| ORIGINAL ARTICLE | | | | Year : 1987 | Volume : 35 | Issue : 2 | Page : 67-70 | | Plasma prostaglandin and diabetic retinopathy OPS Maurya, R Singh, SK Bhattacharya, JK Agarwal C-7, New Medical Enclave Naria, Banaras Hindu University, Varanasi-5, India Correspondence Address: R Singh C-7, New Medical Enclave Naria, Banaras Hindu University, Varanasi-5 India
PMID: 3450622 Abstract | | | Estimation of prostaglandin El (PGE) levels by bioassay technique (Ritcher Crossland) was carried out in 15 normal persons, 15 diabetic patients without Retinopathy, and 30 diabetic patients with Retinopathy. Plasma PGE 1 values were higher in diabetic patients with or without retinopathy than in normal subjects Plasma PGE 1 levels were significantly higher in diabetic with retinopathy than in the control group (p < 0.001), whereas in diabetics without retinopathy the PGE levels did not show a statistically significant difference from controls In diabetic patients with retinopathy, the mean value of PGE 1 was higher in proliferative retinopathy than in background retinopathy, but on statistical analysis, it was not of much significane (P> 0.8). How to cite this article: Maurya O, Singh R, Bhattacharya S K, Agarwal J K. Plasma prostaglandin and diabetic retinopathy. Indian J Ophthalmol 1987;35:67-70 | How to cite this URL: Maurya O, Singh R, Bhattacharya S K, Agarwal J K. Plasma prostaglandin and diabetic retinopathy. Indian J Ophthalmol [serial online] 1987 [cited 2014 Mar 6];35:67-70. Available from: http://www.ijo.in/text.asp?1987/35/2/67/26210 | On reviewing the Ophthalmic Literature, Waitr man[1] (1973) has shown that isolated pigment epithelial cells from the rabbit retina can synthesize relatively large amounts of prostaglandins from linoleic acid. These experiments may provide an explanation for the finding that serum of patients with diabetic retinopathy contained higher concentration of PGF [2] a than that of normal controls, when measured by radioimmune assay method.
David BenEzra (1978) observed the neovasculogenic ability of prostaglandins of the E-series. In diabetes PGE[1] is the most active compound in new vessel proliferation. Thus the above observation shows that there is some relationship between the plasma prostaglandin and diabetic retinopathy, but the relationship between various grades of retinopathy, and levels of plasma prostaglandin is not well defined in Ophthalmic Literature Keeping this in mind the present project has been undertaken to assess the relationship between plasma prostaglandins and various grades of diabetic retinopathy.
Patients & Methods | | |
Estimation of prostaglandin (PG) levels were done in the plasma of 60 cases, which inlcude 45 cases of diabetes and 15 normal subjects as control Out of 45 cases of diabetes, 30 cases were associated with retinopathy, while 15 were without retinopathy. Cases of both sexes aged between 19 and 73 were included in this study. The cases in this series were divided into three groups.
Group - A: Controls
These were 15 patients who attended the Bhuwalka Eye Hospital for the treatment of refractive error, cataract or other disorders and who did not have any ocular infections Their fasting blood sugar level was below 120 mg% and two hours postprandial blood sugar levels below 180 mg% with no sugar in the urine These patients neither complained of polydypsia, polyphagia, polyuria, loss of weight or weakness
Group B : Diabetes without Retinopathy
This group inluded 15 patients who were either known cases of diabetes mellitus, who were already taking treatment for diabetes or in whom presence of diabetes had been confirmed Detailed ophthalmoscopic examination was done after full mydriasis to find out diabetic changes in the retina In this group only those cases which did not show diabetic changes in the retina were included.
Group C - Diabetes with Retinopathy
This group included 30 patients of diabetes mellitus, who were taking treatment for diabetes or in whom presence of diabetes had been confirmed. Detailed Ophthalmoscopic examination was done after full mydriasis These patients showed varying grades of diabetic changes in their retinae.
Before proceeding further with the estimation of plasma PG levels, all patients were tested for visual acuity with and without glasses, I.O.P. was taken with Schiotz Tonometer, detailed ophthalmoscopic and bio-microscopic (slit lamp) examination, visual field, blood pressure, general examination to rule out inflammatory lesions and laboratory investigations including blood sugar, TLC, DLC, ESP, blood urea, serum lipids and urine for sugar, albumin and acetone were done. Estimation of PG level was carried out by bioassay technique (Ritcher Crossland) in the Department of Pharmacology, Institute of Medical Sciences, Banaras Hindu University.
Results | | |
Group A (Control Cases)
Highest and lowest values of plasma prostaglandin El in this group were 2.0 ng/ml and 0.6 ng/ml respectively. The mean ± S.E value was 1.41 ± 0.112 ng/mI of plasma [Table - 1].
Group C (Cases of Diabetes with Retinopathy)
Highest and lowest values of plasma prostaglandin El were 4.6 ng/ml and 1.2 ng/ml res pectively. The mean value ± S. E. was 2.38 ± 0.163 ng/ml [Table - 1]. Among the diabetes with retinopathy (Group C), .19 patients had background retinopathy (Group Cl) and 11 patients had proliferative retinopathy (Group C 2).
Group C 1 (Background retinopathy cases)
Highest and lowest values of plasma prostaglandin El were 4.0 ng/ml and 1.2 ng/ml respectively. The mean ±S.E was 2.17 ± 0.167 ng/ml [Table - 2].
Group C 2 (Proliferative retinopathy cases)
Highest and lowest values of plasma prostaglandin El were 4.6 ng/ml and 2.5 ng/ml respectively. The mean value (± S. E) was 3.29 ± 0.179 ng/ml [Table - 2].
Comment | | |
Prostaglandins are generated during the platelet aggregation reaction. Platelets from diabetic patients are synthesising and release more prostaglandins than platelets from non diabetics (Halusjka et al., [3], sub 1976).
Kwann et al [4] (1972) have reported increased platelet aggregation in diabetic retinopathy. It is possible that in diabetic retinopathy some plasma factor may be responsible for increased aggregation which may be AFL (antihemolytic) factor, Vonwillebrand factor (Vlll: vWF) LASS (labile aggregation stimulating substances Thromboxane B 2, the inactive metabolite of platelet thromboxane A 2, is also elevated in the plasma of some diabetics Thromboxane A 2 is produced from platelet membrane arachidonic acid following the exposure of platelets to collagen, thrombin and other platelet aggregating agents Thromboxane A 2 potentiates release of adenosine diphosphate and other platelet granular contents, and therefore augments platelet aggregation.
In the present series, mean plasma prostaglandin (PG) values in diabetics without retinopathy (Group B) and diabetics with retinopathy (Group C) was higher than control (Group A). The mean plasma prostaglandin level expressed as PGE 1 activity (in ng/ml + SE) were 1.41 ± 0.112, 1.92 ± 0.243 and 2.38 ± 0.163 in group A (Control),
Group B (diabetics without retinopathy) and in group C (diabetics with retinopathy). These findings are in complete agreement with Waitzman (1973) who has shown that serum prostaglandin F 2 a was found in a preliminary study to be high in diabetic retinopathy (1.5 ± 2.8 SE ng/ml).
We compared the mean values of plasma prostaglandin (PG) in diabetics without retinopathy (Group B) and diabetics with retinopathy (Group C). These were quite high when compared to the control group (Group A). On statistical analysis these findings were highly significant in diabetics with retinopathy (p < 0.001) while it was not of much significance in diabetics without retinopathy (p 0.10) [Table - 1]. Mean values were also higher in diabetics with retinopathy than in diabetics without retinopathy, but statistical values were not of much significance (p > 0.10) [Table - 1].
The concentration of PG being higher in diabetics with retinopathy than in diabetics without retinopathy group, may be explained on the basis that there is correlation between the severity of retinopathy and degree of platelet aggregation enhancing activity in the plasma of diabetic subjects (Dobbie et al., [5] (1973).
BenEzra (1978) demonstrated that many varieties of prostaglandins particularly of E series shows a strong vasoformative tendency. PGEI shows strong neovasculogenic activity. Thus, the above mentioned studies show that prostaglandins (specially PGEI) have got some relation with proliferative diabetic retinopathy.
In the present series mean PG values in proliferative retinopathy (Group C 2 ) was higher than in background retinopathy (Group C 1 ). The mean P.G. level expressed as PGE 1 activity (in ng/ml + S.E) was 2.17 ± 0.167 and 3.29 ± 0.179 in background retinopathy (Group C 1 ) and proliferative retinopathy (Group C 2) respectively. These findings are again in agreement with BenEzras (1978) obser vations
We compared mean values of PG in background retinopathy (Group C 1) with proliferative retinopathy (Group C 2). The result shows that it was higher in proliferative retinopathy(Group C 2) than in background retinopathy (Group C 1sub ) but on statistical analysis it was not of much significance (p> 0.8) [Table - 2].
The concentration of PG are higher in proliferative retinopathy than in background retinopathy. This may be explained on the basis that increased platelet aggregation in proliferative retinopathy (Heath et al., 1971 6; Kwann et a1 4 1972) synthesized (and released) more endogenous prostaglandins Increased platelet aggregation favours microthrombi formation leading to further development of ischaernic lesions in the retina (Dobbie et al., 1973). These ischaemic or hypoxic lesions lead to further production of prostaglandins (Ashton et aL, 7 1954) which are responsible for further neovascularization[7]. References | | | 1. | Waitzman, MR, Prostaglandin and diabetic retinopathy. Exp. Eye Res 16, 307-313,1973. | 2. | BenEzra D, Neovasculogenic ability of prostaglandins growth factors and synthetic chemoattractants, Am J. Ophthalmol, 86,455, 1978. | 3. | Halushka, V,• Weiser, C, Chamvers, A and ColwellJ, Synthesis of prostaglandin " E-like" in diabetic and normal platelets. Adv. Prostagi Thrombox Res 2 : 853, 1976. | 4. | Kwann, RC Colwell, J.A Cruz, S.: Increased platelet aggregation in diabetes mellitus, J. Lab. Clin Med. 30: 236-246, 1972. | 5. | Dobbie J. G., Kwann, H.C Colwell J. A, Suwenwella, N.: The role of platelets in pathogenesis of diabetic retinopathy. Trans, Am Acad. Ophth. Otolaryng, 77, 43-47, 1973. | 6. | Heath, H., Brigden, W. D., Canever, J.V, Pollack J, Hunnter, P.R., Kelsey, J. and Bloom, A: Platelet adhesiveness and aggregation in relation to diabetic retinopathy. Diabetiologia, 7:308, 1971. | 7. | Ashton, N., Ward B., and Serpell, G : Effect of oxygen on developing retinal vessels with particular reference to the problems of retrolental fibroplasia, Br. J. OphthaL, 38: 397-432, 1954. | Tables [Table - 1], [Table - 2] |