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ARTICLE
Year : 1969  |  Volume : 17  |  Issue : 3  |  Page : 95-98

Effect of topical steroids on Intraocular pressure in young diabetics


Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh, India

Date of Web Publication10-Jan-2008

Correspondence Address:
I S Jain
Department of Ophthalmology, Postgraduate Institute of Medical Education and Research, Chandigarh
India
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Source of Support: None, Conflict of Interest: None


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How to cite this article:
Jain I S, Gill M. Effect of topical steroids on Intraocular pressure in young diabetics. Indian J Ophthalmol 1969;17:95-8

How to cite this URL:
Jain I S, Gill M. Effect of topical steroids on Intraocular pressure in young diabetics. Indian J Ophthalmol [serial online] 1969 [cited 2023 Mar 20];17:95-8. Available from: https://journals.lww.com/ijo/pages/default.aspx/text.asp?1969/17/3/95/38520

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Table 1

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Diabetics both in adult and juvenile age groups have been found to have a rather high mean intraocular pres­sure Christiansson [6] , Jain and Luthra [3] and Safir, Paulson, Klayman and Crestenfeld. [11]

Furthermore some authors, Mooney [10] Jain and Luthra [8] , have re­ported higher intraocular pressures in diabetics without retinopathy than in those with retinopathy i.e. low intra­ocular pressure rather facilitates the development of diabetic retinopathy. Still other authors, Christiansson [6] have been able to demonstrate lower intra­ocular pressure in diabetics having proliferative retinopathy than in those having non-proliferative retinopathy.

The topical use of steroids in the eye, is now known to cause ocular hy­pertension. This observation has been found to have hereditary implication and appears to be genetically deter­mined. Becker and Hahn [1] suggested a recessive mode of inheritance of primary open-angle glaucoma and a close correlation between glau­coma and steroid response. He has also shown that the response in pati­ents with diabetes mellitus, another genetically determined entity, differs from the non-diabetic population, Becker. [3]

Since no such study has been re­ported from India, the authors under­took the present study to explore pos­sible relationship between young diabetics with and without retinopathy, and intraocular pressure before and after topical corticosteroids.


  Material and Methods Top


Fifty selected young diabetics were studied which included juvenile diabe­tics and patients developing diabetes before the age of 35 years, and those who required insulin for their control.

The intraocular pressure was re­corded with a Schiotz tonometer using 5.5 and 10 gin weights and the cor­rected P0 value was noted from the tables based on Friedenwald's nomo­gram of 1955. A repeat check up of intraocular pressure was done on . the following day and the mean of the two recordings were taken. Pupils were then dilated and refraction was done in each case, followed by fundus examination.

Subsequently, every patient was given Betamethasone 0.1% (Betnesol), eye drops to be put in both the eyes, three times a day for four weeks. In­traocular pressure was recorded again after 2 and 4 weeks. Intraocular pres­sure in 60 eyes of non-diabetics of comparable ages were recorded before and after steroids, and served as con­trols.


  Observations and Comments Top


In the present study of 60 eyes (normal) the mean intraocular pressure before steroids and after steroids is as follows:

Before steroids 14.93 S.D. 2.23

After steroids 16.47 S.D. 3.2

This shows an average increase of 1.54 mm of Hg after topical steroids, which is statistically significant (p < 0.05).

The mechanism of this rise of pres­sure after topical steroids is still obs­cure and a matter of speculation. But Goldman, [6] Becker, [3] Armaly [1] suggested that there was some mechanical obst­ruction in the trabecular mesh-work to the outflow of aqueous, the nature of which was not clear. Armaly [1] pro­posed that increased mechanical resi­stance after topical steroids was due to increased thickness of the layer lining the intra-trabecular spaces, of the mesh-work in the eye by the depo­sition of mucopolysaccharides, the source of which is the mast cells.

Recently, Becker [3] considered open-­angle glaucoma as a heritable trait representing the homozygous recessive state (gg) and non-glaucomatous eyes represent the heterozygous (ng) and (nn) the normal dominant state. The genetic postulation was tied to the steroid therapy in the fol­lowing manner. The presence of reces­sive gene as in (ng) or (gg) produce a greater magnitude of hypertension. So normal eyes can be separable into two groups (ng) and (nn), the former can­not be distinguished from glaucoma (gg). The author further speculated the prevalence of the presumed res­ponsive gene in the population.

The response of intraocular pres­sure in diabetics [Table - 2] also show­ed quite comparable results to those of Levieffs [9] , Becker [3] and Becker et al [5] The rise in. pressure in our series of patients is highly significant (p < 0.01).

Levieff [9] studied 34 patients before and after steriods and found pressure of over 20 mm of Hg in 21 per cent and 65 per cent respectively, while Becker et. al. [5] reported 21 per cent and 60 per cent respectively from his study of 52 juvenile diabetics. Our figures are 15.55 per cent and 37.78 per cent respectively.


  Relationship of Corticosteroids Response to Retinopathy Top


28.57 per cent of the eyes having retinopathy developed intraocular pressure more than 21 mm of Hg after the use of topical steroids, while 40.58 per cent of the eyes having no retino­pathy developed intraocular pressure more than 21 mm of Hg after steroids. This observation further strengthens the view that there is greater preva­lence of retinopathy in eyes having lower intraocular pressure and vice versa.

None of the three eyes having proli­ferative retinopathy showed rise of intraocular pressure greater than 21 mm of Hg. Becker Bresnick, Cheo­rette, Kolker, Oaks and Andrea [5] noted that the presence of prolifera­tive retinopathy was clearly associated with lower degree of response to topi­cal steroids as compared to non-pro­liferative retinopathy cases and then the response resembled more closely the non-diabetic population.

In the present study, since the num­ber of eyes having proliferative reti­nopathy were very small, it is difficult to draw any firm conclusion, but cer­tainly is suggestive.

The above observations of Becker [3] and the results of the present study indicate that the gene for glaucoma and steroid responsiveness: protect the diabetic from proliferative retino­pathy.


  Summary Top


Diabetic eyes have been found to have high mean intraocular pressure as compared to non-diabetic eyes.

The response of intraocular pres­sure in the diabetic eyes after the use of topical steroids is highly significant as compared to that observed in non-­diabetic eyes. The response was found to be significant in eyes having no re­tinopathy than in eyes with retino­pathy.

These observations in the present study tend to indicate that the steroid responsiveness may be a useful tool in predicting the development or pro­gress of diabetic retinopathy.

 
  References Top

1.
Armaly, M. F.: Effect of corticosteroids on intraocular pressure and fluid dyna­mics: 1. The effect of Dexamethasone in the normal. Arch. Oph. (Chicago), 70, 782, 1963.  Back to cited text no. 1
    
2.
Armaly, AI. F.: Statistical attributes of the steroid Ii ypertensivc response in the clinically normal eve. Invest. Ophth., 4, 187, 1965.  Back to cited text no. 2
    
3.
Becker, B.: Intraocular pressure res­ponse to topical corticosteroids. Invest. Ophth., 4, 198, 1965.  Back to cited text no. 3
    
4.
Becker, B, and IIahn, K. A.: Topical corticosteroids and heredity in primary open angle glaucoma. Amcr. ,J. Ophth., 57, 543, 196-1.  Back to cited text no. 4
    
5.
Becker, B.; Bresniek, G.; Chevrette, L.; Kolker, A. E.; Oaks, A1. C.; Cibis An­dea: Intraocular pressure and its res­ponse to topical corticosteroids in dia­betes. A.M.A. Arch. Oph., 76, 479, 1966.  Back to cited text no. 5
    
6.
Christiansson. J.: Intraocular pressure in diabetes mellitus. Acta Ophtli., 39, 1.55, 1961.  Back to cited text no. 6
    
7.
Goldman, IL: Cortisone glaucoma. A. M.A. Arch. Ops. (Chicago), 68, 621, 1962.  Back to cited text no. 7
    
8.
Jain, I. S. and Luthra, C. L. Diabetes Mellitus, its relationship with intra­ocular pressure. Arch. Oph. (Chicago), 97, 179, 1967.  Back to cited text no. 8
    
9.
Levieff et al. Personal communica­tions. Quoted by Becker, B, et al. in 5.  Back to cited text no. 9
    
10.
Mooney, A.: Diabetic retinopathy-A challenge. Brit. J. Oph. 47, 513, 1963.  Back to cited text no. 10
    
11.
Safir, A.; Paulson, E. P.; Klayman, J. and Cre.stenfeld, J.: Ocular abnormali­ties in juvenile diabetics. Arch. Oph., 76, 1966.  Back to cited text no. 11
    



 
 
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