Management of posterior segment IOFBs

Letters to the Editor shaped epithelial cells and fibrous tissue confirmed as collagen by their special stains. However, there seems to be a notable absence of epithelial cells at the base of the pyramidal opacity in the example presented, and only an extremely thin lens capsule separates the pyramidal cataract from the anterior cortical lens fibers. This is at variance with their narrative in the Results section, which suggests normal lens epithelium and capsule are present in this area. The authors question why some of these lesions take a peculiar pyramidal shape and why this type cataract develops progressive cortical changes. The pyramidal shape may simply be the natural morphology when a critical mass of tissue with the contractile properties of collagen becomes sequestered in this fashion. The progressive evolution of the cortical cataract can be explained by the absence of cuboidal lens epithelium at the base of the pyramidal lesion, which is necessary to maintain the viability of the adjacent cortical fibers. My second concern is the result of using a textbook chapter2 rather than an original citation as a reference to define the baseline histology of anterior polar cataract. Unfortunately, the brief textbook description of the histology of this lesion is incomplete and misleading. For example, the textbook never once mentions the word collagen or acknowledges that fibrous tissue is a component. Rather, it emphasizes the point that lens epithelium does not undergo fibrous metaplasia as suggested by Henkind,3 a point that, although correct, distracts from the discussion. As a result, the importance of fibrosis in this lesion is lost and may have been overlooked by Wheeler et al.1 Font and Brownstein4 have shown by electron microscopy that although the lens epithelium in polar cataracts may superficially resemble fibrous tissue and produce collagen, the altered hyperplastic cells retain some anatomic features not characteristic of true fibrocytes. Nevertheless, collagen is present and presumably being produced by these altered epithelial cells. It is reasonable to assume this collagen has similar behavior to that produced by fibrocytes. The lesions studied by Font and Brownstein were apparently nonprogressive and also demonstrated anatomically normal appearing lens epithelium between the capsule and anterior cortex at the base of the polar lesions. Notwithstanding the statement in the article, I do not believe this kind of epithelium is confirmed in this pyramidal cataract, and its absence might account for the progressive nature of this lesion. I do not intend for these comments to in any way to detract from this fine research effort, which I believe is a definite enhancement of our understanding of this interesting problem. GERALD R. CHRISTENSEN, MD Omaha, Nebraska References 1. Wheeler DT, Mullaney PD, Awad A, Zwaan J. Pyramidal anterior polar cataracts. Ophthalmology 1999;106:2362–7. 2. Worgul BV. Lens. In: Tasman W, Jaeger EA, eds. Duane’s Foundations of Clinical Ophthalmology, rev. ed. Philadelphia: Lippincott Williams & Wilkins, 1998; vol. 1, chap. 15. 3. Henkind P, Prose P. Anterior polar cataract. Electron-micro-

scopic evidence of collagen. Am J Ophthalmol 1967;63:768 – 71. 4. Font RL, Brownstein S, A light and electron microscopic study of anterior subcapsular cataracts. Am J Ophthalmol 1974;78: 972– 84.

Author’s reply Dear Editor: The pathogenic mechanism(s) underlying the progressive nature of this unique form of anterior polar cataract remain uncertain. Dr. Christensen’s suggestion that this behavior is the result of a loss of cuboidal epithelium at the base of the pyramidal lesion is an equally valid interpretation of the histologic evidence presented in the article. It is our opinion that there were no differences in histologic findings between pyramidal and flat anterior polar cataracts, although the photomicrographs presented in the article do not fully illustrate this fact. Nevertheless, the concept that lens epithelial cell dysfunction is involved in pyramidal cataract formation and progressive cortical opacification is logically sound and entirely plausible. The authors also agree that the textbook reference cited in our discussion of anterior polar cataract histology may not have been ideally chosen, and we appreciate Dr. Christensen bringing an additional article to our attention and to that of the readers of Ophthalmology. DAVID T. WHEELER, MD Portland, Oregon PAUL B. MULLANEY, FRCOPHTH, FRCS(I) Sligo, Ireland ABDULAZIZ AWAD, MD Riyadh, Saudia Arabia JOHAN ZWAAN, MD, PHD San Antonio, Texas

Management of Posterior Segment IOFBs Dear Editor: In the guest editorial, “Posterior Segment Intraocular Foreign Bodies: Management in the Vitrectomy Era” (Ophthalmology 2000;107:821–2), the authors state that, “For decades, plain x-ray films were the only method for detecting invisible intraocular foreign bodies (IOFBs).” In fact, there were methods to pinpoint and gently remove foreign bodies decades before the widespread use of computed tomography (CT). The Sweet x-ray localization and even the four-point Comberg contact shell made exact localization possible. As a young resident physician in Cologne, I recall that Prof. Neubauer perfectly localized IOFBs with x-ray picture enhancement in the mid 1970s. In several cases, he was able to remove them with good functional results. In other cases, Dr. Heimann operated consecutive endophthalmitis with the newly learned vitrectomy. It was fascinating to see the tension between Dr. Neubauer’s sophisticated but old method and, at that time, the complex but revolutionary vitrectomy. The CT and vitrectomy have truly opened a new chapter in the handling of IOFB, but for the expert, good localization methods other than x-ray film existed for a long time. ZOLTAN SZIGETI, MD Budapest, Hungary

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