Diagnosis, Classification and Prevention

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Diagnosis, classification andprevention of diabetes



Diagnosis and typesSlide 2 of 48


Definition of diabetes

Characterized by hyperglycaemia

• Defects in insulin production

• Autoimmune or otherdestruction of beta cells

• Insulin insensiti ity• Impaired action of insulin on

target tissues



Diagnosis and typesSlide ! of 48


Definition of diabetes

Chronic hyperglycaemia associated"ith long#term damage to$

• %yes

• &idneys

• 'er es• (eart and blood essels





The diabetes epidemic

• 2!0 million affected in 200)

• !*0 million "ithin 20 years

• +ost rapid in Indian and Asiansubcontinents

ID, Diabetes Atlas



Diagnosis and typesSlide * of 48

World Statistics:



Diagnosis and typesSlide ) of 48

Normal Pancreatic Islet:

ß cellsß cells (Insulin) αα cellscells (Glucagon)

δδ cellscells (Somatostatin) pp Cellspp Cells (pan prot)

ßß αα



Diagnosis and typesSlide - of 48Insulin # Anabolic Steroid

• .ransmembrane transport of glucose

• /i er muscle 1 fat ↓ blood glucose

• /i er 1 s eletal muscle # ↑ glycogen

• Con erts glucose to triglycerides

• 'ucleic acid 1 3rotein synthesis

• DiabetesDiabetes Increased catabolism.Increased catabolism.• (yperglycemia ↓ protein synthesis /ipolysis

"asting "eight loss






Cellular 6lucose pta e

Insulin "e#uiring

• Striated $uscle

• %ardiac $uscle

• &ibroblasts• & T

Non'Insulin "e#uiring

• 5lood 9essels

• 'er es

• &idney• %ye /ens



Diagnosis and typesSlide :0 of 48

Patholog( in Diabetes:

• )o* glucose inside cell ; decreased cell metabolism <muscle

li er=

• High glucose outside; 6lycosylation damage <59=; 3olyol products ; osmotic damage>



Diagnosis and typesSlide :: of 48


%lassification

• .ype : diabetes

; autoimmune

; /ADA

; idiopathic

• .ype 2 diabetes





?ther specific types

• +?D@

• Defects in insulin action• Diseases of the pancreas

• %ndocrine disorders

• Drug# or chemical#induced• Infections

%lassification



Diagnosis and typesSlide :! of 48


• ncommon forms of immune#mediated diabetes

• ?ther genetic syndromes

• 6estational diabetes

%lassification





Insulin

6luconeogenesis6lycogenolysis6lycogen synthesis

6lucose upta e6lycogensynthesis

5lood glucose

Insulin and glucose disposal

,ree fatty acid release



Diagnosis and typesSlide :* of 48

T(pe + Diabetes

• 5eta cell destruction

• Absolute insulin deficiency

• sually immune#mediated

• Circulating mar ers of immune destruction<ICA IAA 6AD antibodies=

• arely obese at onset

• Associated "ith other autoimmune diseases<6ra eBs (ashimotoBs AddisonBs 3A itiligo=



Diagnosis and typesSlide :) of 48

Pathogenesis of T(pe I D$GeneticGenetic

HLA-DR3/4HLA-DR3/4 EnvironmentEnvironmentViral infe..?Viral infe..?

Insulin deficiencInsulin deficienc! "e I / IDD#! "e I / IDD#

Autoimmune InsulitisAutoimmune InsulitisA$ to % cells/insulinA$ to % cells/insulin

ß cellß cellDestructionDestruction

• 3S 6lomerulonephritis• 6ra es (ashimoto thyroiditis• heumatic heart disease• S/% Collagen ascular disease• heumatoid arthritis







6lucose upta e 6lycogenolysis 6luconeogenesis <amino acids= &etone production <fatty acids=

6lucose upta e 3rotein degradation → amino acids

5lood glucose

Insulin deficienc( int(pe + diabetes

.riglyceride degradation → fatty acids





Pathogenesis of t(pe + diabetes

• Immunological acti ation

• 3rogressi e beta#cell destruction

• Insufficient beta#cell function

• Dependent on e ogenous insulin

• is of etoacidosis





Diagnosis and typesSlide 2: of 48


5eta#cellmass

Pathogenesis of t(pe + diabetes

.ime <months # years=

.rigger

6enetic

3re#diabetes (oneymoonB

%hronicphase

%linicaldiabetes

Immunologicalabnormalities





Idiopathic t(pe + diabetes

'on#autoimmune type : diabetes

• 'o autoimmune mar ers

• 3ermanent insulinopenia

• &etoacidosis

• 3eople of African and Asian origin



Diagnosis and typesSlide 2! of 48


pidemiolog( of t(pe + diabetes

• Increasing in recent years

• 6eographic ariation

• elati e affluence

• /ac of treatment

ID, Diabetes Atlas





• Age of onset pea s

; preschool; puberty

• AutumnE"inter pea s

pidemiolog( of t(pe + diabetes



Diagnosis and typesSlide 2* of 48T(pe - Diabetes

• +ost ha e insulin resistance

• Insulin secretory defect

• elati e insulin deficiency

• 'o immune mar ers

• +ost are obese at onset

• &etosis may occur "ith stress

• 3rogressi e• 3art of Fdysmetabolic syndromeG

• Accounts for 70#7*H of ne" cases

i i d



Diagnosis and typesSlide 2) of 48

T(pe - diabetes

• Characterized by chronic hyperglycemia

• Associated "ith micro ascular and macro ascularcomplications

• 6enerally arises from a combinationof insulin resistance andβ#cell dysfunction

Definition Diagnosis and Classification of Diabetes +ellitus and its Complications Department of 'oncommunicable Disease Sur eillanceorld (ealth ?rganization 6ene a :777 A ailable at$ http$EE""" diabetes org u EinfocentreEcarerecEdiagnosi doc

Di i d



Diagnosis and typesSlide 2- of 48

IDD#IDD#

Genetic /Genetic / % cell defect% cell defect

Pathogenesis of T(pe II D$&$esit /&$esit /

Life st le ?Life st le ?

% cell% celle'(austione'(austion

! "e II )IDD#! "e II )IDD#

A$nor. *ecretionA$nor. *ecretionInsulin ResistanceInsulin Resistance

RelativeRelative

Insulin Def.Insulin Def.

Di i d





6lucose upta e

6lycolysis

6luconeogenesis <amino acids=


5lood glucose

Insulin insensitivit( in tt(pe - diabetes

Di i d t





5lood glucose

6lucose upta e

Insensitivit( to insulin intt(pe - diabetes

6lucose upta e 6lycolysis



Di i d t



Diagnosis and typesSlide !0 of 48


5lood glucoseCon erted to triglycerides

ffect of insulin resistance in tt(pe - diabetes

6lucose upta e 6lycolysis



6lucose upta e



Major defect in individuals with type 2diabetes 1

Reduced biological response to insulin 1–3

Strong predictor of type 2 diabetes 4

Closely associated with obesity

hat is insulin resistanceJ

I"

: American Diabetes Association Diabetes Care :778K 2:$!:0;!:425ec #'ielsen ( 1 6roop /C J Clin Invest :774K 74$:-:4;:-2: ! 5loomgarden L. Clin Ther :778K 20$2:);2!:

4(affner S+ et al. Circulation 2000K :0:$7-*;780 *5oden 6 Diabetes :77-K 4)$!;:0



What is -cell dysfunction?

Major defect in individuals with type 2diabetes

Reduced ability of β!cells to secrete insulinin response to hyperglyce"ia

De,ronzo A et al. Diabetes Care :772K :*$!:8;



Insulin resistance and -cell dysfunctionare core defects of type 2 diabetes

Insulinresistance

!eneticsusceptibilit(,

obesit(, Westernlifest(le

T(pe - diabetes

I" 'cell

d(sfunction

hodes CM 1 hite +, Eur J Clin Invest 2002K !2 <Suppl !=$!;:!



#nsulin resistance – reduced response tocirculating insulin

Insulinresistance

!lucose output ↓ !lucose upta e ↓ !lucose upta e

H(pergl(cemia

)iver $uscle diposetissue

I"



$hy does the β!cell fail%

%hronich(pergl(cemia

/versecretion ofinsulin tocompensate forinsulin resistance +,-

Highcirculatingfree fatt( acids

!lucoto0icit( -

Pancreas

)ipoto0icit( 1

'celld(sfunction

: 5oden 6 1 Shulman 6I Eur J Clin Invest 2002K !2$:4;2!2&aiser ' et al. J Pediatr Endocrinol Metab 200!K :)$*;22

! ,inegood D. 1 .opp 5 Diabetes Obes Metab 200:K ! <Suppl :=$S20;S2-

Diagnosis and types



Diagnosis and typesSlide !) of 48


T(pe - diabetes

• 70H#7*H of people "ithdiabetes

• Insulin insensiti ity andrelati e insulin deficiency

• ?besity or o er"eight

• Complications often presentat diagnosis

Diagnosis and types



Diagnosis and typesSlide !- of 48


Pathogenesis of t(pe - diabetes

• +ultiple genes in ol ed

• (yperinsulinaemia

• 3oor fetal nutrition → ↓ beta#cellformation

• /o" birth "eightE"eight change

• F.hrifty geneG

• -H beta#cell loss

Diagnosis and types





Age <years=

%ndogenousinsulin

InsulinreNuirements

5eta#cell loss

The natural histor( oft(pe - diabetes

↑ Insulin

reNuirements"ith age

3rimaryfailure

Diagnosis and types





Age <years=

%ndogenousinsulin

InsulinreNuirements

5eta#cell loss

Insulininsensiti ity

(yper#

insulinaemia


↑ Insulin


Diagnosis and types





Age <years=

%ndogenousinsulin

InsulinreNuirements

Secondaryfailure


%ffect oforal drugs

↑ Insulin


5eta#cell loss

(yper#

insulinaemia

Insulininsensiti ity

Diagnosis and types



Diagnosis and typesSlide 4: of 48


pidemiolog( of t(pe - diabetes

• Dramatic increase

• Aging population

• Disturbing trends parallel obesityepidemic

• %specially in adolescents andminority groups

• Increasing in young people



Type-I Type-II

&ess co""onChildren ' 2 (ears#nsulin! )ependent)uration* $ee+s

,cute Metabolicco"plications

,utoantibody* (es-a"ily .istory* /o#nsulin levels* very low#slets* #nsulitis

0 in twins

More co""on ,dult 2 (ears#nsulin #ndependent Months to years

Chronic ascularco"plications5/o(es/or"al or high /or"al 6 78haustion90!:0 in twins



Insulitis – Type I

InsulinitisInsulinitis



Islets in Type II Diabetes:

Loss of ß cells, replaced by Amyloid deposits (hyalinization)Loss of ß cells, replaced by Amyloid deposits (hyalinization)



Islets in Type II Diabetes:

Loss of ß cells, replaced by Amyloid deposits (hyalinization)Loss of ß cells, replaced by Amyloid deposits (hyalinization)

Diagnosis and types



g ypSlide 4) of 48


"is factors for t(pe - diabetes

• Age O 40 years

• ,irst#degree relati e "ith diabetes

• +ember of high ris population

• (istory of impaired glucose toleranceimpaired fasting glucose

• 9ascular disease

• (istory of gestational diabetes

• (istory of deli ery of macrosomicbaby

CDA 200!

Diagnosis and types



g ypSlide 4- of 48


• (ypertension

• Dyslipidaemia

• Abdominal obesity• ? er"eight

• 3olycystic o ary disease

• Acanthosis nigricans

• Schizophrenia

"is factors for t(pe - diabetes

Diagnosis and types



g ypSlide 48 of 48


• 3olydipsia

• 3olyuria

• 'octuria

• 9isual disturbance

• ,atigue

• eight loss

• Infections

Signs and s(mptoms

Diagnosis and types



g ypSlide 47 of 48


Diagnosing diabetes

'ormal Impaired fasting glucose>

Impaired glucosetolerance>>

Diabetes

,36 P) :mmolE/

P::0mgEd/

) : to ) 7mmolE/>

::0 to :2)mgEd/

Q- 0mmolE/

Q:2)mgEd/

2hr 36 P- 8mmolE/

P:2)mgEd/

- 8 to ::mmolE/>>

:2) to 200mgEd/

Q:: :mmolE/

Q200mgEd/

CDA 200! ADA 2004 (? 2002

Diagnosis and types



g ypSlide *0 of 48


Impaired glucose toleranceImpaired fasting glucose

• Intermediate states

• Increased ris of de eloping diabetes• 3re ention strategies to pre ent or

delay progression

• Increased ris of cardio asculardisease

Diagnosis and types



Slide *: of 48


2ncertain diagnosis:/ral glucose tolerance test

• -* g glucose load after 8 hours

fasting

• eadings ta en in fasting stateand at : and 2 hours

• 3ossible problems

Diagnosis and types



Slide *2 of 48


• rinary etones

• Antibodies

• C#peptide

Tests for differential diagnosis

Diagnosis and types



Slide *! of 48


$etabolic s(ndrome

• Cluster of ris factors or syndrome

• .ype 2 diabetes

• Different criteria

• .hree#fold increase in heartdisease and stro e

• ."o#fold increase in cardio asculardisease deaths

Diagnosis and types



Slide *4 of 48


Prevention of t(pe + diabetes

• %arly e posure to co"s milprotein

• 'icotinamide

Diagnosis and typesl d f



Slide ** of 48


Prevention of t(pe + diabetes

Insulin

• Diabetes 3re ention .rial

• Diabetes 3rediction and3re ention 3roRect

Diagnosis and typesSlid *) f 48



Slide *) of 48


Prevention of t(pe - diabetes

/ifestyle modification

• Da ing Study

• ,innish Diabetes 3re ention Study

Diagnosis and typesSlid * f 48



Slide *- of 48


Prevention of t(pe - diabetes

/ifestyle s medication

• Diabetes 3re ention 3rogram

• S.?3#'IDD+



Complications:

Short ter" Co"plications* ;"etabolic<.ypoglyce"ia)iabetic =etoacidosis/on =etotic hyperos"olar diabetic co"a&actic acidosis

&ong ter" Co"plications *;,ngiopathy<Microngiopathy ! Retinopathy>/ephropathy> /europhathy> der"atopathy5Macroangiopathy – ,therosclerosis5



Microangiopathy athogenesis:

.yperglyce"ia chronic5?lycosylation of base"ent "e"braneproteins &ea+y blood vessels5

78cess deposition of proteins –glycosylation cycle5@hic+ and &ea+y blood vessels5/arrow lu"en#sche"ic Argan da"age555



Diabetic Microangiopathy'ormal

Diabetic

6lucose6lycosylation5+ damage lea

A6%B deposition



!europathy

Sensory Motor ;"yelin<Beripheral /europathy"ilateral# symmetric

rogressi$e# irre$ersible

araesthesia# pain# muscleatrophy

isceral neuropathyCranial ner$e – diplopia# "ell palsy

%IT- constipation# diarrhoeaC&' – orthostatic hypotension



!europathy

+yelin loss in ner e





Diabetic (myotrophy

3ainful muscle "asting



Diabetic !europathic ulcer



!europathic ulcer

%tiology$peripheral sensory

neuropathy .rauma1 deformity,actors$

Ischemia callusformation andedema



!europathic ulcers

FEATURES:

Painless, surrounded by callusAt pressure points.associated with good foot pulsesMay not be associated with gangrene



!ephropathy

/odular ?lo"eruloSclerosis5Co""on "orbidity "ortality5

)eposition of D,?7E ,dvanced ?lycosylation7nd!products as nodules5/ephrotic syndro"eByelonephritis7nd stage renal failure



)iabetic /ephropathy

Microangiopathy> atherosclerosis infections*)iffuse or nodular diabeticglo"erulosclerosis ;=i""elstiel $ilson Sy<Renal arteriolosclerosis atherosclerosis/ecrotiFing renal papillitis5Byelonephritis57nd stage +idney5

!odular %lomerulosclerosis



!odular %lomerulosclerosis –)W lesion*







Diabetic %lomerulosclerosis

Hyaline nodulesHyaline nodules



Diabetic %lomerulosclerosis

l



!ormal +etina

l f $ h



!on roliferati$e +etinopathyenous dilation and s"all red dots posterior retinal

pole ! capillary "icro!aneurys"s5Dot and blot retinal he"orrhages and deep!lyingede"a and lipid e8udates i"pair "acular function5&ate generaliFed di"inution of vision due toischemia and macular edema ! co""on cause ofvisual defect ;best detected by fluoresceinangiography<Cotton-,ool spots ;soft e8udates< ! "icroinfarctsdue to ische"ia5 @hey are white and obscureunderlying vessels5 .ard e8udates are caused bychronic ede"a5 @hey are yellow and generally deepto retinal vessels5

lif i$ i h



roliferati$e +etinopathy/eovasculariFation ! which grows into the vitreouscavity5#n advanced disease> neovascular "e"branes canoccur> resulting in a traction retinal detach"ent5

itreous he"orrhages "ay result5sudden severe loss of vision can occur when there isintravitreal he"orrhage5Boor visual prognosis if severe retinal ische"ia>e8tensive neovasculariFation> or e8tensive fibroustissue for"ation5Banretinal photocoagulation "ay di"inish oreli"inate proliferative retinopathy

i h



+etinopathy

/on BroliferativeMicroaneurys"s>)ot blot he"orrhages.ard and soft e8udates

Cotton wool – infarctsMacular ede"a5

Broliferative5/eovasculariFation&arge he"orrhagesRetinal detach"ent5

Di b i i h



Diabetic +etinopathy

eo!ascularization Cotton "ool

spots

Di b i i h




Dot blot ; (emorrhages <+icroaneurysms=

Di b i i h




3re retinal (emorrhage # detachment

Di b ti + ti th




Ad anced fibrous plaNues



The past cannot be changed# but thefuture can** by actions in the present

time*. !!G=

ast is history#ast is history#

/uture is mystery/uture is mysteryresent is the gift01resent is the gift01

b l th di *



abel the diagram*15253545

5

(ard dep?ptic disc+acula5lot hem

Cotton "ool

M i h h l i



Macroangiopathy ,therosclerosis

)yslipide"ia↓ .)&

/on!7nFy"atic ?lycosylation

↑ Blatelet ,dhesiveness

↑ @hro"bo8ane , 2

↓ Brostacyclin

3ndothelial damage (therosclerosis

M#> C ,> ?angrene of &eg ;B )<> Renal

#nsufficiency

(th l i



(therosclerosis:



'lide 'ho,



/ g l i f ti C didi i



/ungal infections: Candidiasis

Macrosomia



Macrosomia

ith 3olycythemia

"lood $essel calcification:



lood $essel calcification:

Amputated thumb



(canthosis !igricans




Insulin resistanceT





Insulin resistanceT

abel the diagram*



abel the diagram*15253545

Capillary'odule ; A6%5o"man caps(yaline

arteriolosclerosis inarteriole

Infections in Diabetes:



Infections in Diabetes:

)ecreased "etabolis" – low i""unity5)ecreased function of ly"phocytes neutrophils – glycosylation5?lycosylation of i""une "ediators5 ,bCapillary thic+ening – i"paired infla""ation5#sche"ia infarctions5

#ncreased glucose ;alone is not the cause <

)iabetes State of i""unosuppression5

aboratory Diagnosis:



aboratory Diagnosis:

Hrine glucose ! dip!stic+ –ScreeningRando" or fasting blood glucose ;'11<-asting I""ol> Rando" 11""ol

#f -asting level is between I!11 then A?@@

.b,1c ! for follow!up> not for diagnosis

-ructosa"ine ! for long ter" "aintenance5

oints to remember:



oints to remember:

)isorder of "etabolis" – #nsulin@ype!# Children> ,cute> Metabolic co"pl5@ype!## ,dults> Chronic> ascular co"pl5

,ngiopathy ;"icro6"acro<>.eart> Grain> =idney> Retina> S+in> G 5

#ncreased #nfections – +now reasons5

.ypoglyce"ia is "ore dangerous5 /ot hyper ?lucose control is critical -GS> ?@@ .b,1C5

4uestions**



4uestions

.ow – =etoacidosis%.ow – hypoglyce"ia % ,ngiopathy – Macro Micro %

#nfections in@ypes of retinopathy %)iabetes insipidus %

/ephrotic 6 /ephritic syndro"e %=idney da"age in )iabetes %





It5s not that I5m so smart#it5s 6ust that I stay ,ith

problems longer.!!,lbert 7instein

Diagnosis and typesSlide :02 of 48%TI3IT4




.ype 2 diabetes can be delayed inpeople "ith I6.

/ifestyle modification is most

effecti e

hat do you thin could be done atcommunity le el to pre ent or delaydiabetesJ

Diagnosis and typesSlide :0! of 48

S mmar(




Summar(

.ype : diabetes

• esults from progressi e beta#

cell destruction• 3eople "ith type : diabetes need

insulin therapy to li e


Summar(




.ype 2 diabetes

• ?ften characterized by insulin

insensiti ity and relati e ratherthan absolute insulin deficiency

• A progressi e condition

• +ost people "ith type 2 diabetes"ill need insulin "ithin * to :0years of diagnosis

Summar(

Diagnosis and typesSlide :0* of 48

"evie* #uestion




evie* #uestion

: .he pathogenesis for type 2 diabetesincludes$

a Insulin deficiency and insulininsensiti ityb Insensiti ity to insulin and

autoimmune beta#cell destruction

c Autoimmune beta#cell destructionand glucagon deficiencyd Insulin deficiency and glucagon

deficiency

Diagnosis and typesSlide :0) of 48

"evie* #uestion




evie* #uestion

2 A person "ith type 2 diabetes recentlystarted on insulin as s if there is a "ayto measure if heEshe is still producing any

insulin .he correct response "ould be$

a Islet cell antibody tests

b C#peptide test

c (bA :c test

d Serum insulin test

Diagnosis and typesSlide :0- of 48

"evie* #uestion




evie* #uestion

! .he Diabetes 3re ention 3rogram <D33=$

a Included people "ith type :

diabetesb Included only people "ith I6.

c .ested the alue of e ercise

d Included people "ith type 2diabetes


"evie* #uestion




evie* #uestion

4 .ype : diabetes is usually caused by$

a InRury to the pancreas

b An autoimmune reaction

c Insulin insensiti ity in the cells

d (ypersensiti ity to insulin


ns*ers




ns*ers

: a

2 b

! b

4 b

Diagnosis and typesSlide ::0 of 48

"eferences




eferences

: American Diabetes Association Diagnosis and classification of diabetes mellitus Diabetes Care

2004K 2-<suppl :=$ S*#S:02 Canadian Diabetes Association Clinical 3ractice 6uidelines % pert Committee Canadian

Diabetes Association 200! clinical practice guidelines for the pre ention and management ofdiabetes in Canada Can M Diab 200!K 2-<suppl 2=

! Chiasson M/ Mosse 6 6omis et al Acarbose for pre ention of type 2 diabetes mellitus$.he S.?3#'IDD+ randomized trial /ancet 2002K !4)$ !7!#40!

4 Delahanty /+ and (alford 5' .he role of Diet 5eha iours in Achie ing impro ed glycaemic

control in intensi ely treated patients in the Diabetes Control and Complications .rial DiabetesCare :77!K :)<::=$ :4*!#*8

* Diabetes Control and Complications .rial esearch 6roup %ffect of intensi e diabetestreatment on the de elopment and progression of long#term complications in adolescents "ithinsulin dependent diabetes mellitus$ Diabetes Control and Complications .rial .he Mournal of3aediatrics :774K :2*<2=$ :--#88

) Diabetes Control and Complications .rialEepidemiology of diabetes inter entions andcomplications research group intensi e diabetes therapy and carotid intima#media thic ness intype : diabetes mellitus 'e" %ngl M +ed 200!K !48$ 2274#!0!

- Diabetes Control and Complications .rial$ .he effect of intensi e treatment of diabetes on thede elopment and progression of long#term complications in insulin#dependent diabetesmellitus ' %ngl M +ed :77!K !27$ 7--#8)

Diagnosis and typesSlide ::: of 48

"eferences




eferences

8 ,ord %S 6iles ( Dietz ( 3re alence of the metabolic syndrome among S adults$ findingsfrom the third 'ational (ealth and 'utrition % amination Sur ey MA+A 2002K 27-$ !*)#*7

7 Diabetes Atlas 200) 5russels$ International Diabetes ,ederation 200)

:0 Isomaa 5 Almgren 3 .uomi . et al Cardio ascular morbidity and mortality associated "ith themetabolic syndrome Diabetes Care 200:K 24<4=$ )8!#7

:: 3an U /i 6 (u @ et al %ffects of diet and e ercise in pre enting 'IDD+ in people "ith impairedglucose tolerance$ .he Da ing I6. and Diabetes Study Diabetes Care :77-K 20<4=$ *!-#44

:2 eport of a (? Consultation /aboratory Diagnosis and monitoring of Diabetes +ellitus orld

(ealth ?rganisation 2002 http$EE"hNlibdoc "ho intEhNE2002E724:*7048! pdf cited April !0200*

:! .uomilehto M /indstrom M %ri sson M6 et al 3re ention of type 2 diabetes mellitus by changes inlifestyle among subRects "ith impaired glucose tolerance ' %ng M +ed 200:K !44$ :!4!#*0

:4 .he Diabetes 3re ention 3rogram esearch 6roup .he diabetes pre ention 3rogram <D33=Diabetes Care 2002K 2!<:2=$ 2:)*#-:

:* & 3rospecti e Diabetes Study 6roup Intensi e blood#glucose control "ith sulpfonylureas or

insulin compared "ith con entional treatment and ris of complications in patients "ith type 2diabetes /ancet :778K !*2$ 8!-#*!

Diagnosis and typesSlide ::2 of 48

"eferences

http://whqlibdoc.who.int/hq/2002/9241590483.pdf

http://whqlibdoc.who.int/hq/2002/9241590483.pdf



eferences

:) & 3rospecti e Diabetes Study 6roup .ight blood pressure control and ris ofmacro ascular and micro ascular complications in type 2 diabetes &3DS !8 5+M

:778K !:-$ -0!#:!

:- ID, Clinical 6uidelines .as ,orce 6lobal 6uideline for .ype 2 Diabetes 5russels$International Diabetes ,ederation 200*

:8 (arris S5 % oe M+ Ldano"icz @ ebster#5ogaert S 6lycemic Control andmorbidity in the Canadian primary care setting <results of the diabetes in Canadae aluation study= Diab esearch and Clin 3ract 200*K -0$ 70#-

Diagnosis, Classification and Prevention

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