Year : 1975 | Volume
: 23 | Issue : 3 | Page : 9--11
Serum lipids in hypertensive retinopathy
K Singh1, KS Mehra1, KG Gode2,
1 Banaras Hindu University, Varanasi-221005, India
2 Department of Ophthalmology and Pharmacology Institute of Medical Sciences, Banaras Hindu University, Varanasi-221005, India
K S Mehra
4, Medical Enclare, B.H. U., Varanasi-221005
|How to cite this article:|
Singh K, Mehra K S, Gode K G. Serum lipids in hypertensive retinopathy.Indian J Ophthalmol 1975;23:9-11
|How to cite this URL:|
Singh K, Mehra K S, Gode K G. Serum lipids in hypertensive retinopathy. Indian J Ophthalmol [serial online] 1975 [cited 2021 Jun 21 ];23:9-11
Available from: https://www.ijo.in/text.asp?1975/23/3/9/31305
Rajyashree et al  have shown that serum lipids play an important role in causation of diabetic retinopathy. Inspite of much work being done we are still in the dark as to the factors causing changes in the fundus in hypertension. Many a time we find that in some hypertensive patients, there is no evidence of hypertensive ratinopathy while other hypertensive patients having lesser degree of hypertension show lots of fundus changes.
The present study was undertaken with a view to determine whether the serum lipids have a similar role in the pathogenesis of ratinopathy in hypertension.
Material & Methods
The patients of both sexes were included and their age was above 29 years. In these cases body weight, vision, tension, slit lamp and fundus examination under mydriatic and blood pressure examination were carried out.
Group A-50 normal patients without having any evidence of diabetes and hypertension.
Group B-50 patients having hypertensis on without any evidence of hypertensive retinopathy or diabetes.
Group C-50 patients having hypertension with retionpathy and without diabetes.
The various hypertensive pretionathy changes were noted down according to Keith, Wagner and Werner's classification.
Following investigotions were carried out in all the three groups of patients.
(a) Total serum lipids : It was done by the method of Chabrol and Chabronnat as quoted by Debot  .
(b) Serum cholesterol : Estimation of serum cholesterol was done by Zak's Ferric chloride method as modified by Debot  . The estimation was done on the same day of collection of blood.
(c) Free fatty acids ; It was determined by the method of Dole 
[Table 1] shows the levels of serum lipids, serum cholesterol, and serum free fatty acids with standard deviations and standard errors in all the the three groups.
[Table 2] shows that there is no significant difference in free fatty acids of Group A and B but there is a significant difference in serum cholesterol and serum total lipids between A and B groups. It was also observed that as far as cholesterol, serum lipids, and free fatty acids are concerned there was significant difference between Group A and C. Between group B and C there was no significant difference in serum cholesterol and total lipids but free fatty acids showed a significant difference. In relation to grade of hypertensive retinopathy it was observed that there was no significant difference in various grades as far as serum cholesterol and serum lipids are concerned but free fatty acids content were higher with higher grades of hypertensive retinopathy [Table 3].
Rajyashree  has shown that serum fatty acids and total lipids are higher in all cases of diabetic retinopathy and the highest levels are seen in cases of diabetic ratinopathy with hypertension.
In the literature we find that no one has tried to correlate the hypertensive fundus picture with values of total serum lipids, cholesterol, and free fatty acids in hypertensive patients. Some workers have reported that serum total lipids and fatty acids are in higher concentration in patients suffering from hypertension but the literature is silent about the fact whether total serum lipids, cholesterol, and free fatty acids give a helping hand in precipitating hypertensive retinopathy, whether or not these factors are raised, lowered or same in patients showing hypertensive fundus involvement.
With this positive finding in our cases of hypertensive retinopathy we are of the opinion that raised free fatty acids might be altering the ratio of endothelial cells and intramural cells of the capillaries (as in the diabetes mleitus) as 4:2 (normally 1:1) and ultimately giving rise to weakening of the vascular wall due to infiltration, leading to microaneurism formation. Consequent rupture of these microanaeurisms result in retinal haemorrhage. Thus rise of free fatty acids level in the blood may be one of the causative factor for the appearance of hypertensive retinopathy.
But we must keep one thing in mind that though there is raised free fatty acids content in hypertensive retinopathy cases as compared to hypertensive cases without retinopathy, but as far as total serum lipids and cholesterol is concerned there is no difference in the two groups, hence rise in free fatty acids will be at the cost of decrease in phospolipids and triglycerides. This factor has to be worked upon in some future study.
Serum cholesterol, lipids and free fatty acids were estimated in 50 normal persons, 50 hypertensive patients without retinopathy, and 50 hypertensive patients having hypertensive retinopathy. Serum cholesterol and serum lipids were raised while free fatty acids were normal in persons having hypertension without retinopathy in comparison to normal persons. In patients having hypertensive retinopathy the free fatty acids, serum lipids, and serum cholesterol were raised in comparison to normal persons. Further in hypertensive retinopathy cases, in comparison to hypertensive cases without retinopathy, the serum lipids and serum cholesterol were not significantly raised but free fatty acids were significantly raised in hypertensive retinopathy cases-higher the grade of hypertensive retinopathy greater was the concentration of serum free fatty acids. Thus the role of raised serum free fatty acids in precipitating hypertensive retinopathy has been discussed.
|1||Avogaro P., Crephaldi and Conte, N 1961, Panminerva Med. 3,574-576|
|2||Chabrol, E. & R. Charonnat, 1937, Presse Medicale, 4.5 1713. 1913 Quoted by Debut, M.P., Journ of Med. Bordeaux, 137, 253|
|3||Debot M.P.; 1960, Jour. of Med. Boredeaux 137, 253,|
|4|| Dole, V.P,, 1956, Jour. Clin. Invest. 35, 150.|
|5||Keith, N.M., Wagner, H.P. and Burker, N.W., 1953 Amer. J. Med. Sc. 197, 322|
|6||Keys, A., 1953, Jour. Mt. Sinai Hos. 20, 118|
|7||Rajyashree, K , 1968, Thesis submitted for the degree of Master of Surgery, B.H.U., Varanasi-5, India.|