VOL. 78, NO. 5 CORRESPONDENCE 873

lar but actually differ even at the levels examined by electron microscopy in spite of their superficial appearance of similarity (see the legend for Fig. 10).

Congo red or thioflavine-T staining of lesions of granular dystrophy were refer­enced to A. Garner (reference 13), and to M. Ghosh, and W. S. Hunter (reference 14). Congo-red staining of the peripheries of some lesions in typical cases of granular dystrophy did stain positively in our own hands but we preferred to credit this ob­servation to the previous reports.

We agree that filaments, as seen by elec­tron microscopy, are not diagnostic of amy­loid, just as no individual staining method is diagnostic of amyloid.

The formation of the granules in this dystrophy is obviously an extremely slow process as determined by clinical observa­tion. Finding no transition between fila­ments and granules in any individual case would not be surprising. One might specu­late that there is some relationship between the two portions, filamentous and homoge­nous, but only a study that includes time as a factor would be helpful. One method, not available to us, but suggested in our paper, would be to study biopsy specimens of members of a family at different ages, or sequential biopsy specimens as the pa­tient grows older. Our method was to study the newly developing granules in the donor tissue and to compare the granules pro­duced in the single area that underwent re-biopsy, granules which presumably are even younger. From these observations a se­quence of morphologic change was pro­posed.

Finally, the quotation "the looser packing of the macromolecules in a granular dys­trophy suggests a 'younger' stage of the disease process" refers to a comparison of filaments to granules within a single lesion of granular dystrophy alone. Figure 10 compares the lesions of a granular with a typical lattice dystrophy, pointing out their similarities as well as their dissimilarities

which we believe is clearly stated in the legend.

SEYMOUR BROWNSTEIN, M.D. BEN S. F INE, M.D.

MAURICE E. SHERMAN, M.D. LORENZ E. ZIMMERMAN, M.D.

Washington, D.C.

SEVERING SUTURES AFTER CATARACT EXTRACTION

Editor:

I have often found it necessary to sever one or more 10-0 Ethilon sutures to re­duce postcataract extraction astigmatism. During the past several months I have found this can be done with little discom­fort to the patient and without incising the conjunctiva by using the argon laser. A 100-(A spot of approximately 300 mW at 0.1 second time directed to the suture on its scleral side as near to the knot as pos­sible will usually cause immediate separa­tion of the suture.

If the suture is visible with a slit lamp, it is easily severed with the laser, but if there is some slight edema or thick Tenon's membrane, a slight pressure on the conjunc­tiva near the suture will usually make the knot more visible to the laser light. For safety, the 100-fx spot is used with the pupil undilated and the patient looking slightly down and away from the suture. I have had no complications to date and have performed this on more than ten pa­tients.

KENNETH J. FAUST, M.D. Leesburg, Florida

PHOTOCOAGULATION AND RUBEOSIS IRIDIS

Editor:

Pan-retinal-photocoagulation has been re­ported to induce regression of retinal neo-vascularization,1 and indeed is practiced by many ophthalmologists in treating prolifera-tive diabetic retinopathy. Regression of co-existant rubeosis iridis has also been re­ported,2 though descriptions of pre- and

874 AMERICAN JOURNAL OF OPHTHALMOLOGY NOVEMBER, 1974

posttreatment neovascularization and changes in intraocular pressure were not indicated.

Utilizing pan-ret in al-photocoagulation (1045 argon laser burns) we recently treated and successfully caused involution of pre-retinal and disk neovascularization in a pa­tient who had had occlusion of the central retinal vein. Prominent neovascularization of the angle also regressed and the intraocular pressure fell from a preoperative level of 32 to 16 mm Hg postoperatively. The pressure has remained stable in the normal range for three months.

We suggest that perhaps this mode of therapy shows promise in the prevention of the disastrous complications of neovascular glaucoma.

MICHAEL A. CALLAHAN, M.D. GEORGE F. HILTON, M.D. San Francisco, California

REFERENCES

1. Beetham, W. P., Aeillo, L. M., Balodimos, M. C, and Konez, L.: Ruby laser photocoagula-tion of early diabetic neovascular retinopathy. Arch.. Ophthalmol. 83:261, 1970.

2. Krill, E., Archer, D., and Newell, E.: Photo-coagulation in complications secondary to branch vein occlusion. Arch. Ophthalmol. 85 :48, 1971.

BROWNING OF THE LENS IN GENERALIZED ALBINISM

Editor:

In his article, "Browning of the lens in generalized albinism" (Am. J. Ophthalmol. 77:819, 1974), Dr. Marvin Sears described a case of brunescent cataract in a patient with generalized albinism. He emphasized that in this case the brunescence could not have been caused by the action of tyrosinase. This is a crucial point in developing a the­ory of brunescent cataracts for if tyrosinase and tyrosine are not involved we must look elsewhere for an explanation. Gomyo and Fujimaki1 have shown that photooxidation of the tryptophan moity of a protein, lyso-zyme, results in increasing color and de­creasing solubility. There is also some data indicating that photooxidation of trypto­

phan is a precursor to brunescent cataract.2'3

This is consistent with other research that one of the oxidation products of tryptophan, 3-hydroxykynurenine, absorbs in the blue region (giving a brown color to the lens) and also is insoluble when linked to a lens protein.4'5 The photooxidation of tryptophan (and possibly other amino acids) in the lens probably occurs from chronic expo­sure to ultraviolet light.2-6 However, what is unexplained and hard to reconcile with this interpretation is the presence of a brunes­cent cataract in an albino. Since exposure to the levels of ultraviolet light over a pe­riod of time sufficient to produce a brunes­cent cataract would be extremely uncom­fortable to an albino, we must suppose that Dr. Sears' patient had some outdoor occu­pation or there was some special photo-sensitizer in his lens either by diet or by heredity. Possibly any further cases of brunescent lenses in albinos could be tested for tryptophan breakdown products as well as tyrosinase activity. Indeed, the rareness of brunescent cataracts in albinos may be because they are photophobic rather than their lack of tyrosinase.

M. L. WOLBARSHT, P H . D . B. S. YAMANASHI, P H . D .

Durham, North Carolina

REFERENCES

1. Gomyo, T., and Fujimaki, M.: Studies on changes of protein by dye sensitized photooxida­tion. 3. On the photodecomposition products of lysozyme. Agr. Biol. Chem. 34:302, 1970.

2. Zigman, S., Schultz, J., and Yulo, T.: Possi­ble roles of near UV light in the cataractous process. Exp. Eye Res. 15:201,1973.

3. Kurzel, R. B., Wolbarsht, M., Yamanashi, B. S., Staton, G. W., and Borkman, R. F.: Tryp­tophan excited states and cataracts in the human lens. Nature 241:132, 1973.

4. Kurzel, R. B., Wolbarsht, M. L., and Yama­nashi, B. S.: Spectral studies on normal and cataractous intact human lenses. Exp. Eye Res. 17:76, 1973.

5. Pirie, A.: Color and solubility of the proteins of human cataracts. Invest. Ophthalmol. 7:634, 1968.

6. : Formation of N'-formylkynurenine in proteins from lens and other sources by ex­posure to light. Biochem. J. 125:203, 1971.