We read with interest the article by Sarker et al(1) in which they compared the outcomes of trabeculectomy versus Ahmed glaucoma valve (AGV) implantation in Sturge–Weber syndrome (SWS) patients with secondary glaucoma aged 11-62 years. As it noted in the paper, the authors found that complete success rates after 24 months were 80% and 70% in the AGV and trabeculectomy groups, respectively, and qualified success rates were 90% and 85% at same period in the AGV and trabeculectomy groups, respectively. We were delighted to get the conclusion that both AGV implant and trabeculectomy appeared to be safe and efficacious in controlling glaucoma secondary to SWS.
As it reported by Mohamed et al., the complete success rate and qualified success rate (intraocular pressure≤17mmHg) of trabeculectomy reported were 80% and 100% at 12 postoperative follow-up month, respectively(2). However, the qualified success rate (90%) of AGV implantation in SWS patients with secondary glaucoma is higher than that reported by Hamush et al. (79%)(3) and Kaushik et al. (76%)(4) at 2 years of follow-up. Meanwhile, the trabeculectomy with MMC success rate in this study was comparable to other studies about primary glaucoma(5, 6), but the success rate of tube shunt surgery was higher than in prior reports. The qualified success rate of Baerveldt implantation for patients who not had undergone previous incisional ocular surgery was 73% in Primary Tube Versus Trabeculectomy (PTVT) study(6) and 75% rep...
We read with interest the article by Sarker et al(1) in which they compared the outcomes of trabeculectomy versus Ahmed glaucoma valve (AGV) implantation in Sturge–Weber syndrome (SWS) patients with secondary glaucoma aged 11-62 years. As it noted in the paper, the authors found that complete success rates after 24 months were 80% and 70% in the AGV and trabeculectomy groups, respectively, and qualified success rates were 90% and 85% at same period in the AGV and trabeculectomy groups, respectively. We were delighted to get the conclusion that both AGV implant and trabeculectomy appeared to be safe and efficacious in controlling glaucoma secondary to SWS.
As it reported by Mohamed et al., the complete success rate and qualified success rate (intraocular pressure≤17mmHg) of trabeculectomy reported were 80% and 100% at 12 postoperative follow-up month, respectively(2). However, the qualified success rate (90%) of AGV implantation in SWS patients with secondary glaucoma is higher than that reported by Hamush et al. (79%)(3) and Kaushik et al. (76%)(4) at 2 years of follow-up. Meanwhile, the trabeculectomy with MMC success rate in this study was comparable to other studies about primary glaucoma(5, 6), but the success rate of tube shunt surgery was higher than in prior reports. The qualified success rate of Baerveldt implantation for patients who not had undergone previous incisional ocular surgery was 73% in Primary Tube Versus Trabeculectomy (PTVT) study(6) and 75% reported by Islamaj et al(5)at 2 years of follow-up. The qualified success rates of AGV implantation and Baerveldt implantation for patients with refractory glaucoma were 76% and 68% at 2 years of follow-up, respectively(7).
This more favorable result of AGV implantation relative to previous reports may because this small sample size study excluded 8 patients (16.7%), enrolled patients may uncomplete 2 years of review, or most of them are older than 18 years old compared with other study about SWS patients with secondary glaucoma(3, 4). The study enrolled eyes may at lower risk of surgical failure than that excluded from the study. As the authors mentioned, a total of 48 patients in glaucoma associated with SWS were surgically treated and 8 patients were excluded because of unreliable follow-ups and/or incomplete case records. Substantial differences in the success rate of cases with and without follow-up may overestimate the success rates of two surgeries and prove misleading on interpreting the results in this small sample size, retrospective study. What’s more, mean±SD follow-up in the study was 23.15±2.36 (range, 15–24) and 22.95±2.87 (range, 13–24) in the AGV and trabeculectomy groups, respectively, which may indicate incomplete 2 years of review for some patients. Patients who experienced successful surgical treatment at 15 months may subsequently experience treatment failure at 24 months. It’s better to supplement the number of patients at each follow up visit.
In conclusion, since the small sample size, it is better to supplement the outcomes of eight patients excluded from the study and the number of patients at each follow up visit so as to yield more convincing results.
Reference
1. Sarker BK, Malek MA, Mannaf SMA, Iftekhar QS, Mahatma M, Sarkar MK, et al. Outcome of trabeculectomy versus Ahmed glaucoma valve implantation in the surgical management of glaucoma in patients with Sturge-Weber syndrome. Br J Ophthalmol. 2021;105(11):1561-5.
2. Mohamed T, Salman A, Elshinawy R. Trabeculectomy with Ologen implant versus mitomycin C in congenital glaucoma secondary to Sturge Weber Syndrome. International journal of ophthalmology. 2018;11(2):251-5.
3. Hamush N, Coleman A, Wilson M. Ahmed glaucoma valve implant for management of glaucoma in Sturge-Weber syndrome. American journal of ophthalmology. 1999;128(6):758-60.
4. Kaushik J, Parihar J, Jain V, Mathur V. Ahmed valve implantation in childhood glaucoma associated with Sturge-Weber syndrome: our experience. Eye (London, England). 2019;33(3):464-8.
5. Islamaj E, Wubbels R, de Waard P. Primary baerveldt versus trabeculectomy study after 5 years of follow-up. Acta ophthalmologica. 2020;98(4):400-7.
6. Gedde SJ, Feuer WJ, Lim KS, Barton K, Goyal S, Ahmed IIK, et al. Treatment Outcomes in the Primary Tube Versus Trabeculectomy Study after 3 Years of Follow-up. Ophthalmology. 2020;127(3):333-45.
7. Christakis P, Zhang D, Budenz D, Barton K, Tsai J, Ahmed I. Five-Year Pooled Data Analysis of the Ahmed Baerveldt Comparison Study and the Ahmed Versus Baerveldt Study. American journal of ophthalmology. 2017;176:118-26.
Affiliations:
Department of Ophthalmology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA
Division of Ophthalmology, Ann & Robert H. Lurie Children’s Hospital of Chicago, Chicago, Illinois, USA
Conflicts of Interest Disclosure:
APT: Consultant to Ivantis, Sandoz, and Zeiss
Acknowledgment:
APT is supported by an unrestricted departmental grant from Research to Prevent Blindness, NY, NY
Corresponding Author:
Angelo P. Tanna, M.D.
Department of Ophthalmology
Northwestern University Feinberg School of Medicine
645 N. Michigan Ave., Suite 440
Chicago, IL 60611
Telephone: 312-908-8152
Fax: 312-503-8152
E-mail: atanna@northwestern.edu
Dear Editor:
I read with interest the work of Doctor Hashimoto and colleagues on the risk of adverse neonatal outcomes (congenital anomalies, preterm birth, low birth weight) associated with maternal exposure to intraocular pressure-lowering medications during pregnancy.1 They used a large Japanese claims database and state-of-the-art statistical methodology to evaluate the frequency of adverse events in a cohort of live births of 91 women who had “at least one dispensation of IOP-lowering medications during the first trimester,” compared to that observed in 735 women with glaucoma or...
Affiliations:
Department of Ophthalmology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA
Division of Ophthalmology, Ann & Robert H. Lurie Children’s Hospital of Chicago, Chicago, Illinois, USA
Conflicts of Interest Disclosure:
APT: Consultant to Ivantis, Sandoz, and Zeiss
Acknowledgment:
APT is supported by an unrestricted departmental grant from Research to Prevent Blindness, NY, NY
Corresponding Author:
Angelo P. Tanna, M.D.
Department of Ophthalmology
Northwestern University Feinberg School of Medicine
645 N. Michigan Ave., Suite 440
Chicago, IL 60611
Telephone: 312-908-8152
Fax: 312-503-8152
E-mail: atanna@northwestern.edu
Dear Editor:
I read with interest the work of Doctor Hashimoto and colleagues on the risk of adverse neonatal outcomes (congenital anomalies, preterm birth, low birth weight) associated with maternal exposure to intraocular pressure-lowering medications during pregnancy.1 They used a large Japanese claims database and state-of-the-art statistical methodology to evaluate the frequency of adverse events in a cohort of live births of 91 women who had “at least one dispensation of IOP-lowering medications during the first trimester,” compared to that observed in 735 women with glaucoma or suspicion of glaucoma who did not have such an exposure.
The authors discuss the previously used and outdated United States Food and Drug Administration (FDA) risk classification system for drugs used during pregnancy. The FDA required the removal of the pregnancy letter categories – A, B, C, D, and X from all drug product labels in 2015. Instead, for systemically absorbed drugs (which includes all ocular hypotensive medications), the FDA requires labeling to include a summary of the risks of using a drug during pregnancy as well as “risk statements based on data from all relevant sources (human, animal, and/or pharmacologic), that describe, for the drug, the risk of adverse developmental outcomes.”2
The investigators observed any adverse outcome in 17.6% of neonates with and in 13.3% without fetal exposure to IOP-lowering medications. The authors concluded that after propensity score adjustment, IOP-lowering medications were not significantly associated with more frequent adverse events. For example, the adjusted odds ratio for congenital anomalies was 1.43 (95% CI, 0.66 to 3.12).
The investigators only evaluated live births; therefore, the potentially increased risk of spontaneous abortion or fetal demise associated with the use of these agents during pregnancy cannot be known from this analysis. It is possible some of the women in the control cohort may have been exposed to ocular hypotensive agent(s) during the first trimester, using medication already in their possession, without necessarily having been dispensed any such agent during the first trimester. This could confound the comparative analysis.
Finally, the authors report their study had a power > 80% for detecting a two-fold increase in the composite outcome (i.e., the risk of any of the adverse neonatal outcomes studied). This begs the question: How much increased risk is a pregnant woman willing to accept? I believe a much lower threshold is necessary to arrive at a meaningful conclusion. In my experience, many women would reject even a 1% increase in the risk of a congenital anomaly. So then, the concluding message in the abstract that “IOP-lowering medications during the first trimester were not significantly associated with increase in congenital anomalies, preterm birth or low birth weight” is not meaningfully supported by the data. The study only supports the concept that the use of these medications is probably not associated with a doubling of the risk. Patients and society are interested in a higher threshold of safety.
Fortunately, pregnancy is often associated with a spontaneous reduction in intraocular pressure (IOP)4; therefore, continued treatment may not be required. Selective laser trabeculoplasty is also an option to consider for some patients. Moreover, many young patients with glaucoma can tolerate nine months of higher IOP.
Glaucoma in pregnancy is a complex problem that requires complex, collaborative decision-making. Pregnant women, their ophthalmologists and obstetricians must evaluate the potential risks associated with continued use of ocular hypotensive agents during pregnancy and weigh those against the risks of modifying or stopping therapy. I congratulate the authors on exploring this important topic and encourage others to conduct similar studies. Eventually, a meta-analysis may yield evidence that can guide clinical decision-making.
REFERENCES:
1. Hashimoto Y, Michihata N, Yamana H, Shigemi D, Morita K, Matsui H, Yasunaga H, Aihara M. Intraocular pressure-lowering medications during pregnancy and risk of neonatal adverse outcomes: a propensity score analysis using a large database. Br J Ophthalmol. 2021 Oct;105(10):1390-1394. doi: 10.1136/bjophthalmol-2020-316198. Epub 2020 Sep 9. PMID: 32907812.
2. Content and Format of Labeling for Human Prescription Drug and Biological Products;
Requirements for Pregnancy and Lactation Labeling. Department of Health and Human Services. Food and Drug Administration 21 CFR Part 201 [Docket No. FDA-2006-N-0515] RIN 0910-AF11. Available online at http://federalregister.gov/a/2014-28241.
3. Mezawa H, Tomotaki A, Yamamoto-Hanada K, Ishitsuka K, Ayabe T, Konishi M, Saito M, Yang L, Suganuma N, Hirahara F, Nakayama SF, Saito H, Ohya Y. Prevalence of Congenital Anomalies in the Japan Environment and Children's Study. J Epidemiol. 2019 Jul 5;29(7):247-256. doi: 10.2188/jea.JE20180014. Epub 2018 Sep 22. PMID: 30249945; PMCID: PMC6556438.
4. Ziai N, Ory SJ, Khan AR, Brubaker RF. Beta-human chorionic gonadotropin, progesterone, and aqueous dynamics during pregnancy. Arch Ophthalmol. 1994 Jun;112(6):801-6. doi: 10.1001/archopht.1994.01090180099043. PMID: 8002840.
Thank you for raising the issue of abbreviations entering the virological lexicon which might give rise to confusion and misunderstanding. Over a decade has elapsed since our patient report was published and the source material is not retrievable. However, our recollection is the patient was discussed contemporaneously at the MDT and the viral aetiology, radiology findings and medical management determined and documented, from which the data was sourced for the 2008 report. Plausible as it may seem, it is not possible to test the veracity of the suggestion that the names ‘Jamestown Canyon’ and ‘John Cunningham’ might have been transposed during that MDT many years after the event, paper records are not kept indefinitely in NHS practice and ethics in medical publishing demands that patient identifiers are not described or retained in order to preserve anonymity. Perhaps the latter should have been considered over half a century ago when JC virus was first identified in the brain of the unfortunate patient after whom the eponymous pathogen was christened
(Padgett BL, Walker DL; et al. (1971). "Cultivation of papova-like virus from human brain with progressive multifocal leucoencephalopathy". Lancet. 1 (7712):
1257–60. doi:10.1016/S0140-6736(71)91777-6)
I read with interest the article by Jonas et al 1. The main purpose of the authors was to explore associations between a disc size change and other morphological parameters. Indeed, many non-ophthalmic and game-changing parameters are associated with disc size change and other morphological parameters, such as the serum lipids 2 dietary factors (such as lutein, zeaxanthin, and omega-3 fatty acids) 2-4, medications (such as lipid-lowering agents) 2, genetic susceptibility, body mass index, age and sex 3, among which only age and sex are addressed in their retrospective analysis.
According to the authors, decrease in the ophthalmoscopic disc size in the myopic eyes during the 10-year follow up, is likely related to a shift of the Bruch’s membrane opening as the inner of the three optic nerve head canal layers into the direction of the fovea. While their interpretations can be partly true, their attributed mechanism is subject to many biases.
Firstly, changes in ophthalmoscopical optic disc size and Bruch’s membrane are a function of macular pigment optical density 5-7, which in turn is a function of dietary carotenoid intake 8;9. Tong et al 10 have shown before that macular pigment optical density (MPOD) is inversely associated with axial length in Chinese subjects with myopia, suggesting that carotenoid intake, particularly lutein, is associated to axial length as well. Another study with a smaller sample size (45 eyes of 32 patients) with a different mean a...
I read with interest the article by Jonas et al 1. The main purpose of the authors was to explore associations between a disc size change and other morphological parameters. Indeed, many non-ophthalmic and game-changing parameters are associated with disc size change and other morphological parameters, such as the serum lipids 2 dietary factors (such as lutein, zeaxanthin, and omega-3 fatty acids) 2-4, medications (such as lipid-lowering agents) 2, genetic susceptibility, body mass index, age and sex 3, among which only age and sex are addressed in their retrospective analysis.
According to the authors, decrease in the ophthalmoscopic disc size in the myopic eyes during the 10-year follow up, is likely related to a shift of the Bruch’s membrane opening as the inner of the three optic nerve head canal layers into the direction of the fovea. While their interpretations can be partly true, their attributed mechanism is subject to many biases.
Firstly, changes in ophthalmoscopical optic disc size and Bruch’s membrane are a function of macular pigment optical density 5-7, which in turn is a function of dietary carotenoid intake 8;9. Tong et al 10 have shown before that macular pigment optical density (MPOD) is inversely associated with axial length in Chinese subjects with myopia, suggesting that carotenoid intake, particularly lutein, is associated to axial length as well. Another study with a smaller sample size (45 eyes of 32 patients) with a different mean age did not show the same association 5. A detailed explanation of the reasons justifying these differences is provided elsewhere 11.
Secondly, in many medical situations (such as obesity, diabetes, etc.), MOPD is reduced dramatically 12;13. Jonas et al 1 report that only 89 highly myoptic eyes (i.e., 43.6%) were re-examined after 10 years. Although the authors report that the age of cases in 2011 did not differ significantly from the age of their controls in the survey of 2011, no other dietary or medical information is provided in their study. Thus, it is very difficult to draw a firm conclusion.
One can certainly question whether there were any changes in carotenoid intakes and/or any medical situation during a decade-long longitudinal study. In support of this argument, MOPD is reported to significantly increase within 3 months in healthy Japanese individuals supplemented with daily 10 mg of orally administered lutein or zeaxanthin 14. Interestingly, in high myopia, it has been shown that even after a shorter period of lutein supplementation (20 to 40 days), MPOD began to rise uniformly at an average rate of 1.13+/-0.12 milliabsorbance units/day. During this same period, the serum lutein concentration increased tenfold, and then approached a steady state plateau. Most critically, the optical density curve eventually levelled off some 40 to 50 days after the participants discontinued the supplement. Thus, even a modest period of dietary carotenoid intake may produce a 30 to 40% reduction in blue light reaching the photoreceptors, Bruch's membrane, and the retinal pigment epithelium 6.
Substantial differences are reported in terms of dietary carotenoid/lutein intake among Chinese population 15;16. This issue may be even more pronounced in a small sample size a low rate of re-participation.
We agree that geometrical reasons may lead to a decrease in the size of the ophthalmoscopically visible optic disc. However, their presumed mechanism 17 may simply be partially a byproduct of MOPD changes over time.
Reference List
1. Jonas JB, Zhang Q, Xu L et al. Change in the ophthalmoscopical optic disc size and shape in a 10-year follow-up: the Beijing Eye Study 2001-2011. Br.J Ophthalmol. 2021.
2. Renzi LM, Hammond BR, Jr., Dengler M et al. The relation between serum lipids and lutein and zeaxanthin in the serum and retina: results from cross-sectional, case-control and case study designs. Lipids Health Dis. 2012;11:33.
3. Bone RA, Landrum JT, Guerra LH et al. Lutein and zeaxanthin dietary supplements raise macular pigment density and serum concentrations of these carotenoids in humans. The Journal of nutrition 2003;133:992-8.
4. Lin KH, Tran T, Kim S et al. Advanced Retinal Imaging and Ocular Parameters of the Rhesus Macaque Eye. Transl.Vis.Sci Technol. 2021;10:7.
5. Benoudis L, Ingrand P, Jeau J et al. Relationships between macular pigment optical density and lacquer cracks in high myopia. J Fr.Ophtalmol. 2016;39:615-21.
6. Landrum JT, Bone RA, Joa H et al. A one year study of the macular pigment: the effect of 140 days of a lutein supplement. Exp.Eye Res. 1997;65:57-62.
7. Zarubina AV, Huisingh CE, Clark ME et al. Rod-Mediated Dark Adaptation and Macular Pigment Optical Density in Older Adults with Normal Maculas. Curr.Eye Res. 2018;43:913-20.
8. Ajana S, Weber D, Helmer C et al. Plasma Concentrations of Lutein and Zeaxanthin, Macular Pigment Optical Density, and Their Associations With Cognitive Performances Among Older Adults. Invest Ophthalmol.Vis.Sci 2018;59:1828-35.
9. Berendschot TT, Plat J, de JA et al. Long-term plant stanol and sterol ester-enriched functional food consumption, serum lutein/zeaxanthin concentration and macular pigment optical density. Br.J Nutr. 2009;101:1607-10.
10. Tong N, Zhang W, Zhang Z et al. Inverse relationship between macular pigment optical density and axial length in Chinese subjects with myopia. Graefes.Arch.Clin.Exp.Ophthalmol. 2013;251:1495-500.
11. Tong N, Zhang W, Wu X. Reply to the letter by Xing-Ru Zhang and Zhen-Yong Zhang: Comments on "Inverse relationship between macular pigment optical density and axial length in Chinese subjects with myopia". Graefes.Arch.Clin.Exp.Ophthalmol. 2013;251:2287.
12. Hammond BR, Jr., Ciulla TA, Snodderly DM. Macular pigment density is reduced in obese subjects. Invest Ophthalmol.Vis.Sci 2002;43:47-50.
13. Scanlon G, Connell P, Ratzlaff M et al. MACULAR PIGMENT OPTICAL DENSITY IS LOWER IN TYPE 2 DIABETES, COMPARED WITH TYPE 1 DIABETES AND NORMAL CONTROLS. Retina. 2015;35:1808-16.
14. Tanito M, Obana A, Gohto Y et al. Macular pigment density changes in Japanese individuals supplemented with lutein or zeaxanthin: quantification via resonance Raman spectrophotometry and autofluorescence imaging. Jpn.J Ophthalmol. 2012;56:488-96.
15. Ng ALK, Leung HH, Kawasaki R et al. Dietary habits, fatty acids and carotenoid levels are associated with neovascular age-related macular degeneration in Chinese. Nutrients 2019;11:1720.
16. Takata Y, Xiang YB, Yang G et al. Intakes of fruits, vegetables, and related vitamins and lung cancer risk: results from the Shanghai Men's Health Study (2002G_ô2009). Nutrition and cancer 2013;65:51-61.
17. Zhang Q, Xu L, Wei WB et al. Size and Shape of Bruch's Membrane Opening in Relationship to Axial Length, Gamma Zone, and Macular Bruch's Membrane Defects. Invest Ophthalmol.Vis.Sci 2019;60:2591-8.
In their 2008 case report, Muqit, et al. describe a case of “presumptive Jamestown Canyon viral retinitis.”1
Jamestown Canyon virus is a mosquito-borne, single-stranded, ribonucleic acid (RNA) orthobunyavirus that is endemic throughout much of North America.2,3 Infection with Jamestown Canyon virus may be asymptomatic or may result in a general febrile illness, meningitis, and/or meningoencephalitis.2,3 Beyond the above case report by Muqit, et al.,1 and another review article referencing this case report,4 Jamestown Canyon virus has not been reported to cause retinitis or other ocular manifestations.
Upon close review of the case report by Muqit, et al.,1 we believe the authors are likely describing a case of John Cunningham (JC) virus (a ubiquitous, double-stranded, deoxyribonucleic acid [DNA] human polyomavirus known to cause progressive multifocal leukoencephalopathy [PML] among the immunocompromised)5-7 rather than Jamestown Canyon virus.
First, the case patient with viral retinitis had underlying human immunodeficiency virus (HIV) infection and a low CD4 lymphocyte count (240 cells/mm3), making him immunocompromised and susceptible to reactivation of the John Cunningham (JC) virus. Second, the case patient had magnetic resonance imaging (MRI) brain findings (i.e., asymmetric, predominantly posterior, confluent, subcortical white matter hyperintensities involving U-fibers) that are classic for John Cunningham (JC) virus-related PML.6,7 In fact,...
In their 2008 case report, Muqit, et al. describe a case of “presumptive Jamestown Canyon viral retinitis.”1
Jamestown Canyon virus is a mosquito-borne, single-stranded, ribonucleic acid (RNA) orthobunyavirus that is endemic throughout much of North America.2,3 Infection with Jamestown Canyon virus may be asymptomatic or may result in a general febrile illness, meningitis, and/or meningoencephalitis.2,3 Beyond the above case report by Muqit, et al.,1 and another review article referencing this case report,4 Jamestown Canyon virus has not been reported to cause retinitis or other ocular manifestations.
Upon close review of the case report by Muqit, et al.,1 we believe the authors are likely describing a case of John Cunningham (JC) virus (a ubiquitous, double-stranded, deoxyribonucleic acid [DNA] human polyomavirus known to cause progressive multifocal leukoencephalopathy [PML] among the immunocompromised)5-7 rather than Jamestown Canyon virus.
First, the case patient with viral retinitis had underlying human immunodeficiency virus (HIV) infection and a low CD4 lymphocyte count (240 cells/mm3), making him immunocompromised and susceptible to reactivation of the John Cunningham (JC) virus. Second, the case patient had magnetic resonance imaging (MRI) brain findings (i.e., asymmetric, predominantly posterior, confluent, subcortical white matter hyperintensities involving U-fibers) that are classic for John Cunningham (JC) virus-related PML.6,7 In fact, the authors claimed that the MRI brain findings were “confirmatory of the underlying diagnosis.”1 No MRI brain findings are classic or confirmatory for Jamestown Canyon virus infection. Third, the case patient’s cerebrospinal fluid was reportedly positive for viral DNA by polymerase chain reaction. This could only be possible for a DNA virus (i.e., John Cunningham (JC) virus) and not an RNA virus (i.e., Jamestown Canyon virus). Fourth, recovery of John Cunningham (JC) viral nucleic acid from ocular tissues of HIV-infected patients has been previously reported, so there is already precedent for this virus to infect the eye.8 Finally, the case patient had no known travel to or any mosquito exposure in North America, where Jamestown Canyon virus is endemic.2,3
Given John Cunningham (JC) and Jamestown Canyon viruses have different virology, epidemiology, and clinical manifestations, we believe the viruses were mistaken for one another because they share the same first letters of their words (i.e., J and C) and their abbreviations were likely confused. If our suspicion is correct, this case report highlights the possible dangers of abbreviations in medicine and the need to clearly define potentially confusing abbreviations in medical literature.
References
1. Muqit MM, Devonport H, Smith RA, Dhillon B. Presumptive Jamestown Canyon viral retinitis. Br J Ophthalmol. 2008 Dec;92(12):1599-600, 1695-6. doi: 10.1136/bjo.2007.132902. PMID: 19029162.
2. Coleman KJ, Chauhan L, Piquet AL, Tyler KL, Pastula DM. An Overview of Jamestown Canyon Virus Disease. Neurohospitalist. 2021 Jul;11(3):277-278. doi: 10.1177/19418744211005948. Epub 2021 Mar 29. PMID: 34163560; PMCID: PMC8182404.
3. Pastula DM, Hoang Johnson DK, White JL, Dupuis AP 2nd, Fischer M, Staples JE. Jamestown Canyon Virus Disease in the United States-2000-2013. Am J Trop Med Hyg. 2015 Aug;93(2):384-9. doi: 10.4269/ajtmh.15-0196. Epub 2015 Jun 1. PMID: 26033022; PMCID: PMC4530766.
4. Karesh JW, Mazzoli RA, Heintz SK. Ocular Manifestations of Mosquito-Transmitted Diseases. Mil Med. 2018 Mar 1;183(suppl_1):450-458. doi: 10.1093/milmed/usx183. PMID: 29635625.
5. Padgett BL, Walker DL, ZuRhein GM, Eckroade RJ, Dessel BH. Cultivation of papova-like virus from human brain with progressive multifocal leucoencephalopathy. Lancet. 1971 Jun 19;1(7712):1257-60. doi: 10.1016/s0140-6736(71)91777-6. PMID: 4104715.
6. Grebenciucova E, Berger JR. Progressive Multifocal Leukoencephalopathy. Neurol Clin. 2018 Nov;36(4):739-750. doi: 10.1016/j.ncl.2018.06.002. PMID: 30366552.
7. Pinto M, Dobson S. BK and JC virus: a review. J Infect. 2014 Jan;68 Suppl 1:S2-8. doi: 10.1016/j.jinf.2013.09.009. Epub 2013 Oct 8. PMID: 24119828.
8. Eberwein P, Hansen LL, Agostini HT. Genotypes of JC virus, DNA of cytomegalovirus, and proviral DNA of human immunodeficiency virus in eyes of acquired immunodeficiency syndrome patients. J Neurovirol. 2005 Feb;11(1):58-65. doi: 10.1080/13550280590900391. PMID: 15804960.
We read with great interest the article by Forte et al1, "Swept source optical Coherence tomography Angiography in patients treated with hydroxychloroquine: co-relation of the functional and morphological test." Hydroxychloroquine (HCQ) is a widely used drug for the management of systemic lupus erythematosus and rheumatoid arthritis. Non-invasive tests like optical coherence tomography, optical coherence tomography-angiography, 10-2 visual fields and multifocal ERG (mf-ERG) help in the early detection of the toxicity.2 We would like to highlight here importance of adaptive optics, and various studies done for the early detection of HCQ toxicity. In the study by Forte et al, mf-ERG did not co-relate with the flow changes on OCT-A, however in another observation by Penrose et al (n=6) a depression of signals on multifocal ERG was found in the perifoveal region even when the patients had normal visual acuity and a normal fundus.3Costa et al found significant differences between the micro-perimetry in the patients taking hydroxychloroquine and controls.4 It will be interesting to know the authors take on this. Besides these, adaptive optics is emerging as an important tool to detect the early photo-receptor changes in patients with HCQ toxicity. Adaptive optics help in the direct visualization of the cone mosaic. Stepien et al in their observation on 4 patients observed that adaptive optics showed a loss of cone mosaic in the perifoveal region that corresponded with...
We read with great interest the article by Forte et al1, "Swept source optical Coherence tomography Angiography in patients treated with hydroxychloroquine: co-relation of the functional and morphological test." Hydroxychloroquine (HCQ) is a widely used drug for the management of systemic lupus erythematosus and rheumatoid arthritis. Non-invasive tests like optical coherence tomography, optical coherence tomography-angiography, 10-2 visual fields and multifocal ERG (mf-ERG) help in the early detection of the toxicity.2 We would like to highlight here importance of adaptive optics, and various studies done for the early detection of HCQ toxicity. In the study by Forte et al, mf-ERG did not co-relate with the flow changes on OCT-A, however in another observation by Penrose et al (n=6) a depression of signals on multifocal ERG was found in the perifoveal region even when the patients had normal visual acuity and a normal fundus.3Costa et al found significant differences between the micro-perimetry in the patients taking hydroxychloroquine and controls.4 It will be interesting to know the authors take on this. Besides these, adaptive optics is emerging as an important tool to detect the early photo-receptor changes in patients with HCQ toxicity. Adaptive optics help in the direct visualization of the cone mosaic. Stepien et al in their observation on 4 patients observed that adaptive optics showed a loss of cone mosaic in the perifoveal region that corresponded with the OCT findings. OCT findings in their study showed a loss of IS -OS junction with preservation of retinal pigment epithelium and external limiting membrane showing a "sinking hole defect". SD-OCT and adaptive optics also showed defects in the area which were unaffected on 10-2 perimetry, suggesting pre-clinical loss. 5 Similarly, Debellemanière G et al, in their study on eyes found that there was increased cone spacing and moderate cone loss with an increasing cumulative dose of HCQ.6 It will be interesting to know the author's point of view about this, Thus to conclude, the non-invasive investigations may aid in the early detection of HCQ toxicity.
References
1. Forte R, Haulani H, Dyrda A, et al
Swept source optical coherence tomography angiography in patients treated with hydroxychloroquine: correlation with morphological and functional tests. British Journal of Ophthalmology 2021;105:1297-1301.
2. Marmor MF, Kellner U, Lai TY, Melles RB, Mieler WF; American Academy of Ophthalmology. Recommendations on Screening for Chloroquine and Hydroxychloroquine Retinopathy (2016 Revision). Ophthalmology. 2016 Jun;123(6):1386-94
3. Penrose PJ, Tzekov RT, Sutter EE, Fu AD, Allen AW Jr, Fung WE, Oxford KW. Multifocal electroretinography evaluation for early detection of retinal dysfunction in patients taking hydroxychloroquine. Retina. 2003 Aug;23(4):503-12.
4. Martínez-Costa L, Victoria Ibañez M, Murcia-Bello C, Epifanio I, Verdejo-Gimeno C, Beltrán-Catalán E, Marco-Ventura P. Use of microperimetry to evaluate hydroxychloroquine and chloroquine retinal toxicity. Can J Ophthalmol. 2013 Oct;48(5):400-5. doi: 10.1016/j.jcjo.2013.03.018. PMID: 24093187.
5. Stepien KE, Han DP, Schell J, Godara P, Rha J, Carroll J. Spectral-domain optical coherence tomography and adaptive optics may detect hydroxychloroquine retinal toxicity before symptomatic vision loss. Trans Am Ophthalmol Soc. 2009 Dec;107:28-33. PMID: 20126479; PMCID: PMC2814561.
6. Debellemanière G, Flores M, Tumahai P, Meillat M, Bidaut Garnier M, Delbosc B, Saleh M. Assessment of parafoveal cone density in patients taking hydroxychloroquine in the absence of clinically documented retinal toxicity. Acta Ophthalmol. 2015 Nov;93(7):e534-40
Shang et al. conducted a prospective study to examine the effect of ophthalmic and systemic conditions on incident dementia (1). The adjusted hazard ratios (HRs) (95% confidence intervals [CIs]) of age-related macular degeneration (AMD), cataract, diabetes-related eye disease (DRED), and glaucoma at baseline for incident dementia were 1.26 (1.05 to 1.52), 1.11 (1.00 to 1.24), 1.61 (1.30 to 2.00), and 1.07 (0.92 to 1.25), respectively. Diabetes, heart disease, stroke and depression at baseline were also significantly associated with an increased risk of dementia. In addition, some combinations of ophthalmic and systemic conditions were at the higher risk for incident dementia. I have a comment about the study.
Vision impairment is a risk factor of dementia, and poor vision is independently associated with a decline in cognitive function (2). Shang et al. clarified that AMD, cataract, and DRED were risk of incident dementia, and some combinations with systemic conditions accelerated risk of incident dementia. Although glaucoma was not significantly associated with increased risk of al-cause dementia, it was significantly associated with increased risk of vascular dementia. The authors also conducted analysis by excluding data in the first 5 years of follow-up, consistent results were also specified on the combined effects of ophthalmic and systemic conditions on incident dementia. Although the mechanism of increased risk of dementia in combinations with ophthalmic and...
Shang et al. conducted a prospective study to examine the effect of ophthalmic and systemic conditions on incident dementia (1). The adjusted hazard ratios (HRs) (95% confidence intervals [CIs]) of age-related macular degeneration (AMD), cataract, diabetes-related eye disease (DRED), and glaucoma at baseline for incident dementia were 1.26 (1.05 to 1.52), 1.11 (1.00 to 1.24), 1.61 (1.30 to 2.00), and 1.07 (0.92 to 1.25), respectively. Diabetes, heart disease, stroke and depression at baseline were also significantly associated with an increased risk of dementia. In addition, some combinations of ophthalmic and systemic conditions were at the higher risk for incident dementia. I have a comment about the study.
Vision impairment is a risk factor of dementia, and poor vision is independently associated with a decline in cognitive function (2). Shang et al. clarified that AMD, cataract, and DRED were risk of incident dementia, and some combinations with systemic conditions accelerated risk of incident dementia. Although glaucoma was not significantly associated with increased risk of al-cause dementia, it was significantly associated with increased risk of vascular dementia. The authors also conducted analysis by excluding data in the first 5 years of follow-up, consistent results were also specified on the combined effects of ophthalmic and systemic conditions on incident dementia. Although the mechanism of increased risk of dementia in combinations with ophthalmic and systemic conditions might be difficult to be explained, medical care on both ophthalmic and systemic conditions will be indispensable to avid acceleration of cognitive decline.
References
1. Shang X, Zhu Z, Huang Y, et al. Associations of ophthalmic and systemic conditions with incident dementia in the UK Biobank. Br J Ophthalmol 2021 Sep 13. doi: 10.1136/bjophthalmol-2021-319508
2. Lim ZW, Chee ML, Soh ZD, et al. Association Between Visual Impairment and Decline in Cognitive Function in a Multiethnic Asian Population. JAMA Netw Open 2020;3(4):e203560.
We read with interest the recent publication by Bertolin et al. (“In vitro establishment, validation and characterisation of conjunctival epithelium outgrowth using tissue fragments and amniotic membrane”). Their validated conjunctival analogue of the simple limbal epithelial transplantation does represent a promising advance in the field. It is, however, interesting to note that the established tissue application was mainly validated on its growth potential and not specifically on its ability to reinstate a healthy ocular mucosal surface.
Functional validation is of utmost importance, especially as the glued fragments are directly transplanted. This approach circumvents the need for expensive cell culture but also bypasses the stringent release criteria for cell therapies or tissue-engineered transplantation products. We would suggest that before this technique can be considered fully validated, it should be demonstrated that the obtained conjunctival cells contribute to the first line of mucosal defence, i.e. barrier formation. Several conjunctival barriers can be identified, such as intercellular junction complexes, glycocalyx and secreted mucins. Bertolin et al. demonstrated the presence of tight junctions (cfr. ZO-1 protein) and a glycocalyx (cfr. membrane-associated mucin-1), but failed to address the presence of goblet cells. As goblet cells are responsible for the secretion of mucin 5AC, which is the most abundant mucin in the mucin la...
We read with interest the recent publication by Bertolin et al. (“In vitro establishment, validation and characterisation of conjunctival epithelium outgrowth using tissue fragments and amniotic membrane”). Their validated conjunctival analogue of the simple limbal epithelial transplantation does represent a promising advance in the field. It is, however, interesting to note that the established tissue application was mainly validated on its growth potential and not specifically on its ability to reinstate a healthy ocular mucosal surface.
Functional validation is of utmost importance, especially as the glued fragments are directly transplanted. This approach circumvents the need for expensive cell culture but also bypasses the stringent release criteria for cell therapies or tissue-engineered transplantation products. We would suggest that before this technique can be considered fully validated, it should be demonstrated that the obtained conjunctival cells contribute to the first line of mucosal defence, i.e. barrier formation. Several conjunctival barriers can be identified, such as intercellular junction complexes, glycocalyx and secreted mucins. Bertolin et al. demonstrated the presence of tight junctions (cfr. ZO-1 protein) and a glycocalyx (cfr. membrane-associated mucin-1), but failed to address the presence of goblet cells. As goblet cells are responsible for the secretion of mucin 5AC, which is the most abundant mucin in the mucin layer of the tear film, its presence is crucial to obtain a normal, hydrated ocular surface. Presence of mucin-producing goblet cells is so characteristic of the conjunctiva that it is a cardinal feature of impression cytology techniques in the diagnosis of corneal limbal stem cell deficiency. We therefore consider goblet cells (and their associated mucin production) in 2D and 3D cultures the “sine qua non” for conjunctival epithelium and propose that it should be a core element of the validated characterization process.
As functional goblet cells are difficult to maintain in culture, it could be debated that the absence of goblet cells in the outgrowth does not implicate their absence during in vivo expansion. If conjunctival stem cells in the outgrowth could be shown to have bipotent properties, it is reasonable to assume that conjunctival goblet cells can differentiate from these bipotent stem cells and that they can be preserved once they are placed in their natural tightly regulated environment, including the conjunctival innervation of the epithelium. Do the authors have any experience with goblet cell maturation? In any case, these properties would have to be well proven before this technique can be relied on in the clinic.
We like to congratulate Mullany et al. for their paper on normal-tension glaucoma is associated with cognitive impairment.1 To link normal-tension glaucoma (NTG) to cognitive impairment and therefore to a neurodegenerative process opens a new vista and research approach for glaucoma research. NTG indeed is an intriguing optic neuropathy that presents with a glaucomatous optic disc appearance and visual field loss similar to that seen in primary open angle glaucoma. The main risk factor for glaucoma however, increased intraocular pressure is missing.
Unlike other cranial nerves the optic nerve is a white matter tract of the brain, enveloped in the meninges (dura, arachnoid and pia mater) and surrounded by cerebrospinal fluid (CSF) on its entire length. And CSF indeed may be the link that connects the neurodegenerative process leading to cognitive impairment and the glaucomatous optic neuropathy in NTG. Recent research demonstrated a relationship between decreased CSF flow, measured in the ventricles and the spinal cord, and cognitive deficit in the elderly.2 In NTG, impaired CSF dynamics was demonstrated with computer assisted cisternography in the subarachnoid space of the intraorbital optic nerve most pronounced in the bulbar region behind the eye globe.3 In a recent publication we found an elevated L-PGDS concentration in the subarachnoid space of the optic nerve in NTG patients with optic nerve sheath compartment syndrome that results in a reduced CSF turnover.4...
We like to congratulate Mullany et al. for their paper on normal-tension glaucoma is associated with cognitive impairment.1 To link normal-tension glaucoma (NTG) to cognitive impairment and therefore to a neurodegenerative process opens a new vista and research approach for glaucoma research. NTG indeed is an intriguing optic neuropathy that presents with a glaucomatous optic disc appearance and visual field loss similar to that seen in primary open angle glaucoma. The main risk factor for glaucoma however, increased intraocular pressure is missing.
Unlike other cranial nerves the optic nerve is a white matter tract of the brain, enveloped in the meninges (dura, arachnoid and pia mater) and surrounded by cerebrospinal fluid (CSF) on its entire length. And CSF indeed may be the link that connects the neurodegenerative process leading to cognitive impairment and the glaucomatous optic neuropathy in NTG. Recent research demonstrated a relationship between decreased CSF flow, measured in the ventricles and the spinal cord, and cognitive deficit in the elderly.2 In NTG, impaired CSF dynamics was demonstrated with computer assisted cisternography in the subarachnoid space of the intraorbital optic nerve most pronounced in the bulbar region behind the eye globe.3 In a recent publication we found an elevated L-PGDS concentration in the subarachnoid space of the optic nerve in NTG patients with optic nerve sheath compartment syndrome that results in a reduced CSF turnover.4 Reduced CSF turnover is thought to result in malnutrition of axons, neurons and glial cells as well as in accumulation of toxic waste products on the other hand. An experimental induced optic nerve sheath compartment in an animal model demonstrated the most impressive damage to axons and glial cells not on the site where the compartment was created (close to optic canal), but behind the lamina cribrosa in an area densely packed with mitochondria.5 A toxic damage following the CSF compartmentation seems to be the most likely explanation.
We encourage to focus in further studies on CSF dynamics in both, dementia and NTG.
References:
1. Mullany S, Xiao L, Qassim A, Marshall H, Gharahkhani P, MacGregor S, Hassall MM, Siggs OM, Souzeau E, Craig JE. Normal-tension glaucoma is associated with cognitive impairment. Br J Ophthalmol. 2021 Mar 29:bjophthalmol-2020-317461. doi: 10.1136/bjophthalmol-2020-317461. Epub ahead of print. PMID: 33781990.
2. Attier-Zmudka J, Sérot JM, Valluy J, Saffarini M, Macaret AS, Diouf M, Dao S, Douadi Y, Malinowski KP, Balédent O. Decreased Cerebrospinal Fluid Flow Is Associated With Cognitive Deficit in Elderly Patients. Front Aging Neurosci. 2019 Apr 30;11:87. doi: 10.3389/fnagi.2019.00087. PMID: 31114494; PMCID: PMC6502902.
3. Pircher A, Montali M, Wostyn P, Pircher J, Berberat J, Remonda L, Killer HE. Impaired cerebrospinal fluid dynamics along the entire optic nerve in normal-tension glaucoma. Acta Ophthalmol. 2018 Aug;96(5):e562-e569. doi: 10.1111/aos.13647. Epub 2018 Mar 12. PMID: 29532640.
4. Pircher A, Neutzner A, Montali M, Huber A, Scholl HPN, Berberat J, Remonda L, Killer HE. Lipocalin-type Prostaglandin D Synthase Concentration Gradients in the Cerebrospinal Fluid in Normal-tension Glaucoma Patients with Optic Nerve Sheath Compartmentation. Eye Brain. 2021 Apr 14;13:89-97. doi: 10.2147/EB.S297274. PMID: 33883963; PMCID: PMC8053785.
5. Jaggi GP, Harlev M, Ziegler U, Dotan S, Miller NR, Killer HE. Cerebrospinal fluid segregation optic neuropathy: an experimental model and a hypothesis. Br J Ophthalmol. 2010 Aug;94(8):1088-93. doi: 10.1136/bjo.2009.171660. Epub 2010 May 27. PMID: 20508039
We would like to congratulate Uwaydat et al. on their large series of spontaneously closed macular holes (MH), which adds new information to the literature.(1) It reinforces the observation that traumatic MH can spontaneously close and that a period of observation in these eyes, where the results of surgery are not clear, is a worthwhile option. However, we disagree with their conclusion that eyes with recent onset small primary MHs should also be observed. The authors don’t suggest a time period for observation but found that the median time for closure for these small holes was 4.4 months.
The report by Uwaydat et al. has 40 authors and the 60 cases of idiopathic MH were collected over at least a two-year period. Assuming a conservative number of 25 MH cases seen per surgeon per annum, this would give a spontaneous closure rate of ~3%, which is similar to the published literature as the authors review in their article.
MH are known to enlarge with time, even in the short term. Madi et al, reported that 83% enlarged, by a median of 105 microns in 8 weeks. (2) Similarly, Berton et al recently estimated that holes less than 250 microns enlarge by a mean of 1.67 microns per day, resulting in a similar 100-micron increase in 2 months.(3)
The anatomical and visual outcomes of surgery are dependent on MH diameter and duration. Holes greater than 300 microns, and with a duration more than four months are less likely to regain 0.3 logMAR or better.(4)...
We would like to congratulate Uwaydat et al. on their large series of spontaneously closed macular holes (MH), which adds new information to the literature.(1) It reinforces the observation that traumatic MH can spontaneously close and that a period of observation in these eyes, where the results of surgery are not clear, is a worthwhile option. However, we disagree with their conclusion that eyes with recent onset small primary MHs should also be observed. The authors don’t suggest a time period for observation but found that the median time for closure for these small holes was 4.4 months.
The report by Uwaydat et al. has 40 authors and the 60 cases of idiopathic MH were collected over at least a two-year period. Assuming a conservative number of 25 MH cases seen per surgeon per annum, this would give a spontaneous closure rate of ~3%, which is similar to the published literature as the authors review in their article.
MH are known to enlarge with time, even in the short term. Madi et al, reported that 83% enlarged, by a median of 105 microns in 8 weeks. (2) Similarly, Berton et al recently estimated that holes less than 250 microns enlarge by a mean of 1.67 microns per day, resulting in a similar 100-micron increase in 2 months.(3)
The anatomical and visual outcomes of surgery are dependent on MH diameter and duration. Holes greater than 300 microns, and with a duration more than four months are less likely to regain 0.3 logMAR or better.(4)
Surgery achieves closure rates of over 98% for small and medium sized holes, and a risk of a worse visual outcome than preoperatively is very low.(4)
Taking this information together, observing a 200 micron hole with a 2-month duration, for even 2 months would likely result in a 100-micron size increase, and a four-fold reduction in the chances of achieving 0.3logMAR or better, set against a 5% chance of observing spontaneous closure.
The spontaneous closure rate in smaller holes is likely to be higher than previously stated however, it is not a common observation, and delaying surgery carries real risks for the patient. Although the options should be discussed with the patient, we advocate prompt surgery for all primary macular holes, including small ones, as the best means of achieving good functional results.
1. Uwaydat, S. H. et al. Clinical characteristics of full thickness macular holes that closed without surgery. Br. J. Ophthalmol. (2021) doi:10.1136/bjophthalmol-2021-319001.
2. Madi, H. A., Dinah, C., Rees, J. & Steel, D. H. W. The Case Mix of Patients Presenting with Full-Thickness Macular Holes and Progression before Surgery: Implications for Optimum Management. Ophthalmol. J. Int. d’ophtalmologie. Int. J. Ophthalmol. Zeitschrift fur Augenheilkd. 233, 216–221 (2015).
3. Berton, M., Robins, J., Frigo, A. C. & Wong, R. Rate of progression of idiopathic full-thickness macular holes before surgery. Eye (Lond). 34, 1386–1391 (2020).
4. Steel, D. H. et al. Factors affecting anatomical and visual outcome after macular hole surgery: findings from a large prospective UK cohort. Eye (Lond). 35, 316–325 (2021).
We read with interest the article by Sarker et al(1) in which they compared the outcomes of trabeculectomy versus Ahmed glaucoma valve (AGV) implantation in Sturge–Weber syndrome (SWS) patients with secondary glaucoma aged 11-62 years. As it noted in the paper, the authors found that complete success rates after 24 months were 80% and 70% in the AGV and trabeculectomy groups, respectively, and qualified success rates were 90% and 85% at same period in the AGV and trabeculectomy groups, respectively. We were delighted to get the conclusion that both AGV implant and trabeculectomy appeared to be safe and efficacious in controlling glaucoma secondary to SWS.
Show MoreAs it reported by Mohamed et al., the complete success rate and qualified success rate (intraocular pressure≤17mmHg) of trabeculectomy reported were 80% and 100% at 12 postoperative follow-up month, respectively(2). However, the qualified success rate (90%) of AGV implantation in SWS patients with secondary glaucoma is higher than that reported by Hamush et al. (79%)(3) and Kaushik et al. (76%)(4) at 2 years of follow-up. Meanwhile, the trabeculectomy with MMC success rate in this study was comparable to other studies about primary glaucoma(5, 6), but the success rate of tube shunt surgery was higher than in prior reports. The qualified success rate of Baerveldt implantation for patients who not had undergone previous incisional ocular surgery was 73% in Primary Tube Versus Trabeculectomy (PTVT) study(6) and 75% rep...
Title: Management of Glaucoma During Pregnancy
Author: Angelo P. Tanna
Affiliations:
Department of Ophthalmology, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA
Division of Ophthalmology, Ann & Robert H. Lurie Children’s Hospital of Chicago, Chicago, Illinois, USA
Conflicts of Interest Disclosure:
APT: Consultant to Ivantis, Sandoz, and Zeiss
Acknowledgment:
APT is supported by an unrestricted departmental grant from Research to Prevent Blindness, NY, NY
Corresponding Author:
Angelo P. Tanna, M.D.
Department of Ophthalmology
Northwestern University Feinberg School of Medicine
645 N. Michigan Ave., Suite 440
Chicago, IL 60611
Telephone: 312-908-8152
Fax: 312-503-8152
E-mail: atanna@northwestern.edu
Dear Editor:
I read with interest the work of Doctor Hashimoto and colleagues on the risk of adverse neonatal outcomes (congenital anomalies, preterm birth, low birth weight) associated with maternal exposure to intraocular pressure-lowering medications during pregnancy.1 They used a large Japanese claims database and state-of-the-art statistical methodology to evaluate the frequency of adverse events in a cohort of live births of 91 women who had “at least one dispensation of IOP-lowering medications during the first trimester,” compared to that observed in 735 women with glaucoma or...
Show MoreThank you for raising the issue of abbreviations entering the virological lexicon which might give rise to confusion and misunderstanding. Over a decade has elapsed since our patient report was published and the source material is not retrievable. However, our recollection is the patient was discussed contemporaneously at the MDT and the viral aetiology, radiology findings and medical management determined and documented, from which the data was sourced for the 2008 report. Plausible as it may seem, it is not possible to test the veracity of the suggestion that the names ‘Jamestown Canyon’ and ‘John Cunningham’ might have been transposed during that MDT many years after the event, paper records are not kept indefinitely in NHS practice and ethics in medical publishing demands that patient identifiers are not described or retained in order to preserve anonymity. Perhaps the latter should have been considered over half a century ago when JC virus was first identified in the brain of the unfortunate patient after whom the eponymous pathogen was christened
(Padgett BL, Walker DL; et al. (1971). "Cultivation of papova-like virus from human brain with progressive multifocal leucoencephalopathy". Lancet. 1 (7712):
1257–60. doi:10.1016/S0140-6736(71)91777-6)
I read with interest the article by Jonas et al 1. The main purpose of the authors was to explore associations between a disc size change and other morphological parameters. Indeed, many non-ophthalmic and game-changing parameters are associated with disc size change and other morphological parameters, such as the serum lipids 2 dietary factors (such as lutein, zeaxanthin, and omega-3 fatty acids) 2-4, medications (such as lipid-lowering agents) 2, genetic susceptibility, body mass index, age and sex 3, among which only age and sex are addressed in their retrospective analysis.
According to the authors, decrease in the ophthalmoscopic disc size in the myopic eyes during the 10-year follow up, is likely related to a shift of the Bruch’s membrane opening as the inner of the three optic nerve head canal layers into the direction of the fovea. While their interpretations can be partly true, their attributed mechanism is subject to many biases.
Firstly, changes in ophthalmoscopical optic disc size and Bruch’s membrane are a function of macular pigment optical density 5-7, which in turn is a function of dietary carotenoid intake 8;9. Tong et al 10 have shown before that macular pigment optical density (MPOD) is inversely associated with axial length in Chinese subjects with myopia, suggesting that carotenoid intake, particularly lutein, is associated to axial length as well. Another study with a smaller sample size (45 eyes of 32 patients) with a different mean a...
Show MoreIn their 2008 case report, Muqit, et al. describe a case of “presumptive Jamestown Canyon viral retinitis.”1
Jamestown Canyon virus is a mosquito-borne, single-stranded, ribonucleic acid (RNA) orthobunyavirus that is endemic throughout much of North America.2,3 Infection with Jamestown Canyon virus may be asymptomatic or may result in a general febrile illness, meningitis, and/or meningoencephalitis.2,3 Beyond the above case report by Muqit, et al.,1 and another review article referencing this case report,4 Jamestown Canyon virus has not been reported to cause retinitis or other ocular manifestations.
Upon close review of the case report by Muqit, et al.,1 we believe the authors are likely describing a case of John Cunningham (JC) virus (a ubiquitous, double-stranded, deoxyribonucleic acid [DNA] human polyomavirus known to cause progressive multifocal leukoencephalopathy [PML] among the immunocompromised)5-7 rather than Jamestown Canyon virus.
First, the case patient with viral retinitis had underlying human immunodeficiency virus (HIV) infection and a low CD4 lymphocyte count (240 cells/mm3), making him immunocompromised and susceptible to reactivation of the John Cunningham (JC) virus. Second, the case patient had magnetic resonance imaging (MRI) brain findings (i.e., asymmetric, predominantly posterior, confluent, subcortical white matter hyperintensities involving U-fibers) that are classic for John Cunningham (JC) virus-related PML.6,7 In fact,...
Show MoreWe read with great interest the article by Forte et al1, "Swept source optical Coherence tomography Angiography in patients treated with hydroxychloroquine: co-relation of the functional and morphological test." Hydroxychloroquine (HCQ) is a widely used drug for the management of systemic lupus erythematosus and rheumatoid arthritis. Non-invasive tests like optical coherence tomography, optical coherence tomography-angiography, 10-2 visual fields and multifocal ERG (mf-ERG) help in the early detection of the toxicity.2 We would like to highlight here importance of adaptive optics, and various studies done for the early detection of HCQ toxicity. In the study by Forte et al, mf-ERG did not co-relate with the flow changes on OCT-A, however in another observation by Penrose et al (n=6) a depression of signals on multifocal ERG was found in the perifoveal region even when the patients had normal visual acuity and a normal fundus.3Costa et al found significant differences between the micro-perimetry in the patients taking hydroxychloroquine and controls.4 It will be interesting to know the authors take on this. Besides these, adaptive optics is emerging as an important tool to detect the early photo-receptor changes in patients with HCQ toxicity. Adaptive optics help in the direct visualization of the cone mosaic. Stepien et al in their observation on 4 patients observed that adaptive optics showed a loss of cone mosaic in the perifoveal region that corresponded with...
Show MoreShang et al. conducted a prospective study to examine the effect of ophthalmic and systemic conditions on incident dementia (1). The adjusted hazard ratios (HRs) (95% confidence intervals [CIs]) of age-related macular degeneration (AMD), cataract, diabetes-related eye disease (DRED), and glaucoma at baseline for incident dementia were 1.26 (1.05 to 1.52), 1.11 (1.00 to 1.24), 1.61 (1.30 to 2.00), and 1.07 (0.92 to 1.25), respectively. Diabetes, heart disease, stroke and depression at baseline were also significantly associated with an increased risk of dementia. In addition, some combinations of ophthalmic and systemic conditions were at the higher risk for incident dementia. I have a comment about the study.
Vision impairment is a risk factor of dementia, and poor vision is independently associated with a decline in cognitive function (2). Shang et al. clarified that AMD, cataract, and DRED were risk of incident dementia, and some combinations with systemic conditions accelerated risk of incident dementia. Although glaucoma was not significantly associated with increased risk of al-cause dementia, it was significantly associated with increased risk of vascular dementia. The authors also conducted analysis by excluding data in the first 5 years of follow-up, consistent results were also specified on the combined effects of ophthalmic and systemic conditions on incident dementia. Although the mechanism of increased risk of dementia in combinations with ophthalmic and...
Show MoreTo the editor,
We read with interest the recent publication by Bertolin et al. (“In vitro establishment, validation and characterisation of conjunctival epithelium outgrowth using tissue fragments and amniotic membrane”). Their validated conjunctival analogue of the simple limbal epithelial transplantation does represent a promising advance in the field. It is, however, interesting to note that the established tissue application was mainly validated on its growth potential and not specifically on its ability to reinstate a healthy ocular mucosal surface.
Functional validation is of utmost importance, especially as the glued fragments are directly transplanted. This approach circumvents the need for expensive cell culture but also bypasses the stringent release criteria for cell therapies or tissue-engineered transplantation products. We would suggest that before this technique can be considered fully validated, it should be demonstrated that the obtained conjunctival cells contribute to the first line of mucosal defence, i.e. barrier formation. Several conjunctival barriers can be identified, such as intercellular junction complexes, glycocalyx and secreted mucins. Bertolin et al. demonstrated the presence of tight junctions (cfr. ZO-1 protein) and a glycocalyx (cfr. membrane-associated mucin-1), but failed to address the presence of goblet cells. As goblet cells are responsible for the secretion of mucin 5AC, which is the most abundant mucin in the mucin la...
Show MoreWe like to congratulate Mullany et al. for their paper on normal-tension glaucoma is associated with cognitive impairment.1 To link normal-tension glaucoma (NTG) to cognitive impairment and therefore to a neurodegenerative process opens a new vista and research approach for glaucoma research. NTG indeed is an intriguing optic neuropathy that presents with a glaucomatous optic disc appearance and visual field loss similar to that seen in primary open angle glaucoma. The main risk factor for glaucoma however, increased intraocular pressure is missing.
Unlike other cranial nerves the optic nerve is a white matter tract of the brain, enveloped in the meninges (dura, arachnoid and pia mater) and surrounded by cerebrospinal fluid (CSF) on its entire length. And CSF indeed may be the link that connects the neurodegenerative process leading to cognitive impairment and the glaucomatous optic neuropathy in NTG. Recent research demonstrated a relationship between decreased CSF flow, measured in the ventricles and the spinal cord, and cognitive deficit in the elderly.2 In NTG, impaired CSF dynamics was demonstrated with computer assisted cisternography in the subarachnoid space of the intraorbital optic nerve most pronounced in the bulbar region behind the eye globe.3 In a recent publication we found an elevated L-PGDS concentration in the subarachnoid space of the optic nerve in NTG patients with optic nerve sheath compartment syndrome that results in a reduced CSF turnover.4...
Show MoreWe would like to congratulate Uwaydat et al. on their large series of spontaneously closed macular holes (MH), which adds new information to the literature.(1) It reinforces the observation that traumatic MH can spontaneously close and that a period of observation in these eyes, where the results of surgery are not clear, is a worthwhile option. However, we disagree with their conclusion that eyes with recent onset small primary MHs should also be observed. The authors don’t suggest a time period for observation but found that the median time for closure for these small holes was 4.4 months.
The report by Uwaydat et al. has 40 authors and the 60 cases of idiopathic MH were collected over at least a two-year period. Assuming a conservative number of 25 MH cases seen per surgeon per annum, this would give a spontaneous closure rate of ~3%, which is similar to the published literature as the authors review in their article.
MH are known to enlarge with time, even in the short term. Madi et al, reported that 83% enlarged, by a median of 105 microns in 8 weeks. (2) Similarly, Berton et al recently estimated that holes less than 250 microns enlarge by a mean of 1.67 microns per day, resulting in a similar 100-micron increase in 2 months.(3)
The anatomical and visual outcomes of surgery are dependent on MH diameter and duration. Holes greater than 300 microns, and with a duration more than four months are less likely to regain 0.3 logMAR or better.(4)...
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