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 Table of Contents  
ORIGINAL ARTICLE
Year : 2017  |  Volume : 12  |  Issue : 2  |  Page : 121-132

Prevalence and risk factors – Hemoglobin A1c, serum magnesium, lipids, and microalbuminuria for diabetic retinopathy: A rural Hospital-based study


Department of Ophthalmology, Jawaharlal Nehru Medical College, DMIMS (DU), Wardha, Maharashtra, India

Date of Web Publication8-Sep-2017

Correspondence Address:
Prerana Phadnis
Department of Ophthalmology, Jawaharlal Nehru Medical College, DMIMS (DU), Sawangi (Meghe), Wardha, Maharashtra
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jdmimsu.jdmimsu_59_17

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  Abstract 

Objective: To study the risk factors responsible for diabetic retinopathy (DR). Material and Methods: One hundred and six cases of DR were included for the study. Detailed history including age and sex of the patient, duration of diabetes, anterior segment, and detailed fundus examination was carried out. Fasting blood sugar (FBS), postmeal blood sugar (PMBS), hemoglobin A1c (HbA1c), serum magnesium, lipid profile, and microalbuminuria were performed. Results: Of 106 patients of DR, 69.81% were males and 30.18% females. Average duration of diabetes was 7.67 years. Average age was 57.16 years. Nonproliferative DR (NPDR) was present in 87.73% and proliferative DR (PDR) in 12.26%. Raised FBS was present in 78.30%, raised PMBS in 69.81%, raised HbA1c in 77.35%, hypomagnesemia in 22.64%, and microalbuminuria in 7.55% patients. Raised low-density lipoprotein was present in 32.11% NPDR, 3.67% PDR, 19.81% clinically significant macular edema (CSME). Raised triglycerides were present in 37.74% NPDR, 1.88% PDR, and 21.70% CSME. Raised total cholesterol was present in 28.30% NPDR, 1.88% PDR, and 18.87% CSME. Conclusion: Risk factors for developing DR were duration of diabetes, uncontrolled blood sugar, raised HbA1c, hypomagnesemia, presence of microalbuminuria, and raised serum lipids. Therefore, good glycemic control with early diagnosis and management is required to prevent DR.

Keywords: Diabetic retinopathy, hypomagnesemia, microalbuminuria, serum lipids


How to cite this article:
Phadnis P, Kamble MA, Daigavane S, Tidke P, Gautam S. Prevalence and risk factors – Hemoglobin A1c, serum magnesium, lipids, and microalbuminuria for diabetic retinopathy: A rural Hospital-based study. J Datta Meghe Inst Med Sci Univ 2017;12:121-32

How to cite this URL:
Phadnis P, Kamble MA, Daigavane S, Tidke P, Gautam S. Prevalence and risk factors – Hemoglobin A1c, serum magnesium, lipids, and microalbuminuria for diabetic retinopathy: A rural Hospital-based study. J Datta Meghe Inst Med Sci Univ [serial online] 2017 [cited 2019 Oct 18];12:121-32. Available from: http://www.journaldmims.com/text.asp?2017/12/2/121/214196


  Introduction Top


The International Diabetes Federation's Diabetes  Atlas More Details reports that India has the highest number of people with diabetes (nearly 25%) in the world and hence considered to be the “Diabetes Capital of the World.” Currently, 40.9 million Indians are estimated to be suffering from diabetes. By 2025, this number will rocket to 69.9 million and potentially 85 million by 2030. In addition, 35 million Indians are at risk for diabetes. It is considered that nearly 14%–22% of the population across India falls in the prediabetic condition. These people could get diabetes within a decade.[1]

Although the pathogenesis is not fully understood various risk factors that affect its progression such as age, sex, and duration of diabetes, which has been known to be the most important one, the longer the period, the more likely are the chances to develop diabetic retinopathy (DR). Approximately 15 years after the initial diagnosis, more than 80% of patients have some degree of DR.[2]

Poor glycemic control results in microvascular complications such as retinopathy, nephropathy, and peripheral neuropathy. In addition, improving glycemic control improves these complications as suggested by many randomized trials done previously. However, fasting blood sugar (FBS) and postmeal blood sugar (PBMS) gauge hyperglycemia for a short duration which may be fallacious in describing a chronic and complex clinical condition.[3] Hence, glycosylated hemoglobin A1c (HbA1c) is presently the gold standard parameter which detects the mean blood glucose level over a period of 6–8 weeks and predicts the potential angiopathic complications. The measurement of HbA1C equals the assessment of hundreds (virtually thousands) of fasting glucose levels and also captures postprandial glucose peaks; therefore, it is a more robust and reliable measurement than fasting and postprandial glucose level.[3]

Hyperlipidemia contributes to DR and macular edema by endothelial dysfunction and breakdown of the blood–retinal barrier, leading to exudation of serum lipids and lipoproteins,[4] and is therefore considered as a metabolic risk factor.

Magnesium is involved on multiple levels in insulin secretion, binding, and activity. Low levels of magnesium can reduce secretion of insulin by the pancreas [5] and can promote the severity of DR.

Microalbuminuria is widely accepted as the first sign of diabetic nephropathy. As it progresses, microalbumiuria is converted to macroalbuminuria resulting in decreased glomerular filtration rate, but its additional effect in predicting retinopathy is questionable and needs to be studied.[6]

These risk factors have the potential to influence the onset, severity of DR, and vision. Hence, this study is carried out to understand the way they meticulously work to ruin our vision and help us keep these factors in check by making sincere efforts to undergo regular health checkup for early diagnosis and prompt management, which is a choice that we can always make to prevent the blinding consequences.

Aims and objectives

  • To study the prevalence of DR in relation to age and sex of the patients
  • To study the prevalence of various types of DR and its correlation with duration of diabetes mellitus (DM)
  • To explore the correlation of DR with risk factors such as serum HbA1c, blood glucose levels, serum magnesium levels, serum lipid profile, and urine microalbuminuria
  • To study the effect of DR on visual acuity (VA).



  Materials and Methods Top


Study setting

Ophthalmology outpatient department (OPD), Acharya Vinoba Bhave Rural Hospital (AVBRH) attached to Jawaharlal Nehru Medical College under DMIMS Sawangi, Wardha.

Design and source of study

This was a cross-sectional prospective clinical-based study of DR patients attending eye OPD and referral from diabetic OPD and indoor patients.

Study type

Noninterventional.

Study duration

Two years (August 2013–August 2015).

Sample size

One hundred and six patients of DR.

Inclusion criteria

  1. Diabetic patients attending eye OPD, referral from diabetic OPD, and indoor patients at AVBRH
  2. Patients between 20 and 80 years of age
  3. Patients who are accessible.


Exclusion criteria

  1. Patients with hazy media impairing visualization of fundus
  2. Patients in whom dilatation of pupil is contraindicated, i.e., angle closure glaucoma.


Study procedure

  • History
    • Relevant history was taken regarding symptomatology, i.e., blurring of vision, diminution of vision, loss of vision, floaters, diplopia, and change of refractive error
    • Loss of sensations, polyphagia, polydipsia, polyuria, and tingling sensations in periphery
    • History of any medication for DM, family history of similar complaints.
  • General and systemic examination was done
  • Ocular examination
    • VA: unaided, aided, and with pin hole were recorded
    • Any other incidental findings of lid, lacrimal apparatus, and ocular movements were noted
    • Anterior segment examination under diffuse torch light illumination and detailed examination was done under high magnification of slit lamp to rule out any pathology of conjunctiva, sclera, cornea, iris, anterior chamber, pupil, lens, anterior vitreous face, and any evidence of uveitis
    • Slit-lamp biomicroscopy with + 78 D + 90 D
    • Fundus examination by direct and indirect ophthalmoscope after dilatation of pupil
    • Intraocular pressure was recorded with a Topcon noncontact tonometer.
  • Diagnosed cases of diabetes after history and ocular examination underwent blood investigations:
    1. FBS
    2. PMBS
    3. Serum HbA1c
    4. Serum magnesium level
    5. Serum fasting lipid profile
    6. Urine microalbuminuria.
  • Fasting and postmeal blood samples were investigated by Rx Imola Randox machine for calibrating values of blood sugar, HbA1c, serum magnesium and lipid profile
  • Urine (24 h) sample was tested for the presence/absence of microalbuminuria using DIRUIH11-MA (microalbumin) dipstick method
  • Fundus pictures were taken using a Topcon fundus camera.


Statistical analysis

Statistical analysis was done using descriptive and inferential statistics using Chi-square test and Z-test for proportion. The software used in the analysis was SPSS 17.0 version (SPSS Inc, Chicago, IL) and GraphPad Prism 5.0 and P < 0.05 is considered as level of significance.





[Table 1] shows prevalence of DR. The study included 106 patients of DR out of 543 patients of DM who attended eye OPD and diabetic OPD. The prevalence was calculated to be 19.52%.
Table 1: Prevalence of diabetic retinopathy

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[Table 2] shows age-wise distribution of 106 patients of DR. Maximum number of cases were in 51–60 years of age group, followed by 61–70 years of age group. No patients below 20 years and above 80 years showed DR. Average age was 57.36 years.
Table 2: Age-wise distribution of patients

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[Table 3] shows gender-wise distribution of 106 patients of DR. Of 106 patients, 69.81% were males and 30.18% were females. It shows a male preponderance of DR in our study with male: female ratio of 2:1.
Table 3: Gender-wise distribution in diabetic retinopathy

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[Table 4] shows duration of DM in 106 patients of DR. Maximum number of patients, i.e., 44.33% of DR, were in 6–10 years of duration, followed by 0–5 years which included 32.07% patients. 16.03% of patients were between 11 and 15 years of duration of DM, while only 7.54% were between 16 and 20 years of duration of DM.
Table 4: Duration of diabetic mellitus in diabetic retinopathy

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[Table 5] shows type of DR in 106 patients. 93 (87.73%) patients were of nonproliferative DR (NPDR), of which 52 (49.05%) patients were of mild NPDR, 34 (32.07%) moderate NPDR, and 7 (6.60%) severe and very severe NPDR. However, 13 (12.26%) patients were of proliferative DR (PDR), of which 6 (5.66%) were mild-moderate PDR, 3 (2.83%) high-risk PDR, and 4 (3.77%) patients advanced PDR.
Table 5: Type of diabetic retinopathy

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[Table 6] shows correlation of severity of DR with duration of DM of 106 patients of DR. Mild NPDR was seen in 28.30% patients between 0 and 5 years of duration of DM. Moderate NPDR was maximum in 21.70% patients between 6 and 10 years of duration of DM. Severe and very severe NPDR was seen in 3.77% patients between 11 and 15 years and 1.89% patients between 6 and 10 years of duration of DM. PDR was seen in 3.77% patients in 16–20 years and 1.89% each of mild-moderate PDR, high-risk PDR, and advanced PDR between 11 and 15 years of duration of DM. Clinically significant macular edema (CSME) was seen maximum in 14.15% in 6–10 years of duration of DM. Since P < 0.0001, it signifies a strong association of severity of DR with duration of DM.
Table 6: Correlation of severity of diabetic retinopathy with duration of diabetic mellitus

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[Table 7] shows total number of CSME patients out of 106 patients of DR. It was present in 26.41% patients of DR. Z-value was significant.
Table 7: Clinically significant macular edema in diabetic retinopathy

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[Table 8] shows blood sugar levels in 106 patients of DR. FBS was raised in 78.30% patients, while PMBS was raised in 69.81% of 106 DR patients. Z-value was statistically significant.
Table 8: Blood sugar levels in diabetic retinopathy

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[Table 9] shows correlation of HbA1c in DR. It was more than cutoff value 6.5% of HbA1c in 77.35% of DR patients while only 22.64% with DR had below 6.5%. Z-value using statistical analysis was significant.
Table 9: Glycosylated hemoglobin in diabetic retinopathy

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[Table 10] shows correlation of HbA1c with type of DR out of 106 patients of DR. Maximum number of patients, i.e., 18.87% of mild NPDR, were in the range of 4%–6.5% of HbA1c; moderate NPDR were seen in 16.98% patients between 6.6% and 8.5% of HbA1c. Severe and very severe NPDR was seen in 3.77% patients between 8.6% and 10.5% and maximum patients of PDR 8.49% had above 10.5% of HbA1c. P < 0.001 signifies strong correlation of HbA1c with severity of DR.
Table 10: Correlation of glycosylated hemoglobin with type of diabetic retinopathy

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[Table 11] shows serum magnesium level in 106 patients of DR. 22.64% patients had hypomagnesemia, while 77.35% patients of DR had normal magnesium levels. Z-value was statistically significant.
Table 11: Magnesium levels in diabetic retinopathy

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[Table 12] shows correlation of serum magnesium with DR of 106 patients. Normal magnesium levels were present in maximum patients of mild NPDR (45.28%) and moderate NPDR (27.36%). As the severity of DR increased, hypomagnesemia was seen in 4.72% of severe and very severe NPDR, 3.77% patients each of mild-moderate PDR and adverse PDR, and 1.89% of high-risk PDR. 8.49% patients of CSME had hypomagnesemia while 17.92% patients of CSME had normal magnesium levels. P < 0.0001 signifies that serum magnesium is strongly associated with severity of DR.
Table 12: Correlation of magnesium with type of diabetic retinopathy

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[Table 13] shows urine microalbuminuria in DR of 106 patients of DR included. It was positive in 17.92% patients while remaining 82.07% had no microalbuminuria on dipstick test. Z-value was statistically significant.
Table 13: Microalbuminuria in diabetic retinopathy

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[Table 14] shows correlation of urine microalbuminuria with type of DR. It was positive in urine sample of 4.72% patients of severe and very severe NPDR and 4.72% of mild-moderate PDR, 1.89% of high-risk PDR, and 3.77% of advanced PDR as compared to 2.83% patients of moderate NPDR. It was absent in patients having mild NPDR. P < 0.0001 signifies a strong correlation with urine microalbuminuria with type of DR.
Table 14: Correlation of urine microalbuminuria with type of diabetic retinopathy

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[Table 15] shows lipid profile estimation done in 106 patients of DR. Low-density lipoprotein (LDL), triglycerides (TGs), and total cholesterol (TC) levels were raised in 36.79%, 39.62%, and 30.18% of patients of DR, respectively. Very LDL (VLDL) was raised in only 13.20% patients of DR, while high-density lipoprotein (HDL) levels were present in 7.54% patients. Z-value using statistical analysis was borderline significant for HDL, while it was significant for LDL, TGs, VLDL, and TC levels.
Table 15: Lipid profile in diabetic retinopathy

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[Table 16] shows correlation of lipid profile with DR in 106 patients. LDL was maximally raised in moderate NPDR (24.53%), severe and very severe NPDR (3.77%), and in patients of CSME (19.81%). TGs were raised in moderate NPDR (21.70%), mild NPDR (13.21%), and in patients of CSME (21.70%). TC was raised in moderate NPDR (19.81%), severe and very severe NPDR (2.83%), and in patients of CSME (18.87%). P < 0.0001 signifies strong association of LDL, TGs, and TC in patients of moderate NPDR, severe and very severe NPDR, and in CSME patients.
Table 16: Correlation of lipid profile with type of diabetic retinopathy

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[Table 17] shows VA with type of DR. Maximum patients of mild NPDR (35.85%) had VA between 6/6 and 6/12. 8.49% patients of moderate NPDR had VA between 6/18 and 6/24. 11.32% patients of moderate NPDR had VA between 6/36 and 6/60 while 10.37% of PDR patients had VA <6/60. 12.26% patients of CSME had VA between 6/36 and 6/60. P < 0.0001 is statistically significant and signifies gross reduction in VA with increased severity of DR. (The observation of the study in graphical forms are depicted in the [Graph 1],[Graph 2],[Graph 3],[Graph 4],[Graph 5],[Graph 6],[Graph 7],[Graph 8],[Graph 9],[Graph 10],[Graph 11],[Graph 12],[Graph 13],[Graph 14],[Graph 15],[Graph 16],[Graph 17])
Table 17: Visual acuity in diabetic retinopathy

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  Discussion Top


Of 543 patients of DM, 106 had DR which shows prevalence of 19.52%. The prevalence of DR in India is 12%–22.4%.[7],[8],[9] The neighboring Asian countries also showed a similar trend approximately 15%.[10],[11],[12] In one study conducted in Southern India, the prevalence was high 26.2%,[13] and in Japan,[14] 38%, which were both in a self-reported population with diabetes. In other countries such as the United States, the United Kingdom, Australia, and the West Indies, the prevalence of DR was estimated to range from 28.5% to 50.3%,[15],[16],[17],[18] while countries that are somewhat closer to India such as Singapore or Mauritius, it was 21.8% and 30%. Our study correlates with other studies done in India and Asian countries [Table 1].

Maximum number of cases was in 51–60 years (31.13%) of age, followed by 61–70 years (28.30%) and 41–50 years (26.41%). After 70 years, only 9.43% patients showed DR. No patients below 20 years had DR. This shows that age is an important risk factor. This pattern may be because many subjects of severe diabetes with secondary complications may not survive beyond the age of 80 years. The prevalence of DR did not show much linear trend with age. There was a decrease in prevalence in the sixth decade of life; however, in the seventh decade, it leveled off and later it dropped [Table 2].

In a study conducted in Sankara Netralaya, the prevalence of DR among patients with diabetes between 40 and 49 years of age was 13.4%; between 50 and 59 years of age, the prevalence was 20.9%; and between 60 and 69 years of age, the prevalence was 20.5%; and for those older than 70 years, the prevalence was 14.8%.[19] Similar trends also were observed by the Eye Diseases Prevalence Research Group's report on the prevalence of DR in the United States, the Barbados Eye Study, the Beaver Dam Study, and the Wisconsin Epidemiologic Study of DR (WESTDR).[19]

Prevalence of DR was seen more in male patients (69.81%) as compared to females (30.18%) with male: female – 2:1. The exact reason for male predominance has not been determined probably because of sociological factors and early presentation of males for health checkup.

This observation of male preponderance is in correlation with the findings of other population-based studies such as the Chennai Urban Rural Epidemiology Study, the Andhra Pradesh Eye Disease Study, and United Kingdom Prospective Diabetes Study [Table 3].[19]

Maximum number of patients with DR was in 6–10 years of duration (44.33%), followed by 0–5 years of duration (32.07%). Of 106 patients of DR, 30 (28.30%) patients were of mild NPDR and 4 (3.77%) patients of moderate NPDR had duration of DM between 0 and 5 years. Of 28 patients, CSME was present in 6 (5.66%) patients and none of the patients of severe and very severe NPDR and PDR was in this category [Table 4] and [Table 6].

Duration of DM between 6 and 10 years was present in 22 (20.75%) patients of mild NPDR, 23 (21.70%) of moderate NPDR, and 2 (1.89%) patients of severe and very severe NPDR. Of 28 patients, CSME was present in 15 (14.15%) patients while none of the patients of PDR was within this range.

Duration of DM between 11 and 15 years was present in 7 (6.60%) patients of moderate NPDR, 4 (3.77%) of severe and very severe NPDR, 2 (1.89%) of mild-moderate PDR, 2 (1.89%) of high-risk PDR, and 2 (1.89%) of advanced PDR. Of 28 patients, CSME was present in 7 (6.60%) patients. None of the patients of mild NPDR was in this range.

Duration of DM between 16 and 20 years was present in 1 (0.94%) patient of severe NPDR, 4 (3.77%) of mild-moderate PDR, 1 (0.94%) of high-risk PDR, and 2 (1.89%) of advanced PDR. None of the patients of mild and moderate NPDR and CSME was in this range. This suggests that the severity of retinopathy increased with the duration of DM in the present study, probably due to prolonged exposure to hyperglycemia and other risk factors.

The mean duration of diabetes in our study was 7.67 years. It correlates with the study conducted at Sankara Netralaya [19] with mean duration of 6.7 years, while the Wisconsin study [19] showed 11.8 years. In a study conducted in Pakistan, patients with duration 5–10 years had five times more chances to have nonproliferative retinopathy and 2 × 106 times (odds ratio) more chances for advanced retinopathy than patients with duration < 5 years and no retinopathy. Similarly, patients with duration more than 10 years had 32 times more chances to have nonproliferative retinopathy and 2 × 108 times (odds ratio) more chance to have proliferative retinopathy than patients with duration < 5 years and no retinopathy.[20]

Of 106 patients of DR, maximum number of patients, i.e., 93 (87.73%) were of NPDR, of which 52 (49.05%) patients were of mild NPDR, 34 (32.07%) moderate NPDR, and 7 (6.60%) severe and very severe NPDR. However, only, 13 (12.26%) patients were of PDR, of which 6 (5.66%) were of mild-moderate PDR, 3 (2.83%) high-risk PDR, and 4 (3.77%) advanced PDR [Table 5].

FBS was raised in 83 patients (78.30%) and 74 patients (69.81%) had raised PMBS, showing poor glycemic control in these patients. Of 106, only 29 patients (27.53%) were on medication due to unawareness of the disease among the rural population. Improvement in glycemic control among the patients on medications showed control in the retinopathy [Table 8].

Blood sugar levels were useful for spot diagnosis of diabetes; however, FBS and PMBS gauge hyperglycemia for a short duration, which may be fallacious in describing a chronic and complex clinical condition.[3]

In our study, 24 (22.64%) DR patients had HbA1c below 6.5%, of which 20 (18.87%) had mild NPDR and 4 (3.77%) had moderate NPDR. No patients of severe and very severe NPDR and PDR were below 6.5%. Rest 82 (77.35%) DR patients were above 6.5% of HbA1c [Table 9] and [Table 10].

HbA1c levels between 6.6% and 8.5% were seen in 17 (16.04%) patients of mild NPDR, 18 (16.98%) of moderate NPDR, and 1 (0.94%) of severe NPDR. No patients of PDR were in this range.

HbA1c level between 8.6% and 10.5% was observed in 14 (13.21%) patients of mild NPDR, 11 (10.38%) of moderate NPDR, 4 (3.77%) of severe and very severe NPDR, 2 (1.89%) of mild-moderate PDR, and 1 (0.94%) patient each of high-risk and advanced PDR.

HbA1c levels were more than 10.5% in 1 (0.94%) patient of mild NPDR, 1 (0.94%) of moderate NPDR, 2 (1.89%) of severe and very severe NPDR, 4 (3.77%) of mild-moderate PDR, 2 (1.89) of high-risk PDR, and 3 (2.83%) patients of advanced PDR.

11 (13.41%) patients of CSME were between 6.6% and 8.5% of HbA1c, 9 (8.49%) between 8.6% and 10.5% of HbA1c, 6 (5.66%) between 6.6% and 8.5% of HbA1c, and 2 (1.89%) more than 10.6% of HbA1c.

Lower levels of HbA1c showed milder degree of retinopathy while raised levels of HbA1c were associated with increased severity in the present study, suggesting that measuring HbA1c can help detect DR at an early stage and its constant high levels may also be responsible for severity of retinopathy. HbA1c detects the mean blood glucose level over a period of 6–8 weeks and predicts the potential angiopathic complications. The measurement of HbA1C equals the assessment of hundreds (virtually thousands) of fasting glucose levels and also captures postprandial glucose peaks; therefore, it is a more robust and reliable measurement than fasting and postprandial glucose level.[3]

Kowall and Rathmann [21] found that prevalence of any retinopathy was 2.5–4.5 times as high in persons with HbA1c-defined type 2 DM. The WESTDR [22] also found that HbA1c (divided into both quartiles and deciles) correlated with a consistent increase in retinopathy from the lowest (5.4%–8.5%) to the highest quartile (11.6%–20.8%) although it did not show any threshold cutoff. Cho et al.[23] however confirmed that the proposed HbA1c cutoff level (6.5%) as proposed by the American Diabetes Association allowed accurate detection of DR.

Of 106 patients, 24 (22.64%) DR patients had hypomagnesemia, of which 4 (3.77%) had mild NPDR, 5 (4.72%) had moderate NPDR, 5 (4.72%) severe and very severe NPDR, 4 (3.77%) mild-moderate PDR, 2 (1.89%) high-risk PDR, and all 4 (3.77%) patients of advanced PDR had hypomagnesemia [Table 11] and [Table 12].

Eighty-two DR (77.35%) patients had normal magnesium levels, of which 48 (45.28%) patients had a mild NPDR, 29 (27.36%) moderate NPDR, 2 (1.89%) severe and very severe NPDR, 2 (1.89%) mild-moderate PDR, and 1 (0.94%) patient was in high-risk category but in the lower range of normal. Our study showed that magnesium levels dropped with the severity of retinopathy suggesting that hypomagnesemia can be an important risk factor.

Hypomagnesemia was present in 9 (8.49%) patients of CSME, while 19 (17.92%) patients had normal serum magnesium levels.

A study [24] has found that diabetic patients, regardless of therapy, had lower concentrations of serum magnesium than healthy people (matched for age) while diabetic subjects with retinopathy had the lowest concentrations of magnesium. In addition, serum magnesium concentrations were affected by the degree of diabetic control; the better the control, the higher was the concentration of magnesium.

Kareem et al.[5] also found to have lower levels of magnesium in diabetics without retinopathy and lowest levels in patients with retinopathy, probably due to increased urinary loss of magnesium due to osmotic effect of glycosuria causing decreased tubular reabsorption of magnesium and also suggested a direct relationship between serum magnesium level and cellular glucose disposal due to increased sensitivity of the tissues to insulin in the presence of adequate magnesium levels.

Microalbuminuria was positive in urine sample of 19 patients (17.92%). Of 19 patients, 5 (4.72%) patients had severe and very severe NPDR, 5 (4.72%) mild-moderate PDR, 2 (1.89%) high-risk PDR, and 4 (3.77%) advanced PDR as compared to those having moderate NPDR, 3 (2.83%) which had positive value. However, 87 (82.07%) patients had no microalbuminuria. It was absent in patients having mild NPDR suggesting that microalbuminuria is more important for predicting proliferative type of DR. However, it is a quantitative assessment done by dip stick which was available at our institute for testing microalbuminuria. Other studies have used qualitative assessment of microalbuminuria which is a more accurate method [Table 13] and [Table 14].

Microalbuminuria was present in 6 (5.66%) patients of CSME and was absent in 22 (20.75%) patients.

Cruickshanks et al.[25] found that microalbuminuria is associated cross-sectionally with the presence of retinopathy in persons with diabetes and with the presence of proliferative disease but in younger-onset individuals. In a cross-sectional study of 4739 type 2 diabetic patients in Shanghai, China, Chang and Chuang [6] reported that a microalbuminuria threshold of 10.7 mg/24 h, which was within the traditional “normal range,” can predict the increased risk for DR development even after adjusting for other risk factors, but it did not show any evidence on predicting the severity of retinopathy.

CSME was present in 28 cases of 106 DR patients. Out of which, 21 (19.81%) patients had raised LDL, 23 (21.69%) had raised TGs, and 20 had raised cholesterol levels (18.86%). These levels were found to be higher in patients having moderate NPDR, i.e., LDL was raised in 26 (24.52%) patients, TGs in 23 (21.69%), and cholesterol in 21 (19.81%) patients [Table 7],[Table 15], and [Table 16].

In patients of severe and very severe NPDR, LDL was raised in 4 (3.77%) patients, TGs were high in 3 (2.83%), and cholesterol in 3 (2.83%) patients, suggesting that the CSME was more prevalent in moderate, severe, and very severe type of retinopathy.

None of the patients of CSME in our study had raised level of HDL and VLDL levels.

This is in consistent with findings of van Leiden et al. showing similar associations between serum TGs and degree of retinopathy in subjects with type 2 DM.[26] Chew et al.[27] stated that patients with high TC and LDL levels were more likely to have retinal hard exudates compared to patients with normal lipid profile. Another study by DCCT/EDIC group showed that severity of retinopathy was associated with serum TGs in subjects with type 1 diabetes.[28] However, Hove et al.[29] reported no significant association between DR, TGs, HDL, and TC in diabetic population in Denmark. Miljanovic et al.[30] reported no lipid profile associated with progression of DR or with PDR.

The mechanism by which high serum lipids may cause progression of DR is not clearly understood. It is suggested that elevation of blood viscosity and alteration of fibrinolytic system occur in hyperlipidemia causing hard exudate formation.[31] There may also be incorporation of TGs into the cell membrane, leading to changes in fluidity and leakage of plasma constituents into the retina, resulting in hemorrhage and edema in retina. This also leads to endothelial dysfunction and local inflammatory response releasing cytokines and growth factors which are responsible for neovascularization in retina.[23],[32]

Of 106 patients of DR, VA was assessed with the severity of DR. VA of range 6/6–6/12 was present in 38 (35.84%) patients of mild NPDR and 8 (7.55%) of moderate NPDR. None of the patients of severe and very severe NPDR and PDR was within this range. Furthermore, 3 (2.83%) of 28 patients of CSME were in this range [Table 17].

VA between 6/18 and 6/24 was present in 7 (6.60%) patients of mild NPDR, 9 (8.49%) of moderate NPDR, and 1 (0.94%) of severe NPDR. None of the patients of PDR was within this range. 4 (3.77%) patients of 28 patients of CSME had VA between 6/18 and 6/24.

VA between 6/36 and 6/60 was present in 4 (3.77%) patients of mild NPDR, 12 (11.32%) of moderate NPDR, 3 (2.83%) of severe and very severe NPDR, and 2 (1.89%) of mild-moderate PDR. No patients of high-risk and advanced PDR were in this range. 13 (12.26%) of 28 patients of CSME had VA between 6/36 and 6/60.

VA <6/60 was present in 3 (2.83%) patients of mild NPDR, 5 (4.72%) in moderate NPDR, 3 (2.83%) in severe and very severe NPDR, 4 (3.77%) in mild-moderate PDR, 3 (2.83%) in high-risk PDR, and 4 (3.77%) in advanced PDR. 8 (7.55%) of 28 patients of CSME were in this range.

VA decreased with increase in the severity of DR and progressed toward blindness in advanced PDR with vision of <6/60. This shows that DR has a severe impact on the vision. In addition, in patients of CSME, vision was found to be decreased even with lesser degree of retinopathy due to involvement of macula and central vision.

Ismail and Whitaker [33] reported a significant difference between VA scores in individuals with progressive DR and controls and when comparing them to groups with diabetes and early DR. However, no significant difference was found when comparing the early DR group with nondiabetic control groups. Therefore, VA is significantly reduced as DR progresses but may not be a sensitive enough approach to detect the early stages of DR.

In addition to microvascular changes, retinal neurodegeneration is now thought to be a component of DR.[34],[35],[36] Histological studies showed that diabetes increases the rate of apoptosis of several types of cells in the retina, including neurons, and lead to the suggestion that DR can be considered a chronic neurodegenerative disease of the retina,[35] which results in fall in the VA.


  Summary Top


A total of 106 patients of DR were studied and various observations were analyzed and findings of the present study are summarized as follows:

  • Of 543 patients of DM, 106 had DR
  • Maximum number of cases was seen in 51–60 years (31.13%) of age, followed by 61–70 years (28.30%) of age.
  • Majority of the patients were males, i.e., 69.81% as compared to females (30.18%), with a male to female ratio of 2:1
  • 44.33% of patients with DR were in 6–10 years of duration, followed by 32.07% between 0 and 5 years of duration
  • Of 106 patients, 87.73% were of NPDR and 12.26% were of PDR
  • Of 87.73% of NPDR 49.05% patients were of mild NPDR, 32.07% were of moderate NPDR, and 6.60% were of severe and very severe NPDR
  • Of 12.26% patients of PDR of which, 5.66% were of mild-moderate PDR, 2.83% high-risk PDR, and 3.77% advanced PDR
  • FBS was raised in 78.30% of the patients and 69.81% had raised PMBS showing poor glycemic control in these patients
  • HbA1c was more than cutoff value, i.e., 6.5% in 77.35% patients of DR, while only 22.64% patients had below 6.5%. HbA1c between 6.6% and 10.5% was present in 61.32% of NPDR, 3.77% of PDR, and 18.87% of CSME, while HbA1c >10.5% was present in 3.77% of NPDR, 8.49% of PDR, and 1.89% of CSME.
  • Hypomagnesemia was seen in 22.64% DR patients, of which 13.21% patients were of NPDR, 9.43% patients of PDR, and 8.49% of CSME
  • Microalbuminuria was positive in urine sample of 7.55% patients of NPDR, 10.38% of PDR, and 5.66% of CSME
  • LDL was raised in 32.11% of NPDR and 3.67% of PDR. TGs were raised in 37.74% of NPDR and 1.88% of PDR. TC was raised in 28.30% of NPDR and 1.88% of PDR
  • CSME was present in 28 cases out of 106 DR, of which 19.81% had raised LDL, 21.70% had raised TGs, and 18.87% patients had raised cholesterol levels
  • VA between 6/6 and 6/24 was present in 59.43% patients of NPDR and 6.6% of CSME; none of the patients of PDR was in this range. VA between 6/36 and <6/60 was present in 28.3% patients of NPDR, 12.26% of PDR, and 19.81% of CSME.



  Conclusion Top


  • Prevalence of DR was 19.52%
  • DR was associated with an increase in age and showed a male preponderance
  • Severity of DR was strongly correlated with duration of diabetes
  • HbA1c is a sensitive diagnostic investigation for estimating blood glucose over a period; lesser value successfully predicted the chances of developing retinopathy at an early stage while higher values strongly predicted its severity
  • Hypomagnesemia was an important risk factor and showed positive correlation with the severity of DR
  • There was a significant correlation of serum TGs, LDL, and TC with moderate and severe and very severe NPDR and CSME.
  • Microalbuminuria was an important marker for the risk of developing severe and very severe NPDR and proliferative type of DR.
  • VA decreased with increased severity of DR and CSME.


Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Mistry P, Vikhe P, Kadu C. Diabetic retinopathy stages detection using fundus images. Int J Eng Res Gen Sci 2015;3:2091-730. Available from: http://www.pnrsolution.org/Datacenter/Vol3/Issue2/6.pdf. [Last accessed on 2015, March-April].  Back to cited text no. 1
    
2.
Massin P, Paques M. Épidémiologie et physiopathologie de la rétinopathie diabétique. EMC Endocrinol Nutr (Elsevier BV) 2004;1:1-6.  Back to cited text no. 2
    
3.
Bonora E, Tuomilehto J. The pros and cons of diagnosing diabetes with A1C. Diabetes Care 2011;34 Suppl 2:S184-90.  Back to cited text no. 3
    
4.
Agroiya P, Philip R, Saran S, Gutch M, Tyagi R, Gupta KK. Association of serum lipids with diabetic retinopathy in type 2 diabetes. Indian J Endocrinol Metab 2013;17 Suppl 1:S335-7.  Back to cited text no. 4
    
5.
Kareem I, Jaweed SA, Bardapurkar JS, Patil VP. Study of magnesium, glycosylated hemoglobin and lipid profile in diabetic retinopathy. Indian J Clin Biochem 2004;19:124-7.  Back to cited text no. 5
    
6.
Chang CH, Chuang LM. Microalbuminuria and diabetic retinopathy in type 2 diabetic patients: From risk association to risk prediction. J Diabetes Investig 2013;4:42-4.  Back to cited text no. 6
    
7.
Ahuja MM, Sivaji L, Garg VK, Mitroo P. Prevalence of diabetes in Northern India (Delhi area). Horm Metab Res 1972;4:321-4.  Back to cited text no. 7
    
8.
Rema M, Premkumar S, Anitha B, Deepa R, Pradeepa R, Mohan V, et al. Prevalence of diabetic retinopathy in urban India: The Chennai Urban Rural Epidemiology Study (CURES) Eye Study, I. Invest Ophthalmol Vis Sci 2005;46:2328-33.  Back to cited text no. 8
    
9.
Ramachandran A, Snehalatha C, Vijay V, King H. Impact of poverty on the prevalence of diabetes and its complications in urban Southern India. Diabet Med 2002;19:130-5.  Back to cited text no. 9
    
10.
Hu YH, Pan XR, Liu PA, Li GW, Howard BV, Bennett PH, et al. Coronary heart disease and diabetic retinopathy in newly diagnosed diabetes in Da Qing, China: The Da Qing IGT and diabetes study. Acta Diabetol 1991;28:169-73.  Back to cited text no. 10
    
11.
Weerasuriya N, Siribaddana S, Dissanayake A, Subasinghe Z, Wariyapola D, Fernando DJ, et al. Long-term complications in newly diagnosed Sri Lankan patients with type 2 diabetes mellitus. QJM 1998;91:439-43.  Back to cited text no. 11
    
12.
Jamal-u-Din, Qureshi MB, Khan AJ, Khan MD, Ahmad K. Prevalence of diabetic retinopathy among individuals screened positive for diabetes in five community-based eye camps in Northern Karachi, Pakistan. J Ayub Med Coll Abbottabad 2006;18:40-3.  Back to cited text no. 12
    
13.
Narendran V, John RK, Raghuram A, Ravindran RD, Nirmalan PK, Thulasiraj RD, et al. Diabetic retinopathy among self reported diabetics in Southern India: A population based assessment. Br J Ophthalmol 2002;86:1014-8.  Back to cited text no. 13
    
14.
Kuzuya T, Akanuma Y, Akazawa Y, Uehata T. Prevalence of chronic complications in Japanese diabetic patients. Diabetes Res Clin Pract 1994;24 Suppl:S159-64.  Back to cited text no. 14
    
15.
Klein R, Klein BE, Moss SE. The Wisconsin epidemiological study of diabetic retinopathy: A review. Diabetes Metab Rev 1989;5:559-70.  Back to cited text no. 15
    
16.
Kohner EM, Aldington SJ, Stratton IM, Manley SE, Holman RR, Matthews DR, et al. United Kingdom prospective diabetes study, 30: Diabetic retinopathy at diagnosis of non-insulin-dependent diabetes mellitus and associated risk factors. Arch Ophthalmol 1998;116:297-303.  Back to cited text no. 16
    
17.
Cugati S, Kifley A, Mitchell P, Wang JJ. Temporal trends in the age-specific prevalence of diabetes and diabetic retinopathy in older persons: Population-based survey findings. Diabetes Res Clin Pract 2006;74:301-8.  Back to cited text no. 17
    
18.
Leske MC, Wu SY, Hyman L, Li X, Hennis A, Connell AM, et al. Diabetic retinopathy in a black population: The Barbados Eye Study. Ophthalmology 1999;106:1893-9.  Back to cited text no. 18
    
19.
Raman R, Rani PK, Reddi Rachepalle S, Gnanamoorthy P, Uthra S, Kumaramanickavel G, et al. Prevalence of diabetic retinopathy in India: Sankara Nethralaya Diabetic Retinopathy Epidemiology and Molecular Genetics Study report 2. Ophthalmology 2009;116:311-8.  Back to cited text no. 19
    
20.
Niazi MK, Akram A, Naz MA, Awan S. Duration of diabetes as a significant factor for retinopathy. Pak J Ophthalmol 2010;26:82-186. 16.  Back to cited text no. 20
    
21.
Kowall B, Rathmann W. HbA1c for diagnosis of type 2 diabetes. Is there an optimal cut point to assess high risk of diabetes complications, and how well does the 6.5% cutoff perform? Diabetes Metab Syndr Obes 2013;6:477-91.  Back to cited text no. 21
    
22.
Klein R, Klein BE, Moss SE, Davis MD, DeMets DL. Glycosylated hemoglobin predicts the incidence and progression of diabetic retinopathy. JAMA 1988;260:2864-71.  Back to cited text no. 22
    
23.
Cho NH, Kim TH, Woo SJ, Park KH, Lim S, Cho YM, et al. Optimal HbA1c cutoff for detecting diabetic retinopathy. Acta Diabetol 2013;50:837-42.  Back to cited text no. 23
    
24.
Ceriello A, Giugliano D, Dello Russo P, Passariello N. Hypomagnesemia in relation to diabetic retinopathy. Diabetes Care 1982;5:558-9.  Back to cited text no. 24
    
25.
Cruickshanks KJ, Ritter LL, Klein R, Moss SE. The association of microalbuminuria with diabetic retinopathy. The Wisconsin epidemiologic study of diabetic retinopathy. Ophthalmology 1993;100:862-7.  Back to cited text no. 25
    
26.
van Leiden HA, Dekker JM, Moll AC, Nijpels G, Heine RJ, Bouter LM, et al. Blood pressure, lipids, and obesity are associated with retinopathy: The Hoorn study. Diabetes Care 2002;25:1320-5.  Back to cited text no. 26
    
27.
Chew EY, Klein ML, Ferris FL 3rd, Remaley NA, Murphy RP, Chantry K, et al. Association of elevated serum lipid levels with retinal hard exudate in diabetic retinopathy. Early Treatment Diabetic Retinopathy Study (ETDRS) report 22. Arch Ophthalmol 1996;114:1079-84.  Back to cited text no. 27
    
28.
Lyons TJ, Jenkins AJ, Zheng D, Lackland DT, McGee D, Garvey WT, et al. Diabetic retinopathy and serum lipoprotein subclasses in the DCCT/EDIC cohort. Invest Ophthalmol Vis Sci 2004;45:910-8.  Back to cited text no. 28
    
29.
Hove MN, Kristensen JK, Lauritzen T, Bek T. The prevalence of retinopathy in an unselected population of type 2 diabetes patients from Arhus County, Denmark. Acta Ophthalmol Scand 2004;82:443-8.  Back to cited text no. 29
    
30.
Miljanovic B, Glynn RJ, Nathan DM, Manson JE, Schaumberg DA. A prospective study of serum lipids and risk of diabetic macular edema in type 1 diabetes. Diabetes 2004;53:2883-92.  Back to cited text no. 30
    
31.
Kawamura M, Heinecke JW, Chait A. Pathophysiological concentrations of glucose promote oxidative modification of low density lipoprotein by a superoxide-dependent pathway. J Clin Invest 1994;94:771-8.  Back to cited text no. 31
    
32.
Rema M, Sujatha P, Pradeepa R. Visual outcomes of pan-retinal photocoagulation in diabetic retinopathy at one-year follow-up and associated risk factors. Indian J Ophthalmol 2005;53:93-9.  Back to cited text no. 32
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33.
Ismail GM, Whitaker D. Early detection of changes in visual function in diabetes mellitus. Ophthalmic Physiol Opt 1998;18:3-12.  Back to cited text no. 33
    
34.
Barber AJ, Lieth E, Khin SA, Antonetti DA, Buchanan AG, Gardner TW, et al. Neural apoptosis in the retina during experimental and human diabetes. Early onset and effect of insulin. J Clin Invest 1998;102:783-91.  Back to cited text no. 34
    
35.
Barber AJ. A new view of diabetic retinopathy: A neurodegenerative disease of the eye. Prog Neuropsychopharmacol Biol Psychiatry 2003;27:283-90.  Back to cited text no. 35
    
36.
Barber AJ, Gardner TW, Abcouwer SF. The significance of vascular and neural apoptosis to the pathology of diabetic retinopathy. Invest Ophthalmol Vis Sci 2011;52:1156-63.  Back to cited text no. 36
    



 
 
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