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Slide 1
Initiating Diabetes Treatment with OADs
Lecture:
Dr.dr.Agus Yuwono SpPD-KEMD,I!ASIM
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Initiating Diabetes Treatment with OADs"e#ture
Main Learning Points
• Understand the different classes ofOADs and when to use which OADs –either as monotherapy or incombination with other OAD’s / Insulin
Slide 2
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Factors to onsider when hoosing an Anti!h"#ergl"cemic agent
Slide $
%&&ecti'eness in lowering glucose
%(tragl"caemic e&&ects that ma" reduce long!term com#lications
Sa&et" #ro&ile
Tolerabilit"
ost
%&&ect on bod" weight
Nathan DM et al. Diabetes Care 2006;29(8):1963-72.
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Slide )
Treatment thera#ies &or T"#e 2 diabetes$hen and %ow to start treatment
Adated !r"# $a%%ah et al. Diabetes Metab $es $e& 2007;23:2'7.
Li&est"le *Met&ormin
*!other OADor +LP!1agonists
,bA1c -./0
asal
asalInsulin
Premi(Insulin
asal *olus
Insulin
STA&T T&EATME!T OAD T&EATME!T STA&T I!S'"I! I!S'"I! I!TE!SII(ATIO!
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Slide 3
4#dated P%56%7I T"#e 2 Diabetes TreatmentAlgorithm
Diabetes ST%P 1 ST%P 2 ST%P $
Healthy life style Healthy life style
+
ono therapy
Healthy life style+
! OAD "ombination
Healthy life style
+
"ombination ! OAD
+
#asal insulin
InsulinIntensification$
$Intensi%e Insulin& use of basal insulin to'ether with insulin prandial
Healthy life style
+
( OAD "ombination
Alternati%e option) if &
• *o insulin is a%ailable
• he patient is ob,ectin' insulin
• #lood 'lucose is still not optimallycontrolled
7ote:
-. herapy failed iftar'et of HbA-c 01 is not achie%edwithin !2( monthsfor each step
!. In case of no HbA-ctest) the use of blood'lucose le%el is alsopermitted. A%era'eblood 'lucose le%elfor a few #3 test inone day can becon%erted to HbA-c4ref& ADA !5-56
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Slide 8
Main #atho#h"siological de&ects in t"#e 2 DM
hepaticglucoseproduction
peripheral'lucoseupta7e
pancreaticinsulinsecretion
pancreatic'luca'onsecretion
'utcarbohydratedeli%ery andabsorption
incretinefect
Hyperglycemia
?
LiverMuscle
PancreasIntestines
Adipose
Brain
Kidney
Glucosereabsorpsion
Adated !r"#:n*%%hi +, +herin $+. Diabetes Mellit*s. n: /"ld#an A*siell" D eds. Ce%il etb"" "! Medi%ine. 23rd,dn. 4hiladelhia 4a: +a*nders ,lse&ier; 2007.
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Slide .
urrent a'ailable OADs and non!Insulin in9ectables inIndonesia
• etformin
• 8ulfonylureas 48Us6 and 'linides
• 92'lucosidase inhibitors 4A3Is6
• 3luca'on2li7e peptide2- 43:;2-6 a'onists
• hia<olidinediones 4=Ds6
• Dipeptidyl peptidase2> inhibitors 4D;;2>
inhibitors6
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Slide
Primar" sites o& action o& currentl" a'ailable oral anti!diabetic agents and non!insulin in9ectables
Chen5 A ant*s /. Can Med Ass"% 200';172:21326.. arnett A. nt Clin 4ra%t 2006;60:1'70. 4re <e / et al.Ne!r"l"5ia. 2010;30:6182'.
Liver
Muscle
PancreasIntestines
Circulatory System
Glucose
FFA
Metformin
TZG l u c o s e r e l e a s e
FFArelease
D e f e c t i v
e
i n s
u l i n
s e c
r e t i o
n
!LP"# agonist
Insulinrelease
A!I
Glucoseabsorption
Intestinallipase in$i%itor
F F A
a b s o
r p t i o
n
Carbohydrates
Fat
I m p a
i r e d g l u c
o s e
u p t a k e
T;D
Metformin
G l u
c o s e
u p t a k
e
Bloc&s
Promotes
PP"'in$i%itor
Adipose
A/: =-5l*%"sidase inhibit"rs; D44-: dietid>l etidase-; A: !ree !att> a%id; ?D: thia"lidinedi"ne
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Slide <
Met&orminMode o) A#tion
The #rimar" e&&ects o& met&ormin are to decrease he#aticglucose #roduction and increase insulin!mediated #eri#heral
glucose u#ta=e
@rent A aile> C. Dr*5s 200';6':38'11.
A: att> A%ids
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Slide 10
Met&ormin(*ini#a* O+er+iew and (ontraindi#ations
Met&ormin
?fficacy$
8afety)olerability andAdherence
"ontraindications Ad%anta'es
• HbA-c reduction
of -2!1
• @;3 reduction of>5205 m'/dl
• Associated with
diarrhea and
abdominaldiscomfort
• :actic acidosis if
improperly
prescribed
• enal
insufficiency
• :i%er failure• Heart failure• 8e%ere
'astrointestinal
disease
• Do not cause
hypo'lycaemia
when used asmono2therapy
• Do not cause
wei'ht 'ainB may
contribute towei'ht loss
@rent A aile> C. Dr*5s 200';6':38'11.
,!!i%a%> deends "n eistin5 bl""d 5l*%"se le&els
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Slide 11
Met&orminTitration
MET-XRMET-IR
1. Nathan DM et. al. Diabetes Care 2009;32:193203. 2. abb"*r + ?irin5 . 4"st5rad*ate Medi%ine 2011;123:1'23.
id: ti%e dail>; 4/: !astin5 las#a 5l*%"se; /: 5astr"intestinal; M,-$: i##ediate release #et!"r#in; M,-B$:etended release #et!"r#in; d: "n%e dail>.
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Slide 12
Met&ormin"itt*e bene)it i) an - to go abo+e ./// mg
Fasting Plasma +lucose ,bA1c
h a n g e
' s / P l a c e b o > m g ? d l @
2300mg2000mg1300mg1000mg300mg
/arber A A# Med 1997;102:91-7.
Met)ormin Dose
h a n g
e ' s / P l a c e b o > 1 @
2300mg2000mg1300mg1000mg300mg
Met)ormin Dose
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Slide 1$
S4s and +linidesMode o) A#tion
• 8ulfonylureas 48Us6 and'linides increaseendo'enous insulin secretionby bindin' to pancreatic C2cells and tri''erin' a
cascade of intracellulare%ents-–(
• he mode of action of 8Usand 'linides is similar) butstimulation of insulinsecretion is more rapid and
short2actin' with 'linides• 8U receptors are also found
on other cells) includin' thecardiac myocytes
1. /allit arin5 -E. Diabetes Fbes Metab 2010;12:111. 2. +%h*it C et al. Diabetes 2001;'0:111. 3. @rent A aile> C. Dr*5s 200';6':38'11.
+E: s*l!"n>l*rea; /E: 5l*%"se trans"rter.
Pancreatic ("cell
!lucoseupta&e
Insulin release
Voltage-gatedcalcium channel
ATP-sensitivepotassium channel
S)s *glinides
!lycolysisrespiration
e p o
l a r
i + a
t i o
n
!luco&inase
ATP
Ca,-
ATP = orangeCa! = light green
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Slide 1)
S4s and +linides(*ini#a* O+er+iew
Sul#hon"lurea
?fficacy$
8afety)olerability andAdherence
• HbA-c reductionof -2!1
• @;3 reduction of
>5205 m'/dl
• Associated withhypo'lycaemia
and wei'ht 'ain
@rent A aile> C. Dr*5s 200';6':38'11. Nathan DM et al. Diabet"l"5ia. 2009;'2:1730. $"senst"% et al. DiabetesCare. 200;27:126'70.
,!!i%a%> deends "n eistin5 bl""d 5l*%"se le&els
+linides
?fficacy$
8afety)olerability andAdherence
• HbA-c reductionof 5.2-.1
• @;3 reduction of
!52E5 m'/dl• ;;3 reduction of
02-55 m'/dl
• Associated withhypo'lycaemia
and wei'ht 'ain• @reFuent
administration
4with e%erymeal6 is
reFuired.
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Slide 13
Al#ha glucosidase inhibitorsMode o) A#tion
• 8low di'estion of sucroseand starch and thereforedelay absorption
• 8low post2meal rise in blood'lucose
• 8ide effects
• @latulence) abdominaldiscomfort ) diarrhoea
• As mono2therapy will notcause hypo'lycaemia
• Hypo'lycaemia when usedwith other medicine 4e.'. asulphonylurea6
1. /allit arin5 -E. Diabetes Fbes Metab 2010;12:111. 2. +%h*it C et al. Diabetes 2001;'0:111. 3. @rent A aile> C. Dr*5s 200';6':38'11.
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Slide 18
Al#ha glucosidase inhibitors(*ini#a* O+er+iew
Al#ha glucosidase inhibitors
?fficacy$8afety) olerability andAdherence
• HbA-c reduction of 5.2
-1• @;3 reduction of -52!5
m'/dl• ;;3 reduction of >525
m'/dl
• Associated with
flatulence) diarrhea andabdominal discomfort
• As mono2therapy will
n"t cause
hypo'lycaemia• @reFuent administration
4with e%ery meal6 is
reFuired.
@rent A aile> C. Dr*5s 200';6':38'11. Nathan DM et al. Diabet"l"5ia. 2009;'2:1730. $"senst"% et al. DiabetesCare. 200;27:126'70.
,!!i%a%> deends "n eistin5 bl""d 5l*%"se le&els
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Slide 1.
Thiaolidinediones >T;Ds@Mode o) A#tion
Thiaolidinediones >T;Ds@ increase the sensiti'it" o& muscleand adi#ose cells to insulin and su##ressing he#atic glucose
#roduction
@rent A aile> C. Dr*5s 200';6':38'11.
?D: hia"lidinedi"nes
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Slide 1
Thiaolidinediones(*ini#a* O+er+iew
@rent A aile> C. Dr*5s 200';6':38'11. Dr*5 Class $e&ie: hia"lidinedi"nes. A&ailable at:htt:GGhar#a%>."re5"nstate.ed*Gdr*5H"li%>Ga5esGd*rHb"ardGre&iesGarti%lesG?DHClass$e&ie.d! . $i" M et al. ,ert Fin4har#a%"ther. 2008;9:229'303.
,!!i%a%> deends "n eistin5 bl""d 5l*%"se le&els
Thiaolidinediones
?fficacy$
8afety)olerability andAdherence
"ontraindications Ad%anta'es
• HbA-c reduction
of 5.2-.1
• @;3 reduction of!52 m'/dl
• Associated with
wei'ht 'ain and
edema• "ontraindicated
in patients with
abnormal li%er
function• Garnin's
re'ardin' ris7 of
fractures• ay eacerbate
or precipitate
con'esti%e heart
failure
• :i%er disease)
heart failure or
history of heartdisease
• ;re'nancy and
breast feedin'
• educed le%els of
:D:2cholesterol
and increasedle%el of HD:2
cholesterol
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Slide 1<
DPP!) inhibitorsMode o) A#tion
Dr*%er D et al. Nat*re 2006;368:169670'. dris et al. Diabetes Fbes Metab 2007;9:1'36'. arnett A. nt Clin 4ra%t2006;60:1'70. /allit et al. Diabetes Fbes Metab 2010;12:111.
D44-: dietid>l etidase-; /: 5astr"intestinal; /4:5l*%"se-deendent ins*lin"tr"i% "l>etide; /4-1: 5l*%a5"n-lie etide
Increases and prolongs!LP"# e.ect on α"cells
Increases and prolongs !LP"#and !IP e.ects on ("cells
Food inta"e
Stomac$
G# tract
Intestine
α"cells
Pancreas
Glucose-dependent insulinsecretion
("cells
PP"'in$i%itor
Glucose-dependent glucagon secretion
#ncretins$G%P-&' G#P(
DPP!)/et e.ect0
%lood glucose
) G#P does not inhibit glucagon secretion by α-cells
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Slide 20
DPP!) inhibitors(*ini#a* O+er+iew
DPP!) inhibitors
?fficacy$8afety) olerability andAdherence
• HbA-c reduction of 5.2
-1• @;3 reduction of !5
m'/dl• ;;3 reduction of >2
m'/dl
• 3enerally well tolerated• :ow ris7 of
hypo'lycemia• *ot associated with
wei'ht 'ain• Upper respiratory tract
infection has beenreported in clinical
studies
• ost reFuire only oncedaily administration
AhrIn . ,ert Fin ,#er5 Dr*5s 2008;13:'93607. /allit et al. Diabetes Fbes Metab 2010;12:111. A#"ri $, etal. AMA 2007;298:19206. +aa5litin DAJs ,nd"%rin"l"5i% and Metab"li% Dr*5s Ad&is"r> C"##ittee rie!in5 D"%*#ent!"r Aril 2009 Meetin5: NDA 22-3'0. A&ailable at: htt:GG.!da.5"&GF$M+GDFC@,+Ga%G09Gbrie!in5G2009-22b1-02-rist"l.d!. (a%%essed N"& 2010). As%hner 4 et al. Diabetes Care 2006;29:26327.
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Slide 21
+LP 1 AgonistMode o) A#tion
1. D">le M, ,5an M. 4har#a%"l her 2007;113(3):'693.
/4-1: 5l*%a5"n-lie etide
+lucagon!li=e #e#tide!1 >+LP!1@ agonist acti'ates the +LPrece#tor in the #ancreas/ This increases insulin release &romthe #ancreatic B!cellsC while inhibiting glucagon release b"
the #ancreatic !cells
α-cell
Pancreas
• Glucose-dependent insulin biosynthesisand secretion
• β-cell proliferation
β-cells
• Glucagon secretion• β-cell apoptosis
GLP-1 agonistNet effect:
blood glucose
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Slide 22
+LP 1 Agonist(*ini#a* O+er+iew
DPP!) inhibitors
?fficacy$8afety) olerability andAdherence
• HbA-c reduction of -2!1• @;3 reduction of E2-!
m'/dl• ;;3 reduction of E2-
m'/dl
• Associated with
moderate and transient
nausea) %omitin' anddiarrhea
• :ow ris7 of
hypo'lycemia and no
e%idence of increased"J ris7
• Associated with wei'ht
reduction• Associated with
reduction in #;
/arber A. Diabetes Care 2011;3 (+*l 2):+2798. M"rett" et al. Clin her 2008;30:1860. Dr*%er D. Cell Metab2006;3:1'36'. A#"ri $, et al. AMA 2007;298:19206.
,!!i%a%> deends "n eistin5 bl""d 5l*%"se le&els
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Slide 2$
The Princi#les o& OAD ombination Theor"
• wo 4or more6 oral blood 'lucose2lowerin'medicines that ha%e different mechanisms ofaction
• wo medications is better rather than increasein initial medicine to maimum dosa'e
• @ewer side effects than mono2therapy at hi'herdoses
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Slide 2)
Diabetes in elderl" #eo#le
• Always start with the lowest doseof any blood 'lucose2lowerin'
medicine and increase 'radually
• Usin' shorter2actin' medicinesthat reduces the ris7 ofhypo'lycaemia
• Hypo'lycaemia may increase the
ris7 of falls and heart attac7 inolder people
emember the possibility of
• @or'etfulness• ;oor moti%ation
• Depression
• "o'niti%e deficits
• ;oly2pharmacy
• educed manual deterity
•hese factors impact on the ability tomaintain self2care and achie%emaimum benefits from blood'lucose2lowerin' medicines.
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OADEs a Guic= summar" o& the di&&erent mechanism o&actions
!+lucosidase inhibitorsDelay intestinal carbohydrateabsorption
!+lucosidase inhibitorsDelay intestinal carbohydrateabsorption
ThiaolidinedionesIncrease 'lucose upta7e ins7eletal muscle anddecrease lipolysis inadipose tissue
ThiaolidinedionesIncrease 'lucose upta7e ins7eletal muscle anddecrease lipolysis inadipose tissue
Sul&on"lureasIncrease insulin secretionfrom pancreatic β2cells
Sul&on"lureasIncrease insulin secretionfrom pancreatic β2cells
GLP = glucagon-like peptide.
Adapted from heng and !antus. CMAJ . "##$%&'"("&)*""+.
MeglitinidesIncrease insulin secretion frompancreatic β2cells
MeglitinidesIncrease insulin secretion frompancreatic β2cells
2iguanide >met&ormin@Decreases hepatic 'lucose production and increasesupta7e
2iguanide >met&ormin@Decr eases hepatic 'lucoseproduction and increasesupta7e
Incretins :+LP!1 analogue>e(en!atide@?DPP!) inhibitors Im#ro'esglucose!de#endent insulinsecretion from pancreatic B!cells) suppresses g*u#agon se#retion )rom -#e**s) slows 'astric emptyin'
Incretins :+LP!1 analogue>e(en!
atide@?DPP!) inhibitors Im#ro'esglucose!de#endent insulinsecretion from pancreatic B!cells) suppresses g*u#agon se#retion )rom -#e**s) slows 'astric emptyin'
Slide 23
Slid 28
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Pro#erties o& a'ailable glucose!lowering agentsthat ma" guide treatment choice in T"#e 2Diabetes
lass om#ounds>s@ ellularmechanism Primar"Ph"siologicalaction>s@
Ad'antages Disad'antages
iguanides Met&ormin Acti'atesAMP!=inase
,e#atic +lucoseProduction ↓
%(tensi'e%(#erience
7o weight gain
7o h"#ogl"cemia
Li=el" HD %'ents ↓
+astrointestinal sidee&&ects
Lactic acidosis ris=
>rare@
Hitamin 12de&icienc"
Multi#le
contraindications:
6DC acidosisCh"#o(iaC
deh"dration etc/
Sul&on"lureas +libenclamide ?
gl"buride+li#iide
+liclaide
+lime#iride
loses 6ATP
channels onbeta cell
#lasme
membranes
Insulin secretion %(tensi'e
e(#erienceMicro'ascular 5is= ↓
>46PDS@
,"#ogl"cemia
eight gainlunts m"ocardial
ischaemic
#reconditioning J
Low durabilit"
Meglitinides 5e#aglinide
7ateglinide
loses 6ATP
channels onbeta cell
#lasme
membranes
Insulin secretion Post#randial
glucose e(cursions ↓
Dosing &le(ibilit"
,"#ogl"cemia
eight gainlunts m"ocardial
ischaemic
#reconditioning JFreGuent dosing
schedule
n*%%i +, et al. Diabet"l"5ia. 2012
Slide 28
I n c l u d
e d i n t
h e
2 i n d e r
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Pro#erties o& a'ailable glucose!lowering agentsthat ma" guide treatment choice in T"#e 2Diabetes cont/
lass om#ounds>s@ ellular
mechanism
Primar"
Ph"siologicalaction>s@
Ad'antages Disad'antages
Thiaolidinedi
ones
Pioglitaone
5osiglitaone
Acti'ates the
nuclear
transcri#tion&actor PPA5!"
Insulin Sensiti'it" 7o h"#ogl"cemia
Durabilit"
,DL!
Triac"lgl"cerols ↓
>#ioglitaone@HD %'ents ↓J
eight +ain
Oedema ? ,eart
Failureone Fractures
LDL!
>rosiglitaone@
Mn >meta!
anal"sesCrosiglitaone@ladder ancer J
>#ioglitaone@
a!+lucosidaseInhibitors
AcarboseMigitol
Hoglibose
Inhibitsintestinal a!
glucosidase
Slows intestinalcarboh"drate
digestions ?
absor#tion
7o h"#ogl"cemiaPost#randial
glucose
e(cursions ↓
HD %'ents ↓
7on!s"stemic
Modest ,bA1ce&&icac"
+astrointestinal side
e&&ects >&latulenceCdiarrhoea@
FreGuent dosing
schedule
DPP!)
Inhibitors
Sitagli#tin
Hildagli#tinSa(agli#tin
Linagli#tin
Alogli#tin
Inhibits DPP!)
acti'it"Cincreasing
#ost#randial
acti'e incretin>+LP!1C +IP@
concentrations
Insulin secretion
>glucose!de#endent@
+lucagon secretion ↓
>glucose!de#endent@
7o h"#ogl"cemia
ell tolerated
Modest ,bA1c
e&&icac"4rticardia?Angio!
oedema
Pancreatitis J
n*%%i +, et al. Diabet"l"5ia. 2012
Slide 2.
I n c l u d
e d i n t
h e
2 i n d e r
Slide 2
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Pro#erties o& a'ailable glucose!lowering agentsthat ma" guide treatment choice in T"#e 2Diabetes cont/
lass om#ounds>s@ ellularmechanism
Primar"Ph"siologicalaction>s@
Ad'antages Disad'antages
+LP!1
5ece#tor
Agents
%(enatide
Liraglutide
Acti'ates +LP!
1 rece#tors
Insulin secretion
>glucose!de#endent@
+lucagon secretion ↓
>glucose!de#endent@
Slows gastricem#t"ing
Satiet"
7o h"#ogl"cemia
eight reduction
Im#ro'ed betacell mass ?
&unction J
ardio'ascular
#rotecti'eactions J
+astrointestinal side
e&&ects >nausea ?
'omiting@Acute #ancreatitis J
cell h"#er#lasia ?
medullar" th"roid
tumoursIn9ectable
Training
5eGuirements
Insulin ,uman 7P,,uman 5egular
Lis#ro
As#art+luisine
+largine
Determir
Pre!mi(ed>se'eral t"#es@
Acti'atesinsulin
rece#tors
+lucose dis#osal
,e#atic glucose#roduction ↓
4ni'ersall"e&&ecti'e
Theoreticall"
unlimitede&&icac"
Micro'ascular
5is= ↓ >46PDS@
,"#ogl"cemiaeight gain
Mitogenic e&&ects J
In9ectableTraining
5eGuirements
KStigmaE &or #atients
n*%%i +, et al. Diabet"l"5ia. 2012
Slide 2
I n c l u d
e d i n t
h e
2 i n d e r
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OADEs and Incretins$or0shop
Main Learning Points
• Understand the different classes ofOAD’s and when to use which OAD’s –either as monotherapy or incombination with other OAD’s / Insulin
Summar"
• Different start and intensificationoptions for OADs eist dependin' on theneed for the indi%idual patient
• etformin will 'enerally be the first
dru' of choice
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