Journal List > J Korean Med Sci > v.19(6) > 1019880

Kwon and Kim: Reply
Reply:
We thank Dr. Najjar for his comment. Achievement of significant visual improvement as well as symptomatic relief in the patients with calcific band keratopathy (CBK) by Najjar et al. is valuable (1). We agree with their description of EDTA chelation, when used properly, as a simple, effective and inexpensive treatment for CBK, and that it is used for treatment of corneal calcific lesion, in which calcium impacted superficially and locally. However, we intended to report the severe and complicated case of band keratopathy and to describe the successful operating techniques of EDTA chelation, superficial keratectomy and amniotic membrane transplantation (2). In our two cases, one patient had been diagnosed as band keratopathy accompanied with Vogt-Koyanagi-Harada syndrome, and the other had a band keratopathy accompanied with partial limbal deficiency, endothelial decompensation, and pseudopterygium. The visual acuities of the two patients were very poor with light perception and the other with hand motion perception. The band keratopathy developed 10 and 8 yr ago in two patients, and had been aggravated, respectively. Slit lamp examination revealed that calcium plaque was deposited densely, broadly and deeply in the stroma layer. On the basis of these findings, we considered how we could infiltrate EDTA to the deposited calcium plaque, and decided to trephine the stroma sufficiently to facilitate the infiltration of EDTA solution. We could, therefore, remove the calcified plaque by blunt spatula to permit a clear, smooth surface without any scraping in either case. Our sufficient trephining into the stromal layer allowed EDTA to dissolve into the pathologic potent space between the destroyed stroma by calcium plaque. There could be possibility of toxicity of EDTA to corneal wound healing in a long term application as well as corneal endothelial decompensation.
Regarding the comment on the recurrence time, we agree that the absence of any recurrences in our cases was attributed to the short follow-up period. However, as you reported that the recurrent time ranged from 1 month to 26 yr (mean time of 17.7 yr), the band keratopathy's cause and condition were very various and changeable, and were possibly induced secondarily by other disease. Anderson et al. (3) reported that the return of calcific deposits was noted in four of 16 (25%) eyes at 1.5, 2, 5, and 13 months postoperatively. The recurrence rate was variable according to the reports. It is possible to explain all those recurrence of band keratopathy, but we can only assume that the recurrence of band keratopathy is attributed to the different and various pathologic causes and/or conditions. Therefore, we consider that further research into this issue is required for clarification.
Conclusively, we aspire toward the perfectly treatment for band keratopathy patients and hope to be able to thoroughly investigate more relevant cases regarding the nature and characteristics of this elusive disease.

References

1. Najjar DM, Cohen EJ, Rapuano CJ, Laibson PR. EDTA chelation for calcific band keratopathy: results and long-term follow-up. Am J Ophthalmol. 2004. 137:1056–1064.
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2. Kwon YS, Song YS, Kim JC. New treatment for band keratopathy: superficial lamellar keratectomy, EDTA chelation and amniotic membrane transplantation. J Korean Med Sci. 2004. 19:611–615.
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3. Anderson DF, Prabhasawat P, Alfonso E, Tseng SC. Amniotic membrane transplantation after the primary surgical management of band keratopathy. Cornea. 2001. 20:354–361.
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