thy Diabetica Fib

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THE CORRELATION BETWEEN DIABETES

MELLITUS AND RETINOPATHY

Composed by:

Aditya Angga Dharma

030.06.010

Supervised by:

dr. Husnun , SpM

Fakultas Kedokteran

Universitas Trisakti

Jakarta

2010

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PREFACE

Firstly, I would like to praise and thank The Lord for His grace and mercy so I can

finally finish this paper on time.

Secondly, I would like to thank both of my parents, my sister and brother for all

support that they have been given to me during this paper was been composed.

Last but not least, I would like to commit my greatest thanks to Dr. Hj. Martiem

Mawie, MS as my lecturer and supervisor. Under his guidance, I could explore and

create more fresh ideas to compose this paper.

This paper was firstly made to accomplish my final English task before graduating

from Trisakti Medical Faculty. The subject that I explore is currently one of major

concern in medical world due to its frequently outbreak. Diabetes mellitus (DM) is a

major medical problem throughout the world. Diabetes causes an array of long-term

systemic complications, which have considerable impact on both the patient and the

society because it typically affects individuals in their most productive years.

Ophthalmic complications of diabetes include corneal abnormalities, glaucoma, iris

neovascularization, cataracts, and neuropathies. However, the most common and

potentially most blinding of these complications is diabetic retinopathy.

Finally, I realize that this paper is far from excellent. Therefore I would like to

apologize if there are mistakes or lack of information in this paper. Critics and

suggestions will be truly admired and welcomed.

Writer,

Aditya Angga Dharma

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CONTENT

Preface.. 2

Content. 3

Abstract 4

I. Introduction. 5

II. Diabetes Mellitus 6

a. Definition....... 6

b. Clasification .. 6

c. Diagnosis. 7

e. Complication 11

III. Diabetes mellitus and Nephropathy.......................................... 12

a. Definition.. 12

b. Risk factors 13

c. Patofisiology ..... 13

d. Pathogenesis ... 14

e. Diagnosis 15

f. Treatment. 18

g. Prevention... 20

h. Evaluation. 22

IV. Conclusion. 24

V. Reference 25

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ABSTRACT

Diabetic retinopathy is a common complication of diabetes affecting the blood

vessels in the retina (the thin light-sensitive membrane that covers the back of the

eye). If untreated, it may lead to blindness. If diagnosed and treated promptly,

blindness is usually preventable.

Patients with type 2 diabetes should have an initial dilated and comprehensive

eye examination by an ophthalmologist or optometristshortly after diabetes diagnosis.

Subsequent examinations for both type 1 and type 2 diabetic patients should be

repeated annually by an ophthalmologist or optometrist who is knowledgeable and

experienced in diagnosing the presence of diabetic retinopathy and is aware of its

management. Less frequent exams (every 2-3 years) may be considered with the

advice of an eye care professionalin the setting ofa normal eye exam. Examinations

will be requiredmore frequentlyif retinopathy is progressing. This follow-upinterval

is recommendedrecognizing that there are limited dataaddressing this issue.

Patients who experience vision loss from diabetes should be encouraged to

pursue visual rehabilitation with an ophthalmologistor optometristwho is trained or

experienced in low-vision care.

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INTRODUCTION

Over 135 million individuals are afflicted with diabetes across the world. In the U.S.,

diabetes affects over 18.2 million people(or 6.3% of the total population) and 800,000

new cases of type 2 diabetes are diagnosed each year(1)(2). Retinopathy is the most

common microvascular complication of diabetes, resulting inblindness for over

10,000 people with diabetes per year. Epidemiological studies have described the

natural history of and treatmentfor diabetic retinopathy. During thefirst two decades

of disease, nearly all patients with type1 diabetes and >60% of patients with type 2

diabetes have retinopathy. In the Wisconsin Epidemiologic Study of Diabetic

Retinopathy (WESDR), 3.6% of younger-onset patients (type 1 diabetes) and 1.6% of

older-onset patients (type 2 diabetes)were legally blind. In the younger-onset group,

86% of blindnesswas attributable to diabetic retinopathy. In the older-onsetgroup, in

which other eye diseases were common, one-third ofthe cases of legal blindness were

due to diabetic retinopathy. There is evidence that retinopathybegins to develop at

least 7 years before the clinical diagnosis of type 2 diabetes. Clinical trials have

demonstrated the effectiveness of photocoagulation, vitrectomy, and control of

hyperglycemia and hypertension for diabetic retinopathy.

DIABETES MELLITUS

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A. Definition

Diabetes is a chronic disease that occurs when the pancreas does not produce enough

insulin, or alternatively, when the body cannot effectively use the insulin it produces.

Insulin is a hormone that regulates blood sugar. Hyperglycaemia, or raised blood

sugar, is a common effect of uncontrolled diabetes and over time leads to serious

damage to many of the body's systems, especially the nerves and blood vessels.(1,10)

B. The clasification of diabetes mellitus may include :

1. Type 1 diabetes (previously known as insulin-dependent or childhood-onset)

is characterized by a lack of insulin production. Without daily administration

of insulin, Type 1 diabetes is rapidly fatal.(1,2,10)

o Symptoms include excessive excretion of urine (polyuria), thirst

(polydipsia), constant hunger, weight loss, vision changes and fatigue.

These symptoms may occur suddenly.

2. Type 2 diabetes (formerly called non-insulin-dependent or adult-onset)

results from the bodys ineffective use of insulin. Type 2 diabetes comprises

90% of people with diabetes around the world, and is largely the result of

excess body weight and physical inactivity.(1,2,10)

o Symptoms may be similar to those of Type 1 diabetes, but are often

less marked. As a result, the disease may be diagnosed several years

after onset, once complications have already arisen.

o Until recently, this type of diabetes was seen only in adults but it is

now also occurring in obese children.

3. Gestational diabetes is Gestational diabetes starts when your body is not able

to make and use all the insulin it needs for pregnancy. Without enough insulin,

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glucose cannot leave the blood and be changed to energy. Glucose builds up in

the blood to high levels. This is called hyperglycemia. (1,2,10)

o Symptoms of gestational diabetes are similar to Type 2 diabetes.

Gestational diabetes is most often diagnosed through prenatal

screening, rather than reported symptoms.

Impaired Glucose Tolerance (IGT) and Impaired Fasting Glycaemia (IFG) are

intermediate conditions in the transition between normality and diabetes. People with

IGT or IFG are at high risk of progressing to type 2 diabetes, although this is not

inevitable. (1,2,3)

C. Diabetes Mellitus Diagnosis

The following tests are used for diagnosis:

A fasting plasma glucose (FPG) test measures blood glucose in a person who

has not eaten anything for at least 8 hours. This test is used to detect diabetes

and pre-diabetes. Diabetes is diagnosed if higher than 126 mg/dL on 2

occasions. (5)

Random Plasma Glucose Test (non-fasting) blood glucose level -- diabetes

is suspected if higher than 200 mg/dL and accompanied by the classic

symptoms of increased thirst, urination, and fatigue (this test must be

confirmed with a fasting blood glucose test). (5)

An oral glucose tolerance test (OGTT) measures blood glucose after a

person fasts at least 8 hours and 2 hours after the person drinks a glucose-

containing beverage. This test can be used to diagnose diabetes and pre-

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diabetes. Diabetes is diagnosed if glucose level is higher than 200 mg/dL after

2 hours. (5)

Test results indicating that a person has diabetes should be confirmed with a second

test on a different day.

FPG Test

The FPG test is the preferred test for diagnosing diabetes because of its convenience

and low cost. However, it will miss some diabetes or pre-diabetes that can be found

with the OGTT. The FPG test is most reliable when done in the morning. Results and

their meaning are shown in Table 1. People with a fasting glucose level of 100 to 125

milligrams per deciliter (mg/dL) have a form of pre-diabetes called impaired fasting

glucose (IFG). Having IFG means a person has an increased risk of developing type 2

diabetes but does not have it yet. A level of 126 mg/dL or above, confirmed by

repeating the test on another day, means a person has diabetes.

Table 1. FPG test

Plasma Glucose Result (mg/dL) Diagnosis

99 or below Normal

100 to 125

Pre-diabetes

(impaired fasting glucose)

126 or above Diabetes*

*Confirmed by repeating the test on a different day. (1,2,10)

OGTT

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Research has shown that the OGTT is more sensitive than the FPG test for diagnosing

pre-diabetes, but it is less convenient to administer. The OGTT requires fasting for at

least 8 hours before the test. The plasma glucose level is measured immediately

before and 2 hours after a person drinks a liquid containing 75 grams of glucose

dissolved in water. Results and their meaning are shown in Table 2. If the blood

glucose level is between 140 and 199 mg/dL 2 hours after drinking the liquid, the

person has a form of pre-diabetes called impaired glucose tolerance (IGT). Having

IGT, like having IFG, means a person has an increased risk of developing type 2

diabetes but does not have it yet. A 2-hour glucose level of 200 mg/dL or above,

confirmed by repeating the test on another day, means a person has diabetes.

Table 2. OGTT

2-Hour Plasma Glucose Result (mg/dL) Diagnosis

139 and below Normal

140 to 199Pre-diabetes

(impaired glucose tolerance)

200 and above Diabetes*

*Confirmed by repeating the test on a different day. (1,2,10)

Gestational diabetes is also diagnosed based on plasma glucose values measured

during the OGTT, preferably by using 100 grams of glucose in liquid for the test.

Blood glucose levels are checked four times during the test. If blood glucose levels

are above normal at least twice during the test, the woman has gestational diabetes.

Table 3 shows the above-normal results for the OGTT for gestational diabetes. (1,2,10)

Table 3. Gestational diabetes: Above-normal

results for the OGTT*

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When Plasma Glucose Result (mg/dL)

Fasting 95 or higher

At 1 hour 180 or higher

At 2 hours 155 or higher

At 3 hours 140 or higher

Note: Some laboratories use other numbers for this test.

*These numbers are for a test using a drink with 100 grams of glucose. (1,2,10)

Random Plasma Glucose Test ( non fasting )

A random, or casual, blood glucose level of 200 mg/dL or higher, plus the presence of

the following symptoms, can mean a person has diabetes:

increased urination

increased thirst

unexplained weight loss

Other symptoms can include fatigue, blurred vision, increased hunger, and sores that

do not heal. The doctor will check the persons blood glucose level on another day

using the FPG test or the OGTT to confirm the diagnosis. (1,2,10)

D. The complications

Over time, diabetes can damage the heart, blood vessels, eyes, kidneys, and nerves.

Diabetic retinopathy is an important cause of blindness, and occurs as

a result of long-term accumulated damage to the small blood vessels in

the retina. After 15 years of diabetes, approximately 2% of people

become blind, and about 10% develop severe visual impairment.

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Diabetic neuropathy is damage to the nerves as a result of diabetes,

and affects up to 50% of people with diabetes. Although many

different problems can occur as a result of diabetic neuropathy,

common symptoms are tingling, pain, numbness, or weakness in the

feet and hands.

Combined with reduced blood flow, neuropathy in the feet increases

the chance offoot ulcers and eventual limb amputation.

Diabetes is among the leading causes of kidney failure. 10-20% of

people with diabetes die ofkidney failure.

Diabetes increases the risk ofheart disease and stroke. 50% of people

with diabetes die of cardiovascular disease (primarily heart disease and

stroke).

The overall risk of dying among people with diabetes is at least double

the risk of their peers without diabetes. (1,3,5,7)

RETINOPATHY IN DIABETES MELLITUS

A. Natural History of Diabetic Retinopathy

Diabetic retinopathy progresses from mild nonproliferative abnormalities,

characterized by increased vascular permeability, to moderate and severe

nonproliferative diabetic retinopathy (NPDR), characterizedby vascular closure, to

proliferative diabetic retinopathy (PDR), characterized by the growth of new blood

vessels on the retina and posterior surface of the vitreous. Macular edema,

characterized by retinal thickening from leaky blood vessels, can develop at all stages

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of retinopathy. Pregnancy, puberty, blood glucosecontrol, hypertension, and cataract

surgery can accelerate thesechanges.(1,3,5)

Vision-threatening retinopathy is rare in type 1 diabetic patients in the first 3-5 years

of diabetes or before puberty. During the next two decades, nearly all type 1 diabetic

patients develop retinopathy. Up to 21% of patients with type 2 diabetes have

retinopathy at the time of first diagnosis of diabetes, and most develop some degree of

retinopathy over time. Vision loss due to diabetic retinopathy results from several

mechanisms. Central vision may be impaired by macular edema or capillary

nonperfusion. New blood vessels of PDR and contraction of the accompanying

fibrous tissue can distort the retina and lead to tractional retinal detachment, producing

severe and oftenirreversible vision loss. In addition, the new blood vesselsmay bleed,

adding the further complication of preretinal or vitreous hemorrhage. Finally,

neovascular glaucoma associatedwith PDR can be a cause of visual loss.(5)

B. Risk Factor

The duration of diabetes is probably the strongest predictor for development and

progression of retinopathy. Among younger-onset patients with diabetes in the

WESDR (Wisconsin Epidemiologic Study of Diabetic Retinopathy), the prevalence of

any retinopathywas 8% at 3 years, 25% at 5 years, 60% at 10 years, and 80% at 15

years. The prevalence of PDR was 0% at 3 years and increased to 25% at 15 years.

The incidence of retinopathy also increased with increasing duration. The 4-year

incidence of developing proliferative retinopathy in the WESDR (Wisconsin

Epidemiologic Study of Diabetic Retinopathy) younger-onset group increased from

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0% during the first 5 years to 27.9% during years 13-14 of diabetes. After 15 years,

the incidence of developing PDRremained stable.(5)

C. Patophysiologi

Several biochemical pathways have been proposed to link hyperglycemia and

microvascular complications. These include polyol accumulation, formation of

advanced glycation end products (AGEs), oxidative stress, and activation of protein

kinase C (PKC). These processesare thought to modulate the disease process through

effectson cellular metabolism, signaling, and growth factors.(3,5)

Polyol accumulation

Accumulation of polyol occurs in experimental hyperglycemia, which in rats and

dogs is associated with the development ofbasement thickening, pericyte loss, and

microaneurysm formation. High concentrations of glucose increase flux throughthe

polyol pathway with the enzymatic activity of aldose reductase, leading to an

elevation of intracellular sorbitol concentrations. This rise in intracellular sorbitol

accumulation has been hypothesizedto cause osmotic damage to vascular cells. (3,5)

AGEs

Another well-characterized pathway is damage resulting from accumulation of

AGEs. High serum glucose can lead to nonenzymaticbinding of glucose to protein

side chains, resulting in theformation of compounds termed AGEs. After 26 weeks

of induced hyperglycemia, the retinal capillaries of diabetic rats have marked

accumulation of AGEs as well as a loss of pericytes.(3,5)

Oxidative damage

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Diabetes and hyperglycemia can also lead to oxidative stress and formation of

reactive oxygen species (ROS), leading to vasculardamage. (3,5)

D. Pathogenesis

Diabetic retinopathy is result of microvascular retinal changes. Hyperglycemia-

induced pericyte death and thickening of the basement membrane lead to

incompetence of the vascular walls. These damage change the formation ofblood

retinal barrier and also make retinal blood vessel become more permiable.

Small blood vessels such as those in the eye are especially vulnerable to poor

blood glucose control. An overaccumulation ofglucose and/orfructose damages the

tiny blood vessels in the retina. During the initial stage, called nonproliferative

diabetic retinopathy (NPDR), most people do not notice any changes in their vision.

Some people develop a condition called macular edema. It occurs when the damaged

blood vessels leak fluid and lipids onto the macula, the part of the retina that lets us

see detail. The fluid makes the macula swell, which blurs vision.

As the disease progresses, severe nonproliferative diabetic retinopathy enters an

advanced, or proliferative, stage. The lack ofoxygen in the retina causes fragile, new,

blood vessels to grow along the retina and in the clear, gel-like vitreous that fills the

inside of the eye. Without timely treatment, these new blood vessels can bleed, cloud

vision, and destroy the retina. Fibrovascular proliferation can also cause tractional

retinal detachment. The new blood vessels can also grow into the angle of the anterior

chamber of the eye and cause Neovascular Glaucoma. Nonproliferative diabetic

retinopathy shows up as cotton wool spots, or microvascular abnormalities or as

superficial retinal hemorrhages. Even so, the advanced proliferative diabetic

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retinopathy (PDR) can remain asymptomatic for a very long time, and so should be

monitored closely with regular checkups.(4)

E. Diagnosis

Many techniques are used in the detection of diabetic retinopathy, including direct

and indirect ophthalmoscopy, fluorescein angiography,stereoscopic digital and color

filmbased fundus photography, and mydriatic or nonmydriatic digital color or

monochromaticsingle-field photography.(4)

Ophthalmoscopy is the most commonly used technique to monitor for

diabetic retinopathy. However, undilated ophthalmoscopy,especially by non

eye care providers has poor sensitivitycompared with stereoscopic seven-field

color photography .Under typical clinical conditions, direct ophthalmoscopy

by

nonophthalmologists has a sensitivity of 50% for the detection

of

proliferative retinopathy.(4)

Ocular Coherence Tomography or OCT: This is a scan similar to an

ultrasound which is used to measure the thickness of the retina. It produces a

cross section of the retina and can determine if there is any swelling or

leakage.

(4)

Tonometry: A standard test that determines the fluid pressure (intraocular

pressure) inside the eye. Elevated pressure is a possible sign ofglaucoma,

another common eye problem in people with diabetes.(4)

Slit Lamp Biomicroscopy Retinal Screening Programs: Systematic programs

for the early detection of diabetic retinopathy using slit-lamp biomicroscopy.

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These exist either as a standalone scheme or as part of the Digital program

(above) where the digital photograph was considered to lack enough clarity for

detection and/or diagnosis of any retinal abnormality. (4)

The Inoveon Diabetic Retinopathy system compared SSF photographsof 290

diabetic patients recorded on 35-mm film and on theirproprietary system. The

sensitivity and specificity of the digital system in detecting threshold events

were 98.2 and 89.7%, respectively.Although Inoveons diabetic retinopathy-

3DT system provideshighly accurate diabetic retinopathy referral decisions,

the requirement for dilation and the cost both reduce its usefulness as a

screening tool.(4)

The DigiScope is a semiautomated instrument that acquires fundus images,

evaluates visual acuity, and transmits the data to a remote reading center

through telephone lines. A pilot study in normal eyes of normal volunteers and

17 consecutivediabetic patients showed that the visualization of many retinal

lesions present in diabetic retinopathy can be visualized by the DigiScope.

Further studies are needed to evaluate the test characteristics of this

technology.(4)

The use of single-field fundus photography has also been usedas a detection tool for

diabetic retinopathy.

Table 2International Clinical Diabetic Retinopathy Disease Severity Scale.(6)

Proposed disease severity

level Findings observable upon dilated ophthalmoscopy

No apparent retinopathy No abnormalities

Mild NPDR Microaneurysms onlyModerate NPDR More than just microaneurysms but less than severe

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NPDR

Severe NPDR Any of the following:

>20 intraretinal hemorrhages in each of 4 quadrants

Definite venous beading in 2+ quadrants

Prominent intraretinal microvascular abnormalities in

1+ quadrant

And no signs of proliferative retinopathy

PDR One or more of the following:

Neovascularization

Vitreous/preretinal hemorrhage

F. Management

There are three major treatments for diabetic retinopathy, which are very

effective in reducing vision loss from this disease. In fact, even people with

advanced retinopathy have a 90 percent chance of keeping their vision when they

get treatment before the retina is severely damaged. Still, the best way of

addressing diabetic retinopathy is to monitor it vigilantly and ensure that it does

not happen in the first place by careful blood glucose control and limitation of

dietary fructose.

These three treatments are laser surgery, injection of triamcinolone into the

eye and vitrectomy. It is important to note that although these treatments are very

successful, they do not cure diabetic retinopathy. Caution should be exercised in

treatment with laser surgery since it causes a loss of retinal tissue. It is often more

prudent to inject triamcinolone. In some patients it results in a marked increase of

vision, especially if there is an edema of the macula.

Avoiding tobacco use and correction of associated hypertension are important

therapeutic measures in the management of diabetic retinopathy. (3,4,5,6)

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The many kind of theraphy diabetes retinopathy among other :

1. Laser surgery

A type of laser surgery called panretinal photocoagulation, or PRP, is used to treat

severe macular edema and proliferative retinopathy. The goal is to create 1 000 - 2

000 burns in the retina with the hope of reducing the retina's oxygen demand, and

hence the possibility of ischemia. In treating advanced diabetic retinopathy, the burns

are used to destroy the abnormal blood vessels that form at the back of the eye.

Before the surgery, the ophthalmologist dilates the pupil and applies anesthetic drops

to numb the eye. In some cases, the doctor also may numb the area behind the eye to

prevent any discomfort. The lights in the office are also dimmed to aid in dilating the

pupil. The patient sits facing the laser machine while the doctor holds a special lens to

the eye. During the procedure, the patient may see flashes oflight. These flashes may

eventually create an uncomfortable stinging sensation for the patient. After the laser

treatment, patients should be advised not to drive for a few hours while the pupils are

still dilated. Vision may remain a little blurry for the rest of the day, though there

should not be much pain in the eye. (4)

2. Scatter laser treatment

Rather than focus the light on a single spot, the eye care professional may make

hundreds of small laser burns away from the center of the retina, a procedure called

scatter laser treatmentorpanretinal photocoagulation. The treatment shrinks the

abnormal blood vessels. Patients may lose some of their peripheral vision after this

surgery, but the procedure saves the rest of the patient's sight. Laser surgery may also

slightly reduce colour and night vision.

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A person with proliferative retinopathy will always be at risk for new bleeding as well

as glaucoma, a complication from the new blood vessels. This means that multiple

treatments may be required to protect vision. (4)

3. Vitrectomy

Instead of laser surgery, some people need an eye operation called a vitrectomy to

restore vision. A vitrectomy is performed when there is a lot of blood in the vitreous.

It involves removing the cloudy vitreous and replacing it with a saline solution made

up ofsalt and water. Because the vitreous is mostly water, there should be no change

between the saline solution and the normal vitreous.

Studies show that people who have a vitrectomy soon after a large hemorrhage are

more likely to protect their vision than someone who waits to have the operation.

Early vitrectomy is especially effective in people with insulin-dependent diabetes,

who may be at greater risk of blindness from a hemorrhage into the eye.

Vitrectomy is often done under local anesthesia. The doctor makes a tiny incision in

the sclera, or white of the eye. Next, a small instrument is placed into the eye to

remove the vitreous and insert the saline solution into the eye.

Patients may be able to return home soon after the vitrectomy, or may be asked to stay

in the hospital overnight. After the operation, the eye will be red and sensitive, and

patients usually need to wear an eyepatch for a few days or weeks to protect the eye.

Medicated eye drops are also prescribed to protect. (4)

G. Prevention

The prevention can do with any method include :

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1. Glycemic Control

The Diabetes Control and Complications Trial (DCCT) investigated the effect of

hyperglycemia in type 1 diabetic patients, as well as the incidence of diabetic

retinopathy, nephropathy,and neuropathy. A total of 1,441 patients who had either no

retinopathy at baseline (primary prevention cohort) or minimal-to-moderateNPDR

(secondary progression cohort) were treated by either conventionaltreatment (one or

two daily injections of insulin) or intensivediabetes management with three or more

daily insulin injectionsor a continuous subcutaneous insulin infusion. In the primary

prevention cohort, the cumulative incidence of progression in retinopathy over the

first 36 months was quite similar between the two groups. After that time, there was a

persistent decreasein the intensive group. Intensive therapy reduced the mean riskof

retinopathy by 76%. In the secondary intervention cohort, the intensive group had a

higher cumulativeincidence of sustained progression during the first year. However,

by 36 months, the intensive group had lower risks of progression. Intensive therapy

reduced the risk of progression by 54%.(5)

The protective effect of glycemic control has also been for confirmed patients with

type 2 diabetes. The U.K. Prospective Diabetes Study (UKPDS) demonstrated that

improved blood glucose control reduced the risk of developing retinopathy and

nephropathy and possibly reduces neuropathy. The overall rate of microvascular

complications was decreased by 25% in patients receiving intensive therapy versus

conventional therapy. Epidemiological analysis of the UKPDS data showed a

continuous relationship between the risk of microvascular complications and

glycemia, such thatfor every percentage point decrease in HbA1c (e.g., from 8 to7%),

there was a 35% reduction in the risk of microvascularcomplications.(5)

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2. Blood Pressure Control

The The U.K. ProspectiveDiabetes Study (UKPDS) also investigated the influence of

tight blood pressure control. A total of 1,148 hypertensive patients with type 2

diabetes were randomized to less tight (


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potentially blinding disorders. Detection of these problems adds value to the

examination but is rarely considered in analyses of screening interval. Patient

education also occurs during examinations. Patients know the importance of

controllingtheir blood glucose, blood pressure, and serum lipids, and thisimportance

can be reinforced at a time when patients are particularly aware of the implications of

vision loss. In addition, long intervals between follow-up visits may lead to

difficultiesin maintaining contact with patients. Patients may be unlikely to remember

that they need an eye examination after severalyears have passed.

After considering these issues, and in the absence of empirical data showing

otherwise, persons with diabetes should have an annual eye examination.(3,5)

Table 1Ophthalmologic examination schedule(7)

Patient group Recommended first examination

Minimum routine follow-

up*

Type 1 diabetes Within 35 years after diagnosis of

diabetes once patient is age 10 years

or older

Yearly

Type 2 diabetes At time of diagnosis of diabetes Yearly

Pregnancy in

preexisting diabetes

Prior to conception and during first

trimester

Physician discretion

pending results of first

trimester exam

* Abnormal findings necessitate more frequent follow-up.

Some evidence suggests that the prepubertal duration of diabetes may be important in

the development of microvascular complications; therefore, clinical judgment should

be used when applying these recommendations to individual patients

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CONCLUSIONS

Diabetic retinopathy is still a leading cause of blindness.

However, our understanding

of the pathophysiology of the diseaseis increasing as new biochemical pathways are

identified. Our ability to diagnosis and classify retinopathy is also improving.

Treatment modalities exist that can prevent or delay the onset of diabetic retinopathy,

as well as prevent loss of vision,in a large proportion of patients with diabetes. The

DCCT and the UKPDS established that glycemic, blood pressure and serum lipid

controlcan prevent and delay the progression of diabetic retinopathy in patients with

diabetes. Timely laser photocoagulation therapy can also prevent loss of vision in a

large proportion of patients with severe NPDR and PDR and/or macular edema.

Because a significantnumber of patients with vision-threatening disease may not have

symptoms, ongoing evaluation for retinopathy is a valuable andrequired strategy. In

the near future, clinical trials of several pharmacologic agents may lead to the

introduction of additional treatmentsand reduction in the frequency of visual loss.

.

23


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REFERENCES

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3. Diabetes Care: Retinopathy in Diabetes. Available from

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January 2009.

4. South-West Vision Center: Diabetic Retinopathy. Available from

http://swvc.net/eye_conditions_swvc.htm. Accessed 3 January 2009.

5. Diabetes Care: Diabetic Retinopathy. Available fromhttp://care.diabetesjournals.org/cgi/content/full/27/10/2540?. Accessed 2

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7. National Diabetes Information Clearinghouse: Diagnosis of Diabetes.

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9. Gabbay KH: Hyperglycemia, polyol metabolism, and complications of

diabetes mellitus.Annu Rev Med26:521536, 1975.

10. World Health Organization (WHO): Diabetes. Available from

http://www.who.int/mediacentre/factsheets/fs312/en/index.html. Accessed 2

January 2009 .

11. Early Treatment Diabetic Retinopathy Study Research Group: Grading

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http://care.diabetesjournals.org/cgi/content/full/27/suppl_1/s84http://swvc.net/eye_conditions_swvc.htmhttp://care.diabetesjournals.org/cgi/content/full/27/10/2540http://care.diabetesjournals.org/cgi/content-nw/full/27/10/2540/T2.%20Accessed%202%20January%202009http://care.diabetesjournals.org/cgi/content-nw/full/27/10/2540/T2.%20Accessed%202%20January%202009http://diabetes.niddk.nih.gov/dm/pubs/diagnosis/http://www.who.int/mediacentre/factsheets/fs312/en/index.htmlhttp://care.diabetesjournals.org/cgi/content/full/27/suppl_1/s84http://swvc.net/eye_conditions_swvc.htmhttp://care.diabetesjournals.org/cgi/content/full/27/10/2540http://care.diabetesjournals.org/cgi/content-nw/full/27/10/2540/T2.%20Accessed%202%20January%202009http://care.diabetesjournals.org/cgi/content-nw/full/27/10/2540/T2.%20Accessed%202%20January%202009http://diabetes.niddk.nih.gov/dm/pubs/diagnosis/http://www.who.int/mediacentre/factsheets/fs312/en/index.html

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