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    The study investigated the effect of corneal collagen crosslinking (CXL) in thinner corneas less than 400 μm thick. They found a significant loss of endothelial cells postoperatively but no clinically significant corneal edema. At follow-up, topographic stabilization of ectasia was seen. The authors did not suggest extending CXL to thinner corneas but commented that many keratoconic patients have thin corneas that do not meet standard CXL criteria. Zhang's comments on CXL in thin corneas were general and not specifically in response to this study.

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    The study investigated the effect of corneal collagen crosslinking (CXL) in thinner corneas less than 400 μm thick. They found a significant loss of endothelial cells postoperatively but no clinically significant corneal edema. At follow-up, topographic stabilization of ectasia was seen. The authors did not suggest extending CXL to thinner corneas but commented that many keratoconic patients have thin corneas that do not meet standard CXL criteria. Zhang's comments on CXL in thin corneas were general and not specifically in response to this study.

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    1 s2.0 S0002939412000669 Main

    Uploaded by

    Cupris23
    The study investigated the effect of corneal collagen crosslinking (CXL) in thinner corneas less than 400 μm thick. They found a significant loss of endothelial cells postoperatively but no clinically significant corneal edema. At follow-up, topographic stabilization of ectasia was seen. The authors did not suggest extending CXL to thinner corneas but commented that many keratoconic patients have thin corneas that do not meet standard CXL criteria. Zhang's comments on CXL in thin corneas were general and not specifically in response to this study.

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    In our study we investigated the effect of CXL in thinner corneas, with central pachymetry less than 400 m.

    1 The main conclusions of our study were that in those patients a signicant endothelial cell count loss was evident postoperatively, not related with clinically signicant corneal edema, and that at the last follow-up examination, a topographic stabilization of the ectasia was apparent in our patient series. In our article we did not suggest an extension of the protocol in thinner corneas; we merely commented on the fact that a large percentage of keratoconic and post-LASIK ectasia patients has thin corneas that apparently do not fulll the criteria for the standard CXL procedure.1 Zhang and associates comments on the standard corneal collagen cross-linking procedure for the patient with a thin cornea are not specically addressed as a response to our article and can be considered general comments on the subject of the enhancement of safety when performing the standard CXL procedure.
    GEORGE D. KYMIONIS

    preservatives in glaucoma medications, they mentioned in the article that elevated and exposed blebs can aggravate OSD symptoms. I think this merits more discussion and explanation: McDonald and Brubaker previously suggested tear meniscus and meniscus-induced thinning, and ocular surface irregularities had ectopic meniscus and a thinned meniscus area and resultant staining.2 They reported that tear lm fractured in these thin areas. Also, they predicted that perilimbal elevations such as ltering blebs have secondary tear menisci and adjacent thinning area. I think the ectopic meniscus and thinning area can be demonstrated by video-meniscometer.3,4 Irregularities or redundant tissue on ocular surface can have punctate keratopathy, uorescein staining, and even corneal erosions without ndings of aqueous deciency. Therefore, OSD is caused not only by topical eye drops and their preservatives but also by irregularities or protrusion on ocular surface in glaucoma patients. Frequent instillation of articial tears or elimination of elevated tissue on the ocular surface can increase patients comfort.
    HALIT OGUZ

    Heraklion, Crete, Greece


    CONFLICT OF INTEREST DISCLOSURES: SEE THE ORIGINAL article1 for any disclosures of the authors.

    S anlurfa, Turkey
    CONFLICT OF INTEREST DISCLOSURES: THE AUTHOR HAS completed and submitted the ICMJE Form for Disclosure of Potential Conicts of Interest and none were reported.

    REFERENCES

    1. Kymionis GD, Portaliou DM, Diakonis VF, Kounis GA, Panagopoulou SI, Grentzelos MA. Corneal collagen crosslinking with riboavin and ultraviolet-A irradiation in patients with thin corneas. Am J Ophthalmol 2012;153(1): 24 28. 2. Wollensak G. Crosslinking treatment of progressive keratoconus: new hope. Curr Opin Ophthalmol 2006;17(4):356 360.

    REFERENCES

    Ocular Surface Disease and Quality of Life in Patients With Glaucoma


    EDITOR: I READ WITH INTEREST THE VALUABLE CROSS-SECTIONAL

    1. Skalicky SE, Goldberg I, McCluskey P. Ocular surface disease and quality of life in patients with glaucoma. Am J Ophthalmol 2012;153(1):19. 2. McDonald JE, Brubaker S. Meniscus-induced thinning of tear lms. Am J Ophthalmol 1971;72(1):139 146. 3. Oguz H, Yokoi N, Kinoshita S. The height and radius of the tear meniscus and methods for examining these parameters. Cornea 2000;19(4):497500. 4. Oguz H. Noninvasive tear meniscometry in dry eye patients with Sjgren syndrome. Am J Ophthalmol 2008;145(1):184.

    study performed by Skalicky and associates1 in the January 2012 issue of the Journal. The authors investigated the relationship between ocular surface disease and glaucomarelated quality of life, glaucoma severity, and treatment in patients with open-angle glaucoma. They found that ocular surface disease index (OSDI) scores and the number of patients with ocular surface disease (OSD) increased with increasing glaucoma severity. In addition, OSDI was signicantly correlated with Glaucoma Quality of Life-15 summary score, glaucoma severity, multiple topical glaucoma medications, worse eye mean deviation and pattern standard deviation, use of topical beta blockers, topical carbonic anhydrase inhibitors, daily dose of benzalkonium chloride, and glaucoma ltration surgery. In addition to VOL. 153, NO. 5

    REPLY
    WE THANK PROFESSOR OGUZ FOR COMMENTING ON OUR

    paper.1 While dysesthetic blebs following glaucoma drainage surgery contribute to symptomatic ocular surface disease (OSD), there is little data regarding the specic etiology.2,3 It is likely to be multifactorial. Budenz and associates,2 investigating 97 patients with unilateral trabeculectomy blebs, found that young age, bleb exposure in the interpalpebral ssure, height of the bleb adjacent to the cornea, and bubbles in the tear lm on blinking were predictive of dysesthesia. Only 2 patients had adjacent dellen and 6 an epithelial defect; hence, no signicant results were obtained regarding these proposed mechanisms. Surprisingly, the type of antibrotic agent used 1003

    CORRESPONDENCE

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