- Email: [email protected]
Extended-Wear Contact Lenses After Corneal Grafts: Reply
119
CORRESPONDENCE
VOL. 91, NO. 1
2. Yannuzzi, L. A., Gitter, K. A., and Schatz, H. : The Macula. A Comprehensive Text and Atlas. New York, Williams and Wilkins, 1979, pp. 134-142. 3. Gass, J. D. M.: Lamellar macular hole. A complication of cystoid macular edema after cataract extraction. A clinicopathologic case report. Trans. Am. Ophthalmol. Soc. 73:231, 1975. 4. Appen, R. E., de Venecia, G., and Ferwerda, J.: Optic disk vasculitis. Am. J. Ophthalmol. 90:352, 1980.
Reply We appreciate Dr. Schatz bringing a point of semantics to our attention. The anomalous vessels we described appear to be collateral vessels which function to shunt (verb) or divert blood to an alter nate route. We propose that this shunting is via anomalous optic disk capillaries that serve as collaterals. Our findings concur with Dr. Schatz's observation that cystoid maculopathy is a major cause of decreased visual acuity in young individuals with occlusion of the central retinal vein. Our retrospective study involved a relatively small number of patients who were not managed by a definitive treatment protocol. We were unable to provide statistical conclusions about final visual acuity with respect to the use of warfarin, corticosteroids, or o t h e r agents. A controlled d o u b l e masked prospective study is needed to confirm Dr. Schatz's observation that sys temic corticosteroids lessen the severity of cystoid maculopathy associated with occlu sion of the central retinal vein. IRA A. PRILUCK, D E N N I S M. ROBERTSON, ROBERT W. H O L L E N H O R S T ,
Rochester,
M.D. M.D. M.D.
Minnesota
Extended-Wear Contact Lenses After Corneal Grafts Editor: In his article, "The effect of extendedwear aphakic hydrophilic contact lenses
after penetrating keratoplasty" (Am. J. Ophthalmol. 90:331, 1980), M. A. Lemp elucidated a significant problem that should be given serious consideration. Six aphakic keratoplasty patients whom I fitted with hydrophilic contact lenses (Hydrocurve 11-55) at various intervals after keratoplasty developed superficial vascularization of the cornea and mild stromal edema. One patient spontane ously developed an endothelial graft re jection; another patient developed a small Staphylococcus aureus corneal ul cer and the inflammation touched off an endothelial graft rejection. In 90 patients with simple surgical aphakia whom I fitted with extendedwear Hydrocurve 11-55 and Hydrocurve II contact lenses there was less vascular ization and stromal edema than in these post-keratoplasty patients. The grafted cornea appears to respond poorly to extended-wear hydrophilic con tact lenses and I strongly agree with Dr. Lemp that "alternative methods of cor recting visual acuity be considered in patients with aphakia who have received corneal grafts." J O H N J. P U R C E L L , J R . ,
St. Louis,
M.D.
Missouri
Reply Editor: I was very interested in Dr. Purcell's letter relating problems he experienced in post-keratoplasty patients fitted with extended-wear hydrophilic lenses. This confirmation of my finding further strengthens the caution which I urged for clinicians in fitting extended-wear lenses in patients with grafts. It should be remembered that currently available extended-wear lenses with a high water content, that is, 70% to 80%, can provide minimal oxygen requirements for normal corneal epithelium. Contact lenses
120
AMERICAN JOURNAL OF OPHTHALMOLOGY
with a lower water content, that is, 55% (such as those fitted by Dr. Purcell) would be expected to provide even less oxygen. These lenses do not allow for ideal oxygen conditions for the corneal epithelium but merely minimal needs in the normal cor nea. The grafted cornea probably has a different metabolism with different oxygen needs. Moreover, there is relatively little exchange of tears beneath a hydrophilic contact lens. This suggests that a possible build-up of metabolic products beneath the lens may further add to corneal damage in these patients. My thanks to Dr. Purcell for sharing his experiences with us. M I C H A E L A . LEMP,
Washington,
JANUARY, 1981
developing proliferative retinopathy was 1.3 in HLA-B15-positive and 2.6 in HLADR4-positive diabetic patients. Detailed results of this study are in press. 2 JÖRG BERTRAMS,
Essen, West
M A N F R E D SPITZNAS,
Los Angeles,
M.D.
Germany M.D.
California
REFERENCES 1. Bertrams, J., and Spitznas, M.: Association between malignant diabetic retinopathy and HLADRw4, abstract. Excerpta Med., 1979, No. 481, p. 22. 2. Bertrams, J., Dewald, G., Spitznas, M., and Rittner, C : HLA-A,B,C,DR,Bf and C2 alleles in insulin dependent diabetes mellitus with prolifera tive retinopathy. Immunobiology, In press.
M.D.
D.C.
HLA Antigens in Diabetic Retinopathy Editor: We were most interested in the excel lent study, "Histocompatibility antigen frequencies in diabetic retinopathy" (Am. J. Ophthalmol. 90:148, 1980), by J. Barbosa, R. C. Ramsay, W. H. Knobloch, H. L. Cantrill, H. Noreen, R. King, and E. Yunis. Their main observa tion was a significant positive association between HLA-B15 and proliferative dia betic retinopathy. We reported identical findings at the Tenth Congress of the International Diabetes Federation in 1979. x In addition to the HLA-A, -B and -C antigens, we tested the HRL-DR determinants, which are known to be primarily associated with insulin-dependent diabetes. Both under normal conditions and in type I diabetes, HLA-DR4 is genetically linked to HLAB15. In contrast to patients with nonproliferative retinopathy, however, patients with proliferative diabetic retinopathy had a stronger association with HLA-DR4 than with HLA-B15. The relative risk for
Reply Editor: We are glad that Drs. Bertrams and Spitznas found an association between proliferative retinopathy and HLA anti gen, a result compatible with our find ings. Schernthaner and associates 1 have also reported an association between HLA-DR4 and proliferative retinopathy. These independent confirmations make sampling bias less likely. Thus, three independent groups have now shown data suggesting a genetic contribution to severe retinopathy. Since the relative risks mentioned by Bertrams and Spitznas are low, it would be interesting to know if stratification of their patients in a way similar to that we performed would increase the strength of the association as it did in our study. As we have mentioned previously, 2 several published reports suggest a higher fre quency of HLA-B15 in patients with proliferative retinopathy, but failure to stratify patients by age at diagnosis may have led to the inability to detect an association. JOSE BARBERA, R O B E R T C. RAMSAY,
Minneapolis,
M.D. M.D.
Minnesota
CORRESPONDENCE
VOL. 91, NO. 1
2. Yannuzzi, L. A., Gitter, K. A., and Schatz, H. : The Macula. A Comprehensive Text and Atlas. New York, Williams and Wilkins, 1979, pp. 134-142. 3. Gass, J. D. M.: Lamellar macular hole. A complication of cystoid macular edema after cataract extraction. A clinicopathologic case report. Trans. Am. Ophthalmol. Soc. 73:231, 1975. 4. Appen, R. E., de Venecia, G., and Ferwerda, J.: Optic disk vasculitis. Am. J. Ophthalmol. 90:352, 1980.
Reply We appreciate Dr. Schatz bringing a point of semantics to our attention. The anomalous vessels we described appear to be collateral vessels which function to shunt (verb) or divert blood to an alter nate route. We propose that this shunting is via anomalous optic disk capillaries that serve as collaterals. Our findings concur with Dr. Schatz's observation that cystoid maculopathy is a major cause of decreased visual acuity in young individuals with occlusion of the central retinal vein. Our retrospective study involved a relatively small number of patients who were not managed by a definitive treatment protocol. We were unable to provide statistical conclusions about final visual acuity with respect to the use of warfarin, corticosteroids, or o t h e r agents. A controlled d o u b l e masked prospective study is needed to confirm Dr. Schatz's observation that sys temic corticosteroids lessen the severity of cystoid maculopathy associated with occlu sion of the central retinal vein. IRA A. PRILUCK, D E N N I S M. ROBERTSON, ROBERT W. H O L L E N H O R S T ,
Rochester,
M.D. M.D. M.D.
Minnesota
Extended-Wear Contact Lenses After Corneal Grafts Editor: In his article, "The effect of extendedwear aphakic hydrophilic contact lenses
after penetrating keratoplasty" (Am. J. Ophthalmol. 90:331, 1980), M. A. Lemp elucidated a significant problem that should be given serious consideration. Six aphakic keratoplasty patients whom I fitted with hydrophilic contact lenses (Hydrocurve 11-55) at various intervals after keratoplasty developed superficial vascularization of the cornea and mild stromal edema. One patient spontane ously developed an endothelial graft re jection; another patient developed a small Staphylococcus aureus corneal ul cer and the inflammation touched off an endothelial graft rejection. In 90 patients with simple surgical aphakia whom I fitted with extendedwear Hydrocurve 11-55 and Hydrocurve II contact lenses there was less vascular ization and stromal edema than in these post-keratoplasty patients. The grafted cornea appears to respond poorly to extended-wear hydrophilic con tact lenses and I strongly agree with Dr. Lemp that "alternative methods of cor recting visual acuity be considered in patients with aphakia who have received corneal grafts." J O H N J. P U R C E L L , J R . ,
St. Louis,
M.D.
Missouri
Reply Editor: I was very interested in Dr. Purcell's letter relating problems he experienced in post-keratoplasty patients fitted with extended-wear hydrophilic lenses. This confirmation of my finding further strengthens the caution which I urged for clinicians in fitting extended-wear lenses in patients with grafts. It should be remembered that currently available extended-wear lenses with a high water content, that is, 70% to 80%, can provide minimal oxygen requirements for normal corneal epithelium. Contact lenses
120
AMERICAN JOURNAL OF OPHTHALMOLOGY
with a lower water content, that is, 55% (such as those fitted by Dr. Purcell) would be expected to provide even less oxygen. These lenses do not allow for ideal oxygen conditions for the corneal epithelium but merely minimal needs in the normal cor nea. The grafted cornea probably has a different metabolism with different oxygen needs. Moreover, there is relatively little exchange of tears beneath a hydrophilic contact lens. This suggests that a possible build-up of metabolic products beneath the lens may further add to corneal damage in these patients. My thanks to Dr. Purcell for sharing his experiences with us. M I C H A E L A . LEMP,
Washington,
JANUARY, 1981
developing proliferative retinopathy was 1.3 in HLA-B15-positive and 2.6 in HLADR4-positive diabetic patients. Detailed results of this study are in press. 2 JÖRG BERTRAMS,
Essen, West
M A N F R E D SPITZNAS,
Los Angeles,
M.D.
Germany M.D.
California
REFERENCES 1. Bertrams, J., and Spitznas, M.: Association between malignant diabetic retinopathy and HLADRw4, abstract. Excerpta Med., 1979, No. 481, p. 22. 2. Bertrams, J., Dewald, G., Spitznas, M., and Rittner, C : HLA-A,B,C,DR,Bf and C2 alleles in insulin dependent diabetes mellitus with prolifera tive retinopathy. Immunobiology, In press.
M.D.
D.C.
HLA Antigens in Diabetic Retinopathy Editor: We were most interested in the excel lent study, "Histocompatibility antigen frequencies in diabetic retinopathy" (Am. J. Ophthalmol. 90:148, 1980), by J. Barbosa, R. C. Ramsay, W. H. Knobloch, H. L. Cantrill, H. Noreen, R. King, and E. Yunis. Their main observa tion was a significant positive association between HLA-B15 and proliferative dia betic retinopathy. We reported identical findings at the Tenth Congress of the International Diabetes Federation in 1979. x In addition to the HLA-A, -B and -C antigens, we tested the HRL-DR determinants, which are known to be primarily associated with insulin-dependent diabetes. Both under normal conditions and in type I diabetes, HLA-DR4 is genetically linked to HLAB15. In contrast to patients with nonproliferative retinopathy, however, patients with proliferative diabetic retinopathy had a stronger association with HLA-DR4 than with HLA-B15. The relative risk for
Reply Editor: We are glad that Drs. Bertrams and Spitznas found an association between proliferative retinopathy and HLA anti gen, a result compatible with our find ings. Schernthaner and associates 1 have also reported an association between HLA-DR4 and proliferative retinopathy. These independent confirmations make sampling bias less likely. Thus, three independent groups have now shown data suggesting a genetic contribution to severe retinopathy. Since the relative risks mentioned by Bertrams and Spitznas are low, it would be interesting to know if stratification of their patients in a way similar to that we performed would increase the strength of the association as it did in our study. As we have mentioned previously, 2 several published reports suggest a higher fre quency of HLA-B15 in patients with proliferative retinopathy, but failure to stratify patients by age at diagnosis may have led to the inability to detect an association. JOSE BARBERA, R O B E R T C. RAMSAY,
Minneapolis,
M.D. M.D.
Minnesota