Serum lipoprotein cholesterol profile in diabetic retinopathy

SP Dhir; Rajvir Dahiya; Jagat Ram; RJ Dash; RN Chakravarti

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ORIGINAL ARTICLE

Year : 1984 | Volume : 32 | Issue : 2 | Page : 89-91

Serum lipoprotein cholesterol profile in diabetic retinopathy

SP Dhir, Rajvir Dahiya, Jagat Ram, RJ Dash, RN Chakravarti
Department of Ophthalmology, Experimental Medicine and Endocrinology, Post graduate Institute of Medical Education and Research, Chandigarh, India

Correspondence Address:
S P Dhir
Departments of Ophthalmology, Experimental Medicine and Endocrinology, Postgraduate Institute of Medical Education and Research, Chandigarh
India

Source of Support: None, Conflict of Interest: None

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PMID: 6526472

How to cite this article:
Dhir S P, Dahiya R, Ram J, Dash R J, Chakravarti R N. Serum lipoprotein cholesterol profile in diabetic retinopathy. Indian J Ophthalmol 1984;32:89-91

How to cite this URL:
Dhir S P, Dahiya R, Ram J, Dash R J, Chakravarti R N. Serum lipoprotein cholesterol profile in diabetic retinopathy. Indian J Ophthalmol [serial online] 1984 [cited 2022 Aug 15];32:89-91. Available from: https://www.ijo.in/text.asp?1984/32/2/89/27378

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There are conflicting reports in literature regarding the lipid profile in diabetics[1],[2] Cornwell. Some workers have found elevated levels of cholesterol and no difference was observed in serum phospholipids between diabetics with and without retinopathy[3]. The level of nonesterified fatty acids were significantly higher in diabetic with retinopathy as compared to without retinopathy[3]. Lopes Virella et al[4] found inverse correlation of high density lipoprotein cholesterol (HDL-c) with poorly controlled diabetics. Previous reports have suggested that there is significant increase in cholesterol, phospholipids and triglycerides in diabetics with retinopathy as compared to controls. However, there is hardly any report regarding the lipoprotein profile in patients with diabetic retinopathy. We have estimated triglycerides, total cholesterol and lipoprotein cholesterol in diabetic patients with and without retinopathy.

Materials and method

All the patients were selected from the Endocrinology out-patients department.

Patients with renal failure and heart disease were excluded from the study. Direct ophthalmoscopic examination was carried out after mydriasis with phenylephrine (5%) instilled twice. Total of 82 patients were studied, out of which 51 formed diabetic group and remaining 31 formed control group. Out of 51 diabetics, 26 were with retinopathy and 25 without retinopathy. Scott's classification (years) was used for the grading of diabetic retinopathy. Diabetes in all these patients was confirmed by estimating fasting and post-prandial blood sugar. The blood samples from over night fasting patients were obtained in EDTA vials (l mg/ ml of blood). Different fractions of lipoprotein were separated by using heparin manganese chloride and sodium dodecyl sulfate double precipitation technique. Total cholesterol and cholesterol content of lipoprotein fractions was estimated by the met by the method of Abell et al.[5] Triglyceride was estimated by the technique of Van Handel and Zilversmit[6].

Observations

Mean values of blood pressure, triglyceride, total cholesterol, cholesterol content of HDL, LDL and VLDL and the ratio of total cholesterol/HDL-c are shown in [Table - 1]. It was observed that there was significant increase in blood pressure, triglyceride, total cholesterol, LDL-c and VLDL-c (P<0.01) with decrease in HDL-c (P<0.01) in diabetic patients as compared to normal subjects. But no significant increase was observed when all these parameters were compared between diabetics with and without retinopathy, though all these values were slightly elevated in diabetic retinopathy group as compared to without diabetic retinopathy.

Discussion

Low HDL-c level has been found to be a significant risk factor for arteriosclerotic disease and ischaemic heart disease.[7],[8] The present study demonstrates that diabetics have significantly increased serum total cholesterol, LDL-c, VLDL-c and triglyceride as compared to normal subjects, HDL-c showed a significant decrease as compared with normal subjects. These findings are in accordance with the previous report.[4] However, comparison of all these parameters between diabetics with and without retinopathy did not reveal any significant difference, though all these values were slightly elevated in diabetic retinopathy group as compared to diabetics without retinopathy.

We have recently reported that low levels of HDL-c is a significant risk factor for ocular arteriosclerotic changes as well as for retinal vascular complications in these patients.[9] It is prudent to ask whether low level of HDL-c is also a significant risk factor in the evolution of diabetic retinopathy. From the present study, it appears that low HDL-c levels do not carry any additional risk, for the development of diabetic retinopathy in diabetic patients. However, retinal arteriosclerosis and vascular complications are common in diabetics. Diabetic retinopathy seems to be of independent evolution from that of arteriosclerosis and retinal vascular complications like venous occlusion and ischaemic optic neuropathy.

Summary

Total cholesterol, triglycerides and lipoprotein cholesterol were measured in 51 diabetic patients and 31 control subjects. Out of 51 diabetic patients, 26 were with retinopathy and 25 without retinopathy. The result showed a significant increase in blood pressure, triglycerides, total cholesterol, LDL-c and VLDL-c (P<0.01) and decrease in HDL-c (P<0.01) in diabetic patients as compared to controls. However, low HDL-c levels were not found to be significant risk factor in patient with diabetic retinopathy.

References

1.	Furman RH., Howard RP., Jakshimi K and Novcla L.N., 1961, Amer. J. Clin. Nutr. 9: 73.
2.	Cornwell D.G., Kruger F.A., Hamwi G.J. and Brown J.B., 1961. Amer. J. Clin. Nutr. 9: 41.
3.	Kulshreshta O.P., Nayar S.K., Sharma D.P., 1979. Ind. J. Ophthalmol. 27: 116.
4.	Lopes-Virella M.F.L., Stoye P.G. and Colwell J.A, 1977. Diabetologia 13: 285.
5.	Abell L.L., Levy B.B., Brodie B.B. and Kendall F.E., 1952. J. Biol. Chem. 195: 357.
6.	Van-Handel E. and Zilversmit D.B., 1957. J. Lab. Clin. Med. 50:152.
7.	Miller G.J. and Miller N.E., 1975. Lancet (i): 16.
8.	Rhoads G.G., Gulbrandsen C.C. and Kagen A, 1976. New Engl. J. Med. 294: 293.
9.	Dhir S.P., Ram J., Dahiya, Rajvir, Jain I.S. and Chakravarti R.N., 1983. Current Eye Res. (In press).