinopathy is low (0.24 cases per million population) in the
United Kingdom, and that in half of the cases visual acuity improves by at
least 2 Snellen lines in 6 months.
The authors’ data, however, need careful interpretation. We investigated
the clinical characteristics, histological features and prognostic
significance of retinopathy of pancreatitis (Purtscher’s retinopathy
associated with acute pancreatitis) in several studies. [2][3] We found
that most of our cases were visually asymptomatic, since the patients were
in severe or terminal status in intensive care units. We also found that
retinopathy of pancreatitis was an indicator of multi-organ failure and
lethal outcome. Our data suggest that pancreatitis associated Purtscher’s
retinopathy is more common than reported by Doctors Agrawal and McKibbin,
and that the visual outcome may be worse than found by the authors who
used data reported by ophthalmologists. One may suppose that the reporting
ophthalmologists might have seen only those cases which were associated
with less severe systemic damage, and therefore the patients were able to
realise their visual symptoms. It is probable that Purtscher’s retinopathy
is more frequent than reported by the authors for the United Kingdom, and
that the visual outcome is different from that indicated in their article,
if all cases are considered.
Correspondence to: Gábor Holló, Department of Ophthalmology,
Semmelweis University, Budapest; hg@szem1.sote.hu
The author has no commercial interest in any product mentioned in the
article or the comment.
References
1.Agrawal A, McKibbin M. Purtscher’s retinopathy: epidemiology,
clinical features and outcome. Br J Ophthalmol 2007;91:1456-1459.
2.Holló G, Bobek I. Clinicopathology of a case with retinopathy of
pancreatitis. Acta Ophthalmol (Copenh) 1993;71:422-425.
3.Holló G, Tarjányi M, Varga M, et al. Retinopathy of pancreatitis
indicates multiple-organ failure and poor prognosis in severe acute
pancreatitis. Acta Ophthalmol (Copenh) 1994;72:114-117.
Re: van Leeuwen R, Eijkemans MJC, Vingerling JR, Hofman A, de Jong
PTVM, Simonsz HJ Risk of bilateral visual impairment in individuals with
amblyopia: the Rotterdam study BJO 2007;91 (11): 1450
Josefin Nilsson The negative impact of amblyopia from a population
perspective: untreated amblyopia almost doubles the lifetime risk of
bilateral visual impairment. BJO 2007;91 (11): 1417
Re: van Leeuwen R, Eijkemans MJC, Vingerling JR, Hofman A, de Jong
PTVM, Simonsz HJ Risk of bilateral visual impairment in individuals with
amblyopia: the Rotterdam study BJO 2007;91 (11): 1450
Josefin Nilsson The negative impact of amblyopia from a population
perspective: untreated amblyopia almost doubles the lifetime risk of
bilateral visual impairment. BJO 2007;91 (11): 1417
Dear Editor
It is not surprising that amblyopes are at higher risk of bilateral
visual impairment since impaired visual functions of the fellow eye have
been previously demonstrated. Leguire et al warned that “In future
studies of amblyopia, whether in children or in adults, caution is advised
in assuming that the nonamblyopic eye is normal because acuity is normal.”
[2] Johnson found that both amblyopic and fellow eyes had central
scotomata, even after apparently successful treatment, [3] and concluded
that “ocular effects of amblyopia may not be strictly limited to the
amblyopic eye.” [4] Anomalous optic discs, reduced axial lengths,[5] and
anatomic abnormalities involving the axial length to optic disc area have
been reported as present to different degrees in amblyopic and fellow
eyes.[6,7] Moreover, amblyopia is commonly associated with systemic
disorders such as prematurity and low birth weight[8] even in the absence of
retinopathy. [9] These anatomic and functional factors put both eyes at
risk makes them more susceptible to vision loss.
Nilsson’s editorial implies that lack of screening and treatment of
amblyopia cause a lifelong handicap[10] and that treatment offer a
significant cost / benefit gain.[11,12] These beliefs employed several
unsupported assumptions. Among them is that treatment results in final
visual acuity sufficient to perform all tasks and that untreated amblyopia
has a financial handicap equivalent to workman’s compensation scales for
loss of an eye. Actually, treatment of severe amblyopia rarely results in
functionally useful vision.[13] PEDIG studies showed that approximately 25
percent of their treated patients had no or very limited improvement at
the end of their initial observation period.[14,15] Initial successes were
reduced by an anticipated 50 percent rate of recidivism.[16,17]
Furthermore, the assumption that improved Snellen acuity reflects
functional improvement is challenged by findings that reading speed is
significantly less than normal even when final acuity was comparable with
the controls. [18]
A retrospective demographic investigation concluded that “No
functionally or clinically significant differences existed between people
with and without amblyopia in educational outcomes, behavioral
difficulties or social maladjustment, participation in social activities,
unintended injuries (school, workplace, or road traffic accidents as
driver), general or mental health and mortality, paid employment, or
occupation based social class trajectories.”[19]
There is an absolute need for effective allocation of medical
resources.[20] Increased bilateral vision impairment among people with
initial anatomic ocular defects in both eyes must motivate efforts to
prevent those prenatal conditions leading to impaired ocular anatomy.
Respectfully submitted,
Philip Lempert, MD
References
1. van Leeuwen R, Eijkemans MJC, Vingerling JR, Hofman A, de Jong PTVM,
Simonsz HJ Risk of bilateral visual impairment in individuals with
amblyopia: the Rotterdam study BJO 2007;91 (11): 1450
2. Leguire LE, Rogers GL, Bremer DL Amblyopia: the normal eye is not
normal. J Pediatr Ophthalmol Strabismus 1990;27(1):32-38
3. Johnson DA Relative scotomata in the "normal" eye of functionally
patients. A scanning laser ophthalmoscope (SLO) micreperimetric study.
Binocul Vis Strabismus Q. 2007;22(1):17-48.
4. Johnson DA The use of the scanning laser ophthalmoscope in the
evaluation of amblyopia (an American Ophthalmological Society thesis).
Trans Am Ophthalmol Soc. 2006;104:414-36.
5. Lempert P. Porter L. Dysversion of the optic disc and axial length
measurements in a presumed amblyopic population J Amer Acad Ped
Ophthalmol Strabismus 1998;2:207-213
6. Lempert P. Axial length – disc area ratio in esotropic amblyopia. Arch
Ophthalmol 2003; 121:821-824
7. Lempert P The axial length / disc area ratio in anisometropic hyperopic
amblyopia: A hypothesis for decreased unilateral vision associated with
hyperopic anisometropia. Ophthalmology 2004:111:304-308
8. Holmström G, M el Azazi M, Kugelberg U Ophthalmological follow up of
preterm infants: a population based, prospective study of visual acuity
and strabismus Br J Ophthalmol 1999;83:143-150
9. O’Connor AR, Stephenson TJ, Johnson A, Tobin MJ, Ratib S, Moseley
M, Fielder AR Visual function in low birthweight children . British
Journal of Ophthalmology 2004: 88 (9): 1149 - 1153
10. Josefin Nilsson The negative impact of amblyopia from a population
perspective: untreated amblyopia almost doubles the lifetime risk of
bilateral visual impairment. BJO 2007;91 (11): 1417
11. Joish VN, Malone DC, Miller JM. A cost-benefit analysis of vision
screening methods for preschoolers and school-age children. J AAPOS
2003;7:283-290
12. Membreno JH, Brown MM, Brown GC, Sharma S, Beauchamp GR. A cost-
utility analysis of therapy for amblyopia.Ophthalmology. 2002;109(12):2265
-2271.
13. Ingram RM Amblyopia: the need for a new approach Brit J. Ophthalmol
1979:63:236-237
14. PEDIG A randomized trial of atropine vs. patching for treatment of
moderate amblyopia in children. Arch Ophthalmol 2002;120:268-278
15. Pediatric Eye Disease Investigator Group. The course of moderate
amblyopia treated with patching in children: experience of the amblyopia
treatment study. Am J Ophthalmol. 2003;136(4):620-629
16. Simons K. Amblyopia characterization, treatment, and prophylaxis.
Surv Ophthalmol. 2005;50(2):123-66
17. Rutstein RP, Fuhr PS Efficacy and stability of amblyopia therapy. Optom
Vis Sci 1992;69(10):747-754
18.Stifter E, Burggasser G, Hirmann E, Thaler A, Radner W. Monocular and
binocular reading performance in children with microstrabismic amblyopia.
Br J Ophthalmol. 2005;89(10):1324-9
19. J S Rahi, P M Cumberland, and C S Peckham Does amblyopia affect
educational, health, and social outcomes? Findings from 1958 British birth
cohort BMJ 2006; 332: 820-825
20. Woolf SH Potential Health and Economic Consequences of Misplaced
Priorities. JAMA 2007;197(5) 523-526
We read with great interest the report by Raftery et al on
Ranibizumab (Lucentis) versus bevacizumab (Avastin): modelling cost
effectiveness. The authors raise the very pertinent point in respect to
a single company owning two competing drugs and the inherent cost to tax
payers. The authors conclude their abstract with "Public pressure may be
the most potent weapon in persuading Genentech to license bevaciz...
We read with great interest the report by Raftery et al on
Ranibizumab (Lucentis) versus bevacizumab (Avastin): modelling cost
effectiveness. The authors raise the very pertinent point in respect to
a single company owning two competing drugs and the inherent cost to tax
payers. The authors conclude their abstract with "Public pressure may be
the most potent weapon in persuading Genentech to license bevacizumab
for AMD".
We would like to suggest what forms this public pressure may take.
The pharmaceutical industry claims to educate the medical profession on
conditions and its drugs to treat them. Should we be relying on a
business to give us unbiased evaluations of products it is selling? Most
doctors who accept free lunches and merchandise will claim to be
unaffected.
However, doctors who have frequent contact with drug representatives are
more willing to prescribe new drugs, do not like ending consultations
with advice only, and are more likely to agree to prescribe a drug that
is not clinically indicated. [1] Doctors are now dependent on drug
companies for education and funding for research.
Research funded by drug companies has been found to be less likely to be
published than research funded by other sources. Studies sponsored by
pharmaceutical companies were found to be four times more likely to have
outcomes favouring the sponsor than were studies with other sponsors.
[2]
We have an unhealthy relationship with the pharmaceutical industry
which undermines our ability to make patient centered decisions. To
prevent more profit centered drugs coming to market rather than patient
centered drugs, we as a profession must take responsibility. When
published financial reports indicate pharmaceutical industry spending in
marketing is three times that of Research and Development, alarm bells
should be ringing.
To reduce this influence we must no longer accept free lunches,
merchandise or holidays, look for alternate means of funding research
and educational meetings and most of all become educated on the role
drug companies play in our decision making. Accepting our need for the
pharmaceutical industry should not mean accepting dependence upon them,
if we wish to see drugs such as bevacizumab being licensed it is time we
make our boundaries clear.
Suggested reading: The Truth About the Drug Companies by Marcia
Angell (Former Editor of the New England Journal of Medicine)
www.nofreelunch.org
References
1. Watkins C, Moore L, Harvey I, Carthy P, Robinson E, Brawn R.
Characteristics of general practitioners who frequently see drug
industry
representatives: national cross sectional survey. BMJ 2003;326: 1178-9
2. Lexchin J, Bero LA, Djulbegovic B, Clark O. Pharmaceutical
industry sponsorship and research outcome and quality: systematic
review.
BMJ 2003;326: 1167-70
We appreciated the paper by Iriyama et al.[1] The authors have
investigated the role of anti vascular endothelial growth factor (VEGF)
antibodies on retinal ganglion cells in rats. It is an interesting and
relevant paper considering the clinical use of anti-VEGF antibodies in a
variety of ocular conditions.[2] However, there are a couple of issues
that require further clarification.
We appreciated the paper by Iriyama et al.[1] The authors have
investigated the role of anti vascular endothelial growth factor (VEGF)
antibodies on retinal ganglion cells in rats. It is an interesting and
relevant paper considering the clinical use of anti-VEGF antibodies in a
variety of ocular conditions.[2] However, there are a couple of issues
that require further clarification.
The authors demonstrate, in figure 1, that bevacizumab (AvastinTM;
Genentech Inc. San Francisco, CA) is unable to bind to murine VEGF and
they provide evidence by doing Western blot on rat ocular tissue (retina
and choroid) using anti-rat VEGF antibody (R&D systems, Minneapolis) and
bevacizumab. Membranes were developed using rabbit anti mouse IgG and
anti-goat IgG. Authors demonstrate that only anti rat VEGF antibody was
able to detect rat VEGF and not bevacizumab. Although the authors have
not mentioned it in their paper, the anti-rat VEGF antibody that the
authors used is raised in goat according to the information provided by
the source. It justifies the use of anti-goat secondary antibody. It is
not clear why and where they used anti-mouse IgG. On the other hand,
bevacizumab is a humanized antibody and it should be detected by
anti-human IgG 3, which was not used by the authors. This might explain
why they could not detect bevacizumab binding with rat VEGF. Consistent
with this argument, Bock et al. in a recent paper[4] have been able to
show that bevacizumab binds to murine VEGF. They used a similar
technique (Western blot), and by using anti-human IgG were able to
detect bevacizumab bound to the murine VEGF. They further confirmed
their results using additional techniques such as ELISA (again utilizing
anti-human IgG) and surface Plasmon resonance (BIAcore assay).
Also, the figure legend of Figure 2 does not match the figure, nor
does the legend for Figure 4. It seems figures have switched.
Rajesh K Sharma, MD, PhD
Kakarla V Chalam, MD, PhD, MBA, FACS
Department of Ophthalmology
University of Florida, College of Medicine
Jacksonville FL
References
1. Iriyama A, Chen YN, Tamaki Y et al. Effect of anti-VEGF antibody on retinal ganglion cells in rats. Br.J.Ophthalmol. 2007;91:1230-3.
2. Aggio FB, Farah ME, Silva WC et al. Intravitreal
bevacizumab for exudative age-related macular degeneration after multiple treatments.
Graefes Arch.Clin.Exp.Ophthalmol. 2006.
3. Heiduschka P, Fietz H, Hofmeister S et al. Penetration of bevacizumab through the retina after intravitreal injection in the monkey.
Invest Ophthalmol.Vis.Sci. 2007;48:2814-23.
4. Bock F, Onderka J, Dietrich T et al. Bevacizumab as a potent inhibitor of inflammatory corneal angiogenesis and lymphangiogenesis.
Invest Ophthalmol.Vis.Sci. 2007;48:2545-52.
We read with great interest the report by Alwitry et al [1] on severe
decompression retinopathy after medical treatment of acute angle closure.
The authors have speculated that the mechanism of the ‘preretinal’
haemorrhage in this case was similar to the scattered ‘intraretinal’
haemorrhages seen in ocular decompression retinopathy. Although we agree
with them that the haemorrhage was caused by sudd...
We read with great interest the report by Alwitry et al [1] on severe
decompression retinopathy after medical treatment of acute angle closure.
The authors have speculated that the mechanism of the ‘preretinal’
haemorrhage in this case was similar to the scattered ‘intraretinal’
haemorrhages seen in ocular decompression retinopathy. Although we agree
with them that the haemorrhage was caused by sudden lowering of
intraocular pressure (IOP), we believe that the exact pathophysiological
mechanism, as well the clinical signs, in this case were different from
the condition originally described by Fechtner et al [2].
It can be hypothesised that a pupillary block caused the volume of
aqueous humor in the posterior chamber to increase markedly. The vitreous
gel was therefore pushed toward the posterior pole. Following medical
therapy the pupillary block was reversed and the aqueous humor moved
rapidly through the pupil from the posterior chamber to the anterior
chamber. This coupled with decreased aqueous production due to
administration of aqueous suppressants allowed the vitreous body to move
forward rapidly. This induced a rapid posterior vitreous detachment (PVD),
disrupting small vessels on the retinal surface or optic disc, and
resulted in the subhyaloid haemorrhage. In the present case the very short
duration of raised IOP makes significant impairment of autoregulation of
retinal vasculature unlikely and the absence of multiple intraretinal
haemorrhages rules out a general compromise of mechanical stability of
retinal capillaries. Obana et al [3] were the first to demonstrate a
subhyaloid haemorrhage caused by PVD induced after laser iridectomy for
primary angle-closure glaucoma and it should be distinguished from ocular
decompression retinopathy.
This leads to an interesting conclusion that a sudden lowering of IOP
may cause posterior segment bleeding by three different mechanisms. Ocular
decompression retinopathy is caused by overwhelming of capacitance of
retinal capillaries and results in multiple intraretinal haemorrhages. The
second mechanism and clinical picture is similar to a central retinal vein
occlusion [4,5]. A sudden change in hydrostatic equation between the
posterior and anterior chambers, induces a rapid PVD and may result in
subhyaloid haemorrhage, as in this case.
Figure 1 Three different mechanisms of posterior segment
bleeding after sudden lowering of intraocular pressure
References
1. Alwitry A, Khan K, Rotchford A et al. Severe decompression
retinopathy after medical treatment of acute primary angle closure. Br J
Ophthalmol 2007;91:121
2. Fechtner RD, Minckler D, Weinreb RN et al. Complications of
glaucoma surgery. Ocular decompression retinopathy. Arch Ophthalmol
1992;110:965-8
3. Obana A, Gohto Y, Ueda N, Miki T, Cho A, Suzuki Y. Retinal and
subhyaloid hemorrhage as a complication of laser iridectomy for primary
angle-closure glaucoma. Arch Ophthalmol. 2000 Oct;118:1449-51
4. Suzuki R, Nakayama M, Satoh N. Three types of retinal bleeding as
a complication of hypotony after trabeculectomy. Ophthalmologica.
1999;213:135-8
5. Dev S, Herndon L, Shields MB. Retinal vein occlusion after
trabeculectomy with mitomycin C. Am J Ophthalmol. 1996 Oct;122:574-5
I read with interest the article by Pedroza-Seres M and associates
who assessed the pathogenic roles of peripheral CD57+ natural killer T
(NKT) cell in pars planitis.[1] The authors compared the frequencies of
CD57+ NKT cell in peripheral blood between pars planitis patients and
healthy controls, and then evaluated the effector-related surface
molecules and functions of CD57+ NKT cells derived from pa...
I read with interest the article by Pedroza-Seres M and associates
who assessed the pathogenic roles of peripheral CD57+ natural killer T
(NKT) cell in pars planitis.[1] The authors compared the frequencies of
CD57+ NKT cell in peripheral blood between pars planitis patients and
healthy controls, and then evaluated the effector-related surface
molecules and functions of CD57+ NKT cells derived from patients. The
authors conclude that CD57+ NKT cell subsets may function as memory-effector T cells during pars planitis immunopathogenesis. My experience of
using similar methods to investigate the phenotypes and functions of
CD8brightCD56+ T cells in Behçet uveitis supports the notion that
NK-typed CD8+ T cells play an effector role in chronic uveitis.[2] I would
like to offer my opinion to their interpretation of experimental results.
I observed that CD8bright CD56+ cells in peripheral blood were composed of
more than 95% TCRαβ cells and that CD8dimCD56+ cells consisted of
natural killer cells and γδTCR+ cells.[2,3] Because the authors used the
different gate of CD8 expression in figure 1 and 3, it is possible to
overestimate the frequencies of peripheral CD8+CD57+ T cells including
CD8dim populations. Likewise CD56+ cells, CD8dimCD57+ cells may not be
TCRαβcells, which require confirmation of TCR expression.
As shown in Figure 4 and Table 3, the authors found that CD57+CD8+ T cells
significantly produced IL-4 after nonspecific stimulation. However, these
results are not compatible with the idea that terminally differentiated NK-typed CD8+ T cells are polarized to produce cytokines, like CD56+CD8+ T cells.[2] Apoptosis of ex vivo CD57+CD8+ T cells may contribute to these
findings because of smaller cell counts after stimulation (thick lines).
The authors described that stimulared or unstimulated immune cells were
used for intracellular staining of perforin. Because CD8+CD56+ T cells
shed the preformed intracellular
perforin after in vitro stimulation, the authors should measure the
amounts of intracellular perforin in unstimulated cells.
I agree with the authors that NK-typed CD8+ T cells exert potent effector
functions over conventional CD8+ T cells. CD56+ T cells are recruited into
eye, particularly in Behçet uveitis, which are different from other
etiologies of uveitis.[3] Moreover, these cells show phenotypical or
functional changes after immunosuppresive treatments.[4] However, I did not
observe upregulation of CD56+ T cells in aqueous or peripheral blood in
patients with intermediate uveitis.[3] The specific roles of CD57+CD8+ T
cells in pars planitis pathogenesis are not definite because the authors
did not evaluate phenotypical or functional differences of CD57+CD8+ T
cells according to the disease activity or compare their results with
other etiologies of uveitis. Therefore, further investigations are needed
to identify the pathogenic roles of CD57+CD8+ T cells in pars planitis.
References
1. Pedroza-Seres M, Linares M, Voorduin S, et al. Pars planitis is
associated with an increased frequency of effector-memory CD57+ T cells.
Br J Ophthalmol 2007;91:1393-8.
2. Ahn JK, Chung H, Lee DS, Yu YS, Yu HG. CD8brightCD56+ T cells are
cytotoxic effectors in patients with active Behçet's uveitis. J
Immunol 2005;175:6133-42.
3. Yu HG, Lee DS, Seo JM, et al. The number of CD8+ T cells and NKT cells
increases in the aqueous humor of patients with Behçet's uveitis.
Clin Exp Immunol 2004;137:437-43.
4. Ahn JK, Park YG, Park SW, et al. Combined low dose cyclosporine and
prednisone down-regulate natural killer cell-like effector functions of
CD8brightCD56+ T cells in patients with active Behçet's uveitis.
Ocul Immunol Inflamm 2006;14:267-275.
We read with interest the article by Aisenbrey et al [1] who have described the results of surgical treatment of peripapillary choroidal neovascularisation in eight patients.
As reported, peripapillary choroidal neovascularisation is a relatively uncommon entity that can be a variant of macular choroidal neovascularisation in elderly patients.
Accordingly to the MPSG[2], early small peripapilla...
We read with interest the article by Aisenbrey et al [1] who have described the results of surgical treatment of peripapillary choroidal neovascularisation in eight patients.
As reported, peripapillary choroidal neovascularisation is a relatively uncommon entity that can be a variant of macular choroidal neovascularisation in elderly patients.
Accordingly to the MPSG[2], early small peripapillary choroidal neovascularisation should be first treated with red thermal laser photocoagulation. If applied by an experienced specialist the risk of burning the interpapillomacular bundle is limited.
However, the therapeutical approach is more delicate for laser resistant, extended and/or very exsudative peripapillary choroidal neovascularisation.
In their study, Aisenbrey et al report good clinical outcome after surgical treatment. Nevertheless, as published by Rosenblatt et al [3], photodynamic therapy with Verteporfin can also be a good option because of its efficacy and very limited risk. This is also our clinical experience.
Figure 1 shows the left eye of a male patient in his early seventies with very exsudative peripapillary choroidal neovascularisation before and one year after one photodynamic therapy with Verteporfin. The current parameters for choroidal neovascularisation and a spot of 4200 µ covering a great part of the optic nerve were used. This case looks very similar to the illustrated case of Aisenbrey et al, except the fact that we first unsuccessfully tried to treat the lesion with thermal laser.
Figure 1: left eye of a male patient in his early seventies with very exsudative peripapillary choroidal neovascularisation before (a) and one year after one photodynamic therapy with Verteporfin (b).
Figure 1a
Figure 1b
In our experience with Verteporfin we have never noted any clinical damage to the optic nerve after partial exposition and it has been shown by Schmidt-Erfurth et al [4] that optic nerve can be exposed to a light dose twice as high as conventionally used without showing histopathological alterations.
Regarding the potential major risks of the surgical approach of peripapillary choroidal neovascularisation we suggest that PDT could be the first therapeutical choice in these cases.
References
1. Aisenbrey S, Gelisken F, Szurman P, et al. Surgical treatment of
peripapillary choroidal neovascularisation. Br J Ophthalmol 2007;91:1027- 1030.
2. The Macular Photocoagulation Study Group. Laser photocoagulation
for neovascular lesions nasal to the fovea. Results from clinical trials for lesions secondary to ocular histoplasmosis or idiopathic causes.
Macular Photocoagulation Study Group. Arch. Ophthalmol. 1995; 113:56-61.
3. Rosenblatt BJ, Shah GK, Blinder K. Photodynamic therapy with
verteporfin for peripapillary choroidal neovascularisation. Retina. 2005; 25:33-37.
4. Schmidt-Erfurth U, Laqua H, Schlotzer-Schrehard U, et al.
Histopathological changes following photodynamic therapy in human eyes.
Arch. Ophthalmol. 2002 Jun; 120(6):835-44.
In a reply to my editorial in the November issue, Dr Lempert raises several valid concerns regarding vision screening for amblyopia. I would like to thank Dr Lempert for his reply and this possibility for a discussion on a difficult and important topic!
I was, however, slightly surprised to find that the reply is written as a rebuttal of my arguments, while I am of the same opinion as Dr Lempert, and have...
Dear Editor
We read with interest the editorial by Miller which comments on the paper, ‘Epidemiology of giant-cell arteritis in an Arab population: a 22-year study’[1]. The author of the editorial comments on geographical variation in the incidence of giant cell arteritis and cites evidence supporting both genetic and environmental aetiologies.
We re-examined the data from our 5 year study[2] looking at...
Dear Editor:
We read with great interest the recent commentary by Stewart et al [1] describing the evidence of the blood flow disturbances in the pathogenesis of the glaucomatous damage. Although I agree with some of the findings of this excellent review, there are some important points that should be addressed:
1.After reading this article, one may think that there is not evidence that ocular bl...
Dear Editor,
In their article Doctors Agrawal and McKibbin evaluate the one-year frequency and the clinical outcome data of Putscher’s retinopathy through the British Ophthalmological Surveillance Unit. [1] All their 15 cases were visually symptomatic. Twelve cases were associated with trauma and 3 cases with acute pancreatitis. The authors conclude that the incidence of Purtsher’s retinopathy is low (0.24 case...
Re: van Leeuwen R, Eijkemans MJC, Vingerling JR, Hofman A, de Jong PTVM, Simonsz HJ Risk of bilateral visual impairment in individuals with amblyopia: the Rotterdam study BJO 2007;91 (11): 1450
Josefin Nilsson The negative impact of amblyopia from a population perspective: untreated amblyopia almost doubles the lifetime risk of bilateral visual impairment. BJO 2007;91 (11): 1417
Dear Editor
...
Dear Editor
We read with great interest the report by Raftery et al on Ranibizumab (Lucentis) versus bevacizumab (Avastin): modelling cost effectiveness. The authors raise the very pertinent point in respect to a single company owning two competing drugs and the inherent cost to tax payers. The authors conclude their abstract with "Public pressure may be the most potent weapon in persuading Genentech to license bevaciz...
Dear Editor,
We appreciated the paper by Iriyama et al.[1] The authors have investigated the role of anti vascular endothelial growth factor (VEGF) antibodies on retinal ganglion cells in rats. It is an interesting and relevant paper considering the clinical use of anti-VEGF antibodies in a variety of ocular conditions.[2] However, there are a couple of issues that require further clarification.
The author...
Dear Editor,
We read with great interest the report by Alwitry et al [1] on severe decompression retinopathy after medical treatment of acute angle closure. The authors have speculated that the mechanism of the ‘preretinal’ haemorrhage in this case was similar to the scattered ‘intraretinal’ haemorrhages seen in ocular decompression retinopathy. Although we agree with them that the haemorrhage was caused by sudd...
Dear Editor
I read with interest the article by Pedroza-Seres M and associates who assessed the pathogenic roles of peripheral CD57+ natural killer T (NKT) cell in pars planitis.[1] The authors compared the frequencies of CD57+ NKT cell in peripheral blood between pars planitis patients and healthy controls, and then evaluated the effector-related surface molecules and functions of CD57+ NKT cells derived from pa...
Dear Editor
We read with interest the article by Aisenbrey et al [1] who have described the results of surgical treatment of peripapillary choroidal neovascularisation in eight patients.
As reported, peripapillary choroidal neovascularisation is a relatively uncommon entity that can be a variant of macular choroidal neovascularisation in elderly patients. Accordingly to the MPSG[2], early small peripapilla...
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