VOL. 93, NO. 5 CORRESPONDENCE 663

tion," by J . F. Weiss and M. Belkin (Am. J . Ophthalmol. 92:625, 1982), comple-ments material my associates and I re-ported in 19801 regarding the effect of penicillamine on the solubility of vitreous collagen. Using control animals and ani-mals treated with 0.5 mg/day of penicilla-mine and measuring soluble and insolu-ble vitreous collagen, we found that 47% of the vitreous collagen became soluble after treatment with penicillamine com-pared with 6% in the control group.

These findings were similar to those presented by Moorhead and associates2

regarding the effect of aminopropri-onitrile on conjunctival scarring by inhi-bition of collagen cross-linking. Beta-minoproprionitrile has an effect on collagen cross-linking similar to that of penicillamine, but we were unable to obtain significant results on vitreous col-lagen with this substance.

A. RAYMOND PILKERTON, M.D.

Washington, D.C.

REFERENCES

1. Brancato, L. J . , Lukac, J. , Pilkerton, A. R., and Rao, N. A. : Effect of d-rjerncillamine on solubili-ty of vitreous collagen. ARVO Abstracts. Supplement to Invest. Ophthalmol. Vis. Sei. St. Louis, C. V. Mosby, 1980, p. 46.

2. Moorhead, L. C , Patsalos, P. N., Steglich, M. C , Brockman, D., and Wiggins, R. C : The treatment of conjunctival scarring by inhibition of collagen crosslinking, abstract. Ophthalmology 87:121, 1980.

Reply

Editor: I thank Dr. Pilkerton for drawing at-

tention to those who preceded us in their interest in the use of penicillamine in ophthalmology. There are many exciting potential uses for agents that can control fibrosis and collagen formation, and I hope that our study will stimulate further research along these lines. Drs. Pilkerton

and Moorhead deserve commendation for their pioneering efforts in this area.

JOSEPH F. WEISS , M.D.

Memphis, Tennessee

Choyée VIII Intraocular Lens

Editor: In the article, "A histopathologic study

of the Choyce VIII intraocular lens," by R. J . Olson, D. Sevel, and D. Stevenson (Am. J . Ophthalmol. 92:781, 1981), I noted that the implant used on the sec-ond eye was too short and had to be changed. The implant was found to be 12 |xm and not 12.5 u,m as had been thought at the time of the first operation. Manufacturers' quality control is superior to the standards of a few years ago, but here was one mistake that could have been avoided if the implant length had been checked before use. Fortunately, no harm was done to the eye by the ex-change procedure.

The most valuable aspect of the article was the pathologic findings and it was reassuring to find that:

The micropathologic findings in the two eyes we studied suggested that with time a lens of the proper length would actually move away from the corneal endothelium. With this kind of stability, contact between the intraocular lens and the corneal endo-thelium would be unlikely except in instances of severe trauma or with a flexible anterior chamber lens.

My own clinical and pathologic experi-ence confirms this statement.

Unfortunately, a significant proportion of Mark VIII intraocular lens implanta-tions result in some degree of iris tuck. This iris tuck should not be confused with the slight overall effect on the pupil along the long axis of the implant that indicates the implant was slightly too long (0.3 to 0.4 mm). The tucking is basically the result of poor surgical technique and has been considerably reduced in recent

664 AMERICAN JOURNAL OF OPHTHALMOLOGY MAY, 1982

years by the use of the following: (1) the Mark IX implant which, because of its considerably reduced dimensions, is much easier to insert but as stable as the Mark VIII; (2) acetylcholine chloride (Miochol) to minimize and centralize the pupil before implantation; and (3) sodium hyaluronate (Healon) to create the anteri-or chamber if air is not retained. Even if air is readily retained, lubricating the distal foot plates with sodium hyaluronate reduces still further the likelihood of iris tuck. However, even when iris tuck does occur, the effect is more cosmetic than functional, although the surgeon's pride is likely to be hurt.

Finally, Olson, Sevel, and Stevenson mention the possibility (based on their micropathologic findings) of late hemor-rhage caused by uveal erosion. This pos-sibility no longer bothers me because in my observations of approximately 2,000 Mark VIII implants (inserted since 1963) and 650 Mark IX implants (first used four years ago), there have been no instances of this late complication other than those resulting from direct trauma severe enough to rupture the globe in some cases.

D. P. CHOYCE, M.S., F.R.C.S. London, England

Reply

Editor: We thank Dr. Choyce for his comments

and are pleased to learn that in his experi-ence late hemorrhage resulting from uveal erosion is not a problem. The histo-pathologic findings certainly suggested that this might be a concern, which is the reason we raised this issue. Dr. Steven-son's experience with more than 1,000 Choyce Mark VIII anterior chamber in-traocular lens implantations also indicates

that early or late hemorrhage is not a problem.

RANDALL J. OLSON, M.D.

Salt Lake City, Utah DAVID SEVEL, M.D.

DARA STEVENSON, M.D.

San Diego, California

Chloramphenicol and Aplastic Anemia

Editor: Although I agree with the statement by

M. P. Dutro in his Letter to the Editor, "Chloramphenicol and aplastic anemia" (Am. J . Ophthalmol. 92:870, 1981), that the risk-benefit ratio of a drug must be carefully considered before administra-tion and, more specifically, that the least toxic drug is indicated when it is equally effective, I do not believe that the danger of aplastic anemia following topical chlo-ramphenicol therapy is as great as he suggested.

A review of the three cases1"3 cited as evidence for chloramphenicol-associated aplastic anemia following ocular therapy disclosed that this association is not only rare, but invariably includes many other factors that may have been contributory.

For example, Abrams, Degnan, and Vinciguerra1 reported a fatal case of mar-row aplasia following topical application of chloramphenicol ointment. However, the patient had abnormal findings on liver function tests performed at the time of admission to the hospital. This may have been significant in that aplastic ane-mia following hepatitis is well known.4,5

Additionally, other antimicrobials (poly-myxin B and tetracycline) had been taken by the patient. Although neither of these agents has been implicated as a causal agent in aplastic anemia, they may have contributed to this unusual reaction. Fi-nally, the patient had features of the reversible, dose-related form of chloram-phenicol toxicity (reticulocytopenia and