A metastizing adenocarcinoma of the retinal pigment epithelium in a 37-year-old man with Down syndrome (DS) has recently been reported in the
British Journal of Ophthalmology [1]. In the article the authors underlined
an unusual and atypical aggressive behaviour of the tumour which was the
first well documented adenocarcinoma of the retinal pigment epithelium
with metastases. Although solid tumours are...
A metastizing adenocarcinoma of the retinal pigment epithelium in a 37-year-old man with Down syndrome (DS) has recently been reported in the
British Journal of Ophthalmology [1]. In the article the authors underlined
an unusual and atypical aggressive behaviour of the tumour which was the
first well documented adenocarcinoma of the retinal pigment epithelium
with metastases. Although solid tumours are globally less frequent in
persons with DS than in the general population [2] this does not seem to
apply to ocular neoplasms. Including Heindl's et al report 30 cases of
primary or secondary malignant tumours of the eye and orbit have been
reported so far, two thirds being retinoblastoma [3]. Unfortunately, but
interestingly, some neoplasms in patients with DS may have a rapid
progression as observed in a low grade glioma [4]. The reason for this
unfavourable course in some patients remains unknown. Nonetheless, as
ocular malignant neoplasm could be more frequent in children and adults
with DS, and since some of these tumours may have an unexpected aggressive
behaviour, we want to attract attention on them to allow a precocious
diagnosis and early treatment.
The study on tumors in DS is supported by the Fondation Jérôme
Lejeune.
References
1. Heindl LM, Naumann GO, Kruse FE, Holbach LM. Aggressive
metastasising adenocarcinoma of the retinal pigment epithelium with
trisomy 21. Br J Ophthalmol. 2008;92:389-91
2. Patja K, Pukkala E, Sund R, Iivanainen M, Kaski M. Cancer
incidence of persons with Down syndrome in Finland: a population-based
study. Int J Cancer. 2006;118:1769-72
3. Satgé D, Lacombe D, Vekemans M, Bonnet A, Réthoré M-O, Munier F. A
survey of ocular tumors in Down syndrome alone or associated with another
genetic affection. Int J Disabil Human Dev 2006;5:311-7
4. Satgé D, Monteil P, Sasco AJ, Vital A, Ohgaki H, Geneix A, Malet
P, Vekemans M, Réthoré MO. Aspects of intracranial and spinal tumors in
patients with Down syndrome and report of a rapidly progressing Grade 2
astrocytoma. Cancer. 2001;91:1458-66
We thank Dr Ayata for the thoughtful comments of our article. He
had three questions that we would like to answer as follows:
1) Figure 1 was quite important for the paper because it shows the
exact
location of the macular pigment in monkeys (courtesy of Francois Delori,
PhD). We are sorry for the lack of the image in the on-line paper
version but it was probably due to the PDF saving...
We thank Dr Ayata for the thoughtful comments of our article. He
had three questions that we would like to answer as follows:
1) Figure 1 was quite important for the paper because it shows the
exact
location of the macular pigment in monkeys (courtesy of Francois Delori,
PhD). We are sorry for the lack of the image in the on-line paper
version but it was probably due to the PDF saving process.
2) We do not think there is any inconsistency between results and
conclusion because that was exactly what we expected. If a pseudohole is
a macular lesion where there is no loss of foveal tissue, the presence
of foveal AF indicates the absence of macular pigment in the fovea.
Being the pigment located in the outer plexiform layer and outer nuclear
layer in the fovea (fig 1), that means we were dealing with lamellar
rather than pseudo macular holes. Our paper just underlined the finding
that OCT alone is inadequate to differentiate pseudo from lamellar
holes. As to this respect AF imaging may be useful because reveals a
loss of foveal tissue.
3) We are aware of the different aspects of AF-imaging after dark
and
light adaptation. As Dr Ayata properly pointed out, the visible changes
in AF imaging in light and dark adapted eyes are minimal in the fovea
and the lack of macular pigment in lamellar macular hole is in the
fovea. The AF ratio was used to correlate AF intensities with residual
retinal thickness at the bottom of the defect. The reason why we did not
use raw images for AF quantitative measurements was related to the great
difficulties in visualizing foveal defect in non normalized images. The
ratio could have affected the results of these correlations but not the
presence of foveal AF itself.
We thank again Dr Ayata for his interest in our article.
Epigenetic regulation of tumor suppressor genes provides an
attractive mechanism for tumors in which mutations and structural changes
are rare. The latter may apply to uveal melanoma for which little is known
of the genes that contribute to tumor development. In the search for
genes, uveal melanoma is often compared to its counterpart in the skin,
cutaneous melanoma. One of the major cuteneous melan...
Epigenetic regulation of tumor suppressor genes provides an
attractive mechanism for tumors in which mutations and structural changes
are rare. The latter may apply to uveal melanoma for which little is known
of the genes that contribute to tumor development. In the search for
genes, uveal melanoma is often compared to its counterpart in the skin,
cutaneous melanoma. One of the major cuteneous melanoma genes is the p16
encoding CDKN2A gene for which mutations and deletions are the major
mechanisms of inactivation. Deletions and mutations in CDKN2A are however
rare in uveal melanoma; still p16 expression is lacking in half of the
cell lines[1]. Using methylation analysis and methylation inhibition in cell
culture, we have shown that the underlying mechanism of loss of p16
expression in these cell lines is methylation of CDKN2A. This observation
is not disputed but controversy arises when primary tumors are analyzed
and estimates are given for the extend of CDKN2A methylation in uveal
melanoma[2,3]. The study by Moulin et al is an example of a study that
displays some remarkable deviations from results we and others have
achieved previously[4,5]. We would like to comment on some of the technical
and biological factors that may contribute to the lack of consistency in
the results that are achieved in the field of uveal melanoma epigenetics.
The molecular mechanism of epigenetic gene regulation is complex and
characterized by multiple molecular events that are functionally
connected. Hence, the analysis of only one of these events will never be
sufficient to fully explain the downregulation of tumor suppressor genes.
Whereas tumor cell lines probably present the endpoint of epigenetic
silencing and commonly display a homogeneous methylation profile, primary
tumors in contrast frequently present a more heterogeneous pattern of
methylation. We presume that this heterogeneity is correlated with the
progress of epigenetic silencing. On the one hand it is possible that
only a fraction of the tumor cells carries methylated tumor suppressor
genes, on the other hand the degree of CpG methylation may vary over a
broad range, depending on the advance of the epigenetic silencing. Despite
this heterogeneity, methylation can be used as molecular marker and may
have an important role in the pathogenesis of uveal melanoma.
The heterogeneity of the methylation requires sensitive techniques to
reveal this methylation in primary tumors. With the advent of bisulfite
modification of DNA, the analysis of methylation has increased enormously.
Most commonly applied techniques are the methylation-specific PCR (MSP)
and bisulfite sequence analysis. MSP is a technique with a high
sensitivity that is based on PCR primers that are specific for methylated
and unmethylated DNA. A drawback of this method is the false positive rate
due to illegitimate polymerization of methylation-specific primers that
are hybridized to unmethylated DNA which is a common event due to the
error rate of the polymerase. Therefore, we propose that MSP requires
validation by an additional technique. Initially we have used restriction
enzyme analysis for validation of internal CpG’s [1]. Recently, we turned to
melting temperature analysis of bisulfite PCR reactions that amplify both
methylated and unmethylated DNA. Analysis of these PCR reactions provides
insight into the degree of methylation and the quantity of methylated and
unmethylated fractions in tumor tissue[6]. Reanalysis of primary uveal
melanoma with melting point analysis for CDKN2A (previously analyzed with
MSP) indicated that the methylated fraction rarely exceeded 10% of the
tumor DNA (unpublished). Because of this low percentage, most of the
tumors will not test positive with the assay used by Moulin et al.
Loss of p16 expression is observed in many tumors and marks a
critical event in tumor development. Epigenetic silencing of the CDKN2A
gene (or any other tumor suppressor gene of interest) in uveal melanoma
should therefore be recognized even if it is only present in a minority of
cells as it may represent the malignant component of the tumor.
References
1. van der Velden,P.A. et al. Promoter Hypermethylation: A Common
Cause of Reduced p16(INK4a) Expression in Uveal Melanoma. Cancer Res 61,
5303-5306 (2001).
2. Lamperska,K. et al. Expression of p16 in sporadic primary uveal
melanoma. Acta Biochim. Pol. 49, 377-385 (2002).
3. Edmunds,S.C., Kelsell,D.P., Hungerford,J.L. & Cree,I.A.
Mutational analysis of selected genes in the TGFbeta, Wnt, pRb, and p53
pathways in primary uveal melanoma. Invest Ophthalmol. Vis. Sci. 43, 2845-
2851 (2002).
4. Merhavi,E. et al. Promoter methylation status of multiple genes
in uveal melanoma. Invest Ophthalmol. Vis. Sci. 48, 4403-4406 (2007).
5. Moulin,A.P., Clement,G., Bosman,F.T., Zografos,L. &
Benhattar,J. Methylation of CpG island promoters in uveal melanoma. Br. J.
Ophthalmol. 92, 281-285 (2008).
6. Maat,W. et al. Epigenetic Inactivation of RASSF1a in Uveal
Melanoma. Invest Ophthalmol. Vis. Sci. 48, 486-490 (2007).
Thank you for your comments. Two cases with the exfoliation syndrome
and one with pigmentary glaucoma were included in our study. As you
mentioned, dilatation of the pupil often causes a rise of intraocular
pressure in such cases. However, none of the three individuals in our
study had a significant rise of intraocular pressure or progression of
glaucoma.
Sincerely,
George Sp...
Thank you for your comments. Two cases with the exfoliation syndrome
and one with pigmentary glaucoma were included in our study. As you
mentioned, dilatation of the pupil often causes a rise of intraocular
pressure in such cases. However, none of the three individuals in our
study had a significant rise of intraocular pressure or progression of
glaucoma.
Sincerely,
George Spaeth M.D.
We thank Dr Kesarwani for the interest in our article.
In response to the points raised:
1. Inclusion criteria
We attempted to recruit children with X(T) measuring more than 20 prism
dioptres when fixing a 6 metre target, as angles under this amount are
usually felt not to require treatment. However, Dr Kesarwani is correct to
point out that, at the baseline assessme...
We thank Dr Kesarwani for the interest in our article.
In response to the points raised:
1. Inclusion criteria
We attempted to recruit children with X(T) measuring more than 20 prism
dioptres when fixing a 6 metre target, as angles under this amount are
usually felt not to require treatment. However, Dr Kesarwani is correct to
point out that, at the baseline assessment following recruitment to the
study, some children had angles of strabismus measuring < 20 pd. We
were interested to see how the score performed in children with small
angle X(T) and so decided not to exclude them.
2. Stereoacuity values
The reason the distance stereoacuity mean is lower than the near is
probably due to the range of stereoacuities each test provides. For
values of less than 200" for distance
the score will be negative as this is the largest disparity possible (if
tested at 3m) however, one can test up to (down to) a disparity of 600" on
the FNS.
3. Median distance stereoacuity values included values calculated
with adjustment for interpupillary distance.
Once again, we thank Dr Kesarwani for attentive reading of our paper
We read with great interest the recently published article by Bottoni
and associates. However, we would like to express our concerns regarding
their article entitled “Diagnosis of macular pseudoholes and lamellar
macular holes: is optical coherence tomography the gold standard?” Br. J.
Ophthalmol. published online 1 Feb 2008; doi:10.1136/bjo.2007.127597. [1]
In this article, the authors investigate...
We read with great interest the recently published article by Bottoni
and associates. However, we would like to express our concerns regarding
their article entitled “Diagnosis of macular pseudoholes and lamellar
macular holes: is optical coherence tomography the gold standard?” Br. J.
Ophthalmol. published online 1 Feb 2008; doi:10.1136/bjo.2007.127597. [1]
In this article, the authors investigate whether fundus autofluorescence
imaging (FAF) differentiates between macular pseudo hole (MPH) and
lamellar macular hole (LMH).
(First of all, figure 1 has not been presented. I guess it could be a
technical error owing to the PDF rendering process).
Second, although corrected value of the foveal AF intensity was not
found to be significantly different between the two groups (ie,
pseudoholes and lamellar holes), authors concluded that AF imaging may add
useful information as to the differential diagnosis of MPH from LMH.
Moreover, they stated that the presence of foveal AF is consistent with a
loss of foveal tissue and therefore a diagnosis of LMH. We believe there
is an inconsistency between results and
conclusion.
Third, several factors should be considered for evaluating FAF
intensities in different examination and patient. Detector gain, pupillary
alignment, refraction of the eye, lens status and number of the averaged
image could be interfere pixel intensity of the FAF signal and those
should be standardized before quantitative analyses of FAF images. [2] In
the aforementioned article, standardization of the FAF images has not been
clearly stated.
Ratio between the region of interest and background intensity appears
reliable for single mean image quantification. However, bleaching of the
photopigments due to the continuous visible light excitation may influence
results and leads miscalculation. Bleaching with blue light is minimal at
the fovea and is maximum approximately 12 degrees away from the fovea in
the horizontal and vertical meridians. [3] Increment of the pixel
intensity of the FAF image is depending on excitation time and amplitude
of the fotobleaching is related amount of the photopigment and varies
individually. According to our results (article in process), nearly 40%
increment (range 18.8 % to 75.9 %) in FAF luminosity occurs during first
thirty seconds of the excitation. For this reason, obtaining standard FAF
images with accurate luminosity requires at least 30 second fundus
illumination to bleach the photoreceptor pigments.
Considering these biasing factors (acquiring standardized FAF images,
using accurate raw image processing algorithm) may provide more reliable
results. Different analyse technics (i.e. circularity, eccentricity or
transition pattern analyse) may grant the difference.
We thank Bottoni and his associates for their interesting article.
References
1. Bottoni F, Carmassi L, Cigada M, Moschini S, Bergamini F.
Diagnosis of macular pseudoholes and lamellar macular holes: is optical
coherence tomography the gold standard? Br J Ophthalmol. 2008 Feb 1; [Epub
ahead of print] doi:10.1136/bjo.2007.127597
2. Schmitz-Valckenberg S, Holz FG, Fitzke FW. Perspectives in Imaging
Technologies. In: Atlas of Fundus Autofluorescence Imaging, Holz FG,
Spaide RF, Bird AC (editors). Springer – Verlag, Berlin 2007:325-34
I appreciate the letter by Dr. Lempert regarding Dr. Nilsson's
Editorial to our study of the extension of the period of bilateral visual
impairment (BVI) in persons with untreated amblyopia, and the response by
Dr. Nilsson. A slight misunderstanding may arise, however, from the first
sentence of Dr. Lempert's letter: "It is not surprising that amblyopes are
at higher risk of bilateral visual impairm...
I appreciate the letter by Dr. Lempert regarding Dr. Nilsson's
Editorial to our study of the extension of the period of bilateral visual
impairment (BVI) in persons with untreated amblyopia, and the response by
Dr. Nilsson. A slight misunderstanding may arise, however, from the first
sentence of Dr. Lempert's letter: "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."
This may seem to imply that we reported extension of the period of
BVI caused by impaired function of the fellow eye. Instead, we reported
that for untreated amblyopes the lifetime risk of BVI was 18% while they
lived on average 7.2 years with BVI, while for non-amblyopes, these
figures were 10% and 6.7 years, respectively. Hence, untreated amblyopia
extended the average expected period living with BVI from 0.7 to 1.3
years. This extension was only or primarily caused by the fact that they
already had decreased function of their amblyopic eye.
We agree with the authors’ recommendation on the need for a sleep
history in the eye clinic and probably having a lower threshold for
referral to sleep physicians for further sleep studies.[1] However, we would
like to bring to their attention other epidemiological studies where
screening tools/sleep history have shown a high prevalence of sleep
disorders in patients with ocular disorders other than...
We agree with the authors’ recommendation on the need for a sleep
history in the eye clinic and probably having a lower threshold for
referral to sleep physicians for further sleep studies.[1] However, we would
like to bring to their attention other epidemiological studies where
screening tools/sleep history have shown a high prevalence of sleep
disorders in patients with ocular disorders other than non- arteritic
anterior ischaemic optic neuropathy (NAION). These include primary open
angle glaucoma (POAG), normal tension glaucoma (NTG), floppy eye lid
syndrome (FES) and more recently central serous chorio-retinopathy
(CSCR).[2-5] The evidence from these studies is summarized in table 1.
The
literature shows a higher prevalence of sleep disorder than that reported
in the general population in the United Kingdom by Ohayon et al (1.9% of
population sample, n=4972) based on the minimal criteria of the
International Classification of Sleep Disorders.[6]
We note the authors have adjusted the statistical analysis for
glaucoma among other factors, but the proportion of patients diagnosed
with glaucoma in the study and control groups is not mentioned. They also
do not mention the ocular diagnosis of the randomly selected control group
from the ophthalmology clinics and if any exclusion criteria, other than
NAION was used. This may be the reason for their study having a lower
proportion of patients with symptoms consistent with SAS than previously
reported. The other reason can be the different screening methods used in
these studies.
Also, the authors do not mention if the patients scoring positive on
the Sleep Apnoea scale of the Sleep Disorders Questionnaire (SA-SDQ) were
referred for sleep studies. Offering polysomnography or even limited sleep
study to the study sample and comparing the outcomes with the SA-SDQ
scores could provide the required evidence or validation, as mentioned by
the authors, on the need for lower cut-off points for this patient sub-group.
We recently conducted a similar study in the general eye clinic
population, which is under consideration for publication at the present
time. Following a review of the various components of the screening
questionnaire; patients with glaucoma were more likely to report episodes
of apnoea, morning headaches, short term memory loss and poor
concentration. We therefore suggest the authors also do a further analysis
of the responses obtained to the 8 questions addressing the specific
symptoms of SAS in the SA-SDQ, as they might be able to provide an
additional weighted score for screening in their patient subgroup.
References
1. Li J, McGwin G, Vaphiades MS, Owsley C. Non-arteritic anterior
ischaemic optic neuropathy and presumed sleep apnoea syndrome screened by
the Sleep Apnoea scale of the Sleep disorders Questionnaire (SA-SDQ). Br J
Ophthalmol 2007; 91:1524-1527.
2. Hakki Onen S, Mouriaux F, Berramdane L, Dascotte JC, Kulik JF,
Rouland JF. High prevalence of sleep disordered breathing in patients with
primary open angle glaucoma. Acta Ophthalmol Scand 2000; 78: 638-641.
3. Marcus DM, Costarides AP, Gokhale P, Papastergiou G, Miller JJ,
Johnson MH, Choudhary BA. Sleep Disorders: A risk factor for normal
tension glaucoma. J Glaucoma 2001; 10: 177-183.
4. McNab AA, The eye and sleep. Clinical Experimental Ophthalmology
2005; 33: 117-25.
5. Leveque TK, Yu L, Musch DC, Chervin RD, Zacks DN. Central serous
chorioretinopathy and risk for obstructive sleep apnoea. Sleep Breath
2007; 11: 253-257.
6. Ohayon MM, Guilleminault C, Priest RG, Caulet M (1997) Snoring and
breathing pauses during sleep: telephone interview survey of a United
Kingdom population sample. BMJ, 314, 860–863.
We want to thank Drs. Martinez and Sanchez for the response to our recent editorial. We are in agreement with them that evidence does exist that blood flow is altered in glaucoma and is suggestive of a
pathogenetic role[1]. We also agree that a variety of methods are being used to evaluate blood flow and these techniques certainly have improved over the last decade and a half.
We want to thank Drs. Martinez and Sanchez for the response to our recent editorial. We are in agreement with them that evidence does exist that blood flow is altered in glaucoma and is suggestive of a
pathogenetic role[1]. We also agree that a variety of methods are being used to evaluate blood flow and these techniques certainly have improved over the last decade and a half.
I would also like to thank Drs. Martinez and Sanchez for calling attention to their article in Acta Ophthalmologica[2] detailing their prospective analysis of blood flow in glaucoma. They are to be congratulated on their work. Unfortunately, in an editorial, space is limited and not all research could be highlighted
to the extent that we would have desired.
The article mentioned by Dr. Martinez and Sanchez is an elegant early step in attempting to prospectively determine blood flow-based risk factors for progression over the mid-term in patients with untreated primary open angle glaucoma. In the 49 patients evaluated by
the authors(23 progressed and 26 non-progressed over three years) differences in
resistivity index as measured with color Doppler, but not baseline
intraocular pressure as in the Early Manifest Glaucoma Trial, predicted
approximately 80-90% of patients who ultimately progressed or remained
stable[2,3].
This work highlights ocular hemodynamics as a possible risk factor
for glaucomatous progression. Their response letter confirms the need
for a more definitive evaluation of blood flow in glaucoma to determine
any relationship to its pathogenesis and if improving this parameter
improves long-term visual outcomes. By doing so we hope that, in the
future, our patients may be more specifically and adequately treated.
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. 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.
Dr Buck et al must be commended for this wonderful article[1] which
takes us one step closer to deciding intervention based on Newcastle
scoring system previously described.[2] However, we seek a few
clarifications.
1.Inclusion criteria: The authors have described the inclusion
criteria for the study to be intermittent exotropia X(T)) of more than or
equal to 20 prism dioptres (pd), for...
Dr Buck et al must be commended for this wonderful article[1] which
takes us one step closer to deciding intervention based on Newcastle
scoring system previously described.[2] However, we seek a few
clarifications.
1.Inclusion criteria: The authors have described the inclusion
criteria for the study to be intermittent exotropia X(T)) of more than or
equal to 20 prism dioptres (pd), for distance fixation and X(T) of less
than or equal to 20 pd at near. A closer look of the results reveals that
the range of values is 0 to 40 pd and 6 pd.to 50 pd for near and distance
respectively (table 2).Has the inclusion criteria been adhered to?
2.As per the table cited, the median and mean stereoacuity values are
more for near than for distance which is contrary to what is expected in a
case of intermittent exotropia. We would request the authors to elucidate
more on this aspect.
3.Median values are 110 sec of arc and 75 sec of arc at baseline and
follow up respectively for near stereoacuity by Frisby test. Similarly
median values are 34 sec of arc and 23 sec of arc for distance
stereoacuity at baseline and follow up by FD2TM distance stereoacuity. We
would like the authors to clarify their testing protocols because these
values are not included in the testing protocols usually followed for
administering these tests.
References
1.Buck D, Hatt SR, Haggerty H, Hrisos S, Strong NP, Steen NI, Clarke MP.
The use of the Newcastle Control Score in the management of intermittent
exotropia. Br J Ophthalmol 2007;91:215-218
2.Haggerty H, Richardson S, Hrisos S, et al. The Newcastle Control
Score: a new
method of grading the severity of intermittent exotropia. Br J Ophthalmol
2004;88:233¨C5.
Dear Editor
A metastizing adenocarcinoma of the retinal pigment epithelium in a 37-year-old man with Down syndrome (DS) has recently been reported in the British Journal of Ophthalmology [1]. In the article the authors underlined an unusual and atypical aggressive behaviour of the tumour which was the first well documented adenocarcinoma of the retinal pigment epithelium with metastases. Although solid tumours are...
Dear Editor
We thank Dr Ayata for the thoughtful comments of our article. He had three questions that we would like to answer as follows:
1) Figure 1 was quite important for the paper because it shows the exact location of the macular pigment in monkeys (courtesy of Francois Delori, PhD). We are sorry for the lack of the image in the on-line paper version but it was probably due to the PDF saving...
Dear editor,
Epigenetic regulation of tumor suppressor genes provides an attractive mechanism for tumors in which mutations and structural changes are rare. The latter may apply to uveal melanoma for which little is known of the genes that contribute to tumor development. In the search for genes, uveal melanoma is often compared to its counterpart in the skin, cutaneous melanoma. One of the major cuteneous melan...
Dear Dr Radcliffe and colleagues,
Thank you for your comments. Two cases with the exfoliation syndrome and one with pigmentary glaucoma were included in our study. As you mentioned, dilatation of the pupil often causes a rise of intraocular pressure in such cases. However, none of the three individuals in our study had a significant rise of intraocular pressure or progression of glaucoma. Sincerely, George Sp...
Dear Editor
We thank Dr Kesarwani for the interest in our article.
In response to the points raised:
1. Inclusion criteria
We attempted to recruit children with X(T) measuring more than 20 prism dioptres when fixing a 6 metre target, as angles under this amount are usually felt not to require treatment. However, Dr Kesarwani is correct to point out that, at the baseline assessme...
Dear Editor,
We read with great interest the recently published article by Bottoni and associates. However, we would like to express our concerns regarding their article entitled “Diagnosis of macular pseudoholes and lamellar macular holes: is optical coherence tomography the gold standard?” Br. J. Ophthalmol. published online 1 Feb 2008; doi:10.1136/bjo.2007.127597. [1] In this article, the authors investigate...
Dear Editor,
I appreciate the letter by Dr. Lempert regarding Dr. Nilsson's Editorial to our study of the extension of the period of bilateral visual impairment (BVI) in persons with untreated amblyopia, and the response by Dr. Nilsson. A slight misunderstanding may arise, however, from the first sentence of Dr. Lempert's letter: "It is not surprising that amblyopes are at higher risk of bilateral visual impairm...
Dear Editor,
We agree with the authors’ recommendation on the need for a sleep history in the eye clinic and probably having a lower threshold for referral to sleep physicians for further sleep studies.[1] However, we would like to bring to their attention other epidemiological studies where screening tools/sleep history have shown a high prevalence of sleep disorders in patients with ocular disorders other than...
Dear editor,
We want to thank Drs. Martinez and Sanchez for the response to our recent editorial. We are in agreement with them that evidence does exist that blood flow is altered in glaucoma and is suggestive of a pathogenetic role[1]. We also agree that a variety of methods are being used to evaluate blood flow and these techniques certainly have improved over the last decade and a half.
I would also lik...
Dear Editor,
Dr Buck et al must be commended for this wonderful article[1] which takes us one step closer to deciding intervention based on Newcastle scoring system previously described.[2] However, we seek a few clarifications.
1.Inclusion criteria: The authors have described the inclusion criteria for the study to be intermittent exotropia X(T)) of more than or equal to 20 prism dioptres (pd), for...
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