Indian Journal of Ophthalmology

ORIGINAL ARTICLE
Year
: 1989  |  Volume : 37  |  Issue : 3  |  Page : 134--141

Systemic aspirin and systemic vitamin E in senile cataracts : cataract V


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

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

Abstract

We undertook a prospective study in senile cataract patients using systemic aspirin and systemic vitamin E. Vitamin E treated eyes did show less progression of PSC opacities extent and less new nuclear opacities during the follow-up, but overall vitamin E treated eyes did no better than the control group eyes. More eyes in systemic aspirin treated group maintained the initial vision and loss of vision in the aspirin group was also less marked. Aspirin also caused a significant less mean increase in cortical opacity extent, nuclear/opacity and density and PSC opacity extent and density as well as in ophthalmoscopically graded opacity extent and density. We suggest that aspirin is a potential drug which should be further evaluated in large double blind photodocumentated studies. The present data does not justify the recommendation that aspirin be prescribed for slowing down cataract progression. This must await large studies and confirmation.



How to cite this article:
Sharma Y R, Vajpayee R B, Bhatnagar R, Mohan M, Azad R V, Kumar M, Nath R. Systemic aspirin and systemic vitamin E in senile cataracts : cataract V.Indian J Ophthalmol 1989;37:134-141


How to cite this URL:
Sharma Y R, Vajpayee R B, Bhatnagar R, Mohan M, Azad R V, Kumar M, Nath R. Systemic aspirin and systemic vitamin E in senile cataracts : cataract V. Indian J Ophthalmol [serial online] 1989 [cited 2019 Oct 22 ];37:134-141
Available from: http://www.ijo.in/text.asp?1989/37/3/134/26068


Full Text

 INTRODUCTION



Retrospective studies have suggested that use of sys­temic aspirin may slow down the progression of cata­ract [1],[2],[3],[4]. These studies were conducted because plasma tryptophane was found to be elevated in cataract pa­tients [5],[6]. This was not confirmed in another study but a later study indicated that free tryptophane levels were higher in cataract patients after an oral load of trypto­phane [7],[8]. Aspirin lowers the plasma tryptophane [9]. Among other aspirin actions which have been sug­gested as possibly anti-cataractogenic include aldose reductase inhibition [10], acetylation of lens crystallin [11], prevention of carbamylation of lens proteins and pre­vention of cyanate induced phase separation opacities [12] and numerous other effects [13]. Aspirin when admini­stered systemically binds to lens proteins and is retained by the lens for upto 24 hours [14]. The report that aspirin decelerates cataract progression attracted widespread attention [15] but also lead to acrimony and disagreement [16],[17]. A recent retrospective study has indicated that use of Aspirin reduces the risk of cataract formation [18]. Recently also, the role of oxidative stress in aetiopatho­genesis of cataract formation has been emphasisied [19],[20],[21] The enzyme superoxide dismutase is present in the lens and has been suggested to protect against the oxidative stress [22] However, in a prospective study superoxide dismutase was found ineffective in preventing canine cataracts [23]. Vitamin E, another natural antioxidant has been shown to prevent photo peroxidation of lens lip­ids [20]- Vitamin E has also been shown to slow down cata­ract progression in emory mice 19

We conducted prospective studies using systemic aspi­rin and Vitamin E to note any possible effect on senile cataract progression.

 MATERIAL AND METHODS



The methodology and cataract classification system used in this study have been described 26,27Cataract patients seen in the cataract cell who consented to participate in the study involving systemic use of medications were randomly assigned to one of three groups. The control group was put on one placebo tablet containing aspirin tablet excipients tid PC, the second group was put on one tablet of Vitamin E 400 mg od AC and third group was put on one 325 mg. aspirin tablet tid PC. The control group receiving three placebo tablets daily served as control for both vitamin E and aspirin groups. The ne­cessity of using such a control group stemmed from our inability to obtain similar looking placebo tablets as that of vitamin E which were available to us in bright green pearl form as a proprietary preparation. Each patient was coded and 60 patients each were randomly assigned to one of three groups and each patient was requested to come for monthly follow up (some were permitted to come at 3 month intervals). At each follow up corrected visual acuity and detailed slit lamp and ophthalmoscopic examination was recorded on a printed proforma with­out referring to previous records. For inclusion in the study normal fundus examination and absence of any other significant ocular disorder were essential prerequisites. Initially a two years follow up for each patient was planned but at the conclusion of the study we chose to analyse data of all patients who completed at least 3 months follow up. In ten percent of patients in each group lens photographs using Zeiss slit lamp camera or Nikon zoom anterior segment camera were taken.

 RESULTS



This study was again marred by high drop out rate though it was less than we had in senile cataract patients who were also diabetic and were put on topical sulindac therapy 28. In control group 39 patients (76 eyes), in vitamin E group 42 patients (80 eyes) and in aspirin group 43 cataract (81 eyes) completed at least three months follow up (Table 1). Some patients in the study were one eyed or the second eye was not considered in data analysis because of preexisting unilateral pathology and some developed unilateral pathology during the follow up in the three groups ranged from 3 to 23 months with mean of 9.25 months in control group, 10.45 months in vitamin E group and 10.55 months in aspirin group (Table 2). The majority of cataracts in all three groups initially was such that no separate date analysis was possible for pure groups (Table 3). The distribution of cortical and PSC opacities initially and finally was simi­lar in all the three groups, but increase in the percentage of nuclear opacities was significantly less in both vita­min E and aspirin groups as compared to the control group ([Table 4] ; P [1],[2],[3],[4] Those data were based on retrospective studies and have been criticized [16] An independent study also supported that long term usage of aspirin and aspirin-like drugs lessens the risk of cataract. [18] This study ,vas also based on retrospective data analysis. We undertook this prospective study primarily to study what effect aspirin has on cataract progression. Various constraints precluded proper photodocumentation and a double blind protocol 26,27 For the same reason, vitamin E studies were not possible using a suitable placebo and for both aspirin and vita­min E groups, a single control group had to be used. We recognise the various pitfalls of our studies though all possible steps were taken to obviate (lessen) observer bias. Because a number of parameters were studied objectively by more than one observer and because previous patient data was never referred to during follow up, we suggest our data to be fairly reliable. The present study clearly indicates that more aspirin treated eyes maintain the same vision and visual loss in them tends to be less marked than in control group eyes. This was not noted in the vitamin E group. Development of new nuclear opacities during follow up was significantly less in both vitamin E and aspirin groups. Other than this the only parameter studied where vitamin E treated eyes showed less mean increase was PSC opacity extent. But in the vitamin E group cortical opacity extent, nu­clear opacity extent and density and ophthalmoscopi­cally graded opacity density all showed a significant more increase than control group. In the aspirin group cortical opacity extent, nuclear opacity density, PSC opacity extent and density and ophthalmoscopically graded opacity extent and density all showed signifi­cant less mean increase compared to control group eyes.

The data indicates that aspirin, whatever its exact mode of action, is a potential drug which should be further tested in large double blind photo-documented mul­ticentric studies. The present data does not justify the recommendation that systematic aspirin be used in medical management of senile cataracts. This must await further studies and confirmation.

While in vitamin E treated eyes increase in PSC opacity extent was considerably less and development of new nuclear opacities during follow up was less, overall the present data does not justify further large scale clinical cataract studies with vitamin E. This must await more basic data and more definitive data suggesting use of vitamin E for studies on medical therapy of cataracts.

 ACKNOWLEDGEMENT



We thank E. Merck India for supplying us vitamin E tablets generously. We gratefully thank ICMR, India, for partly supporting this study. During part of this study, Dr. Y. R. Sharma was appointed under supernumerary research cadre scheme at Dr. R. P. Centre. We also thank all residents who referred their cases to the cataract cell.

 NOTE



None of the authors has any kind of proprietary interest in any form in any of the drugs studied. This includes glutathione, sulindac, aspirin and vitamin E.

References

1Collier E. Rheumatoid arthritis and cataract surgery. Int. Ophthalmol; 2:127-129,1980.
2Cotlier E, Sharma Y. R. Aspirin and senile cataracts in rheumatoid arthritis. The lancet; Feb 7: 338-339, 1981.
3Cotlier E. Senile cataracts : Evidence for acceleration by diabetes and deceleration by salicylate. Am J pphthalmol; 16:113-118, 1981.
4Cotlier E. Aspirin effect on cataract formation in patients with rheumatoid arthiritis or combined to diabetes. Int. ophthalmol; 3:173-177,1981.
5Cotlier E, Sharma Y R Zuckerman J, Puklin J, Teasely B, Irvine J. Plasma tryptophane in humans with diabetic and senile cataracts. Exp eye res; 33 247-252, 1981.
6Chadwick C, Phipps D A, Powell C. Serum Tryptophane and cataract. The Lancet; Sept 21: 583, 1981.
7Allergi E, Angi M. Plasma Tryptophane in senile cataract. The Lancet; July 18:157,1981.
8Rinaldl E, Miele L, Pulcini D, Menna A, Pletra F D, Cotticelli L, et al. Alteration of serum tryptophane metabolism in patients suffering from senile cataract. Metab ophthalmol - Paed and syst; 8 : 16-19, 1984.
9Smith HG, Lakatos C. Effects of acetylsalicylic acid on serum proteinbinding and metabolism of Tryptophan in man. J pharm pharmacol; 23: 180-189, 1971.
10Sharma Y R, Cotlier E. Inhibition of lens and cataract aldose reductase by protein-bound anti-rheumatic drugs: Salicylate, indomethacin, oxyphenbutazone, Sulindac. Exp eye res; 35: 21-27,1982.
11Rao G N, Lardis M P, Cotlier E. Acetylation of lens crystallins: A possible mechanism by which aspirin could prevent cataract formation. Biochem Biophys res comm; 128:1125-1132,1985.
12Crompton M, Rixa K C, Harding J. J. Aspirin prevents carbamylation of lens protiens and prevents cyanate induced phase separation opacities in vitro: A possible mechanism by which aspirin could prevent cataract. Exp eye res; 40: 279-311,1985.
13Cotlier E., Aspirin and cataracts : from the laboratory to clinical trials. Proceedings of the centennial year of University of Illinois : 207-215, 1981.
14Collier E, Sharma Y R, Niven T, Brescia M. Distribution of salicylate in lens and intraocular fluids and its effects on cataract formation. Am. J. Med, 74 :83-90,1983.
15Medical News. Study to begin on whether aspirin can delay senile cataract formation. JAMA;244 : 2593-2594, 1980.
16Seigal D, Sperduto R D, Ferris F Cm. Aspirin and cataracts. Ophthalmol, 89 :47A-48A, 1982.
17Collier E. Reply to view point. Ophthalmol; 89: 48A-49A, 1982.
18Heyningen R V, Harding J J. Do aspirin like analgesics protect against cataract. The lancet; May 17:1111-1113,1986.
19Varma S D, Chand D, Sharma YR, Kuck R D, Richards R D. Oxidative stress on lens : Role of light and oxygen. Current eye res; 3:35-57, 1984.
20Varma S D, Srivastava V K, Richards R D. Photoperoxidation in lens and cataract formation: Preventive role of superoxide dismutase, catalase and vitamin C. Ophth res; 14:167-175,1982.
21Jernigan HM. Role of hydrogen peroxide in Riboflavin-sensitised photodynamic damage to cultured rat lenses. Exp eye res; 41:121-129,1985.
22Bhuyan K C, Bhuyan D K. Superoxide dismutase of the eye. Biochim et Biophys Acta; 542: 28-38,1978.
23Brainard J, Hanna C, Petursson G. Evaluation of superoxide dismutase in medical treatment of canine cataract. Arch Ophthalmol; 100: 1832-1834, 1982.