eLetters

636 e-Letters

published between 2016 and 2019

  • Confounding effect of anterior chamber depth on assessment of dynamic air-puff applanation results in glaucoma patients

    We read the study by Vinciguerra et al. on cornea biomechanical properties of open angle glaucoma, ocular hypertension, normal tension and normal eyes assessed with dynamic air-puff applanation [1]. The study reported significant correlations between the properties and types of glaucoma. Most of the study patients were also under anti-glaucoma medication. Interestingly, the study did not assess the potential confounding effects of the anterior chamber on assessment of corneal biomechanical properties [1]. However, we wish to bring to the notice of the authors our earlier study on the same subject [2]. In our study, open and closed angle patients under the anti-glaucoma medication were assessed with air-puff applanation to determine if medication altered corneal biomechanical properties. The highlight of the study was that anterior chamber depth (ACD) was also included as a covariate in addition to other tomographic features [2]. Our study clearly showed that the ACD had a significant effect of the level of bIOP among the different types of glaucoma patient [2]. The ACD is a direct indicator of the volume of vault space between the cornea and the lens. This vault space resisted the inward motion of the cornea during the first half of the applanation. If ACD was lower, then bIOP was greater and vice versa. In patients with angle closure glaucoma, we expect the ACD to be less than NTG and normal eyes [1,2]. Hence, the results from the Vinciguerra et al. study could be skewed...

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  • Choroidal Thickness in Macular Telangiectasia Type 2

    Editor,
    We read with great interest the article titled “Choroidal thickness and vascular density in macular telangiectasia type 2 using en face swept-source optical coherence tomography” by Wang et al.[1] This is an interesting study in which the authors performed multimodal imaging for the diagnosis of macular telangiectasia (MacTel) type 2 and reported similar choroidal thickness (CT) between MacTel type 2 and control eyes using swept-source optical coherence tomography (SS-OCT).[1]
    There are a few concerns that we would like to highlight. Although the authors control for confounders like age and spherical equivalent, axial length is another important confounder that has not been evaluated in this prospectively conducted study. The subfoveal CT has been reported to decrease by up to 58µm per one mm increase in the axial length after adjusting for age and sex.[2] Ignoring the axial length in choroidal thickness analysis may have untoward consequences.
    Although the number of cases was small (n=39 eyes), the stagewise distribution of CT may be of help. A recent study by Kumar et al. using SS-OCT reported different subfoveal CT in non-proliferative and proliferative stages of the disease, although the results were not statistically significant.[3] If a varied distribution is observed between different stages, this may support the role of the choroid in the pathophysiology of this disease.
    Inter-ocular asymmetry does exist in CT[4] as well as in the pr...

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  • Re: Choroidal Thickness in Macular Telangiectasia Type 2

    Dear Editor,

    We appreciate the interest in our paper by Kumawat and Kumar, and the opportunity to address their comments. With regards to axial length, it is certainly known to be correlated with choroidal thickness. However, this information was not routinely obtained in our retina clinic and was not available for most patients in the study. We were able to account for spherical equivalent in our multivariate model, which may serve as a proxy for axial length. We agree that accounting for at least one of these variables is required for studies on choroidal thickness. We appreciate the Kumawat and Kumar’s suggestion to categorize patients based on stage of disease (proliferative vs nonproliferative). We had considered this approach, however the small number of patients with proliferative disease (only 4) made this less ideal from a statistical standpoint. Subretinal neovascularization was included in our univariate analysis but was not found to be statistically significant with regard to choroidal thickness, so it was not further considered in our multivariate assessments. Lastly, while inter-ocular asymmetry in choroidal thickness may exist, eye laterality was not found to be a significant variable affecting choroidal thickness in our univariate analysis (p = 0.87) and thus was also not included in multivariate models. We once again thank Dr. Kumawat and Dr. Kumar for their interest in our work.

  • Intraocular pressure change after injection of intravitreal dexamethasone (Ozurdex) implant

    I read with interest and appreciate the article by Choi et al 1 on 'Intraocular pressure change after injection of intravitreal dexamethasone (Ozurdex) implant in Korean patients'.
    As the study looks at the IOP changes after intravitreal dexamethasone implant, how the IOP was recorded for the patients is very important. The authors have reported that the intraocular pressure (IOP) was measured by non-contact tonometer (NCT) or Goldmann applanation tonometry (GAT) in this study. First, it is not mentioned as to which NCT was used for IOP measurement. If NCT was used to measure pre-injection IOP, was it used to measure post-injection IOP measurement also? Or on different visits IOP recording was done with NCT or GAT, is not clear. As GAT is still considered as a gold standard for IOP measurement, if IOP on NCT is found to be high, ideally it should be rechecked with GAT. Second, it is not mentioned whether a single IOP measurement was taken or multiple IOP measurements were obtained, taking the average value as the final IOP. Third, a s the lower range of age was 16 years (Table 1), was there any correlation of IOP change after the injection with the age?

    Reference

    1. Choi W, Park SE, Kang HG et al. Intraocular pressure change after injection of intravitreal dexamethasone (Ozurdex) implant in Korean patients. Br J Ophthalmol 2018. Epub ahead
    of print. doi:10.1136/ bjophthalmol-2018-312958

  • Collaterals or telangiectasias?

    I read with great interest the paper titled “Collateral vessels on optical coherence tomography (OCT) angiography in eyes with branch retinal vein occlusion (BRVO)” by Suzuki et al.1
    The authors defined collateral vessels as dilated and tortuous capillaries occurring in pre-existing capillary beds and linking the obstructed vessel with the nearest patent vessel, according to previous reports.2-4 The authors demonstrated that collaterals were detected in 23 out of 28 (82%) eyes, all of which already existed at mean 0.95 months after the onset, and that all of the collaterals were observed in both the retinal superficial and the deep layers.
    However, some of the vessels which are pointed out as collaterals in the study1 look like simply dilated/tortuous vessels, because they don’t seem to connect obstructed to non-obstructed adjacent vessels nor by-pass obstructions. In a previous report, the authors found collateral vessels in 18 out of 28 (64%) eyes at mean 25.1 months from the onset, while superficial and deep capillary telangiectasias were detected in 13 and 28 out of 28 eyes, respectively.4 Therefore, I suppose that some of the vessels defined as collaterals in this study1 may be simply telangiectasias.
    Fruend et al.5 defined collateral vessels as the authors did. After excluding collaterals involving the perifoveal vascular ring, they demonstrated that collaterals were found in 23 out of 23 eyes (100%) at median time of 3.79 years from RVO...

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  • Previous Reports of Tyr437His mutation

    Dear Editors,

    The British Journal of Ophthalmology article, “Novel MYOC gene mutation in a Chinese family with primary open angle glaucoma” by Lei and coworkers describes a Tyr437His mutation in the myocilin gene. Contrary to descriptions in the title, abstract, and text of this article, the Tyr437His mutation is not novel. We and others have previously reported the same Tyr437His mutation in several publications dating back to 1997 [1-5].

    1 Stone EM, Fingert JH, Alward WLM, et al. Identification of a Gene That Causes Primary Open Angle Glaucoma. Science 1997;275:668–70.
    2 Alward WL, Fingert JH, Coote MA, et al. Clinical features associated with mutations in the chromosome 1 open-angle glaucoma gene (GLC1A). N Engl J Med 1998;338:1022–7.
    3 Wiggs JL, Allingham RR, Vollrath D, et al. Prevalence of mutations in TIGR/Myocilin in patients with adult and juvenile primary open-angle glaucoma. Am J Hum Genet 1998;63:1549–52.
    4 Fingert JH, Héon E, Liebmann JM, et al. Analysis of myocilin mutations in 1703 glaucoma patients from five different populations. Hum Mol Genet 1999;8:899–905.
    5 Fingert JH, Stone EM, Sheffield VC, et al. Myocilin glaucoma. Survey of Ophthalmology 2002;47:547–61.

  • reply to Previous Reports of Tyr437His mutation

    Dear Editors,
    Thanks for your email and comments for John H Fingert et al.
    In our work, we aim to characterize the genotype(s), phenotype(s) and age-related penetrance in a Chinese family with primary open-angle glaucoma (POAG). We recruited a four-generation Chinese family with 22 participants and identified a novel heterozygous MYOC gene mutation (exon3 c.1309T>C p.Y437H) only among seven POAG patients and one ocular hypertension (OHT) patient. Further, we summarized the exact phenotype characterization of MYOC Y437H mutation and calculated the age-related penetrance of this family. Hopefully, we can do a favor in establishing genotype–phenotype correlations, which play a significant role in predicting the range of phenotypic variation of a specific mutation, in managing the disease better and in genetic counselling.
    To the best of our knowledge, this is the first report of Y437H mutation in Chinese.Thus, we titled our work as “A novel MYOC gene mutation in a Chinese family with primary open-angle glaucoma”, which we really mean is a novel mutation only in Chinese population. We are very sorry about the misunderstanding the inappropriate title of our article may cause. In “Molecular analysis” section, we have affirmed that the Y437H mutation has been reported and referred previous article titled” Identification of a gene that causes primary open angle glaucoma” and so on.
    To avoid above misunderstanding ever happening, if it is possible we’d li...

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  • Author response to “Collaterals or telangiectasias?”

    Dear Editor,

    We appreciate the valuable comments from Dr. Sato regarding our recently published article.1 Dr. Sato’s comments raise important points about definition of collateral vessels in eyes with branch retinal vein occlusion (BRVO).
    As previously reported,2 collateral vessels develop from the pre-existing retinal capillary network to drain a blood flow from an obstructed vein into an adjacent area in eyes with BRVO. Therefore, in the current study, we defined collateral vessels as dilated and tortuous capillaries occurring in pre-existing capillary beds and linking the obstructed vessel with the nearest patent vessel. Thus, the adjacent vessels also seemed to be dilated and tortuous, which had been similarly observed in our previous study.3 We speculate that the pressure gradient between an obstructed vein and neighbouring unobstructed vessels causes collateral vessels formation. The collaterals detection rate in the current study was higher than in the previous study.3 This is because wider optical coherence tomography angiography (OCTA) images, the size of which was 6 ✕ 6 mm in area, were used in the current study.
    Regarding the other comment about the location of collateral vessels, Freund et al4 reported that collateral vessels were observed in only deep retinal capillary layer. However, we confirmed that the collateral vessels were present in both the superficial and the deep capillary layers on B scan images of OCTA. Additionally, fluoresc...

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  • Reply to the letter of Dr. Tarannum Mansoori

    We would like to thank Dr. Tarannum Mansoori for the interest in our study, “Intraocular pressure change after injection of intravitreal dexamethasone (Ozurdex) implant in Korean patients” and highlighting important issues about the intraocular pressure (IOP) measurement methods and the correlation of IOP with age.1
    We used KT-800 Non-Contact Tonometer (Kowa, Tokyo, Japan) to measure IOP initially and rechecked with GAT if necessary. Unless the patient was diagnosed with glaucoma, NCT was initially used to measure both pre- and post-injection IOP.
    As Dr. Tarannum Mansoori has pointed out, we also agree that GAT is the gold standard for IOP measurement. If the IOP measured with NCT was found to be high, it was always rechecked with GAT. GAT was used in 2 situations in our study. First, when the patients had a previous history of glaucoma, and second, when the patients’ IOP as measured with NCT was high (greater than 20). Thus, in cases of high IOP, the measurement involved NCT and was also always double checked with GAT. Moreover, multiple IOP measurements were obtained with GAT in cases of high IOP, and the average value of the measurements was regarded as the final IOP.
    The range of age of the patients for injection of intravitreal dexamethasone was broad, from 16 to 88 years. We know that very young age (less than six years) or an older age are risk factors for steroid-induced glaucoma.2 However, regrettably, we have not performed any further analysis...

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  • Response to Monfermé et al., 2018

    To the Editor:

    We read the recent article in the journal by Monfermé and coauthors (1) on phenotypic associations of TYR R402Q compound heterozygosity with keen interest. Given our own and others previous findings (2-4) that the R402Q-S192Y haplotype seemed to have a stronger biological effect, we were surprised that a triallelic effect was not supported in the clinical discussion by Monfermé et al. When we examined these results more closely, we noted that their sample included 52 S192Y variant allele carriers out of the entire collection of 69 patients, of whom 31 (44.9%) carried the R402Q-S192Y double variant haplotype. In our own collections from the Australian general population (BNMS and BLTS, Duffy et al., in submission), only 6% of R402Q carriers also carried S192Y in cis. When we examined the European 1000 Genomes subsamples, there too only 7% of R402Q haplotypes had the 192Y rather than 192S wild type allele. So, even though Monfermé et al could not detect a statistically significant additive effect on OCA trait severity due to the S192Y polymorphism within their sample, it is clear that the S192 variant allele is markedly overrepresented compared to the general population, suggesting that it must have some relationship to albinism. This genetic association of the TYR R402Q-S192Y double variant haplotype with OCA1 is now clearly causative (2, 3), and explains some of the missing heritability that has previously been seen in OCA patients (4).

    Yours,...

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