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CV: dr.

R Bowo Pramono SpPD KEMD


Lahir TEGAL 27-jan 1959
Istri: dr. Astuti SpS, 2 putri
Dokter Umum: FK UGM

17-01-1985
SPPD : FK UGM 24-11-1997
KEMD : 14-05-2008
Pekerjaan:
1987-2002 PKM Kedung Waringin Bekasi
1999-2004 RSU Selong Lombok Timur
2004-2010 RS DR Sardjito/FK UGM
2006-2013 Sekretaris Bagian Penyakit Dalam FK UGM
2007-2011 Sekretaris PAPDI Cabang Yogyakarta
1

DIAGNOSIS & MANAJEMEN


DM TIPE 2

By 2030, 7 of the 10 Countries with the


Most Diabetic Patients Will Be in Asia
2000
Ranking

1
2
3
4
5
6
7
8
9
10

Country

India
China
USA
Indonesia
Japan
Pakistan
Russian Fed.
Brazil
Italy
Bangladesh

2030
People with
diabetes
(millions)
31.7
20.8
17.7
8.4
6.8
5.2
4.6
4.6
4.3
3.2

Country

India
China
USA
Indonesia
Pakistan
Brazil
Bangladesh
Japan
Philippines
Egypt

People with
diabetes
(millions)
79.4
42.3
30.3
21.3
13.9
11.3
11.1
8.9
7.8
6.7

5
Wild S et al. Diabetes Care 2004;27(5):1047-53.

Type of DM
1. Type 1 (IDDM: insulin dependent DM)
2. Type 2 (NIDDM: non insulin dependent DM)
- obese
- non obese
3. Others (genetic cell function & insulin action,
disease of exocrine pancreas, drugs,
endocrinopathies, infections, immune, others.
4. Gestasional
6

Diagnosis (WHO classification)


Venous plasma glucose (mg/dL)
Normal

Fasting &
2h post-prandial

< 100
< 140

Diabetes mellitus

Fasting &
2h post-prandial

> 126
> 200

Impaired Glucose
Tolerance (IGT)

Fasting &
2h post-prandial

< 100
140-199

Impaired Fasting
Glucose (IFG)

Fasting &
2h post-prandial

100 - 125
< 140

NB:
In the absence of symptom, the diagnosis of DM must be confirmed by a
second
diagnosis test (i.e. fasting, random, or Oral Glucose Tolerance Test (OGTT) on7
a separate day

Assesment of the newly


diagnosed patient
Hystory:
Duration of symptom: thirst, polyuria, weight
loss
Possible secondary causes of diabetes:
acromegaly
Family history
Pressence of complication of diabetes
Risk factor for developing complications:
smoking, hypertension, hyperlipidemia
9


Examination:
BMI (body mass index weight (kg)/height2(m)
Clues for secondary causes
Cardiovascular system (BP + pulse)
Sign of autonomic and peripheral neuropathy
Eyes for retinopathy
Investigation:
Blood test for: urea & electrolytes, liver & thyroid
function, full lipid profil
Urine tests for ketones, macro and (if negative)
micro albuminuria
An ECG in all type 2 DM
10

Type 2 diabetes is NOT a mild disease


Stroke
Diabetic
Retinopath
y cause
Leading
of blindness
in working age
adults1

2 to 4 fold increase
in
cardiovascular
mortality and
stroke3

Cardiovascular
Disease

8/10 diabetic
patients
die from CV events4

Diabetic
Nephropathy
Leading cause of
end-stage renal
disease2

Diabetic
Neuropathy
Leading cause of
non-traumatic lower
extremity
amputations5

Fong DS, et al. Diabetes Care 2003; 26 (Suppl. 1):S99S102. 2Molitch ME, et al. Diabetes Care 2003; 26
(Suppl. 1):S94S98.
11
3
4
Kannel WB, et al. Am Heart J 1990; 120:672676. Gray RP & Yudkin JS. In Textbook of Diabetes 1997.
5
Mayfield JA, et al. Diabetes Care 2003; 26 (Suppl. 1):S78S79.

Multiple Factors Contribute to T2DM


Decreased
glucose
uptake

Hungry & stress

Progressive
-cell
dysfunction

Type 2 Diabetes

Hepatic
glucose production

Impaired
incretin
signaling
1. Bode BW. Postgrad Med. 2009;121:82-93.
2. DeFronzo RA. Ann Intern Med. 1999;131:281-303.
3. DeFronzo RA. Diabetes. 2009;58:773-795.

Increased
lipolysis

Increased
renal
glucose transport

Lack of
cells
glucagon
suppression

Prinsip Dasar Terapi Diabetes


Mellitus
3

PENGATURAN
MAKAN
4

LATIHAN
JASMANI

PENYULUHA
N

OBAT

CANGKOK

Correlation between HbA1c level and mean


plasma glucosa levels on multiple testing
over 2-3 months
HbA1c

Mean plasma glucose (mg/dL)

135

170

205

240

10

275

11

310

12

345

15

HbA1c HbA1c
HbA1c

135 mg/dl

7.8%

HbA1c

135 mg/dl

7.8%

Time

What the Different Measures Tell Us

A1C1
Measures mean glycemia (past 3-4 months)
Reflects risk for T2DM complications

Different glucose profiles can result in similar A1C values 2


FPG and PPG measures allow for daily glucose variations to be
assessed

1. Sacks DB et al. Clin Chem. 2002;48:436-472.


2. Del Prato S. Int J Obes Relat Metab Disord. 2002;26(suppl 3):S9-17. Permission for figure requested.

Hasil dari UKPDS:


Kontrol yang baik pada DM T2 mampu menurunkan resiko
komplikasi
Penurunan 1% HbA1c

Menurunkan resiko*

Kematian karena
diabetes

-21%

Infark miokard

-14%

Komplikasi
mikrovaskuler

-37%

Gangguan pembuluh
darah perifer

-43%

1%

*p<0.0001 n=3,642 type 2 diabetes patients

Stratton IM et al. BMJ 2000;321:405412

PRINSIP PENGOBATAN DIET


Kebutuhan kalori sesuai : kelamin,
umur , berat badan, aktifitas fisik,
pekerjaan, kehamilan, menyusui,
komplikasi
3 kali makan utama dan 3 kali makan
kecil
Jumlah dan waktu makan harus tepat

JADWAL MAKAN DIABETES


Komposisi diet: 60-70 % hidrat arang
20-25 % lemak
10-15 % protein
20%

10%

25%

10%

25%

6.30

9.30

12.00

15.00

19.00

10%

21.00

PRINSIP OLAHRAGA PADA


DIABETES
Pilih olahraga yang disenangi
Melibatkan otot-otot besar
Frekuensi

: Teratur 3-5 kali perminggu

Intensitas

: Ringan sampai sedang

Durasi

: 30 60 menit / 5 X30 menit /minggu

Tipe

: Aerobik (jalan, joging, ber sepeda)

Program Latihan
Teratur (3-4 kali seminggu)
20- 40 menit didahului
pemanasan 5-10 mnt dan
cool-down 10 mnt

CRIPE:
Continous
Rythmis
Interval
Progresif
Endurance

Treatment options for type 2


diabetes
Sulfonylureas
1st generation e.g. chlorpropamide,
tolbutamide
2nd generation e.g. glyburide,
gliclazide, glipizide, gliquidone
3rd generation e.g. glimepiride
Modified release

-glucosidase inhibitors
e.g. acarbose

Glinides/meglitinides
Non-sulfonylureic e.g. repaglinide
Amino acid derivatives e.g. nateglinide

Biguanides
e.g. metformin

Thiazolidinediones
e.g. rosiglitazone, pioglitazone

Insulin
regular
intermediate/long acting
pre-mixed
analogs

rapid acting
long acting

Fixed-dose oral antidiabetic


drug combinations
e.g. glyburide/metformin,
glipizide/metformin,
rosiglitazone/metformin

Metformin
How it works

Decreases hepatic glucose output


Lowers fasting glycemia

Expected HbA1c ~ 1.5%


reduction
Adverse events GI side effects

Lactic acidosis (quite rare)

Weight effects
CV effects

Weight stability or modest weight loss


Unconfirmed beneficial effect
demonstrated in UKPDS

Nathan DM et al. Diabetes Care 2006;29(8):1963-72.

Sulfonylureas
How they work

Enhance insulin secretion

Expected HbA1c
reduction

~ 1.5%

Adverse events

Hypoglycemia (but severe episodes


are infrequent)

Weight effects

~ 2 kg weight gain common when


therapy initiated

CV effects

UGDP suggested potential cause of


increased CVD mortality; not
substantiated by UKPDS
Nathan DM et al. Diabetes Care 2006;29(8):1963-72.

Tabel 3. Jenis Sulfonilurea


Sulfonylurea

Length of
action

Begins of
action

Daily dose
(mg)

Route of
excretion

Glibenclamide

16 24h

2 4h

1,25 15

R = 50%, B = 50%

Gliclazide

10 24h

2 4h

40 320

R = 70%, B = 30%

Glipizide

6 24h

2 4h

2,5 40

R = 80%, B =20%

Chlorpramide

24 72h

2 4h

100 500

Renal

Tolbutamide

6 10h

2 4h

100 1000

Renal

Glimepiride

24h

2 4h

1-6

R = 40%, B =60%

gliquidon

18 - 24h

2 - 4h

30 - 120

R = 5%, B = 95%
26

Glinides
How they work

Stimulate insulin secretion (but


differently from sulfonylureas)

Expected HbA1c
reduction

~ 1.5% (repaglinide)

Adverse events

Hypoglycemia (may be less frequent


than some sulfonylureas)

Weight effects

~ 2 kg weight gain common when


therapy initiated

CV effects

None mentioned in ADA


recommendations

Nathan DM et al. Diabetes Care 2006;29(8):1963-72.

Dipeptidyl Peptidase IV Inhibitors


How they work

Inhibit degradation of endogenous


GLP-1

Expected HbA1c
reduction

~0.8%

Adverse events

Minimal

Weight effects

Neutral

CV effects

Unknown

Nathan DM et al. Diabetes Care 2006;29(8):1963-72.

-Glucosidase Inhibitors
How they work

rate of digestion of polysaccharides in


proximal small intestine (primarily lowering
PPG levels without causing hypoglycemia)

Expected HbA1c
reduction

0.50.8%

Adverse events

Increased gas production


GI symptoms

Weight effects
CV effects

Weight neutral
Unconfirmed report of reduction of
severe outcomes in one clinical trial

Nathan DM et al. Diabetes Care 2006;29(8):1963-72.

Thiazolidinediones
How they work

Increase sensitivity of muscle, fat, and liver to


endogenous and exogenous insulin

Expected HbA1c
reduction

0.51.4%

Adverse events

Weight gain and fluid retention

Weight effects

Increase in subcutaneous adiposity


Redistribution from visceral deposits

CV effects

New / worsened CHF or peripheral edema


(due to fluid retention)
Reduction in some secondary CV endpoints
demonstrated in PROactive study

Nathan DM et al. Diabetes Care 2006;29(8):1963-72.

Glucagon-like Peptide 1 Agonist


(exenatide)

How it works

Stimulates insulin secretion

Expected HbA1c 0.51%


reduction
Adverse events GI side effects (nausea, vomiting,
diarrhea)

Weight effects

Weight loss of ~ 23 kg over 6 months


(may be result of GI effects)

CV effects

None mentioned in ADA


recommendations

Nathan DM et al. Diabetes Care 2006;29(8):1963-72.

Dipeptidyl Peptidase IV Inhibitors


How they work

Inhibit degradation of endogenous


GLP-1

Expected HbA1c
reduction

~0.8%

Adverse events

Minimal

Weight effects

Neutral

CV effects

Unknown

Nathan DM et al. Diabetes Care 2006;29(8):1963-72.

Insulin
How it works

Direct compensation for lack of


insulin sensitivity

Expected HbA1c
reduction

1.52.5%

Adverse events

Hypoglycemia

Weight effects
CV effects

Weight gain of ~ 24 kg

Beneficial effect on TG and HDL


Weight gain may have an adverse
effect on CV risks
Nathan DM et al. Diabetes Care 2006;29(8):1963-72.

Indikasi terapi Insulin:


DM tipe 1
DM tipe 2 yang tidak terkontrol diet, olah raga,
OHO.
DM gestasional
Gangguan faal hati & ginjal yang berat.
Dengan infeksi akut (selulitis, gangren), TBC
berat, penyakit kritis (stroke/AMI)
Dengan KAD/HHS
Dengan fraktur atau pembedahan mayor
Kurus (BB rendah), terkait malnutrisi (DMTM)
Dengan penyakit Graves
Dengan tumor ganas
Dengan pemberian kortikosteroid

100

75
Beta Cell
Function
(%)

IGT

Postpandrial
Hiperglycemi

T-2 DM phase I
Beta Cell function
50 %

50

Stages of Type
2 Diabetes
T2 DM
phase I

25

T2 DM
phase II
T2 DM
phase III

0
-12 -10
14
Lebovitz, 2000

-6

-2

Years From Diagnosis

10
35

Effectiveness of Type 2 Diabetes Therapy


Starting HbA1c

Diet &
Exercise
1.5-2%

Metformin
Insulin
Secretagogues

1%

TZD

Alpha-glucosidase
Inhibitors

Combination
Oral
Agents

Insulin

3-4%

5% or more

<7%

<8%
1-1.5%

<8-10%

>10%

The Importance of treating Type 2 Diabetes


Type 2 diabetes is a progressive disease
Postprandial glucose

Diagnosis
Glucose

Fasting glucose

Insulin

Insulin resistance

Inadequate
-cell function
Microvascular changes
Macrovascular changes
NGT

Prediabetes
(IFG/IGT)

Diabetes

Adapted from Type 2 Diabetes BASICS. International Diabetes Center 2000

Insulin secretion

What is good glycemic control?

Overall aim to achieve glucose levels as close to normal as


possible
Minimise development and progression of microvascular and
macrovascular complications

ADA1

IDF2

PERKENI3

FPG
<130 mg/dL

FPG
<110 mg/dl

FPG
<100 mg/dl

HbA1c
< 7.0%

PPG
<180 mg/dL

HbA1c
< 6.5%

PPG
<145 mg/dL

HbA1c
< 7%

PPG
<140 mg/dl

1. American Diabetes Association Diabetes Care 2009;32 (Suppl 1):S1-S97


2. IDF Clinical Guidelines Task Force. International Diabetes Federation 2005. 3. PERKENI 2011 Konsensus .

The benefits of good blood glucose control are clear

Good control is
7.0% HbA1c
HbA1c measures the
average
blood glucose level
HbA1c
over the
last three months
-1%

Myocardial
infarction

-14%
Microvascular
complications

-37%
Deaths related
to diabetes

-21%
Source: UKPDS = United Kingdom Prospective Diabetes Study. Stratton IM et al.
BMJ. 2000;321(7258):405-412.

Individualized Treatment based on several criteria to control


blood glucose

Slide 40
Inzucci SE, et al. Diabetologia. 2012

New position statement of the ADA and EASD on management


of hyperglycemia in type 2 diabetes

Inzucci SE, et al. Diabetologia. 2012

Updated PERKENI Type 2 Diabetes Treatment Algorithm

Diabetes
Healthy life style

STEP 1

STEP 2

STEP 3

Healthy life style


+
Mono therapy

Note:
1.

2.

Therapy failed if target of


HbA1c < 7% is not
achieved within 2-3
months for each step
In case of no HbA1c test,
the use of blood glucose
level is also permitted.
Average blood glucose
level for a few BG test in
one day can be converted
to HbA1c (ref: ADA 2010)

Healthy life style


+

Healthy life style

2 OAD Combination

+
Combination 2 OAD

Alternative option, if :

No insulin is available

Basal insulin

The patient is objecting insulin


Blood glucose is still not optimally
controlled

Healthy life style


+
3 OAD Combination

*Intensive Insulin: use of Slide


basal insulin
42 together with insulin prandial

Insulin Intensification*

Relative contribution of fasting and prandial


glucose to HbA1c levels

Contribution (%)

Relative contribution of postprandial versus fasting


glycaemia over HbA1c sixtiles

HbA1c sixtiles (%)

Target HbA1c will not be reached without bringing down postprandial hyperglycaemia
Woerle HJ, et al. Diabetes Res Clin Pract 2007;77:2805

Diabetes elevated blood glucose due to insufficient insulin


secretion
Normal glucose and insulin
excursions

Glucose

Insulin

Glucose
120

300

80
60

200

40
100

20

120

06:00 10:00 14:00 18:00 22:00 02:00 06:00

100

Insulin U/mL

Insulin U/mL

100

Insulin

400

Glucose mg/dL

400

Glucose mg/dL

Early Type 2 Diabetes Glucose and


insulin excursions

300

80
60

200

40
100

20
06:00 10:00 14:00 18:00 22:00 02:00 06:00

Dinner

Lunch

Slide 44

Breakfast

Dinner

Lunch

Breakfast

Time of Day

Time of Day

Three Types of Insulin


PRE-MIX

0 4 8 12 16 20 24
Time (h)

Basal Insulin provides a


steady concentration of insulin
in the bloodstream over 24
hours. Initially, basal insulin
should be given at 10 units
per day at night time or in the
morning1

FAST-ACTING

GIR (mg/kg/min)

GIR (mg/kg/min)

GIR (mg/kg/min)

BASAL

0 4 8 12 16 20 24
Time (h)

Premixed insulins contain a


mixture of rapid-acting and
intermediate-acting insulin in
a fixed combination to provide
coverage of prandial and
basal insulin requirements2
Slide 45

0 4 8 12 16 20 24
Time (h)

Fast-acting insulins include single


amino acid replacement that
reduce their ability to self-associate
into dimers and hexamers. This
means that they are quickly
absorbed into the bloodstream,
following subcutaneous injection.3

1. Hompesch M. Diabetes Obes Metab 2006; 8:568; 2. Weyer et al. Diabetes Care 1997;10:16121614.; 3. 1. Heinemann et al. Diabetes Care.
1998;21:19104

Insulin can be initiated at any time


Traditionally, insulin has been reserved as the last line of
therapy
However, considering the benefits of normal glycemic status,
Insulin can be initiated earlier and as soon as possible

Inadequate
Lifestyle

+ 1 OAD

INITIATE INSULIN

+ 2 OAD

+ 3 OAD

Ideal Basal Insulin

Closely mimic normal pancreatic basal insulin secretion


No distinct peak effect
Continued effect over 24 hours
Reduce nocturnal hypoglycemia
Once-daily administration for patient compliance
Predictable absorption pattern

Levemir (Insulin Detemir)

LysB29(N-tetradecanoyl)des(B30)human insulin

C14
(My fatty a
risti
c
c a id cha
cid)
in

Thr

Lys

Pro
Pro

Thr

Tyr

A21

B29
A1

Phe

Phe

Asn

Gly

Cys

Lys

Gly

Arg

Glu

Gly

Cys
Val
Leu

Tyr
Asn

Tyr

Ile

Glu

Leu

Val

Leu

Ala

Gln

Glu

Glu
Gln
Cys

Tyr
Cys

Thr

Ser

Ile

Cys

Ser

Val

Leu

Leu
His
Gly

B1

Phe

Val

Asn

Gln

His

Leu

Cys

Ser

Levemir Dose Titration Guidelines:


3-0-3 Algorithm
Start with Levemir 10 U or 0,1-0,2 U per Kg BB
Dose Adjustment for Each Arm
Mean 3-day FPG (mg/dL)
increase dose

FPG>90 mg/dl (5.0 mm/L)


FPG target range
70-90 mg/dL
FPG <70 mg/dL (3.8 mmol/L)

3 units

FPG>110 mg/dL (6.1 mmol/L)

0 maintain
dose

FPG target range


80-110 mg/dL

decrease dose

3 units

FPG <80 mg/dL (4.4 mmol/L)

Patients who experienced hypoglycemia reduced their daily dose by 3 units

Blonde L et al. Diabetes Obes Metab. 2009; 11(6):623-631.

Insulin Titration schemes


Basal and Fast-Acting Insulin
Fasting Blood Glucose
Content (mg/dl)
<70 mg/dl

Reduce dosage with 2 units

70-130 mg/dl

Maintain dosage

130-180 mg/dl

Increase dosage 2 units per 3 days

>180 mg/dl

Increase dosage 4 units per 3 days

BASAL
INSULIN

Basal Insulin Titration

Once titrated, continue to monitor HbA1c every 3 months

Subsequent pre-meal
Glucose (mg/dl)

Fast-acting Insulin Titration

Start with 4 units / day

Increase by 2 units every 3 days


until target is reached

FAST-ACTING
INSULIN

When starting Fast-acting Insulin, secretagogues should be


discontinued

Slide 50
Source: KONSENSUS: Insulin Treatment 2011

Treatment therapies for Type 2 diabetes

Premixed
Insulin

(Twice daily
Treat to target)

Lifestyle +
Metformin

+-other OAD
or GLP-1
agonists

Basal Insulin
(Basal + 3
prandial)

Basal Insulin
(Once-daily
treat-to-target)

HbA1c
7.0%
1c

Adapted from Raccah et al. Diabetes Metab Res Rev 2007;23:257.

Basal Insulin
(Basal + 1 or 2
prandial)

HbA1c
7.0%, FPG on target, PPG 160 mg/dl
1c

What International guidelines say about Insulin


intensification :
ADA:

FPG on target but HbA1c >7


Add 4U rapid-acting insulin at breakfast, lunch or dinner

AAFP:

FPG on target but HbA1c >7


Add 4U rapid-acting insulin at breakfast, lunch or dinner

AACE:

High HbA1c
Support intensification from basal to premix or basal-bolus
Support intensification from premix to basal-bolus

IDF:

High HbA1c
Support intensification from basal to premix or basal-bolus
Support intensification from premix to basal-bolus

EASD:

Refer to IDF guidelines

add rapid-acting

switch to premix

Insulin Treatment Optimization


How to Optimize Treatment after Basal Initiation

Start with Basal Insulin


10u / daily with meal or
before bedtime. Same
injection time every day

Basal
Basal Insulin
Insulin Only
Only
Usually
with
OAD
Usually with OAD

If glycemic target is not reached titrate


according to Basal Titration Scheme
Basal
Basal Insulin
Insulin Only
Only
Usually
with
OAD
Usually with OAD

If glycemic target is not reached within


2-3 months the intensify Insulin
treatment
Premix Insulin
Usually keep OAD

Switch to Premix twice-daily.


Start with equal basal dose, but
give 50% per injection and
titrate accordingly
Source: PERKENI Insulin Guidelines 2011

Basal
Basal with
with Prandial
Prandial
Usually
keep
Usually keep OAD
OAD

Add Prandial starting with


4u / day either once or
twice-daily and titrate
accordingly

Basal
Basal Bolus
Bolus
Usually
Usually keep
keep OAD
OAD

Switch to Basal Bolus (3


daily prandial) start with 4u
/ day and titrate
accordingly)

Practical guideline on intensification of insulin therapy with BIAsp 30


(NovoMix)
A simple algorithm for the intensification of basal insulin OD or BiD to BIAsp 30 BID

Basal insulin OD or BID


HbA1c 7-8%
FPG >110 mg/dl

Titrate basal insulin to achieve


FPG <110 mg/dl

HbA1c >8%
FPG: 73-110 mg/dl

Switch to BIAsp 30 BID

Practical guideline for swiching from basal insulin OD or BID to


BIAsp 30 BID
1:1 Total dose transfer to BIAsp 30
Split the dose 50:50 prebreakfast and predinner
Titrate the dose preferably once a week
Discontinue sulfonylureas (SUs)
Continue metformin
Consider discontinuing TZDs as per local guideline and practice
Administer BIAsp 30 just before meals

Practical guideline on intensification of insulin therapy with BIAsp 30


(NovoMix)
Practical guideline for swiching from BIAsp 30 BID to TID
Add 2-6 U or 10% of total daily BIAsp 30 dose before lunch
Down-titration of morning (-2 to 4 U) may be needed after adding the lunch dose
Titrate the dose preferably once a week according to the algoritm below
Discontinue sulfonylureas (SUs)
Continue metformin
Consider discontinuing TZDs as per local guideline and practice
Administer BIAsp 30 just before meals

Preprandial blood glucose value


<80 mg/dl
80-110 mg/dl
110-140 mg/dl
141-180 mg/dl
>180 mg/dl

Dose change
-2U
0
+2 U
+4 U
+6 U

When the daily insulin dose in a OD regimen nears 40-50 U, intensifying the regimen to BID
BIAsp 30 distribution = 2:1:3 (breakfast:lunch:dinner)
BIAsp 30 TID: alternative to basal-bolus (fewer daily injection and only one device need)

LOKASI PENYUNTIKKAN

Insulin Regimen Evolution

57

Menurunkan GDP akan menurunkan profil glukosa


darah 24 jam
400

Glukosa Plasma (mg/dl)

T2DM

300

15
200

Hiperglikemi dikarenakan peningkatan GDP

10

100

Normal
0
6

Meal

Meal

10

14

Meal

18

0
22

Waktu (jam)
Comparison of 24-hour glucose levels in control subjects vs patients with diabetes (p<0.001).
Adapted from Polonsky K, et al. N Engl J Med 1988;318:12319.

Glukosa Plasma (mmol/l)

20

INSULIN ANALOG:
1. NovoRapid
2. NovoMix
3. Levemir

Injectables

Current treatments for type 2 diabetes have limitations when renal function declines
Dose Reduction

Insulin
Liraglutide

Dose Reduction

Exenatide
Linagliptin

Oral drugs

Sitagliptin
Vildagliptin
Saxaglipti
n

Dose Reduction

Metformin
Acarbose
Repaglinid
e
Glimepirid
e

Dose Reduction

Dose Reduction Dose Reduction

Gliclazide
Pioglitazo
ne
>60

30 60

Declining GFR

<30

Hemodialysis

Adapted from: Schernthaner G, et al. Nephrol Dial Transplant. 2011;26(2):4547 (in press) and respective EMEA SmPCs

61

ADA/EASD consensus algorithm


Tier 1:

Call to action if HbA1c is 7%

well-validated therapies
At diagnosis:
Lifestyle +
Metformin

STEP 1

Lifestyle + Metformin
+ Basal insulin

Lifestyle + Metformin
+ Intensive insulin

Lifestyle + Metformin
+ Sulfonylurea
STEP 2

STEP 3

Tier 2:

Less well validated


therapies

Lifestyle + Metformin
+ Pioglitazone
No hypoglycaemia
Oedema/CHF
Bone loss

Lifestyle + metformin
+ GLP-1 agonist
No hypoglycaemia
Weight loss
Nausea/vomiting
Nathan DM, et al. Diabetes Care 2009;32 193-203.

Lifestyle + Metformin
+ Pioglitazone
+ Sulfonylurea

Lifestyle + metformin
+ Basal insulin
62

KASUS 1
Seorang wanita penderita Ca Mammae
usia 65 tahun dengan DM sejak 5 tahun
yll. dengan HbA1c 9,2%, GD puasa
225mg%, 2jpp 270 mg%, terapi metformin
3x500mg, Glibenclamid 1 0 0 tidak teratur.
Creatinin 1,9mg%, BUN 59mg%.
1, berapa target HbA1c?
2. TX sebaiknya apa?
Slide 64

Kasus 2.
Seorang Dosen Pria usia 45 tahun
dengan GDN 250mg%, 2jpp 350mg%,
telah mendapat terapi glimepirid 2mg 1-00 selama 2 tahun.
1. berapa target HbA1c?
2. Terapi apa agar HbA1c tercapai?
Slide 65

Kasus 3
Seorang ibu rumah tangga usia 42th, DM
dan HT, dengan kadar gula darah puasa
112 mg%, 2jpp 211mg%, HbA1c 7,0%, T
130/85mmhg terapi insulin basal 22 unit,
irbesartan 1x300mg
Apakah sudah tercapai target?
obat apa yang perlu dirubah atau
ditambah?
Slide 66

Less Hypoglycemia
Less Weight Gain

DM tipe 1
67

1980

1980

2009

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