Letters to the Editor Author’s reply
Dear Editor: We agree that similarity in concept does indeed exist between our use of a sub-conjunctival perfluoropropane bubble as a spacer, and that of Dr. Luttrull’s novel employment of the gas, albeit in association with a drainage implant. We feel that this only emphasizes the potential benefit this technique can confer over a variety of glaucoma filtering operations. We apologize for the typographical oversight pointed out by Drs. Lai and Lam regarding the number of ‘qualified successes’ in our study—the figures in the main text (4 patients requiring supplementary medication) are correct. The percentages quoted in the introductory paragraph do indeed refer to success, and not failure, rates.
Dear Editor: This tumor invariably masquerades as other more common entities. Their interesting case illustrates the tremendous difficulty with clinical observations. Further, standard biopsies are often insufficient to make a correct histologic diagnosis. The need for wide margins and adequate depth cannot be overemphasized. Unfortunately, the correct diagnosis is often only achieved after one or more recurrences and excisions. In response to their preference for the term microcystic adnexal carcinoma, we feel it is interchangeable with sclerosing sweat duct carcinoma. As discussed in the article, these names have developed from different patterns of differentiation seen in various tumors. Whichever pattern predominates usually dictates the assignment of one or the other title. Our cases generally had prominent desmoplasia and sweat duct differentiation. Finally, as they point out, there are no known risk factors for this tumor. It is quite possible that immunosuppression may contribute to its development or spread. None of our patients were clinically immunosuppressed. We encourage the reporting of individual and small case series in the hopes that possible risk factors may become more apparent as more numbers are reported.
STEVE K.L. SEAH, FRCS, FRCOPHTH Singapore
Sclerosing Sweat Duct Carcinoma of the Eyelid Margin: Unusual Presentation of a Rare Tumor Dear Editor: In the paper by Duffy et al1 they describe 4 cases of primary sclerosing sweat duct carcinoma affecting the lower eyelid margin. The risk factors for this tumor are not yet established. We have seen a similar case2 of a 66-year-old female with microcystic adnexal carcinoma (this is a preferred name for the same tumor) on the medial lower lid. It masqueraded as a benign chalazion until a large incisional biopsy showed the histopathologic diagnosis. Our patient was immunosuppressed following retinal transplantation and this may have played a role in the development of her tumor. The benign clinical appearance of this sweat gland malignancy gives very little indication of its true identity and aggressive behavior. A large incisional biopsy is recommended to provide sufficient tissue for histopathologic evaluation. Low magnification is best to identify the solid nests, strands, and cords of dark or clear staining cells in a sclerotic stoma. Smaller biopsies can result in misdiagnosis. Once there is a histopathologic diagnosis, wide excision with horizontal frozen section control (Mohs’ micrographic surgery) with a wide free margin is recommended. Longterm follow up is essential. JANE M. OLVER, FRCOPHTH J.L. BROOKES London, England References 1. Duffy MT, Harrison W, Sassoon J, Hornblass A. Sclerosing sweat duct carcinoma of the eyelid margin: unusual presentation of a rare tumor. Ophthalmology 1999;106:751– 6. 2. Brookes JL, Bentley C, Verma S, et al. Microcystic adnexal carcinoma masquerading as a chalazion [letter]. Br J Ophthalmol 1998;82:196 –7.
MARK DUFFY, MD, PHD ALBERT HORNBLASS, MD Chicago, IL
Acute Corneal Necrosis after Excimer Laser Keratectomy for Hyperopia Dear Editor: In the paper by Meitz et al (Ophthalmology 1999;106:490 – 6), the authors report a case of acute corneal necrosis with signs of apoptosis after excimer laser treatment of the cornea. The authors speculated that this sort of stromal reaction occurs more frequently than previously thought and that the changes are sometimes misinterpreted as infection. We would like to point out that there are many other points that support this observation that were not discussed in the paper. Excimer laser corneal tissue interaction may initiate free radical formation in the cornea.1 There are three possible sources of free oxygen radical production in the cornea during and after excimer laser photoablation. The first one is Ultraviolet radiation (193 nm UV radiation, UV-C) that occurs during excimer laser treatment. The second is excimer laser induced thermal increase in the corneal tissue during photoablation.1,2 The last one is the accumulation of PMNs to the laser ablated surface.3 Excimer laser treatment also changes the corneal Aldehyde dehydrogenase and Glutathione S transferase activities.4 Free radicals cause tissue damage by reacting with lipid components of the cell membranes, nucleic acids, and sulphur containing enzymes. Recent studies demonstrated that reactive oxygen species induce apoptosis in the cornea and other tissues.5,6,7
Ophthalmology Volume 107, Number 2, February 2000 We congratulate Dr. Mietz for this histopathologic report of a case of acute corneal necrosis with signs of apoptosis. KAMIL BILGIHAN, MD UFUK ADIGUZEL, MD AYSE BILGIHAN, MD FIKRET AKATA, MD BERATI HASANREISOGLU, MD Ankara, Turkey References 1. Bilgihan K, Bilgihan A, Akata F, et al. Excimer laser corneal surgery and free oxygen radicals. Jpn J Ophthalmol 1996;40: 154 –7. 2. Niizuma T, Ito S, Hayashi M, et al. Cooling the cornea to prevent side effects of photorefractive keratectomy. J Refract Corneal Surg 1994;10(Suppl. 2):S262– 6. 3. Hayashi S, Ishimoto S, Wu GS, et al. Oxygen free radical damage in the cornea after excimer laser therapy. Br J Ophthalmol 1997;81:141– 4. 4. Bilgihan K, Bilgihan A, Hasanreisog˘lu B, Tu¨rko¨zkan N. Corneal aldehyde dehydrogenase and glutathione S-transferase activity after excimer laser keratectomy in guinea pigs. Br J Ophthalmol 1998;82:300 –2. 5. Cho KS, Lee EH, Choi JS, Joo CK. Reactive oxygen speciesinduced apoptosis and necrosis in bovine corneal endothelial cells. Invest Ophthalmol Vis Sci 1999;40:911–9. 6. Lenaz G. Role of mitochondria in oxidative stress and ageing. Biochim Biophys Acta 1998;1366:53– 67. 7. Stoian I, Oros A, Moldoveanu E. Apoptosis and free radicals. Biochem Mol Med 1996;59:93–7.
Author’s reply Dear Editor: In our report, we discussed several possible reasons that may have contributed to the tissue damage with subsequent apoptosis we found in that case. We also stated that employing this technique of laser ablation, the energy used by the laser system to correct hyperopia is much higher than the energy and amount of tissue removed to treat myopia. This means that the amount of energy delivered to the tissue is high. In that respect, the point raised by Dr. Bilgihan may very well be important, and it might be speculated that the radical production in the tissue may be excessive. A large increase in temperature is usually not present in the corneal tissue, since we do not see any area of coagulative necrosis. In addition, an accumulation of PMNs is usually not observed after treatment. We believe that what Dr. Bilgihan states may be true and important. Talking to a specialist in Laser Physics, however, we believe that, as stated in the paper, the main issue in this case was the treatment of hyperopia. To treat hyperopia, 10-fold energy is delivered by the laser system to the tissue, as compared with energy used in the treatment of myopia. In our opinion, this may be the most important factor. HOLGER MIETZ, MD Koe¨ln, Germany
Intraocular Lens Power Calculation after Corneal Refractive Surgery Remains Challenging Dear Editor: In the article, “Underestimation of intraocular lens power for cataract surgery after myopic photorefractive keratectomy”, published in Ophthalmology 1999;106:693–702, Dr. Seitz et al found that direct corneal power measurements underestimate corneal flattening after PRK by an average of 24%. When these values are entered into IOL power formulas, theoretically hyperopic shift after cataract surgery will occur. We believe that the authors raised an important issue because the number of refractive surgeries is increasing rapidly, and after 20 or 30 years many of these patients will need cataract surgery. Currently, many cataract surgeons have been using refraction-derived keratometric values instead of the measured keratometric values for IOL power calculation in postoperative radial keratotomy (RK) eyes and PRK eyes to avoid or reduce hyperopic shift after cataract surgery. The challenge still remains. We have several questions for the authors regarding this article. The first question is about the study design. The authors mentioned in the Abstract, and Patients and Methods sections that “this is nonrandomized, prospective study.” However, in the conclusion of the abstract and text the authors stated that “because this study is retrospective and theoretical, there is still need for a large prospective investigation to validate our findings.” Furthermore, we do not feel that a randomized prospective study is practical because it may take many years for the study patients to develop cataracts after PRK surgery, making it be difficult to follow these patients to collect follow-up data. To avoid hyperopia after cataract surgery following PRK, the authors suggested that “the calculation method using spherical equivalent change of refraction at corneal plane seems to be the most appropriate method.” Our question is: if calculated corneal powers (according to spherical equivalent change of refraction at the corneal plane and spectacle plane) are so close in Dr. Seitz’s article (Table 1) and no patient had cataract surgery following PRK, how did the authors know that one method is better than the other? We have experienced clinically that the incidence of unplanned hyperopia after cataract surgery in postoperative PRK eyes can be reduced by using the refraction derivedkeratometric value for IOL power calculation (corneal power calculation according to spherical equivalent change of refraction at the spectacle plane rather than at the corneal plane). In the Result section, the authors stated that “keratometric corneal power overestimation (⌬Kcalc-co) and IOLP underestimation (⌬IOLPH, Kcalc-co) correlated significantly with actual difference between preoperative and postoperative pachymetric corneal thickness (P ⫽ 0.05).” We could not find data in the text, Table, or Figure to support this result. In this article, the authors used calculated keratometric values as a gold standard to predict IOL power calculation. Clinically, the calculated keratometric values are not always