When reading the article we were a bit surprised by the
extremely positive declaration of the clinical results after subthreshold
diode micropulse photocoagulation. The authors stated that
subthreshold diode micropulse laser photocoagulation minimises
chorioretinal damage in the management of CSMO and demonstrates a
beneficial effect on visual acuity and CSMO resolution (in 96% of all
treated eyes, n=...
When reading the article we were a bit surprised by the
extremely positive declaration of the clinical results after subthreshold
diode micropulse photocoagulation. The authors stated that
subthreshold diode micropulse laser photocoagulation minimises
chorioretinal damage in the management of CSMO and demonstrates a
beneficial effect on visual acuity and CSMO resolution (in 96% of all
treated eyes, n=95). However, we have
the strong feeling that the presented results may not support this
conclusion. Moreover, the basic mechanism of the proposed laser
interaction is unclear. It is most likely that
nothing than marginal thermal side effects occurred in the retina
during treatment.
Conventional laser therapy is regarded as effective in treating CSMO.
Unwanted side effects as e.g. induction of CNV or subretinal fibrosis
principally do not appear if laser parameters for threshold exposition are
carefully used. Generally a new laser method must measure against this gold
standard, so that at least comparable results are obtained. This seems not to be the case in the present article.
Conclusions such as "visual acuity was stable or improved in 85% of treated eyes" are questionable if Tab.2 shows stabilization in only 76.8% of eyes (+ < 3 ETDRS lines) and only 8.4% achieved significant better visual acuity (also 14.7% lost more
than 3 lines). Regarding Tab.1 and Tab.3 overall visual acuity
became worse and not better and nearly none of the p-values showed
significance (if p-value was significant visual acuity was worse).
As stated by the authors, the validity of this pilot study is
limited by its small size and retrospective nature. In fact no uniform
postoperative patient follow-up was performed and only the "last available
visual acuity measure" was taken for outcome assessment. This value was
obtained between 3 and 29 (mean 12.2 months), which underlines a high variability. In other words, the results
might only reflect the spontaneous untreated course of CSMO. Also
questionable is the postoperative gradation of CSMO as "worse, better and
resolved". There were no OCT scans taken
either pre- or post-operatively to verify macular thickness. Also,
angiography seems to be performed only in patients who appeared to need
additional treatment. Thus from none of the presented results could it be
objectively concluded that CSMO improved in 96% of eyes.
Finally it is
stated in the results section that in "79% of eyes exhibiting complete
resolution of CSMO postoperatively had significantly better visual
outcomes compared to 17% of eyes with persistent and 4% of eyes with
worsening macular oedema (table 8)". However, Tab.8 clearly demonstrates
that only 8% (n=6) with resolved oedema (n=75) gained 3 or more lines,
which is significantly better, but that 84% (n=63) had only stable visual
acuity within + 3 lines visual acuity change, whereas also additional 8%
had significant vision loss (Tab.8). Thus the proposed positive clinical
result in terms of CSMO resolution and visual acuity improvement could not
been followed.
Independent of clinical results, the mechanism of the
micropulse laser method is unclear. Since there
were no ophthalmoscopically nor angiographically visible laser
damage in the tissue, one has to ask, what happens to the fundus
during treatment? As proven in many experimental
studies conventional laser photocoagulation leads to primary destruction
of the RPE since it absorbs about 60% of the energy from a green laser
beam. The RPE damage is repaired within 7 days by migration and
proliferation of neighbour cells and this seems to lead to an enhanced
pump-function of the new RPE cells leading to resolution of CSMO. Bruch´s
membrane usually stays intact, thus no potential CNV induction is
expected. Because of the long laser exposition times of about 100ms during
irradiation, thermal damage to photoreceptors leads to
irreversible laser scotoma.
In both laser treatments (thermal laser and SRT) the primary RPE
damage can be demonstrated by angiography revealing leakage from the
damaged RPE site, thus the mode of action of the laser treatment can
clearly be proven and is comprehensible. This is not the case in the
article by Luttrull et al. who used repetitive laser pulses of 100µs pulse
duration (which are - at required energies for RPE damage - too long to
spare photoreceptors) within an envelope of 300ms. Temperature
calculations for the laser parameters set in this article reveal an
increase of tissue temperature of 1.8°C per pulse within the laser spot
(taken into account that there is just a 20% energy absorption within the
RPE/choroid complex at 810nm wavelength). The mean temperature increase in
the centre of the laser spot is - due to heat accumulation at the high
repetition rate of 500Hz - about only 11°C after 300ms. Neither thermal
nor thermomechanical based tissue alterations are expected for this low
short time temperature increase. Consequently it might be not remarkable
that - as also stated in the discussion section - the angiographical
visible diabetic leakage after therapy mostly persisted. The discussion of possible mechanisms of this kind of
micropulse laser irradiation as e.g. up- and down- regulation of different
growth factors or heat-shock proteins is speculative.
An aim to provide an optimised keratoprosthesis, with excellent
biointegration, and all other properties meeting ideal requirements, is
one we share with the authors of the recent article entitled “Hydroxyapatite promotes superior keratocyte adhesion and proliferation in comparison with current keratoprosthesis skirt materials”.[1] However, the current paper includes some points that require clarificatio...
An aim to provide an optimised keratoprosthesis, with excellent
biointegration, and all other properties meeting ideal requirements, is
one we share with the authors of the recent article entitled “Hydroxyapatite promotes superior keratocyte adhesion and proliferation in comparison with current keratoprosthesis skirt materials”.[1] However, the current paper includes some points that require clarification.
PHEMA (spelled in full: poly(2-hydroxyethyl methacrylate)is a non-toxic polymer of the toxic monomer HEMA, though cytotoxicity is still possible if non-reacted monomer has not been fully removed. The ' polyhydroxyethyl methacrylate' the authors obtained for their study was not fully described, and may have been contact lens blanks, unlikely to have been processed for 'implantable quality'. Whether the samples had been fully extracted was not stated, nor was the hydration of the samples when used for the study. Contact lens blanks are not designed for cell adhesion and the results of this study, with regard to PHEMA, are entirely predictable and have been previously reported.
The commercially available keratoprosthesis AlphaCor is made from a form of PHEMA, specifically modified for its intended purpose within the cornea. In particular, the AlphaCor OPTIC is made from a relatively low water content, but hydrated, microporous form, similar to the samples evaluated by the authors, specifically because it does not encourage cellular adhesion (epithelial coverage is not desired for this model, nor would adherent posterior cells and membranes be desirable).
In contradistinction, the biointegratable SKIRT region of AlphaCor is
made from a macroporous form of PHEMA with a very high water content; this material, with its interconnecting channels, has been optimised to promote viable biocolonisation, which has been extensively described in the literature. The authors of the present article do concede that cells 'may behave differently in colonising a 3-D porous keratoprosthesis skirt': indeed they do. Further, very subtle modifications of the sponge structure significantly affect all aspects of biointegration.
Both early trial results, such as the preliminary cases cited by the authors, and current results for over 250 AlphaCor devices, have been extensively presented and made available to all device users. Histology now available from AlphaCor devices explanted from human recipients confirms that the biointegration process in humans is similar to that previously shown in the animal model, and maintained in the long term. As expected, specific inflammatory processes can cause localised reversal of biointegration in areas of stromal melting. Certainly, porosity itself does not prevent melting processes, as is also seen in relation to hydroxyapatite keratoprostheses and orbital implants.
There is no argument that keratoprosthesis materials and design
require ongoing revision and improvement. The authors' findings in
relation to hydroxyapatite are interesting, although as they note, this
rigid material has its own limitations. Novel approaches are undergoing early evaluation and may offer benefits. However, at present,
in our view, AlphaCor is a device worthy of consideration for those in whom a donor graft would fail.
Disclosure: Celia Hicks is Medical Director of CooperVision Surgical,
manufacturer of AlphaCor. The Biomaterials and Polymer Research department of the Lions Eye Institute has a financial interest with CooperVision Surgical through support of departmental funding, travel and research.
References
1. J S Mehta, C E Futter, S R Sandeman, R G A F Faragher, K A Hing, K E Tanner, and B D S Allan. Hydroxyapatite promotes superior keratocyte adhesion and proliferation in comparison with current keratoprosthesis skirt materials. Br. J. Ophthalmol. 2005; 89: 1356 – 1362.
I appreciate the editorial, “Cataract surgery programmes in Africa”
in response to our paper “Increasing cataract surgery to meet VISION
2020 targets; experience from two rural programmes in East Africa.” I
agree with the need to generate evidence for the effectiveness of public
health interventions and thank you for drawing attention to this. As
pointed out, public health interventions are multifacete...
I appreciate the editorial, “Cataract surgery programmes in Africa”
in response to our paper “Increasing cataract surgery to meet VISION
2020 targets; experience from two rural programmes in East Africa.” I
agree with the need to generate evidence for the effectiveness of public
health interventions and thank you for drawing attention to this. As
pointed out, public health interventions are multifaceted and complex.
Such complexity requires the use of both quantitative and qualitative
methods to describe and understand. Within the space limits of our
paper, we could not provide more detail of either qualitative or
quantitative information we have generated on making changes at the
hospital in order to provide more service. However, this information is
provided in a booklet called “Karibuni Macho: transforming the Eye
Department of KCMC to reach VISION 2020 goals,” which may be downloaded
free at http://www.kcco.net (click Reports) or http://www.iefusa.org.
The article by Al-Hazmi et al.[1] states that combined trabeculotomy-
trabeculectomy with mitomyocin C (CTTM) gave better results than
trabeculotomy alone for primary congenital glaucoma (PCG) at the King
Khaled Eye Specialist Hospital (KKESH) in Riyadh, Saudi Arabia, between
1982 and 2002. For moderate PCG the success rate is stated as 40% and 80%
for trabeculotomy and CTTM, respectively. For severe...
The article by Al-Hazmi et al.[1] states that combined trabeculotomy-
trabeculectomy with mitomyocin C (CTTM) gave better results than
trabeculotomy alone for primary congenital glaucoma (PCG) at the King
Khaled Eye Specialist Hospital (KKESH) in Riyadh, Saudi Arabia, between
1982 and 2002. For moderate PCG the success rate is stated as 40% and 80%
for trabeculotomy and CTTM, respectively. For severe PCG the stated
success rate is 10% and 70% for trabeculotomy and CTTM, respectively.
However, without more specifics regarding when the trabeculotomies were
performed at KKESH, the authors cannot advocate CTTM over trabeculotomy
for moderate and severe PCG.
As the article states, over the years at KKESH the success rate for
trabeculotomy for PCG dramatically improved (29% from 1982-1990; 47% from
1991-94; 82% from 1995-2002) The authors attribute these improved results
over the years to improved primary healthcare facilities within the
kingdom, earlier referrals, better equipment availability, and surgeons
becoming more adapt at surgical intervention. In contrast, CTTM for PCG
was first performed at KKESH in 1994 with less of a “learning curve”; the
success rate from 1994 -2002 was 72%. The complication rate, however, was
higher for CTTM than for trabeculotomy.
Because initial trabeculotomy success for PCG at KKESH has
dramatically increased with time, it is important to know how many of the
reported trabeculotomy failures for moderate and severe PCG were from the
earlier periods of the hospital. This information was not in the
manuscript. It may be that trabeculotomy as currently performed at KKESH
for moderate and severe PCG has a success rate similar to that of CTTM for
the same patient population with less surgical complications.
References
1. Al-Hazmi A, Awad A, Zwaan Z, et al. Correlation between surgical
success rate and severity of congenital glaucoma. Br J Ophthalmol
2005;89:449–453.
We read
with interest the paper published by Boschi, et. al.[1]
in which immunohistochemistry was performed on orbital tissues from
patients with thyroid associated ophthalmopathy (TAO) and compared to
non...
We read
with interest the paper published by Boschi, et. al.[1]
in which immunohistochemistry was performed on orbital tissues from
patients with thyroid associated ophthalmopathy (TAO) and compared to
non-diseased orbital tissue.
Our
laboratory recently reported positive TSH receptor staining within
normal human muscle fibres, using one of the same antibodies (3G4) as
Boschi et. al., (supplied by Costagliola) and a commercial antibody
(3B12) [2].
Our
findings differ from Boschi et. al.’s as no staining of the
muscle fibres was visible in their experience.
Assessing
the techniques used gave some possibilities as to why our findings
differ. Our paraffin-embedded tissues were subjected to a proteolytic
antigen retrieval step, as commonly used in avidin-biotin
staining.[3]
The reason for this is that formalin used in fixation is notorious
for altering protein immunoreactivity, and hence masking protein
expression.[4][5]
Moreover,
the amplification immunohistochemistry kit used in our experiments is
possibly more sensitive than conventional immunohistochemistry used
in the experiments of Boschi, et. al.[6]
We do not
dispute the finding that TSHR expression is elevated in orbital
connective tissue of diseased patients. Combined with our findings,
Boschi et. al.’s paper also suggests that expression of TSH-R
on normal muscle fibres is lower than in the connective tissue of
diseased patients. Boschi et. al. has successfully produced more
evidence that connective tissues in the orbit are active in TAO
affected patients, however the potential role of the extraocular
muscle in the pathogenesis of TAO should also be considered.
Yours
sincerely,
Steven J.
Kloprogge and Albert G. Frauman
References
1
Boschi A, Daumerie C, Spiritus M, et al. Quantification of cells
expressing the thyrotropin receptor in extraocular muscles in
thyroid associated orbitopathy. Br J Ophthalmol 2005;89(6):724-9.
2
Kloprogge SJ, Busuttil BE, Frauman AG. TSH receptor protein is
selectively expressed in normal human extraocular muscle. Muscle
Nerve. 2005;32(1):95-8.
3
Thompson LD, Miettinen M, Wenig BM. Sinonasal-type
hemangiopericytoma: a clinicopathologic and immunophenotypic
analysis of 104 cases showing perivascular myoid differentiation. Am
J Surg Pathol. 2003;27(6):737-49.
4
Fox CH, Johnson FB, Whiting J, et. al. Formaldehyde fixation. J
Histochem Cytochem 1985;33(8):845-53.
5
Puchtler H, Meloan SN. On the chemistry of formaldehyde fixation and
its effects on immunohistochemical reactions. Histochemistry
1985;82(3):201-4.
6Erber
WN, Willis JI, Hoffman GJ. An enhanced immunocytochemical method for
staining bone marrow trephine sections. J Clin Pathol.
1997;50(5):389-93.
We read with interest the paper by Cazabon et al.[1] on the important
emerging problem of sudden visual loss after removal of silicone oil. We
have seen a similar pattern of visual loss in our own patients typically
seen in macula on detachments associated with giant retinal tears. We have
identified 12 cases between 2 units (St Thomas’, London and Sunderland Eye
Infirmary), but 5 of these clearly descr...
We read with interest the paper by Cazabon et al.[1] on the important
emerging problem of sudden visual loss after removal of silicone oil. We
have seen a similar pattern of visual loss in our own patients typically
seen in macula on detachments associated with giant retinal tears. We have
identified 12 cases between 2 units (St Thomas’, London and Sunderland Eye
Infirmary), but 5 of these clearly describe onset of visual loss before
oil removal (onset between 1 month and 5 months after oil insertion).[2]
Results of investigations were very similar to those reported by Cazabon
et al. In 4 of 5 pattern ERG was suggestive of macular dysfunction. The
timing of onset of visual loss obviously alters the potential aetiology,
which as stated is unknown.
In their paper, information on acuity for cases 2 and 3, between 1
week after oil insertion and oil removal is not provided. Did these cases
have visual loss preceding oil removal? Developing cataract can obviously
hinder interpretation of acuity measurements. In our cases the symptoms
described did not fit with cataract (scotoma, red desaturation) and
persisted if any cataract was removed.
We have seen a further case since this report, a 46 year old female
with a giant retinal tear and macula-on retinal detachment affecting the
right eye. Acuity reduced during period of tamponade from 6/6 2 weeks
after oil insertion to 6/36+1, which did not recover after oil removal.
She reported a central negative scotoma. Electrophysiology suggested
macular dysfunction.
We have speculated that photo-toxicity may play a role, as oil
transmits light more in the blue spectrum than aqueous.[3] The fat
soluble macula pigments, lutein and zeaxanthin, are thought to protect the
macula from photo-oxidative damage. Silicone oil has previously been
reported to dissolve fat soluble elements from the retina.[4]
We measured the macular pigment optical density (MPOD) in this case
using a modified confocal scanning laser ophthalmoscope and 2-wavelength
autofluorescence technique 3 weeks after oil removal. The results showed a
substantially reduced MPOD in the eye which had silicone oil compared to
the fellow eye. Although the peak MPOD, at the foveal centre, of both eyes
was similar (0.47 Right vs. 0.52 Left), the MPOD at half-degree, one-degree
and 2-degrees eccentricity from the foveal centre was markedly lower in
the eye which had silicone oil (0.12, 0.06, 0.02 respectively vs. 0.40,
0.22, 0.07).
Although MPOD varies greatly between individuals, there is usually
high inter-ocular symmetry in normal eyes.[5] Further work is required to
determine whether or not this relates to the visual loss and whether
therapeutic supplementation, may reduce the risk of visual loss.
References
1. Cazabon S, Groenewald C, Pearce IA, Wong D. Visual loss following
removal of intraocular silicone oil. Br J Ophthalmol 2005;89:799-802.
2. Herbert EN, Habib M, Steel D, Williamson TH. Central scotoma
associated with intraocular silicone oil tamponade develops before oil
removal. Graefe’s Arch Clin Exp Ophthalmol. DOI 10.1007/s00417-005-0076-6.
3. Azzolini C, Docchio F, Brancato R Trabucchi G. Interactions between
light and vitreous fluid substitutes. Arch Ophthalmol. 1992;110:1468-1471.
4. Refojo MF, Leong FL, Chung H et al. Extraction of retinol and
cholesterol by intraocular silicone oils. Ophthalmology 1998;95:614-8.
5. Bone RA, Sparrock JM.. Comparison of macular pigment densities in
human eyes. Vision Res. 1971;11:1057-1064.
We read with great interest the article by S Cazabon et al. "Visual
loss following removal of intraocular silicone oil".[1]
In all the three patients it would have been better to compare the
visual acuity just before the silicone oil removal than immediate visual
acuity after initial vitrectomy. Because the silicone oil contact with eye
also could be responsible for visual loss as it was known...
We read with great interest the article by S Cazabon et al. "Visual
loss following removal of intraocular silicone oil".[1]
In all the three patients it would have been better to compare the
visual acuity just before the silicone oil removal than immediate visual
acuity after initial vitrectomy. Because the silicone oil contact with eye
also could be responsible for visual loss as it was known to cause optic
nerve damage as described in earlier reports.[2]
Earlier Newsom RS et al also[3] reported unexplained sudden visual
loss following silicone oil removal in seven patients. They also observed
only electrophysiological abnormalities.
May be the unexplained visual loss could be due to optic nerve damage
and diffuse gangilion cell dysfuntion due to silicone oil tamponade effect
on eye rather than procedure of silicone oil removal itself.
References
1. S Cazabon, C Groenewald, I A Pearce, and D Wong. Visual loss following removal of intraocular silicone oil.Br J Ophthalmol 2005; 89: 799-802
2. Budde M, Cursiefen C, Holbach LM, Naumann GO. Silicone oil-associated optic nerve degeneration. Am J Ophthalmol. 2001 Mar;131(3):392-4.
3. Newsom RS, Johnston R, Sullivan PM, Aylward GB, Holder GE, Gregor ZJ. Sudden visual loss after removal of silicone oil.Retina. 2004 Dec;24(6):871-7.
We thank Singh and Raj for their interest and submit the following,
in response to their comments, concerning our report of early
chorioretinal anastomosis in non-ischaemic CRVO[1]:
Of the six patients who underwent laser anastomosis two had a
successful anastomosis following the first treatment at a single site
(33%), two cases were successful after a second attempt at one site (66%),
a furt...
We thank Singh and Raj for their interest and submit the following,
in response to their comments, concerning our report of early
chorioretinal anastomosis in non-ischaemic CRVO[1]:
Of the six patients who underwent laser anastomosis two had a
successful anastomosis following the first treatment at a single site
(33%), two cases were successful after a second attempt at one site (66%),
a further case had two treatments and the second treament was at two
sites, one further patient had two single treatments, followed by a third
treatment at two sites. This left all patients with a functioning
anastomosis (100%) as confirmed with fluorescein angiography.
We considered that the intervention was justified as this group have
a significant risk of visual deterioration.
We did not feel that a sham laser procedure was justified and such a group
would further have diluted results and limited recruitment to the
different groups. As OCT constitutes an objective measure, this may not be
necessary. However in a larger study this may be a practical possibility.
Finally, concerning the reference to Fuller et al.[2], this study
focussed on anterior segment neovascularisation and data analysis centred
on non-perfused (ischaemic) CRVO and excluded perfused (non-ischaemic)
CRVO. It is therefore difficult to comment on this point. Natural history
studies are best conducted on a large scale. In our series of untreated
patients we did not observe any disc collaterals during the treatment
period. This point is, however, of limited significance.
We hope that this information addresses the points raised.
Richard Antcliff, Eric Mayer, Tom Williamson and John Shilling.
References
1. Antcliff RJ, M.E., Williamson TH, Shilling JS., Early
chorioretinal anastomosis in non-ischaemic CRVO: a randomised trial. Br J
Ophthalmol., 2005. 89(6): p. 780-1.
2. Fuller, J.J., et al., Retinochoroidal collateral veins protect
against anterior segment neovascularization after central retinal vein
occlusion. Arch Ophthalmol, 2003. 121(3): p. 332-6.
The recent article on the ocular manifestations of Bloom syndrome by
Bhisitkul and Rizen [1] suggested that macular drusen may be
an integral part of Bloom syndrome. Recently we published the finding of
drusen in a young girl with Bloom syndrome [2]; we suspected that drusen
might be expected in one of the premature aging syndromes, but at
that time found little information on drusen as an ocular
abnor...
The recent article on the ocular manifestations of Bloom syndrome by
Bhisitkul and Rizen [1] suggested that macular drusen may be
an integral part of Bloom syndrome. Recently we published the finding of
drusen in a young girl with Bloom syndrome [2]; we suspected that drusen
might be expected in one of the premature aging syndromes, but at
that time found little information on drusen as an ocular
abnormality in Bloom syndrome.[3] Were drusen a characteristic
ocular finding in Bloom syndrome? Did every Bloom
syndrome patient have drusen? If not, then did Bloom syndrome have
different mutations, some leading to drusen and others not, and was it
necessary to pay greater heed to the Bloom syndrome patients with drusen because of increased risks?
More recently, we had the opportunity to
study a family of two siblings with Bloom syndrome. The diagnosis of the siblings was made based on characteristic clinical and laboratory findings and elevated sister chromatid exchange (SCE) formation. Mutation analysis
was not done. Both siblings with Bloom syndrome also had drusen. A third unaffected sibling didn't have drusen, nor did the parents. The clinical phenotypes of the two affected siblings were completely discordant. The first patient had severe clinical symptoms (chronic lung disease due to pulmonary fibrosis and bronchiectasis) as a clinical
presentation of rapid progress and poor prognosis. The second patient was without symptoms.
Therefore, drusen may be a characteristic ocular abnormality of Bloom syndrome, and can be present in Bloom syndrome patients with different clinical phenotypes. We have yet to understand the prognostic value of drusen, if any, for the clinical course of the disease. It is possible that different mutations might cause drusen and the clinical phenotype is dependent on the type of mutation. To the best of our current knowledge, genetic heterogeneity might be involved in Bloom syndrome.[4,5] The patient described by Bhisitkul and Rizen had drusen and
developed leukemia during the 1 year follow-up period.[1] This gives some support to our opinion that "the probability of developing cancer in Bloom syndrome patients with drusen might be relatively higher than those without drusen". We do not disregard the cancer predisposition potential of the syndrome itself, but it is fair to say that our opinion
expressed above has merit, and it would be prudent to pay greater heed to the Bloom syndrome patients with drusen.
In the light of our experiences and the article published in your
journal, drusen appear to be a typical feature of Bloom syndrome.
However, the significance of this finding remains undetermined.
Deniz Aslan, Sengul Ozdek, Sibel Ozdogan
References
1) Bhisitkul RB, Rizen M. Bloom syndrome: multiple retinopathies in
a
chromosome breakage disorder. Br J Ophthalmol. 2004;88:354-357.
2) Aslan D, Ozturk G, Kaya Z, Bideci A, Ozdogan S, Ozdek S, Gursel
T.
Early-onset drusen in a girl with bloom syndrome: probable clinical
importance of an ocular manifestation. J Pediatr Hematol Oncol.
2004;26:256-257.
3) Dollfus H, Porto F, Caussade P, Speeg-Schatz C, Sahel J,
Grosshans
E, Flament J, Sarasin A. Ocular Manifestations in the Inherited DNA
Repair
Disorders. Surv Ophtalmol. 2003;48:107-122.
4) German J, Ellis NA, Proytcheva M. Bloom's syndrome. XIX.
Cytogenetic and population evidence for genetic heterogeneity. Clin
Genet.
1996;49:223-231.
5) Ellis NA, Lennon DJ, Proytcheva M, Alhadeff B, Henderson EE,
German J. Somatic intragenic recombination within the mutated locus BLM
can correct the high sister-chromatid exchange phenotype of Bloom
syndrome
cells. Am J Hum Genet. 1995;57:1019-1027.
We read with interest the recent report by Barry and Murray on
unregistered visual impairment. It is important to note, however, that
this paper relates to registration instigated by completion of BD8
certificates. In September 2003, Stephen Ladyman, the then Health
Minister, Department of Health, announced changes to the process of
registration, referral and identification for visual impairment...
We read with interest the recent report by Barry and Murray on
unregistered visual impairment. It is important to note, however, that
this paper relates to registration instigated by completion of BD8
certificates. In September 2003, Stephen Ladyman, the then Health
Minister, Department of Health, announced changes to the process of
registration, referral and identification for visual impairment in England
stating that the BD8 was trying to do too much. The BD8 certificate was
replaced by the Certificate of Visual Impairment 2003 in November 2003 and
two referral letters were introduced for use by eye clinics and high
street optometrists to alert social services to the needs of people with
vision impairments in advance of certification. The Welsh Assembly
Government is reported to be awaiting final revisions of the forms before
deciding whether this approach will be adopted also in Wales.
A further issue worth consideration is that any study that attempts
to assess coverage of certification by application of certification
criteria to visual status at one point in time will detect under-registration and "inappropriate" registration. Measures of visual
function show variability – visual acuity can fluctuate greatly in an
individual with diabetic eye disease and the point at which someone
becomes certifiable due to visual field loss in glaucoma is not easy to
determine. Patients need time to come to terms with their loss of vision
and consultants need time to determine whether an individual is
certifiable. One should not underestimate the distress faced by an
individual when told that their condition is certifiable for registration
as blind or partially sighted.
Dear Editor,
When reading the article we were a bit surprised by the extremely positive declaration of the clinical results after subthreshold diode micropulse photocoagulation. The authors stated that subthreshold diode micropulse laser photocoagulation minimises chorioretinal damage in the management of CSMO and demonstrates a beneficial effect on visual acuity and CSMO resolution (in 96% of all treated eyes, n=...
Dear Editor,
An aim to provide an optimised keratoprosthesis, with excellent biointegration, and all other properties meeting ideal requirements, is one we share with the authors of the recent article entitled “Hydroxyapatite promotes superior keratocyte adhesion and proliferation in comparison with current keratoprosthesis skirt materials”.[1] However, the current paper includes some points that require clarificatio...
Dear Editor,
I appreciate the editorial, “Cataract surgery programmes in Africa” in response to our paper “Increasing cataract surgery to meet VISION 2020 targets; experience from two rural programmes in East Africa.” I agree with the need to generate evidence for the effectiveness of public health interventions and thank you for drawing attention to this. As pointed out, public health interventions are multifacete...
Dear Editor,
The article by Al-Hazmi et al.[1] states that combined trabeculotomy- trabeculectomy with mitomyocin C (CTTM) gave better results than trabeculotomy alone for primary congenital glaucoma (PCG) at the King Khaled Eye Specialist Hospital (KKESH) in Riyadh, Saudi Arabia, between 1982 and 2002. For moderate PCG the success rate is stated as 40% and 80% for trabeculotomy and CTTM, respectively. For severe...
Dear Editor,
We read with interest the paper published by Boschi, et. al.[1] in which immunohistochemistry was performed on orbital tissues from patients with thyroid associated ophthalmopathy (TAO) and compared to non...
Dear Editor,
We read with interest the paper by Cazabon et al.[1] on the important emerging problem of sudden visual loss after removal of silicone oil. We have seen a similar pattern of visual loss in our own patients typically seen in macula on detachments associated with giant retinal tears. We have identified 12 cases between 2 units (St Thomas’, London and Sunderland Eye Infirmary), but 5 of these clearly descr...
Dear Editor,
We read with great interest the article by S Cazabon et al. "Visual loss following removal of intraocular silicone oil".[1]
In all the three patients it would have been better to compare the visual acuity just before the silicone oil removal than immediate visual acuity after initial vitrectomy. Because the silicone oil contact with eye also could be responsible for visual loss as it was known...
Dear Editor,
We thank Singh and Raj for their interest and submit the following, in response to their comments, concerning our report of early chorioretinal anastomosis in non-ischaemic CRVO[1]:
Of the six patients who underwent laser anastomosis two had a successful anastomosis following the first treatment at a single site (33%), two cases were successful after a second attempt at one site (66%), a furt...
Dear Editor,
The recent article on the ocular manifestations of Bloom syndrome by Bhisitkul and Rizen [1] suggested that macular drusen may be an integral part of Bloom syndrome. Recently we published the finding of drusen in a young girl with Bloom syndrome [2]; we suspected that drusen might be expected in one of the premature aging syndromes, but at that time found little information on drusen as an ocular abnor...
Dear Editor,
We read with interest the recent report by Barry and Murray on unregistered visual impairment. It is important to note, however, that this paper relates to registration instigated by completion of BD8 certificates. In September 2003, Stephen Ladyman, the then Health Minister, Department of Health, announced changes to the process of registration, referral and identification for visual impairment...
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