|Year : 1982 | Volume
| Issue : 4 | Page : 387-390
Plasma prostaglandin in primary glaucoma
R Singh, MC Rao, SK Bhatatcharya
Department of Ophthalmology, Department of pharmacology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India
C-7, New Medical Enclave, Banaras Hindu University, Varanasi-221005
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Singh R, Rao M C, Bhatatcharya S K. Plasma prostaglandin in primary glaucoma. Indian J Ophthalmol 1982;30:387-90
|How to cite this URL:|
Singh R, Rao M C, Bhatatcharya S K. Plasma prostaglandin in primary glaucoma. Indian J Ophthalmol [serial online] 1982 [cited 2020 May 31];30:387-90. Available from: http://www.ijo.in/text.asp?1982/30/4/387/29479
Waitzman and King noted rise of intraocular pressure and miosis on injecting PGE 2 and PGE 2 directly into anterior chamber of rabbits eye. Beitch and Eaking have observed the effect of prostaglandin E 1 , E 2 , Flα, F2α and A, on rabhits intraocular pressure after intracameral injection. They noticed that all prostaglandin except PGE 1 give rise to long sustained rise of intraocular pressure. Similarly Wyllie and Wyllie have postulated that prostaglandin El may play role in the etiology of .open angle glaucoma. Human aqueous humour was found to contain prostaglandin like activity and this was found to be signiflcantly higher in open angle glaucoma patients than those with cataract. Howevere xcept for very preliminary study by Chiang there is no other report in literature to indicate certain relationship between plasma prostaglandin and glaucoma. The present study was therefore carried out with the object of examining possible relationship between plasma prostagland in levels and raised intraocular pressure in the patients of glaucoma; and in few patient effect of administration of Indomethacin (prostaglandin inhibitor) on intraocular pressure and plasma prostaglandin was also carried out.
| Materials and methods|| |
In the present study estimation of prostaglandin was done in the plasma of 37 cases of primary glaucoma and 11 normal cases which were taken as a control, Cases of both the sexes were included varying in age from 30 to 80 years. From study point of view the cases in this series were divided into three groups.
Group A (Normal Cases)
These were those patients who attended the Bhualika Eye Hospital for the treatment of refractive error, cataract etc. and who did not have any ocular infection. In these patients intraocular pressure was in the range of 15-20 mm of Hg (Schiotz) and they did not show any glaucomatous field changes or glautomatous cupping on fundus examination.
Group B (Case of open angle glaucoma)
In this group of patient proved case of chronic simple glaucoma were included who had not taken any treatment for their intraocular pressure was more than 30 min Hg with fundus changes and field defects of chronic simple glaucoma.
Group C (Cases of narrow angle glaucoma)
This group include patients of proved narrow angle glaucoma and had not taken any treatment for glaucoma so far.
All the cases were subjected to detailed ocular examination including oblique illumination, visual aquity with and without glasses, intraocular pressure with Schiotz tonometer, fundus examination, Peripheral and central fields, gonioscopy, General examination was done to rule out any inflammatory lesions, laboratory investigations like blood sugar, TLC, DLC, ESR were also carried out.
To assess the effect of indomethacin in patients of glaucoma after doing all the above examinations, the patients were given indomethacin in the dose of 25 mg six hourly for 3 days. Intraocular tension before and after indomethacin was noted. Plasma prostaglandin estimation was also done prior to and after the administration of Indomethacin.
Estimation of prostaglandin was carried out by bioassay technique (Richter Crossland).
| Observations|| |
1. Plasma prostaglandin levels in control group (Group A).
Total number of cases for this group were 14. The highest and the lowest levels of plasma prostaglandin recorded in this group A were 2.30 ng/ml and 1.00 ng/ml respectively.
`The mean ( ± SE) was 1.75±0.1073ng/ml [Table - 1].
2. Plasma prostaglandin level in open angle glaucoma patients (Group B).
Total number of cases to this group were 26. The highest and lowest level of plasma prostaglandin were 4.34 ng/ml and 1 00 ng/ ml respectively. The .mean value (± SE) was 2.18 + 0.173 ng / ml of plasma [Table - 1].
3. Plasma prostaglandin level in narrow angle glaucoma patients (Group C).
Total number of cases in the group were 11. The highest and lowest values of prostaglandin in plasma were 3.78 ng/ml and 1.00 ng/ml respectively. The mean value (±SE) was 1.91 + 0.84 [Table - 1].
With the rise in intraocular pressure there was an increase in plasma prostaglandin levels in both open and narrow angle glaucoma patients [Table - 2].
The effect of prostaglandin antagonist (Indomethacin) on plasma prostaglandin and intraocular pressure in primary glaucoma patients (open angle).
The mean plasma prostaglandin levels before and after the in.domethacin administration were 2.23 ng/ml and 1.16 ng/ ml respectively and mean difference was 1.07 ng/ml.
It was also noted that after administration of indomethacin there was fall in IOT ranging from 2.5 mm Hg to 6 mm Hg (Schiotz) [Table 3].
| Discussion|| |
Willie and Wyllie have observed that PGEI may play role in the etiology of open angle glaucoma. He has also reported that aqueous humour was found to contain prostaglandin like activity and it was seen that it was significantly higher in sample obtained from the patients with open angle glaucoma than patients those with cataract. In the present series of our observation shows that mean prostaglandin values of primary glaucoma (both opened and narrow angle) was higher than control group [Table - 1].
The mean prostaglandin expressed as PGE1 activity (in ng/ml ± SE was 2.18 + 0.173, 1.91 ± 0.84 and 1.75 ± 0.107, in open angle narrow angle and controls respectively. These findings are incomplete agreement with that of Chiang (1974). His values were (ng/ml±SE) 3.25 ± 0.5, 2.47 ± 1.05±0.08 open angle, narrow angle and in control respectively.
In our observations values of plasma prostaglandin in control cases were compared to patients of primary glaucoma. The results shows that it was statistically significant in case of open angle glaucoma (p<0.05) while it was statistically not much significant when mean values of control were campare to with narrow angle glaucoma (p>0.05) [Table - 1]. Thus from these observations it is clear that prostaglandin is raised in plasma in cases of both open and narrow angle glaucoma but in open angle glaucoma it is statistically more significant than narrow angle glaucoma.
The rise in IOP in glaucoma patients due to prostaglandin may be due to the prostaglandin leads to increased vasodilation thus pausing breakdown of blood aqueous barrier finally giving in rise of IOP or due stimulation active transport across the ciliary body leading to increased aqueous production. When the mean values of plasma prostaglandin in open and narrow angle glaucoma were compared statistically it was found to be insignificant (p1 > 0.05).
Relationship of plasma prostaglandin to intraocular pressure in these patients shows that there was rise of 1OP with rise in plasma prostaglandin levels in both open and narrow angle glaucoma. Suggesting casual relationship between prostaglandin and 1OP [Table - 2].
Smith and Lands and Vane are of the opinion that certain anti inflammatory substance like indomethacin aspirin and soda salicylate inhibit the synthesis of prostaglandin. In our four cases of primary open angle glaucoma there was marked fall in the level of plasma prostaglandin after administration of Indomethacin the mean fall in the level of plasma prostaglandin having being 1.07 ng/ml along with fall in JOT, mean fall in IOT is 2.5 mm Hg and maximum is 6 mm Hg which appears to be insignificant. The reason may be that this study was carried out in very small number of cases. To establish the effect of indomethacin on JOP further study is needed.
| Summary|| |
Estimation of plasma prostaglandin (PGEi) was carried out in 14 normal individuals, 26 open. angle glaucoma and 11 narrow angle glaucoma patients. The plasma prostaglandin estimated by bio-assay technique. It was Observed that plasma prostaglandin was raised in primary glaucoma (both open and narrow angle glaucoma). Plasma prostaglandin is significantly higher in open angle glaucoma as compared to control group (p < 0.05) where as in narrow angle glaucoma the PGE1 levels do not show any significant difference as compared to the control group. The effect of prostaglandin antegonist like indomethacin on levels of plasma prostaglandin and 1OP levels showed that there was lowering of plasma prostaglandin and slight lowering of IOP.
| References|| |
Waitzman, M.B. and King, C.D., 1967, Amer J. Physiol. 212 :329.
Beitch, B.R. and Eakins. K.E., 1969., Brit. J. Pharmacology, 37 : 158.
Wyllie, A.M. Wyllie, J.H., 1971, Brit. Med. J. 3, 615.
Chiang, T.S. and Thomas, R.P., 1972, Arch. Ophthalmol. 88, 418-420.
Smith, W.L. and Lands, W., 1971, J. Biol. Chem.246 : 6700.
Vane, J.R. 1971. Nature New Biol. 238 :232.
[Table - 1], [Table - 2], [Table - 3]