Indian Journal of Ophthalmology

: 1989  |  Volume : 37  |  Issue : 3  |  Page : 127--133

Topical sulindac therapy in diabetic senile cataracts : cataract IV

YR Sharma, RB Vajpayee, R Bhatnagar, Madan Mohan, RV Azad, Mukesh Kumar, Ram Nath 
 Dr. R. P. Centre for Ophthalmic Sciences, All India Institute for Medical Sciences, Ansari Nagar, New Delhi - 110 029, India

Correspondence Address:
Y R Sharma
Dr. R. P. Centre for Ophthalmic Sciences, All India Institute for Medical Sciences, Ansari Nagar, New Delhi - 110 029


Sulindac, a non-steroidal anti-inflammatory drug has been found to be a potent inhibitor of enzyme aldose reductase. We used sulindac topically in diabetic senile cataract patients to note if it effects the progression of cataracts. More of sulindac treated eyes maintained initial vision and fewer eyes had visual loss of up to two lines or more as compared to control eyes. The extent and density of different opacities showed less progression in sulindac treated eyes but it was not statistically significant except that the ophthalmoscopically observed density of opacity showed statistically very significant lesser mean increase in sulindac treated eyes. We suggest that sulindac is a potential drug which should be further evaluated in large double blind photodocumented studies in diabetic senile cataracts.

How to cite this article:
Sharma Y R, Vajpayee R B, Bhatnagar R, Mohan M, Azad R V, Kumar M, Nath R. Topical sulindac therapy in diabetic senile cataracts : cataract IV.Indian J Ophthalmol 1989;37:127-133

How to cite this URL:
Sharma Y R, Vajpayee R B, Bhatnagar R, Mohan M, Azad R V, Kumar M, Nath R. Topical sulindac therapy in diabetic senile cataracts : cataract IV. Indian J Ophthalmol [serial online] 1989 [cited 2021 Jun 18 ];37:127-133
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Senile cataracts are more common in diabetes mellitus, occur earlier and the progression is faster than in the non-diabetic population [1],[2],[3]. Pivotal role of polyol path­way in sugar cataracts in animals has been established and thus inducted cataracts can be slowed down and prevented with the use of aldose reductase inhibitors [4],[5],[6]. The role of the polyol pathway in human diabetic cataracts has been speculated [3]. Elevated sorbitol levels have been reported in human senile cataracts in diabetic patients [7]. Aqueous humour glucose levels are elevated and could possibly exert an osmotic stress through glucose conversion to sorbitol mediated by the enzyme aldose reductase [8]. Elevated blood glucose levels have been reported in non-diabetic senile cataracts. [9] Sulindac, a nonsteroidal antiinflammatory drug, has been de­scribed as a potent aldose reductase inhibitor. [10] Sulindacs in vitro and in-vivo efficacy has been demonstrated [11],[12],[13] Sorbinil, another potent aldose reductase inhibitor penetrates the lens after topical application. [14] Indometha­cin which like sulindac is a non-steroidal anti-inflam­matory drug and belongs to the same group has been recovered from the aqueous humour for upto six hours after topical application. [15] Topical sulindac penetrates the cornea after topical application and is recoverable from the lens. [16] We used topical sulindac in medical treatment of senile cataracts in diabetic population and reported herein are the results.


Patients seen in the cataract cell with known history of diabetes and who consented to participate in the pro­gramme were eligible to enter the study. Most of these patients were controlled by diet and oral anti-diabetic agents; few were also on insulin treatment. Control of diabetes was not a factor for inclusion in the study since the contralateral eye was used as control. Patients who had diabetic retinopathy of any grade were ex­cluded. The eye judged to have more advanced cataract was put on topical 1 percent sulindac drops qid and placebo drops were prescribed qid for the fellow eye. Sulindac was dissolved in phosphate buffer 0.05M, Ph 8.00. Because sulindac drops were yellow in colour and placebo drops were colourless the vials used were not labeled. The patient was asked to use the "yellow" eye drops in eye having more advanced cataract and col­ourless drops for fellow eye. The methodology and ex­amination procedures have been described previously. [17],[18],[19] Patients were followed up at one month intervals and initially a follow up of two years was planned. 50 patients were included in the study.


Large drop out rate encountered in our studies on medical therapy of cataract was even more marked in the dia­betic group. Of fifty patients, none completed even one year's follow up. Maximum follow up obtained was 9 months. Only 21 out of 50 patients completed a follow up of at least 3 months (5.42+2.01, m+SD). Data on 21 patients who were followed up for 3 months or more was analysed [Table 1]. Very few patients had pure cataracts. Most were of the mixed type. The distribu­tion of cortical and PSC opacities was similar in both group of eyes initially and at final follow up, but in control eyes 11(52.38%) had nuclear cataracts initially and at completion of follow up 16 eyes (76.19%) had them while in sulindac treated eyes, the number of nu­clear cataracts remained same (16=76.19%; [Table 2] p 0.05).

Of 21 control eyes, only 2 maintained the same vision while in sulindac treated eyes 13 of 21 eyes maintained the same vision (P0.05; Tale 5 and [Table 6]). The increase in nuclear opacity density showed no difference in the two groups but mean increase in extent of nuclear opacity was greater in control eyes as compared to sulindac treated eyes but again difference was not statis­tically significant (P > 0.05; [Table 7] & [Table 8]). The difference in mean increase in extent of density of PSC was also not statistically significant though the mean increase in PSC density was greater in sulindac treated eyes. (P > 0.05; [Table 9][Table 10]. The mean increase in ophthalmoscopically observed opacity was similar in two groups but ophthalmoscopically observed density showed a considerably greater increase in control eyes (P [18] None of the 50 patients put on topical sulindac completed the planned two years fol­low up. Maximum follow up obtained was nine months and only 21 patients completed follow up of at last three months. Perhaps greater preoccupation with the dia­betic state accounts for this. The visual status remained better in sulindac treated eyes. a significantly greater number of sulindac treated eyes maintained the initial vision. 19 eyes in the control group had loss of upto two lines or more while in sulindac group only 8 eyes had loss of upto 2 lines or more. Only 2 control eyes main­tained the initial vision. The percentage distribution of cortical and PSC opacities was similar in the two groups, but no eye on sulindac developed nuclear opacity den­ova. This happened in five eyes in control group. Mean increase in percentage visual acuity loss was considera­bly more in control eyes ( p 0.05). Interestingly ophthalmoscopically observed extent of opacity showed approximately similar mean increase bu t sulindac treated eyes showed very significant less mean increase in ophthalmoscopically observed opacity density (p 20 and its membrane stabilising properties."' The reversibility of retinal capillary leak­age in early diabetic retinopathy by use of systemic sulindac has been reported.[22] Sulindac is the only potent aldose reductase inhibitor which is currently clinical use.


We thank Dr. D.E. Duggan of Merck Sharp and Dohme, West Point, Philadelphia for kindly supplying us Sulindac. We gratefully acknowledge, our thanks to ICMR India for partly supporting this study. During part of this study, Dr. Y.R. Sharma was appointed under the supernumerary research cadre scheme at Dr. R.P. Centre. We thank all the residents who referred their cases to the cataract cell[22].


1Caird Fl,Hutchinson M,Pirie A.Cataract and Diabse­tes. Br Med 1 1964; 12:665-668.
2Ederer F, Hitler R, Taylor HR. Senile lens changes and diabetes in two population studies. Am J Oph­thalmol 1981; 91:361-395.
3Caird Fl, Pine A, Rarrasell TG. Diabetes and the eye. Oxford and Edinburgh. Blackwell Scientific Publica­tions, 1969.
4Kinoshita JH. Mechanisms initiating catarct forma­tion. Invest ophthaimol vis Sci 1974; 13: 713-724.
5Kinoshita JH, Kador P, Datiles M. Aldose reductase in diabetic cataracts. JAMA 1981; 246:257-261
6Kador PF, Kinoshita JH. Diabetic and galactosemic cataracts. In: Regnault F'J. Sci Adv. Symposium on the lens. Amsterdam Excerpta Medica, 19:110-123.
7Varma SD, Schocket SS, Richards RD. Implications of aldose reductose in cataracts in human diabetes. invest Ophthalmol vis scl 1979,18:237-242.
8Davies PD< Duncan G, Pynsent PB, Arber DL, Lucas VA. Aqueous humour glucose concentration in car­act patients and the effect on the lens. Exp eye res 1984, 39: 605-609.
9Dugmore LVI, Gun K. Glucose. tolerance test in 200 patients with senile cataracts; Dr. J Ophthalmol 1980, 64:689-692.
10Sharma YR, Cotlier E. Inhibition of lens and ctaract aldose reductase by protein bound anti­-rheumatic drugs: Salicylate, Indomethacin, Oxyphenbu­tazone, Sulindac. Exp eye res 1982, 35:21-27.
11Jacobson M, Sharma YR, Cotlier E, Hollander JD. Diabetic complications in lens and nerve and their prevention by sulindac or sorbinil : Two novel aldose reductase inhibitors. Invest ophthalmot vis sci 1983, 24:1426-1429.
12Sharma YR, Richards RD, Varma SD. Sugar cataracts in gerbil. Effect of quercetin, Sulindac and sulindac sulfide. ARVO abstracts. Invest ophthalmI Vis Sci 1983 : 263.
13Sharma YR, Bhatnagar R, Vajpayee RB, Azad RV, and Mukesh Kumar. The effectivity of sulindac in sugar cataracts. Devel Ophthalmol, In Press.
14Crabbe MJC, Petachey M, Burgess SEP, Cheng H> The penetration of sorbinil, an aldpse reductase inli­bitor into lens, Aqueous humour and enyhrocytes of patients undergoing cataracts extraction. Exp Eye Res 1985, 40: 95-99,
15Hanna C, Sharp JD, Rock L. Ocular absorption of indomethacin by the rabbit. arch ophthalmol 1972, 88:196-198.
16Duggan DE, personal communication 1983.
17Sharma YR, Vaipayee RB, Madan Mohan, Azad RV, Mukesh Kumar. A simple accurate method of cata­ract classification Cataract 1. Manuscript submitted for publication.
18Ibid. Methodology for studies on medical therapyof cataracts : cataract II. Manuscript submitted for publication.
19Ibid. Topical glutathiotlein therapy in sensile cata­ract: Cataract III. Manuscript submitted for publica­tion.
20Frank RN. The mechanism of blood retinal carrier breakdown in diabetes. Arch Ophthalmol 1985: 103:1303-1304.
21Mizushima Y. Sakai S, Yamamura M. Mode of stabi­lising action of non-steroid anti-inflammatory drugs on erythrocycle membrane. Biochem Phermacol 1976; 19:227-234.
22Cunah-Vaz JG, Mota CC, Leite EC et al. Effect of sulindac on permeability of the blood retinal barriers in early diabeticrationapthy. ArchOphthalmol1985; 10: 1307-1311.