Recent eLetters
Displaying 1-10 letters out of 442 published
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Response to `Clinical factors associated with malignancy and HIV status in patients with ocular surface squamous neoplasia at Kililmanjaro Christian Medical Centre, Tanzania'
Submit responseDear Author,
We read your paper entitled `Clinical factors associated with malignancy and HIV status in patients with ocular surface squamous neoplasia at Kililmanjaro Christian Medical Centre, Tanzania' with much interest. It was an interesting insight into the characteristics of OSSN patients in sub-saharan Africa. However, we had some queries and we hope you can share your thoughts on them.
Firstly, we note that patients were selected based on external appearance of lesions and we feel that this creates a selection bias as patients with clinically less prominent lesions are less likely to be recruited into the study. Your groupings of malignant lesions have included mild to moderate dysplasia, many of which may be clinically less prominent than more dysplastic lesions. This creates a bias where patients selected are more likely to be of a higher dysplastic grade. However, we do agree that selecting a large random group of patients from the general population and testing them histologically may not be feasible.
Our second point is that the p value for independent association with HIV status in the text (p = 0.035) is different from that in the table (p = 0.01) Thirdly, we note that you have concluded that HIV positive patients tend to have a higher malignancy grade based on a regression model. However, we were wondering if there was any explanation for the fact that CD4 counts did not show a similar association. Furthermore, you concluded that positive HIV status was associated with longer lesion duration, larger lesion size, leukoplakia and the presence of feeder vessels. However, this raises a few questions. Firstly, most would agree that a lesion of longer duration is more likely to be of a larger size with corresponding feeder vessels and show leukoplakic changes than one present for a shorter duration. If it possible then that, HIV status was associated with the above risk factors(large size, feeder vessels, leukoplakia) as HIV patients themselves were more likely to have a lesion present for a longer duration of time? Also, it is mentioned that women comprised of 69% of HIV patients. We were wondering if in your experience, women in sub-Saharan Africa may have lesser access to medical care which could have contributed to the longer duration of lesions seen in HIV patients.
Lastly, it is stated that HIV patients are more likely to suffer a recurrence. However, if HIV patients are more likely to have a larger lesion for a longer duration, would this contribute to a higher recurrence rate? Also, if HIV status is a postulated risk factor for the development of dysplasia, it is highly conceivable that there are multiple dysplastic foci. It is then possible that a `recurrent lesion' is in fact the progression of a dysplastic lesion of another focus? As such, were all the recurrences in the same spot of excision?
Thank you for your time and we hope to hear your thoughts on the above queries!
References:
1. Clinical factors associated with malignancy and HIV status in patients with ocular surface squamous neoplasia at Kilimanjaro Christian Medical Centre, Tanzania. Makupa II, Swai B, Makupa WU, White VA, Lewallen S. Br J Ophthalmol. 2012 Apr;96(4):482-4. Epub 2011 Nov PMID: 22075543
Conflict of Interest:
None declared
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Re:Brimonidine induced uveitis: Extent of the problem?
Submit responseThe authors thank the respondent for the observations and comments. Most of our patients were referred to us by other ophthalmologists. Unfortunately, as tertiary referral practitioners to the wider ophthalmic community (uveitis: JCR, glaucoma: WHM and DD) we have no way of knowing how many patients in our community are on brimonidine or how many cases of brimonidine induced uveitis may be seen by other consultants. We agree with the respondent that brimonidine rechallenge testing adds to the evidence for causality. This has previously been performed, in case reports by Byles [1] (four patients), Goyal [2] (one patient), Cates [3] (one patient) and Becker [4] (one patient). In all of these cases, uveitis recurred on re-exposure. In our case series, all of the patients had field threatening glaucoma, in one case in an only eye. Given the severity of their alphagan side effects we could not ethically request that any patient voluntarily trial re-exposure to the drug when its implication in uveitis (sometimes hypertensive) is already so well documented. 1. Byles DB, Frith P, Salmon JF. Anterior uveitis as a side effect of topical brimonidine. Am J Ophthalmol. 2000 Sep;130(3):287-91. 2. Goyal R, Ram AR. Brimonidine tartarate 0.2% (Alphagan) associated granulomatous anterior uveitis. Eye (Lond). 2000 Dec;14(Pt 6):908-10. 3. Cates CA, Jeffrey MN. Granulomatous anterior uveitis associated with 0.2% topical brimonidine. Eye (Lond). 2003 Jul;17(5):670-1. 4. Becker HI, Walton RC, Diamant JI, Zegans ME. Anterior uveitis and concurrent allergic conjunctivitis associated with long-term use of topical 0.2% brimonidine tartrate. Arch Ophthalmol. 2004 Jul;122(7):1063- 6.
Conflict of Interest:
None declared
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Brimonidine induced uveitis: Extent of the problem?
Submit responseArticle "Brimonidine (Alphagan) associated anterior uveitis" by McKnight CM et al1 is informative. Cessation of brimonidine eye drops resulted in improvement of uveitis in five cases. This case series has produced further evidence that brimonidine may be responsible for uveitis/ raised IOP in some cases. However a critic may still argue the two events to be coincidental. Unfortunately we have only a few anti glaucoma drugs that can be used in uveitis. For the sake of the rest of glaucoma patients, a few of these patients can be motivated to be volunteers. Restarting the brimonidine in any of these patients and documenting the reappearance of uveitis would produce stronger evidence. Moreover, their 5 patients1 presented with uveitis after using brimonidine for 13, 17, 6, 12 months and 5 years. Earlier reports also suggested that when brimonidine is used, anterior uveitis can occur after approximately 1 year2/ 2 years3 of treatment. Keeping in view the common use of brimonidine, these case reports reflect a very low incidence of uveitis and that too after use for many months. Had authors stated their total number of patients on brimonidine, we would have gained an idea of the frequency/ prevalence of the problem. References: 1. McKnight CM, Richards JC, Daniels D, Morgan WH. Brimonidine (Alphagan) associated anterior uveitis. Br J Ophthalmol. 2012 Jan 18. [Epub ahead of print] 2. Velasque L, Ducousso F, Pernod L, Vignal R, Deral V. [Anterior uveitis and topical brimonidine: a case report]. J Fr Ophtalmol. 2004 Dec;27(10):1150-2. [Article in French] 3. Nguyen EV, Azar D, Papalkar D, McCluskey P. Brimonidine-induced anterior uveitis and conjunctivitis: clinical and histologic features. J Glaucoma. 2008 Jan-Feb;17(1):40-2.
Conflict of Interest:
None declared
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Re:Re:Efficacy of Silicone Punctal Plugs in Children
Submit responseWe thank Dr Shoaib for his comments. In the results we clearly state 'The indication for insertion was based on the presence of ocular surface changes and poor tear film meniscus, with a previous unsuc- cessful management by lubrication and topical medication alone. Overall, 18 of the 25 patients had a concurrent systemic disorder (table 1).' Schirmer's test is , we believe , a poor test for dry eye in children. It often results in reflex tearing and is of little clinical value in children. Tear break up time is only of value if we know what the normal value is in CHILDREN. This is in fact the subject of our next manuscript which is in review as I write this. In children under 12 years of age and over 4 years of age , the non-invasive tear break up time using the Tearscope ( Keeler , Windsor ,UK) is over 25 seconds ( unpublished data as yet). So in children we looked at tear meniscus and ocular surface changes such as PEE. We not only relied on subjective improvement but also objective signs of improvement of ocular surface changes. As for the comparison of cases of BKC, we can only comment on our own paper which Dr Shoaib cites(1) . Please note that the majority of the children in the 'Punctal Plug' manuscript had a systemic disorder which led to secondary lid and corneal changes. In the article cited regarding BKC (1) many of the children had neovascularisation of the cornea and lubrication is clearly mentioned but not punctual plugs. We clearly state here in the 'Punctal Plug' article that children who failed lubrication were offered plugs. None of the cohort from the 2007 manuscript were in this manuscript. Finally, it is precisely because children can be so difficult to assess that there has been no previous manuscript, to the best of our knowledge, discussing punctual plugs exclusively in children.
1 Jones SM, Weinstein JM, Cumberland P, Klein N, Nischal KK. Visual Outcome and Corneal Changes in Children with Chronic Blepharokeratoconjunctivitis. Ophthalmology 2007;114:2271-2280
Conflict of Interest:
None declared
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Re:Efficacy of Silicone Punctal Plugs in Children
Submit responseWe thank Drs Hanovar and Ali for their comments. The main impetus for publishing this data was to show that children are NOT prone to infections with this strategy. In fact while steroid injections were given in cases of severe corneal neovascularisation such as K.I.D. syndrome and ectodermal hypoplasia , the fact that no child got a canaliculitis or other infection even when steroids were used, re-affirms that infection is not a risk that should prevent the clinician from using silicone punctal plugs if appropriate. Furthermore , clinically if spontaneous extrusion occurred after 6 months we often found that the symptoms had improved. We really wanted to know if using the plugs was a redundant manouevre , hence discussing the rate of extrusion within 6 months of placement , which we considered to be high in any case ( 19%). Perhaps the most striking fact is that we were unable to cite any other article dedicated to children with respect to the use of punctal plugs . We hope this article will encourage Drs Ali and Hanovar and others to share their experiences.
Conflict of Interest:
None declared
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Posterior Segment Eye Diseases: A Growing Problem.
Submit responseWe welcome the latest estimates of global visual impairment (VI). (1) Posterior segment eye diseases (PSED): Glaucoma; Age-Related Macular Degeneration (ARMD); and Diabetic Retinopathy (DR) are now recognised as a major cause of VI worldwide and are more prevalent than infectious causes of VI such as trachoma and corneal ulcers. The majority of data collated in the last ten years from which these figures are estimated likely underestimate the true prevalence of PSED for three reasons: (a) The majority of surveys used the WHO coding instructions, which use the "principal disorder responsible for visual loss in the individual after considering disorders in either eye which are most amenable to treatment or prevention"(2), i.e. if a patient has co-existent PSED with cataract it will be deemed that cataract is the primary cause of VI. Therefore most VI prevalence data available in which cataract is the primary cause will underestimate the actual prevalence of PSED; (b) The Rapid Assessment of Avoidable Blindness (RAAB) methodology, which forms one of the most employed methods of gathering VI data in the last ten years (20 published from Africa, Latin America and Asia) does not allow for accurate diagnosis of PSED or differentiation between PSED; and (c) VI surveys have been designed to diagnose the cause of disease in those with varying degrees of visual impairment (?6/18 Snellen acuity) and thus pre-visually impairing disease is not detected. This is particularly important in the detection of PSED where cessation rather than cure is currently our only realistic management option. If VISION 2020: The Right to Sight's aims of alleviating suffering from avoidable blindness is to be met, the growing impact of PSED needs to be a focus of policy makers.
Conflict of Interest:
None declared
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Re:Role of endothelial keretoplasty in penetrating keratoplasty graft rejection?
Submit responseWe thank Dr. Shoaib for his interest in our article.1 We agree that there are various causes of graft rejection and that performing an endothelial keratoplasty (EK) would not resolve the rejection. To clarify our wording for the article, patients who developed endothelial graft rejection with subsequent endothelial failure were offered EK under their penetrating keratoplasty (PK). The rejection episode was resolved at the time of the EK. There were a total of 9 patients that fulfilled this requirement and were included in the study. These patients did not have any epithelial or stromal rejection and did not have stromal opacities. We do feel that EK under PK for immunological endothelial failure is a viable treatment option that should be considered in cases where there are not any stromal opacities.
Jennifer Nottage, MD
Verinder Nirankari, MD
Eye Consultants of Maryland, Owings Mills, MD
1. Nottage JM, Nirankari VS. Endothelial keratoplasty without Descemet's stripping in eyes with previous penetrating corneal transplants. Br J Ophthalmol. 2012 Jan;96(1):24-7
Conflict of Interest:
None declared
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Role of endothelial keretoplasty in penetrating keratoplasty graft rejection?
Submit responseArticle "Endothelial keratoplasty without Descemet's stripping in eyes with previous penetrating corneal transplants" by Nottage JM and Nirankari VS1, is very informative and the authors deserve appreciation for their wonderful work. However one point requires discussion. Authors mentioned that endothelial keratoplasty (EK) was done either for graft rejection (n = 9) or endothelial failure (n = 24). It seems logical to replace endothelium in endothelium failure. The question is how new endothelium can correct graft rejection? Authors mention "An allograft rejection was defined as corneal clouding in association with an epithelial or endothelial rejection line, keratic precipitates and/or anterior chamber cells." Endothelial line reflecting endothelial rejection can qualify as an indication for EK but the rest of the signs can be due to rejection of the other parts of the graft. A further breakdown of the frequency of above mentioned signs of allograft rejection would have been useful. Other authors have been careful not to include the generalized graft rejection cases for EK e.g. Chen ES et al2 mentioned in their Protocal under the heading of Methods, the inclusion criteria "after penetrating keratoplasty (PK) and without significant stromal haze". Similarly Straiko et al3 described inclusion criteria "for failed PK grafts from endothelial failure with minimal stromal Opacities" and "all eyes with a prior standard PK graft that had failed because of immunologic or nonimmunologic endothelial failure". Graft rejection results from host immunologic response against foreign antigen from donor tissue. Li JY et al 4 observed that it can lead to decreased endothelial cell survival and graft failure. They reported a graft rejection rate of 7.3 % and that the greatest number of rejections occurred between postoperative months 12 and 18. An initial improvement due to healthy endothelial can be expected in all cases of EK but antigenic stimulation will continue even after removal of the rejected graft's endothelium. Especially for the one patient regarding whom authors1 of the under discussion article wrote "had multiple previous graft failure, requiring placement of an investigational ciclosporine implant to prevent further rejection." Should we do EK or PK in PK rejection cases? Perhaps a longer follow up will answer this question. References: 1. Nottage JM, Nirankari VS. Endothelial keratoplasty without Descemet's stripping in eyes with previous penetrating corneal transplants. Br J Ophthalmol. 2012 Jan;96(1):24-7 2. Chen ES, Terry MA, Shamie N, Hoar KL, Phillips PM, Friend DJ. Endothelial keratoplasty: vision, endothelial survival, and complications in a comparative case series of fellows vs attending surgeons. Am J Ophthalmol. 2009 Jul;148(1):26-31.e2. Epub 2009 Apr 17. 3. Straiko MD, Terry MA, Shamie N. Descemet stripping automated endothelial keratoplasty under failed penetrating keratoplasty: a surgical strategy to minimize complications. Am J Ophthalmol. 2011 Feb;151(2):233- 7.e2. Epub 2010 Dec 3. 4. Li JY, Terry MA, Goshe J, Shamie N, Davis-Boozer D. Graft rejection after descemet's stripping automated endothelial keratoplasty graft survival and endothelial cell loss. Ophthalmology. 2012 Jan;119(1):90-4. Epub 2011 Nov 23.
Conflict of Interest:
None declared
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CSR or TB?
Submit responseThe article "Oral rifampin utilisation for the treatment of chronic multifocal central serous retinopathy(CSR)"1 by Steinle NC et al is very informative. However a few points require further elaboration. We were told that patient is an African -American but for how long he stayed in Africa and how frequently he or any of his close family members visit any tuberculosis (TB) endemic area? As both CSR and ocular TB are poorly understood diseases, there is a possibility that these were confused with each other or TB was the underlying pathology in this condition which resembled CSR. Furthermore Rifampin did not cure the disease and its discontinuation led to recurrence which is also true in incomplete TB treatment. Recommendations in this case include an appropriate test like QuantiFERON-TB Gold2 or polymerase chain reactions (PCR) of vitreous, to rule out TB and a full six month course of anti TB3 to avoid recurrences. References: 1. Steinle NC, Gupta N, Yuan A, Singh RP. Oral rifampin utilisation for the treatment of chronic multifocal central serous retinopathy. Br J Ophthalmol. 2012 Jan;96(1):10-3. 2. Gineys R, Bodaghi B, Carcelain G, Cassoux N, Boutin le TH, Amoura Z, Lehoang P, Trad S. QuantiFERON-TB gold cut-off value: implications for the management of tuberculosis-related ocular inflammation. Am J Ophthalmol. 2011 Sep;152(3):433-440.e1 3. Sanghvi C, Bell C, Woodhead M, Hardy C, Jones N. Presumed tuberculous uveitis: diagnosis, management, and outcome. Eye (Lond). 2011 Apr;25(4):475-80.
Conflict of Interest:
None declared
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Re:Efficacy of Silicone Punctal Plugs in Children
Submit responseA Mataftsi et al1 published an interesting article regarding punctal plugs in children. One of their aim was to establish the efficacy however they have not mentioned any test (Schirmer, Tear film break-up time, Rose Bengal staining, osmolarity) to confirm the diagnosis of dry eye and to calibrate the tear deficiency. It was only the clinical impression (flouresein staining is not specific for dry eyes and therefore cannot be used as diagnostic). In the follow up also, there was no yardstick to measure and compare the post procedure improvement with the pre procedure status. Only subjective feelings (patients or parents) are difficult to gauge and therefore a scientific test at this stage would have established the exact positive role of the plugs which could have been counterchecked and verified by other workers. These tests could have been done in the same sitting/ anesthesia and would not have required any additional visit or anaesthesia. A few points of this article differed markedly from previous articles. In "Blepharokeratoconjunctivitis in children: diagnosis and treatment"2 by M Viswalingam et al in which patients in Moorfields Eye Hospital, London, UK, were analyzed, there is no mention of dry eye in either the text or Table 1- Classification of the severity of blepharokeratoconjunctivitis (BKC) in children and Table - 3 Clinical symptoms and signs. Punctate erosions were present in only 9 % (all Asian) of their patients. Their patients improved without any dry eye treatment. Similarly in "Visual Outcome and Corneal Changes in Children with Chronic Blepharokeratoconjunctivitis"3 by Jones SM et al, in patients analyzed in Great Ormond Street Hospital for Children, London, UK, from1999 to 2005 (same hospital and almost same time period as is of the present article), there was no mention of dry eye and punctate epithelial erosions (PEE) were found in 31% of eyes. "In the authors' experience, effective treatment for BKC should include a combination of both systemic and topical antimicrobial therapy, along with topical steroids" was the authors' recommendation in the above mentioned article and no punctal plugs were mentioned. Now in the present article, authors have found a lot of dry eyes (out of which 14 required punctual plugs) in BKC (and PEE in 100%) among the almost same record which was used for the above mentioned article and now they claim "plugs were successful in treating a variety of causes of dry eye in our cohort, with more than half of the children presenting with lipid deficiency secondary to meibomian gland dysfunction".
Despite these observations, authors deserve appreciation for introducing the new concept of punctal plug use in children.
References: 1. Mataftsi A, Subbu RG, Jones S, Nischal KK. The use of punctal plugs in children. Br J Ophthalmol 2012;96:90-92. 2. Viswalingam M, Rauz S, Morlet N, Dart JK. Blepharokeratoconjunctivitis in children: diagnosis and treatment. Br J Ophthalmol. 2005 Apr;89(4):400- 3. 3. Jones SM, Weinstein JM, Cumberland P, Klein N, Nischal KK. Visual Outcome and Corneal Changes in Children with Chronic Blepharokeratoconjunctivitis. Ophthalmology 2007;114:2271-2280
Conflict of Interest:
None declared
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