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Diabetic Retinopathy – An Update

Neeti Gupta1, Rohit Gupta2
Department of 1Ophthalmology and 2Medicine,
Himalayan Institute of Medical Sciences, Dehradun, Uttarakhand, India

Abstract: Diabetic retinopathy is the most common complication of diabetes mellitus and a leading cause of blindness in diabetics. Diabetic retinopathy
in Indians presents at a younger age and has genetic predisposition. The present article focuses on the pathophysiology, classification and management
of diabetic retinopathy.

INTRODUCTION two main pathological processes leading to the changes in DR. The
Diabetes Mellitus (DM) and the eye diseases associated with it comprise earliest change seen in diabetes before development of retinopathy is
a set of complex disorder with multi-factorial etiology, where both genetic the breakdown of the blood retinal barrier (BRB). Aldose reductase
and environmental factors play an active role. It is a major cause of present in the pericytes alters the cellular metabolism, resulting in the
avoidable blindness in both the developed and developing countries loss of pericytes. This disrupts the autoregulation and lead to breakdown
.Newly diagnosed diabetic cases are increasing at an alarming rate in the of BRB and leakage of plasma.
developing countries like India due to better life style and the demographic Loss of pericytes also leads to saccular out pouching of the capillary
right shift of the population ,urbanization and disparities in the access walls known as microaneurysms. These microaneurysms tend to gradually
to the health care system. enlarge, thickening and hyalinization of the walls takes place, which
Approximately 382 million people across the world have been estimated eventually lead to auto occlusion by encroachment of the thickened wall
to have DM in 2013 and if no action is taken this number will rise to 592 into the lumen. Other factors responsible for microvascular occlusion
million by 20351. WHO estimates that 19% of the world’s diabetic are capillary endothelial cell damage and proliferation; change in red
population lives in India and 80 million people in India will have diabetes blood cells leading to defective oxygen transport and increased stickiness
by the year 2030. Diabetic retinopathy (DR) is the most common and aggregation of platelets. (Fig 1)
complication of diabetes mellitus. It has been seen that patients having
DR are 25 times more at risk of blindness than a non-diabetic individual.
Timely diagnosis with the help of better screening and referral facilities,
strict control of systemic parameters and timely intervention in the form
of medical and surgical intervention can delay the sight threatening
complication of DR.
EPIDEMIOLOGY
It has been estimated that 30% of people with DM have DR worldwide2.
A pooled analysis of 35 studies showed that the overall prevalence of
DR of any severity is 34.6% and the prevalence of proliferative diabetic
retinopathy (PDR) and diabetic macular edema (DME) is 6.96% and
6.81% respectively2. The presence of diabetic retinopathy is directly
proportional to the duration of DM. Seoul metropolitan city diabetes
prevention programme study estimated that 55.2% patient had DR with
more than 10 yrs of DM as compared to 12.6% with less than 10 yrs of
DM with an approximately three fold increase in the vision threatening Fig 1 : Pathogenesis of DR
DR in patients with more than 10 years of DM3.
RISK FACTORS
The prevalence of DR in India is approximately 5.6 million 4.There may
be 2.9 million people with mild non proliferative diabetic retinopathy Progression of DR depends on various risk factors. The main aim towards
(NPDR), 2.2 million people with moderate NPDR, 111,258 people with delayed progression of DR is to target the modifiable risk factors.
severe NPDR and 296,688 people with PDR4. The prevalence rate of NON MODIFIABLE RISK FACTORS
DR in type 2 DM was reported as 34.1% from south India5. Chennai
urban rural epidemiology study (CURES) estimated that the overall 1. Duration of DM: It has been reported that there a direct correlation between
prevalence of DR in urban population to be 17.6%6. the duration of DM and severity of DR. There is 99% risk of DR in patients
of IDDM of 20 years duration as compared to 60% risk of DR in NIDDM
Several reports suggest that Indians with type 2 DM may differ from patients with same duration.
their European counterparts in many aspects, including younger age of 2. Residual beta cell function: A higher prevalence of PDR in diabetic patients
onset, obesity, insulin resistance and genetic predisposition5. have been reported in patients with low pancreatic beta cell capacity so lower
PATHOPHYSIOLOGY beta cell insulin secretory capacity may be a risk factor for severe DR.
3. Genetic predisposition: A lot of research is in process for understanding the
The vascular disruption of DR is characterised by abnormal vascular
genetic predisposition for DR in DM. A large no of genes and genetic variants
flow, disruption in permeability and closure or non-perfusion of
have been reported but till date no gene have been accepted as a high risk
capillaries. Microvascular leakage and microvascular occlusion are the
gene for DR7. Recently genetic association for susceptibility to DR has been
found in five chromosomal regions and PLXDC2 and ARHGAP22. The
Correspondence: Dr. Neeti Gupta, Assistant Professor, Department of latter two genes are being implicated in the endothelial cell angiogenesis and
Ophthalmology, Himalayan Institute of Medical Sciences, Swami Ram increased capillary permeability in Taiwanese population8. Where as
Nagar, Dehradun, Uttarakhand, India e-mail: [email protected]
chromosomes 13q22.2, 2q31.1 and 2q37.2 are three possible susceptible
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loci for DR in Chinese population9. management of all forms of DM.

4. Insulin resistance: Insulin resistance is an independent specific marker of 8. Pregnancy: Pregnancy is a well established risk factor for progression of
proliferative retinopathy that may characterize patients at increased risk for DR. Pregnant women with type 1 DM have twice the risk of development
blindness. of DR than a non pregnant diabetic female. Risk factors for progression of
MODIFIABLE RISK FACTORS retinopathy during pregnancy include baseline severity of DR, glycaemic
1. Glycemic control: Intensive glycemic control and decreasing the level of control, duration of diabetes and concomitant hypertension. Females with
glycosylated haemoglobin, (HbA1C) is the most effective in delaying the poorest glycaemic control at baseline and greatest reduction in HbA1C in
progression of DR. Diabetes Control and Complications Trial (DCCT) in the first trimester were at increased risk of DR progression.
type 1 DM and United Kingdom Prospective Diabetes Study (UKPDS) in 9. Obstructive Sleep Apnea (OSA): OSA has been found to be independent
type 2DM concluded that optimal metabolic control reduces the incidence predictor of PDR even after adjusting for conventional risk factors and
and progression of DR. novel biomarkers of DR16. With comorbid conditions like obesity and
2. Hypertension: High blood pressure is a major risk factor for DR and DME. hypertension OSA further increases the risk of PDR17.
Progression of DR was associated with higher diastolic blood pressure at 10. Cataract surgery: Patients after cataract surgery show worsening of
baseline and increases in diastolic blood pressure over 4 yrs follow up. The DR. Factors that decrease the risk of DR are myopia of more than 2
UKPDS demonstrated that control of blood pressure lead to reduction in diopters, glaucoma, optic atrophy, carotid artery occlusion, and extensive
progression of DR and reduced need for laser. On the contrary the Action to chorioretinal scarring .Patients having such problems in one eye may
control cardiovascular risk in diabetes (ACCORD) study concluded that present with asymmetrical DR.
control of blood pressure did not reduced the progression of DR. There is no CLINICAL FEATURES OF DIABETIC RETINOPATHY
definitive evidence that any one method of lowering blood pressure is superior. There are many classification system for DR but ETDRS classification is
However blocking the renin angiotensin system (RAS) may reduce the recognized as the “gold standard” for grading the severity of diabetic retinopathy
incidence and progression of retinopathy. It was seen that 5 years of worldwide (Table-1). Because of the complexity of ETDRS classification for
Candesartan treatment reduced the incidence of retinopathy in severity by application and communication in the clinical practices its use in everyday clinical
18% in type 1 DM and 34% regression of retinopathy in type 2DM10. Enalapril practice has not proven to be easy or practical. Another classification system used
and losartan showed decrease in progression of DR by 65% and worldwide clinically is the International Clinical Diabetic Retinopathy Disease
70%respectively apparently independent of change in blood pressure in RASS Severity Scale. (Table 2)
study11.
Table-1: Early Treatment Diabetic Retinopathy Study classification of DR
3. Nephropathy: Wisconsin Epidemiological study of diabetic retinopathy
(WESDR) study predicted about 95% increased risk of developing DME in
the presence of gross proteinuria at baseline. The commonest way of
evaluating renal function is by measuring urinary albumin excretion rate as
urea and creatinine may remain normal until established stage of nephropathy.
Prevalence of PDR was found to be higher in patients with persistent
microalbuminuria.
4. Hyperlipidemia: Increased risk of retinal hard exudates is associated with
increased serum total cholesterol in WESDR but not significant in predicting
the severity of retinopathy. Early Treatment Diabetic Retinopathy Study
(ETDRS) concluded that there is significant correlation between elevated
cholesterol, high density lipids and triglycerides with faster development of
hard exudates. Lipid lowering agents may decrease the risk of vision loss in
DR. Atorvaststin has shown to decrease macular edema, severity of hard
exudates, subfoveal migration of hard exudates and need for macular laser
in patients with type 2 DM and dyslipidemia12. In cases where statins fails,
fibrates might help to reduce the risk. Effect of fenofibrate on the need for
Table-2: International Clinical Diabetic Retinopathy Disease Severity
laser treatment for diabetic retinopathy (FIELD) study showed significant Scale Classification
benefits of fenofibrate on DR in terms of requirement of first laser and
development of DME13, similarly ACCORD study confirmed that addition
of fenofibrate with statins significantly reduced the progression of retinopathy.
5. Anemia: Low haemoglobin level has now been found to be an independent
risk factor for development of high risk PDR and severe vision loss. A diabetic
patient with less than 12 g/dl of haemoglobin has two fold increased risk of
any grade of retinopathy and fivefold increase risk of developing severe
grade of retinopathy in already established DR.
6. Obesity: An increase in Body mass index(BMI) significantly correlates
with deterioration of HbA1C, decrease in HDL, increase in triglyceride and
higher prevalence of hypertension14. Many studies report significant
association of high BMI and obesity with DR.
7. Exercise: Exercise may have a beneficial role in reducing the risk of diabetic
complication by direct and indirect mechanisms but physical exercise may NON-PROLIFERATIVE DR: (FIG 2)
have a detrimental effect on advanced DR. Loss of auto regulation in patients 1. Microaneurysm: The earliest clinical observable lesion in DR is
with PDR may increase the retinal arteriolar perfusion pressure to hemorrhagic microaneurysm which is small outpouching of the retinal capillaries in the
threshold in these abnormal new vessels during exercise and may lead to inner nuclear layer. They are clinically visible when the size is more than
intraretinal, preretinal or vitreous haemorrhage. It was seen that 84% of 30µm and the upper limit is 125 µm.
vitreous haemorrhage were associated with exercise no more strenuous than 2. Intraretinal haemorrhages: Appear secondary to rupture of
walking15. Individually tailored exercise regimens are beneficial in the microaneurysms, capillary or venules and can be dot haemorrhage which
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are seen in outer plexiform and inner nuclear layer. Blot haemorrhages are screening as well as to record the progression of retinopathy. A seven field
seen in inner plexiform and outer plexiform layer of the retina and have less stereo fundus photography is the standard procedure to record the fundus
distinct margins as compared to dot haemorrhage. Flame shaped images. Now a day ultra wide field imaging is used primarily as a screening
haemorrhages occur in the superficial nerve fibre layer. Intra-retinal device in diagnoses of DR18. Wide field imaging allows visualisation of up
haemorrhages are seen scattered throughout the posterior pole and resolves to 200º of peripheral retina captured in a single image.
in 4-6 months. 2. Fundus Fluorescein angiography:
3. Hard Exudates: Comprise of accumulated and condensed plasma made of Fundus fluorescein angiography is not required for screening or diagnosing
serum lipoproteins in the outer plexiform layer and appear as creamy yellow DR as it can be done clinically but it can be used to:
plaque, flecks or dots and have affinity toward macula. • Classify diabetic macular edema (DME) into focal or diffuse and its
4. Cotton wool spots: They are consequence of capillary occlusion in the nerve treatment
fibre layer and appear like a fluffy white cotton wool like lesion. They are • Diagnose cystoid macular edema
almost always seen around the major vascular arcade. • Ischemic maculopathy – in defining the extent of capillary non
5. Venous changes: Venous dilatation and tortusity and beeding, looping perfusion areas
and sausage like segmentation of veins may be seen. As mentioned earlier Ultra wide field fundus angiography imaged 3.9 times more
6. Intra retinal microvascular abnormalities (IRMA): IRMA are dilated non perfusion areas, 1.9 times more neovascularisation and 3.8 times more pan
capillaries running between arteriole and venule adjacent to capillary retinal photocoagulation than the conventional seven standard fields.
non-perfusion area and acts as collaterals channels 3. Optical Coherence Tomography (OCT):
Venous changes, IRMA and multiple cotton wool spots are indicators OCT is a non invasive imaging technique that provides high resolution cross
of retinal ischemia and increase the probability of progression from non section imaging of the retina, retinal nerve fibre layer and optic nerve head.
proliferative to proliferative diabetic retinopathy. OCT helps in early diagnosis of macular oedema as it is more sensitive than
clinically examination, in deciding the treatment options for DME and also
helps to monitor the response of the treatment options available for DME.
DME has been classified into different types according to OCT:
Type 1: Sponge like retinal thickening
Type 2: Cystoid macular edema
Type 3: Serous retinal detachment
Type 4: Tractional macular edema
Type 5: Taut posterior hyaloid membrane
OCT can help in detecting retinal nerve fibre layer loss as well as early
development of oedema by macular thickness measurement in clinically
Fig 2: Moderate NPDR showing Fig 3: PDR - NVD with vitreous asymptomatic patients.
venous beading and IRMA haemorrhage 4. Ultrasonography:
B Scan ultrasonography is a non-invasive tool for imaging intraocular contents
PROLIFERATIVE DR: (FIG 3) in cases of hazy media, leading to difficulty in fundus visualisation. Vitreous
This stage is characterised by formation of new vessels from the surface haemorrhage, posterior vitreous detachments and tractional retinal
of the retina and optic disc due to retinal ischemia. detachments can be easily visualised through B scan.
1. New vessels at disc (NVD): NVD is seen when the area of ischemic retina TREATMENT OF DIABETIC RETINOPATHY
is more than a quarter of the whole retina and is defined as new vessels on Medical management:
the disc and around the disc. These new vessels may be derived from retinal
or choroidal circulation. Control of systemic parameters: As discussed earlier various systemic
2. New vessels elsewhere (NVE): NVE, develop from the venous sides of the parameters like blood glucose level and serum glycosylated haemoglobin
capillary network adjacent to an area of ischemia. These new vessels (HbA1C), systemic hypertension, anaemia, dyslipidaemia and proteinuria are
proliferate between the internal limiting membrane and the posterior hyaloid independent risk factors for progression of retinopathy. Optimal metabolic control
phase and when posterior hyloid contracts it pull these fragile vessels leading of the above systemic parameters showed significant reduction of macular edema
to pre retinal bleed or vitreous haemorrhage. When posterior vitreous and visual improvement even without laser photocoagulation.
detachment occurs it may pull the vessels along with the retina leading to Laser photocoagulation: Principle of laser photocoagulation is to make the
tractional retinal detachment. Sometimes the fibrovascular fronds contracts hypoxic retina anoxic by damaging the retinal pigment epithelium/photoreceptor
and may cause a break in the retina leading to combined tractional- complex, which are the most metabolically active cells in the retina thus improving
rhegmatogenous retinal detachment. In cases of severe retinal ischemia there the oxygenation of the inner retinal layers resulting in vasoconstriction, decrease
may be development of rubeosis iridis leading to neovascular glaucoma. retinal blood flow and decreased vascular leakage19. Diabetic retinopathy study
DIABETIC MACULOPATHY (DRS) concluded that laser photocoagulation reduced the rate of severe vision
loss by 50%.
It is the most common cause of decreased vision in a diabetic patient and is
defined as hard exudates or retinal thickening involving the macula. Indications of laser are
Diabetic maculopathy has been divided into four types • Clinically significant macular edema
• Proliferative diabetic retinopathy
a. Non clinically significant macular edema • Very severe NPDR in situations like:
b. Clinically significant macular edema(CSME). Focal / diffuse • Pregnancy
c. Ischemic maculopathy • Nephropathy
d. Mixed type. • Cardiac failure
OCULAR INVESTIGATION IN DIABETIC • Coronary artery disease
RETINOPATHY • Cataract surgery
• Uncontrolled blood glucose
1. Fundus photography: Diagnosis of DR is essentially clinical but fundus
• Recent initiation of insulin in type 2 DM patients
photography is the best way to record the retinal changes. It helps both in
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- Poor patient follow up PHARMACOTHERAPY

Laser treatment in CSME: Either focal laser for localised leakage or
grid laser for diffuse leakage has been recommended by ETDRS. A Most of the manifestation seen in DR is due to increase vascular
modified grid pattern has also been described where a particular sector permeability and vascular occlusion through various metabolic pathways.
or sectors of retinal thickening is treated rather than general pattern around (Fig 4)
the fovea. Modified grid is preferred than the grid pattern in clinical Role of these pharmacological agents is to block the molecular target
practice. Retreatment with laser for residual macular oedema can be done agents involved in the metabolic pathway in the pathogenesis of DR at
after 4 months various levels and other is corticosteroids which are primarily used as
Laser treatment in PDR: DRS recommended a full scatter an anti inflammatory agent.
photocoagulation also known as pan retinal photocoagulation (PRP) and Anti vascular endothelial growth factors (Anti VEGF):Anti VEGF are
concluded that patient undergoing PRP showed 50% less chance of severe now been clinically used and have promising effect in treatment of
vision loss as compared to those not undergoing laser treatment. complications of DR. Intravitreal administration of anti VEGF - aptamer
Additional PRP is done in cases of persistent or no regression of new pegaptanib sodium (Macugen) and humanized anti VEGF antibodies -
vessels, recurring vitreous haemorrhage, extensive intraretinal ranibizumab (Lucentis) and bevacizumab (Avastin) are been increasing
haemorrhage, and extensive skip areas. used in treatment of DME and regression of neovasularisation of the
Laser treatment in PDR with macular edema: It has been seen that PRP retina and iris, and also in regression of new vessels before vitrectomy
may itself cause macular edema or may increase the pre-existing macular in cases of fibrovascular proliferation and thus decreasing the chances
edema hence PRP is done in two to three sittings and macular edema is of intraoperative bleed.
treated before the completion of PRP. Although Laser is the standard care in treatment of DME, Combination
Surgical Treatment: Pars plana vitrectomy (PPV) is the surgical treatment of PRP with anti VEGF have demonstrated greater efficacy21
procedure indicated in treatment of various complications of PDR. Aim Aflibercept (VEGF Trap- Eye) - a recombinant fusion protein consisting
of surgical treatment is to remove axial opacities, relieve anteroposterior of VEGF binding domain of human VEGF receptor 1&2 fused to fc
and tangential traction, segment or peel epiretinal membrane, treat all domain of human immunoglobulin G1, has approximately 100 folds
retinal breaks and deliver laser treatment20. greater affinity to VEGF- A, than either ranibizumab and bevacizumab22.
Recent studies have showen that VEGF Trap-Eye is clinically equivalent
Indications of PPV are: efficacy to ranibizumab with a longer duration of action for about 2
• Non clearing vitreous haemorrhage months and has a better outcome than laser alone23.
• Fibrovascular proliferation causing tractional retinal detachment Corticosteroids: Corticosteroids have shown to inhibit the expression of
involving, threatening or obscuring the macula both VEGF and VEGF gene and have anti-inflammatory properties which
• Combined tractional and rhegmatogenous retinal detachment explains the rationale to use steroids for DME. Giving systemic steroids
• Recalcitrant macular edema with or without taut posterior hyaloids for long term in management of DME is not feasible as it has adverse
• Epiretinal membrane effect throughout the body. Local delivery of steroids in the form of
• Severe premacular haemorrhage posterior subtenon injection or intravitreal injection causes temporary
• Neovascular glaucoma reduction of DME even before laser treatment. Intravitreal inserts of
Indications of immediate vitrectomy: Fluocinolone acetonide are also being used for slow delivery with
• Type 1 DM when severe vitreous haemorrhage shows no sign of prolonged action in cases of DME24.
spontaneous clearing Protein kinase C inhibitors: Recent studies have shown significant
• No Previous laser treatment given reduction in risk of vision loss in patient treated with ruboxistaurine
• Fibrovascular proliferation complexes are more extensive and appear mesylate also known as LY333531 which is an oral PKC inhibitor but it
more vascular did not prevent DR progression25. It also showed improvement in DME.
• Fellow eye has rapid progressive visual loss
• Fellow eye is blind Aldose reductase inhibitors: They act at the level of Polyol pathway
• Rubeosis iridis with recent vitreous haemorrhage with no prior laser thus decreasing the formation of sorbitol. Aldose reductase inhibitors
treatment. and have shown decrease vascular leakage on angiography but clinically
has little therapeutic success26.
Somatostatin analogues: Octreotide a somatostatin analogue and growth
hormone/Insulin like growth factor-1 antagonist have shown to delay
progression of retinopathy but had little effect on visual acuity and
progression of DME27.
ACE inhibitors: There has been recent evidence that suggest inhibitors
of renin angiotensin system (RAS) by ACE inhibitors (i.e Candesaetan)
may have a beneficial effect on DR which is independent of their
hypotensive properties10.
Screening for DR and criteria for referral: As duration of diabetes is
directly proportional to the severity of DR, and timely treatment of DR
may delay the complication, screening and early detection of DR is very
critical. The recommended eye examination schedule is shown in table
3. The cheapest and most widely available technique for screening is
direct ophthalmoscopy but has low sensitivity. Retinal photography is
the most effective method of screening large population. Earlier 7 field
Fig 4: Metabolic retinal photography was the gold standard but was more time consuming.
pathways involved in Single field fundus photography through non-dilated pupils serves as an
Diabetic retinopathy effective tool for screening of DR28.
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Several clinical tools, namely, multifocal electroretinography (ERG), 12. Gupta A, Gupta V, Thapar S, Bhansali A. Lipid-lowering drug atorvastatin as an adjunct in the man-
agement of diabetic macular edema. Am J Ophthalmol. 2004;137:675–82
flash ERG, contrast sensitivity, colour vision, short-wavelength 13. Keech AC, Mitchell P, Summanen PA, et al. Effect of fenofibrate on the need for laser treatment for
automated perimetry, and OCT, can detect neuronal dysfunction at early diabetic retinopathy (FIELD study): a randomised controlled trial. Lancet. 2007;370:1687e97
14. Kastelan S, Tomic M, Gverovic Antunica A, Ljubic S, Salopek Rabatic J, Karabatic M. Body mass
stages of diabetes index: a risk factor for reti-nopathy in type 2 diabetic patients. Mediators Inflamm 2013; 2013: 436329.
15. Anderson BJr. Activity and diabetic vitreous hemorrhages. Ophthalmology 1980; 87: 173–5.
CONCLUSION 16. Rudrappa S, Warren G,Idris I. Obstructive sleep apnoea is associated with the development and pro-
gression of diabetic retinopathy, independent of conventional risk factors and novel biomarkers for
Diabetic retinopathy is the most common complication of diabetes which diabetic retinopathy.Br J Ophthalmol 2012 ;96(12):1535
may lead to legal blindness and is a major public health problem. Early 17. Shiba T, Takahashi M, Hori Y, Saishin Y, Sato Y, Maeno T. Evaluation of the relationship between
detection through screening, educating the population and timely background factors and sleep-disordered breathing in patients with proliferative diabetic retinopathy.
Jpn J Ophthalmol 2011; 55: 638-642
intervention may decrease the complications in the course of disease. 18. Wessel MM, Aaker GD, Parlitsis G, Cho M, D’Amico DJ, Kiss S. Ultra-wide-field angiography im-
proves the detection and clas-sification of diabetic retinopathy. Retina 2012; 32: 785-91.
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Diabetes Mellitus and Tuberculosis

H. M. Kansal1, Saurabh Srivastava2, S. K. Bhargava3
1
Associate Professor, Department of Pulmonary Medicine, 2Professor, Department of Medicine, 3Professor and
Head, Dept of Radiology and Imaging, School of Medical Sciences and Research, Sharda University, Greater
Noida, Uttar Pradesh, India

Abstract: Diabetes and tuberculosis are the twin epidemics which has a major impact on morbidity and mortality of either disorder. Improved
understanding of the bidirectional relationship is necessary to reduce the dual burden of the disease. The present article focuses on the association of
the two disorders and salient features of the two disorders when they occur together.

INTRODUCTION have been implicated in the occurrence of tuberculosis in Diabetic patients3.

T EPIDEMIOLOGY
uberculosis (TB) and diabetes mellitus (DM) are both important health
issues more so in developing countries where TB is endemic and burden In 2014, 387 million people have diabetes; by 2035 this will rise to 592 million.
of diabetes is also very high. A bidirectional association between them has The greatest numbers of people with diabetes are between 40 and 59 years of age
been demonstrated by many researchers. In early 20th century it was a major 179 million people with diabetes are undiagnosed. Diabetes caused 4.9 million
concern due to lack of proper treatment of both the diseases. With the resurgence deaths in 2014; Every seven seconds a person dies from diabetes. 77% of people
of multi drug resistance tuberculosis, along with presence of human immune with diabetes live in middle and low income countries the prevalence of Diabetes
deficiency virus infection and epidemic of diabetes in these countries, this in India as per International Diabetes Federation (IDF) is 8.6%4.
association has been a major concern in these areas1,2.
Asia is the epicenter of the growing burden of DM and the largest contribution is
India not only faces the public health difficulties associated with newly increasing
from India and China5.
rates of chronic diseases such as DM, but as with other low and middle income
countries, endures sustained rates of infectious diseases (such as TB) which remain Tuberculosis (TB) remains a major global health problem. In 2012, an estimated
to be brought under control. 8.6 million people developed TB and 1.3 million died from the disease. India and
China accounted for 39% of the incident TB patients in 2012.
Depressed cellular immunity, dysfunction of alveolar macrophages, low levels
of interferon gamma, pulmonary microangiopathy, and micronutrient deficiency Challenges to TB control and treatment success include structural factors, such as
suboptimal case detection and non-adherence to therapy, as well as host-level
Correspondence: Dr. H. M. Kansal, Associate Professor, Department of factors, such as HIV and diabetes mellitus (DM), that increase vulnerability to
Pulmonary Medicine, School of Medical Sciences and Research, Sharda active TB6.
University, Greater Noida (U.P) e-mail: [email protected]
Worldwide, 70% of diabetics live in TB endemic countries. In the 22 countries