We thank Konstantopoulos et al. for their interest in our paper and
congratulate them for having conducted such a large study. It should be
noted, however, that we did not actually conclude that older age was not
associated with an increased risk of intraoperative complications, rather
we stated that our data suggest that age alone may not be a major risk
factor for any complication. Clearly absence of...
We thank Konstantopoulos et al. for their interest in our paper and
congratulate them for having conducted such a large study. It should be
noted, however, that we did not actually conclude that older age was not
associated with an increased risk of intraoperative complications, rather
we stated that our data suggest that age alone may not be a major risk
factor for any complication. Clearly absence of statistical evidence can
never be equated to proof of no difference and we were careful to
highlight that our numbers were small ( 9 patients older than 96, 111
greater than 88 years).
If we attempt to summarise data from our study, the Southampton Study
and that by Berler to examine whether or not age greater than 88 is a risk
factor for intra operative complications using meta analysis techniques,
we find that there is significant inconsistency between the studies (test
for heterogeneity Chi-square = 7.54, P = 0.02, I-squared = 73.5 %). It
seems likely therefore that the different findings from our work and that
of Southampton are not simply a reflection of varying study sizes but
arise from other differences between the studies - for example the
populations being operated on, or perhaps the techniques employed.
We would therefore agree with Konstantopoulos that further research
into this interesting subject is needed.
References
1. Robbie SJ, Muhtaseb M, Qureshi K, Bunce C, Xing W, Ionides A.
Introperative complications of cataract surgery in the very old. Br J
Ophthalmol 2006; 90:1516-1518.
2. Berler DK. Intraoperative complications during cataract surgery in
the very old. Trans Am Ophthalmol Soc. 2000; 98:127-30; discussion 130-2.
We read your article titled- 'Socioeconomic status, systemic blood
pressure and intraocular pressure: the Tanjong Pagar Study', with great
interest. The association of the level of education and income with
intraocular pressure in the Chinese population of Singapore has been
discussed in an interesting and detailed manner.
We do appreciate that this is the first report, to assess the
asso...
We read your article titled- 'Socioeconomic status, systemic blood
pressure and intraocular pressure: the Tanjong Pagar Study', with great
interest. The association of the level of education and income with
intraocular pressure in the Chinese population of Singapore has been
discussed in an interesting and detailed manner.
We do appreciate that this is the first report, to assess the
association. However, although the results are interesting, we feel that
caution should be exercised when drawing conclusions from this data.
Table
1 demonstrates that in those with secondary level of education, the
measured IOP was highest for age groups 50-59 years and 60-69 years, and
second highest in the above 70 years age group. Although the measured
IOP
was highest for those with secondary level of education, in 2 out of the 4 groups, and second highest in the third group, the final mean IOP was
lower in the secondary education group than those with primary or no
formal education. The reason behind this fallacy is that the number of
subjects with secondary education in the 50-59 years, 60-69 years and
the
above 70 years age group, was considerably lower than that of the
primary
and no formal education groups while that in the 40-49 years age group
was
considerably higher than the other two groups. As the measured IOP in
the
40-49 years group with secondary education was lowest among the four
groups but the number of subjects was highest, the final mean IOP in the
secondary education group was lower than that in the primary and the no
formal education group. In brief, the final mean IOP could only be
comparable if the number of subjects in all the groups considered would
have been similar. As this was not the case, there appears to be serious
doubts regarding the validity of the conclusions of this study. A more
detailed and clear explanation is warranted in this regard.
We would like to thank Kase et al for their interesting report[1] on
p27 and cyclin expression in pterygium. The authors have reported in
table
1[1] that cyclin D was up-regulated and p27 down-regulated in pterygium,
and concluded that a disorder of epithelial cell proliferation or cell
cycle was involved. However, several important issues have not been
addressed. We would like to highlight 3
points:...
We would like to thank Kase et al for their interesting report[1] on
p27 and cyclin expression in pterygium. The authors have reported in
table
1[1] that cyclin D was up-regulated and p27 down-regulated in pterygium,
and concluded that a disorder of epithelial cell proliferation or cell
cycle was involved. However, several important issues have not been
addressed. We would like to highlight 3
points:
1. p27 is usually regarded as an inhibitor to cyclin E/CDK2 rather
than cyclin D.[2] The down-regulation of p27 was apparently regarded by
the authors[1] to have an inhibitory role on G1-S progression, in such a
scenario, it would be important to report the expression and regulation
of
cyclin E in pterygium.
2. Studies have found that p27 (or members of KIP, CIP) may
positively regulate cyclin D/CDK[4,3] and many tumors show
co-expression
of p27 and cyclin D rather than suppression of p27.[4] Consequently, a
down-regulation of p27 as an upstream event in pterygium may be expected
to reduce cyclin D/CDK4 expression. We noted that the authors found up-regulation of cyclin D, which can easily have been due to fluctuation of
factors other than KIP, such as the INK4 family, usually regarded as the
more important regulators of cyclin D.[5] On the other hand, some tumors have shown binding of p27 to cyclin D2,[6] in such a case, the p27 may
have been sequestered and functionally inhibited, consequently
increasing
activity of cyclin E/CDK2. This illustrates that information on both
cyclin/CDK complexes is essential for a proper understanding of
proliferation-related diseases. It is also interesting that our gene
microarray expression studies (http://www.ncbi.nlm.nih.gov, GDS1758,
GSE2513 and GPL96) show that transcripts for cyclin D2 was significantly
down-regulated in pterygial tissue compared to un-involved conjunctival
tissue.
3. In their discussion, the authors[1] have omitted to cite studies
which did not support cell cycle dys-regulation in pterygium, which we
feel ought to be included for objectivity. For example, a study[7] which
showed no alteration in cell proliferation in pterygium and another[8]
that showed conjunctival and pterygial epithelial cell proliferation
were
not significantly different.
References
1. Kase S, Takahashi S, Sato I, Nakanishi K, Yoshida K, Ohno S.
Expression of p27(KIP1) and cyclin D1, and cell proliferation in human
pterygium. Br J Ophthalmol. 2006 Dec 19; [Epub ahead of print]
2. Xu X, Nakano T, Wick S, Dubay M, Brizuela L. Mechanism of
Cdk2/Cyclin E inhibition by p27 and p27 phosphorylation. Biochemistry.
1999 Jul 6;38(27):8713-22.
3. Bryja V, Pachernik J, Faldikova L, Krejci P, Pogue R, Nevriva I,
Dvorak P, Hampl A. The role of p27(Kip1) in maintaining the levels of D-type cyclins in vivo. Biochim Biophys Acta. 2004 May 3;1691(2-3):105-16.
4. Pignataro L, Sambataro G, Pagani D, Pruneri G.
Clinico-prognostic
value of D-type cyclins and p27 in laryngeal cancer patients: a review.
Acta Otorhinolaryngol Ital. 2005 Apr;25(2):75-85. Review. Erratum in:
Acta
Otorhinolaryngol Ital. 2005 Jun;25(3):following 207.
5. Hirai H, Roussel MF, Kato JY, Ashmun RA, Sherr CJ. Novel INK4
proteins, p19 and p18, are specific inhibitors of the cyclin D-dependent
kinases CDK4 and CDK6. Mol Cell Biol. 1995 May;15(5):2672-81.
6. Kukoski R, Blonigen B, Macri E, Renshaw AA, Hoffman M, Loda M,
Datta MW. p27 and cyclin E/D2 associations in testicular germ cell
tumors:
implications for tumorigenesis. Appl Immunohistochem Mol Morphol. 2003
Jun;11(2):138-43.
7. Karukonda SR, Thompson HW, Beuerman RW, Lam DS, Wilson R, Chew
SJ,
Steinemann TL. Cell cycle kinetics in pterygium at three latitudes. Br J
Ophthalmol. 1995 Apr;79(4):313-7.
8. Tan DT, Liu YP, Sun L. Flow cytometry measurements of DNA
content
in primary and recurrent pterygia. Invest Ophthalmol Vis Sci. 2000
Jun;41(7):1684-6.
We read with interest the article by Robbie et al titled
‘Intraoperative complications of cataract surgery in the very old’.[1] We
agree with the authors that identification of risk factors for cataract
surgery is important, as it has implications for patient care, surgical
training, auditing and revalidation. The authors concluded that older
age was not associated with an increased risk of intraoper...
We read with interest the article by Robbie et al titled
‘Intraoperative complications of cataract surgery in the very old’.[1] We
agree with the authors that identification of risk factors for cataract
surgery is important, as it has implications for patient care, surgical
training, auditing and revalidation. The authors concluded that older
age was not associated with an increased risk of intraoperative
complications. Complication rates in patients >=88 years were not
significantly different to patients <88 (4.5% vs. 6.3%, p=0.54). In
patients >=96 years, although the complication rate was higher than in
patients <96, this was not statistically significant (11.1% vs. 6.3%,
p=0.45). However, the study included only 54 patients older than 90 years
(number of patients older than 88 not stated) and 9 patients older than 96
years.
In a similar study, we identified all phacoemulsification cataract
procedures carried out between 2001 and 2005 at the Southampton Eye Unit.
Intraoperative complications, as classified in the National Cataract
Surgery Survey,[2] were recorded on a computer database for each cataract
procedure. We analysed the same data as the above study,[1] including age
of patient, grade of surgeon and intraoperative complications (defined as
abnormality in wound closure, posterior capsule tear, zonule dehiscence,
anterior chamber haemorrhage, iris trauma or persistent iris prolapse).
Logistic regression analysis was carried out to examine whether age
>=88 and age >=96 years were associated with an increased risk of
complications. SPSS version 14 was used for statistical analysis;
p<0.05 was considered statistically significant.
We identified 9367 consecutive phacoemulsification procedures. The
mean patient age was 76.9 (SD 9.8) years. The overall complication rate
was 3.1%. No significant difference was found between grades of surgeon
and complication rates (trainee vs. consultant: 3.2% vs. 3.1%, p=0.90).
Interestingly, the complication rate in patients >=88 years (837
eyes) was 4.3% compared to 3.0% in patients <88 years (OR 1.4, 95% CI
1.005-2.049, p<0.05). In patients >=96 years (36 eyes) the
complication rate was 8.3% vs. 3.1% in patients <96 years (OR 2.8, 95%
CI 0.858-9.228, p=0.09).
Therefore, in contrast to the above study,[1] our results suggest
that older age may be a risk factor for intraoperative complications
during phacoemulsification surgery. We suggest that the rate of
complications in cataract surgery in different age groups requires further
study and that, in view of our results, experienced surgeons should
preferentially operate on patients older than age 88.
References
1. Robbie SJ, Muhtaseb M, Qureshi K, Bunce C, Xing W, Ionides A.
Introperative complications of cataract surgery in the very old. Br J
Ophthalmol 2006;90:1516-1518.
2. Desai P, Minassian DC, Reidy A. National cataract surgery survey 1997-
8: a report of the results of the clinical outcomes. Br J Ophthalmol
1999;83:1336-1340.
We appreciate the thoughtful comments of Dr Konstantopoulos and
colleagues on our recent article [1]. They raise some
interesting comments that we would like to answer point by point.
Basically, our article published on March 2006 showed a strong association
between NAION and Sleep apnoea syndrome [1]. The first point addressed by
Konstantopoulos et al. was the high prevalence rate (48%) of patients...
We appreciate the thoughtful comments of Dr Konstantopoulos and
colleagues on our recent article [1]. They raise some
interesting comments that we would like to answer point by point.
Basically, our article published on March 2006 showed a strong association
between NAION and Sleep apnoea syndrome [1]. The first point addressed by
Konstantopoulos et al. was the high prevalence rate (48%) of patients
included in the study having a history of fellow eye NAION. They
suggest that this prevalence is unexpectedly high and not representative
of what is encountered in a normal clinical practice. In the Ischemic
Optic Neuropathy Decompression Trial (IONDT) [2] that recruited 418
patients, 19% had previous NAION affecting the fellow eye at baseline.
However, they found a cumulative incidence rate of 14.7% of second eye
NAION over a median patient follow up of 5.1 years. The cumulative
prevalence rate corresponding to the second eye involvement before and
during the study was 30.6%. Others studies found a cumulative prevalence
rate range from 23 to 48% which is closed to the prevalence we had in our
study [3-5]. A subsequent question
was the validity of second eye involvement diagnosis. Regarding this,
Konstantopoulos and colleagues were interested to know whether the visual
field defect was confirmed by perimetry. We can confirm that the diagnosis
of bilateral NAION was documented in all cases by an automated perimetry.
The larger question addressed by Konstantopoulos and colleagues was
whether there was a selection bias in our study. As stated in the article
[1], private practice ophthalmologists and general practitioners are
referring all incident cases of NAION for short duration hospitalization
allowing assessment of associated vascular risk factors and treatment decisions. Based on this, we strongly doubt that only atypical cases
of bilateral NAION were included in our study.
In summary, we have demonstrated a strong association between NAION
and OSA that justifies evaluation of every NAION patient with polysomnography
or at least a sleep questionnaire or other screening methods like
oximetry. OSA per se is one of the factors contributing to cardiovascular risk in the general population and in NAION patients.
For this reason also
hypertension, diabetes or hyperlipemia should be documented. Moreover, CPAP treatment,
independently of NAION improves the patient's quality of life when
suffering severe OSA. Finally, the crucial point is to accumulate in
the next years scientific data to address potential beneficial effects of
CPAP treatment on NAION time course evolution.
References
1. Palombi K, Renard E, Levy P, Chiquet C, et al. Non-arteritic
anterior ischaemic optic neuropathy is nearly systematically associated
with obstructive sleep apnoea. Br J Ophthalmol 2006;90:879-882.
2. Newman NJ, Scherer R, Langenberg P, Kelman S, et al. The fellow
eye in NAION: report from the ischemic optic neuropathy decompression
trial follow-up study. Am J Ophthalmol 2002;134:317-328.
3. Repka MX, Savino PJ, Schatz NJ, Sergott RC. Clinical profile and
long-term implications of anterior ischemic optic neuropathy. Am J
Ophthalmol. 1983;96:478-483.
4. Ellenberg C Jr, keltner JL, Burde RM. Acute optic neuropathy in
older patients. Arch Neurol 1973; 28:182-185.
In their article Pakravan et al. write on the correlation of central
corneal thickness and optic disc size.[1] The authors describe a negative
correlation (r= -0.284) which was statistically significant (p=0.036) for
the 72 eyes investigated. These 72 eyes, however, represent 53 patients.
This means that 19 patients are represented with both eyes and 34
participants with only one eye. The right and the...
In their article Pakravan et al. write on the correlation of central
corneal thickness and optic disc size.[1] The authors describe a negative
correlation (r= -0.284) which was statistically significant (p=0.036) for
the 72 eyes investigated. These 72 eyes, however, represent 53 patients.
This means that 19 patients are represented with both eyes and 34
participants with only one eye. The right and the left eye of the same
person cannot be considered independent from each other. Oppositely, the
two eyes frequently have similar characteristics for many parameters
including central cornea thickness and optic disc size. Using both eyes of
certain individuals and only one eye of others for correlation may lead to
incorrect conclusion due to increased representation of some
characteristics. It is especially important in cases like the authors’
report in which the correlation and the p-value were not extremely strong.
The authors’ are requested to repeat their calculation using one
(preferably randomly selected) eye per patient, and to present their data
(r and p-value). If the significant negative correlation presented in the
original article is reproducible, the conclusion can be maintained, but in
the opposite case revision of the conclusion is necessary.
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. Pakravan M, Parsa A, Sanagou M, et al. Central corneal thickness
and correlation to disc size: a potential link for susceptibility to
glaucoma. Br J Ophthalmol 2007;91:26-28.
I am very interested in Drs. Hayashi and Hayashi's article entitled
'Visual function in patients with yellow tinted intraocular lenses
compared with vision in patients with non-tinted intraocular lenses' that
was published in Br J Ophthalmol 2006; 90:1019-1023. This is a well
designed and controlled clinical study with interesting results. I have a
few comments on the article to the authors as follows...
I am very interested in Drs. Hayashi and Hayashi's article entitled
'Visual function in patients with yellow tinted intraocular lenses
compared with vision in patients with non-tinted intraocular lenses' that
was published in Br J Ophthalmol 2006; 90:1019-1023. This is a well
designed and controlled clinical study with interesting results. I have a
few comments on the article to the authors as follows:
1. It is well known that pupil size and IOL tilt or decentration can
significantly affect glare test results. Since this article did not report
the information for IOL tilt or decentration during follow-up visits and
the information for pupil sizes during the glare test, I did not know if
the authors addressed these issues in their study.
2. The authors have pointed out that one of the weaknesses of this
study was that 'mesopic contrast sensitivity was examined under a higher
luminance level (5 cd/m²) than that typically used for mesopic vision
testing (≤3 cd/m²)' and 'The second limitation of the study described
here is that scotopic contrast sensitivity was not examined'. Previous
studies have demonstrated that visual acuity and contrast sensitivity
performed under a dim light condition are more sensitive than the results
obtained under a bright light condition. A small visual benefit among
aspheric IOL, yellow tinted IOL and conventional IOL may be seen under a
dim light condition but not a bright light condition.
3. Currently, several manufacturers offer yellow tinted IOLs and the
IOL color is not exactly the same. Therefore, the authors should mention
how much blue light this IOL can block and discuss if the remaining blue
light that is not blocked by the IOL can cause potential retinal toxicity
long-term. Furthermore, color vision is always a concern for yellow tinted
IOL implantation. This study did not perform color vision testing.
4. The authors stated, in their article, that five patients (13.9%)
in the non-tinted IOL group noted cyanopsia at 2 weeks after surgery,
while no patient in the yellow tinted IOL group reported this symptom. No
patients in either group, however, reported this symptom at 3 months after
surgery. Clinically, it is no surprise if a patient complains about bright
light or different color images after cataract surgery and IOL
implantation. The symptoms will go away gradually. In Drs. Hayashi and
Hayashi's article, five patients with cyanopsia at 2 weeks after surgery
and the symptom disappeared at 3 months after surgery. Did the patients
get used to the color of the images at 3 months after surgery or were the
patients not able to distinguish a difference in color at 3 months,
because the second eye was operated on? The article did not report the
interval of two eye surgeries.
5. Drs. Hayashi and Hayashi stated in their article that 'because in
vitro studies showed that short wavelength blue light has photo toxicity
for the neural retina and retinal pigment epithelial cells, and that the
blue light absorbing IOL could prevent damage to the retinal pigment
epithelial cells, the yellow tinted IOL is thought to contribute to the
prevention of AMD. Therefore, the use of yellow tinted IOLs is recommended
for eyes at high risk to develop AMD'. It is reasonable to predicate
clinical outcomes based on in vitro results. It is premature to recommend
yellow tinted IOL for prevention of AMD based on the in vitro results,
because in vitro results are not always repeatable in clinical trials.
In summary, this study has provided additional scientific data and
evidence to support the safety and efficacy of yellow tinted IOL in human
eyes. But the beneficial effect of yellow tinted IOL for prevention of AMD
is purely based on a theory. Clinically, it is equally difficult to prove
or disprove this theory. Therefore, the debates and controversy regarding
the beneficial effect of yellow tinted IOL will likely continue for years
to come.
I was interested to read the article by Garcia-Arumi and colleagues
on "Surgical embolus removal in retinal artery occlusion".[1] The authors
claim that "Surgical removal of retinal arterial emboli seems to be an
effective and safe treatment for RAO (retinal artery occlusion)".
Briefly, the study was based on 6 eyes with temporal branch retinal
artery occlusion (BRAO) and one with central re...
I was interested to read the article by Garcia-Arumi and colleagues
on "Surgical embolus removal in retinal artery occlusion".[1] The authors
claim that "Surgical removal of retinal arterial emboli seems to be an
effective and safe treatment for RAO (retinal artery occlusion)".
Briefly, the study was based on 6 eyes with temporal branch retinal
artery occlusion (BRAO) and one with central retinal artery occlusion
(CRAO). The surgery was performed in BRAO eyes 4, 12, 19, 22, 28, and 33
hours after onset and in CRAO eye 29 hours after visual loss. The first
post-operative evaluation, 48 hours after surgery, showed reperfusion of
the occluded branch retinal artery in 4 and none in one; in the
remaining eye,
no evaluation was possible for 2 weeks because of vitreous hemorrhage.
In
the 6 eyes with BRAO, pre-operative visual acuity was: hand motion,
counting fingers, 20/400, 20/200, 20/200 and 20/25, at 48 hours it was
20/200, 20/100, 20/100, 20/200, 20/100 and 20/30 respectively, and final
visual acuity was 20/50, 20/30, 20/80, 20/200, 20/25 and 20/25
respectively; in the CRAO eye, visual acuity remained hand motion all
along.
It is worth noting, initially, that a conclusion based on 6 eyes is
limited. However, the matter of
apparent improvement in visual acuity claimed by the authors deserves
comment.
1. All 6 of the eyes had temporal BRAO. In the vast majority of
temporal BRAO eyes the border between the ischemic and non-ischemic
retina
passes through the fovea, as their figures 2 and 3 show. Also the
fluorescein angiogram in Figure 2 shows a patent cilioretinal artery.
These are extremely important facts in determining whether the visual
improvement noted was result of removal of the embolus or simply the
natural history of the disease. Having studied the natural history of
about
200 BRAO eyes, I recently stated: "In cilioretinal artery occlusion,
branch retinal artery occlusion and CRAO with cilioretinal artery
sparing,
the junction between the infarcted and normal retina may often pass
through the fovea. In many of these eyes, I have seen marked spontaneous
visual acuity improvement occurring within several days or weeks, from
almost 20/200 or worse to even normal. This spontaneous improvement is
often erroneously attributed to an advocated treatment."[2]
When the junction between the normal and infarcted retina passes
through the fovea, in such eyes, the retinal edema associated with
retinal
infarction most probably also involves to some extent the adjacent
normal
foveal retina shortly after the occlusion; over the following weeks the
normal foveal retina recovers spontaneously, resulting in natural visual
improvement. In the series of Garcia-Arumi and colleagues a significant
visual improvement at final visit seen in 4 of 6 eyes is not uncommon in
such eyes, as a part of the natural history in my experience. Moreover,
the eye in figure 2, not only had the junction between the normal and
infracted retinal passing through the fovea but also had patent
cilioretinal artery, which is an important factor in natural visual
acuity
improvement not only in BRAO but also in CRAO[3].
2. Having studied more than 450 patients with BRAO and CRAO, I have
found another common confounding factor involving visual acuity testing.
At the initial visit, because of sudden visual loss, the patient is
emotionally upset, and tends to test poorly; for instance a patient with
only temporal BRAO with the border between the ischemic and normal
retina
passing through fovea should not have hand motion or even 20/400 visual
acuity, if tested properly because the other half of the macula and
retina
is still functioning normally. Moreover, later on it is not unusual to
find patients with central scotoma learning to fixate eccentrically and
show better visual acuity, which may erroneously be interpreted as
genuine
improvement. In my studies on various ocular vascular occlusive diseases
I
have found that unless improvement in visual acuity corresponds with
improvement in central scotoma, it is not a genuine improvement but due
to
eccentric fixation.[4]
3. Since visual acuity testing assesses only the function of the
fovea and not of the entire involved retina, visual fields, particularly
with a Goldmann perimeter, give us much better information about the
extent of visual loss and change. In my study, every eye with BRAO had
visual fields plotted with a Goldmann perimeter; that showed that the
visual fields of BRAO eyes often did show reduction in size of the
visual
field defect as a part of the natural history. Garcia-Arumi and
colleagues
state that they recorded the visual fields with Humphrey perimeter but
give no information on the visual fields of their cases. Moreover,
unlike
the Goldmann perimeter, Humphrey perimeter provides information about
only
the central 240 - 300 and not the entire involved retina.
4. In the series of Garcia-Arumi and colleagues, 6 of 7 eyes had
had
acute retinal ischemia for 12 to 33 hours and in one for 4 hours. We
evaluated the retinal tolerance time to acute ischemia experimentally in
rhesus monkeys[5] and found that in CRAO, ischemic retina can recover
normal
function from acute ischemia of 97 minutes, but after that the longer
the
ischemia, the more extensive the irreversible damage so that acute
ischemia lasting for 240 minutes results in massive irreversible retinal
damage. Therefore, it does not seem logical that restoration of
circulation in BRAO 4 to 33 hours after the occlusion would restore
function in an already irreversibly damaged retina. Moreover, they found
restoration of circulation in 4 of the 6 eyes on fluorescein angiography
first done 48 hours after the surgery. They argue that "in branch RAO
because some degree of perfusion at the macular area may be supplied by
the contralateral temporal artery." [1] This may be true, but it may also
be
another factor in the spontaneous marked visual recovery in such eyes as
a
part of natural history.
In conclusion, based on my studies on the natural history in BRAO
eyes, I feel the visual acuity improvement attributed by Garcia-Arumi
and
colleagues to embolectomy simply represents natural history.
References
1. Garcia-Arumi J, Martinez-Castillo V, Boixadera A, et al.
Surgical
embolus removal in retinal artery occlusion. Br J Ophthalmol
2006;90:1252-
5.
2. Hayreh SS. Prevalent misconceptions about acute retinal vascular
occlusive disorders. Prog Retin Eye Res 2005;24:493-519.
3. Hayreh SS, Zimmerman B. Central Retinal Artery Occlusion: Visual
Outcome. Am J Ophthalmol 2005;140:376-91.
4. Hayreh SS, Zimmerman B, Kardon RH. Visual improvement with
corticosteroid therapy in giant cell arteritis. Acta Ophthalmol Scand
2002;80:355-67.
5. Hayreh SS, Zimmerman MB, Kimura A, et al. Central retinal
artery
occlusion. Retinal survival time. Exp Eye Res 2004;78:723-36.
Yours sincerely,
S.S. Hayreh
Sohan Singh Hayreh, MD, PhD, DSc, FRCS, FRCOphth
Professor Emeritus of Ophthalmology & Director Ocular Vascular
Clinic
We thank Pushpoth and Sandramouli for their wide-ranging critique
of
our paper discussing previous isotretinoin use in potential military
aviator recruits.[1] We cannot agree with their comment that the finding
of 2 of 47 candidates, with clinically abnormal dark adaptation (DA) and
11 with electroretinogram (ERG) abnormalities does not justify further
screening of this population. Aircrew recruits...
We thank Pushpoth and Sandramouli for their wide-ranging critique
of
our paper discussing previous isotretinoin use in potential military
aviator recruits.[1] We cannot agree with their comment that the finding
of 2 of 47 candidates, with clinically abnormal dark adaptation (DA) and
11 with electroretinogram (ERG) abnormalities does not justify further
screening of this population. Aircrew recruits are a selected
population,
to a large degree without any significant history of systemic or ocular
abnormalities. In balance of probability this selection makes it more
likely that the retinal function of these individuals falls within the
age-matched normal population, not less. The candidates had, for the most
part, applied for a career in aviation long after taking isotretinoin,
though we agree that it would have been desirable to prospectively
follow
the ERG and DA changes before and after treatment.
Pushpoth's and Sandramouli's assumption that isotreinoin-related
retinal toxicity is dose-related cannot be made from our retrospective
report; largely for the reasons outlined in their comments on incomplete
dosage information. We do know that none of the individuals had a
history,
or family history of retinal abnormality and that clinical retinal and
visual field measurements were normal. Colour vision tested normal in
all
cases with an Ishihara Pseudoisochromic Plate Test and Lanthony 15 hue
colour vision test.
Our reference to Oner et al.[2] was not to compare the papers
results
but to disagree with the finding that all side-effects of isotretinoin
were short-lived. Had they performed electrophysiology they might have
found a different result.
In this paper we lend support to the findings of other studies that
rod function can be adversely affected by previous isotretinoin
use[3,4].
As aviation is a night-vision critical profession; we consider it
justified at present to check the night vision of aircrew candidates
with
a history of isotretinoin by dark adaptometry, from a flight-safety
point
of view. We agree with Pushpoth and Sandramouli that a prospective study
of the retinal effects of isotretinoin would shed more light on the
problem as much remains to be learnt about the safety of isoretinoin.
Sincerely yours,
Susan P Mollan, Malcolm Woodcock, Peter Good and Robert AH Scott
References
1. Mollan SP, Woodcock M, Siddiqi R, Huntbach J, Good P, Scott RAH.
Does use of isotretinoin rule out a career in flying? Br J Ophthalmol
2006;90:957-959
2. Oner A, Ferahbas A, Karakucuk S, et al. Ocular side-effects
associated with systemic isotretinoin. J Toxicol 2004; 23:189-195
3. Brown RD, Grattan CEH. Visual toxicity of synthetic retinoids.
Br J
Ophthalmol. 1989;73:286-288
4. Weleber RG, Denman ST, Hanifin JM, Cunningham WJ. Abnormal
retinal
function associated with Isotretinoin therapy for acne. Arch Ophthalmol.
1986;104: 831-837
We read with interest the article by Steven et al.[1] on their
finding of secondary paracentral retinal holes following internal limiting
membrane peel. We have also reported on 4 eyes of 4 patients that
developed iatrogenic eccentric macular holes following vitrectomy with ILM
peeling for idiopathic macular holes.[2]
In their report, Steven et al treated 3 of the 7 patients with argon laser
photocoagula...
We read with interest the article by Steven et al.[1] on their
finding of secondary paracentral retinal holes following internal limiting
membrane peel. We have also reported on 4 eyes of 4 patients that
developed iatrogenic eccentric macular holes following vitrectomy with ILM
peeling for idiopathic macular holes.[2]
In their report, Steven et al treated 3 of the 7 patients with argon laser
photocoagulation. Haritoglou et al.[3] reported paracentral scotomata
following vitrectomy with ILM peeling for macular holes. Treatment of
these paracentral holes with argon laser photocoagulation could therefore
make these scotomas worse.
The pathogenesis of these iatrogenic holes is unclear. We believe that
there must be an element of mechanical trauma involved in the formation of
these secondary holes, despite the fact that it is not visible at the time
of surgery. Their speculation of weakening of the glial structure of the
retina caused by decapitation of the Muller cells is interesting and may
also play an important role – as all the holes reported are in the ILM-
denuded area. We note that in the series by Steven et al, all the reported
holes appear temporal to the fovea. In our series, the holes were reported
inferior as well as nasal to the fovea.
We used trypan blue to assist in the peeling of the ILM, and no obvious
areas of retinal trauma were apparent at the time of surgery. The
secondary holes became apparent in the follow-up period; none of them have
had any treatment and have not caused any problems after long-term follow-up (6 years). We recommend that these holes should not be treated, as they
do not appear to lead to retinal detachment.
References
1. Steven P, Laqua H, Wong D, Hoerauf H. Secondary paracentral retinal
holes following internal limiting membrane removal. Br J Ophthalmol
2006;90:293-95.
2. Rubinstein A, Bates R, Benjamin L, Shaikh A. Iatrogenic eccentric full
thickness macular holes following vitrectomy with ILM peeling for
idiopathic macular holes. Eye 2005;19:1333-35.
3. Haritoglou C, Ehrt O, Gass CA, et al. Paracentral scotomata: a new
finding after vitrectomy for idiopathic macular hole. Br J Ophthalmol
2001;85:231-3.
Editor
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We thank Pushpoth and Sandramouli for their wide-ranging critique of our paper discussing previous isotretinoin use in potential military aviator recruits.[1] We cannot agree with their comment that the finding of 2 of 47 candidates, with clinically abnormal dark adaptation (DA) and 11 with electroretinogram (ERG) abnormalities does not justify further screening of this population. Aircrew recruits...
Dear Editor
We read with interest the article by Steven et al.[1] on their finding of secondary paracentral retinal holes following internal limiting membrane peel. We have also reported on 4 eyes of 4 patients that developed iatrogenic eccentric macular holes following vitrectomy with ILM peeling for idiopathic macular holes.[2] In their report, Steven et al treated 3 of the 7 patients with argon laser photocoagula...
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