Role of Low Density Lipoprotein Cholesterol in Progression of Diabetic Retinopathy
Published: April 1, 2018 | DOI: https://doi.org/10.7860/JCDR/2018/27441.11373
Rahul, Narsingh Verma, Mayank Agarwal, Pravesh Kumar, Sandeep Saxena, Anuj Maheshwari
1. Assistant Professor, Department of Physiology, Hind Institute of Medical Sciences, Barabanki, Uttar Pradesh, India.
2. Professor, Department of Physiology, King George's Medical University, Lucknow, Uttar Pradesh, India.
3. Senior Resident, Department of Physiology, Hind Institute of Medical Sciences, Barabanki, Uttar Pradesh, India.
4. Medical Officer, Employee State Insurance Corporation of India, Lucknow, Uttar Pradesh, India.
5. Professor, Department of Ophthalmology, King George's Medical University, Lucknow, Uttar Pradesh, India.
6. Professor, Department of Medicine, Babu Banarsidas Dental University, Lucknow, Uttar Pradesh, India.
Correspondence
Dr. Mayank Agarwal,
Hind Institute of Medical Sciences, Safedabad, Barabanki, Uttar Pradesh, India.
E-mail: ma.gsvm@gmail.com
Introduction: Various cross-sectional studies indicate that dyslipidemia and increased activity of enzyme Aldose Reductase (ALDR-2) are associated with the establishment of Diabetic Retinopathy (DR). However, it remains unclear that among dyslipidemia and ALDR-2 activity, which is more important for the progression of DR from nonproliferative to the proliferative stage.
Aim: The present study was designed to explore the role of dyslipidemia and ALDR-2 activity in the progression of DR.
Materials and Methods: Two hundred subjects were involved in this cross-sectional study, 150 subjects had Type 2 diabetes while 50 had No Diabetes and No Retinopathy (NDNR) and acted as controls. On the basis of fundus examination, diabetic subjects were further divided equally into those having: No Retinopathy (DNR), Non-Proliferative DR (NPDR), and Proliferative DR (PDR). Fasting lipid profile, ALDR-2 level, fasting and postprandial blood sugar were measured using a standard protocol. Data were analysed using both descriptive and inferential statistics using unpaired t-test.
Results: ALDR-2 level was significantly (p-value=0.0001) higher in NPDR than DNR. Low-Density Lipoprotein Cholesterol (LDL-C) was significantly (p-value=0.0235) higher in PDR than NPDR. Fasting Blood Sugar (FBS), Postprandial Blood Sugar (PPS), and LDL-C were significantly higher in DNR than NDNR while high-density lipoprotein cholesterol was significantly lower in DNR than NDNR group.
Conclusion: Persistent hyperglycaemia causes an increased ALDR-2 activity that has a significant role in the establishment of DR. However, dyslipidemia is more important as a risk factor for progression of NPDR to PDR. Hypolipidemic drug as an adjunctive therapy could prevent the progression of DR from NPDR to PDR.
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