Curriculum Vitae

Nama : Dr. Alwi Shahab, SpPD-KEMD

Tgl Lahir : Palembang, 8 Januari 1955
Riwayat Pendidikan :
1983 : Lulus Dokter Umum (FK Unsri)
1995 : Lulus Spesialis Peny. Dalam (FK Unsri)
2006 : Konsultan Endokrin Metabolisme
Diabetes (KEMD)  Kolegium Ilmu Penyakit
Dalam Indonesia

Riwayat Pekerjaan / Jabatan :

1995-2004 : Sekretaris KPS I. Peny. Dalam FK Unsri

2003-2006 : Ka Div.Yan Med RSMH Palembang
2006-2009 : Ka Instalasi Teknologi Informasi RSMH Plg
2004 – sekarang : Koordinator Pendidikan Spesialis (KPS) Ilmu Penyakit Dalam
FK Unsri / RSMH Palembang

E-mail address : shahabalwi@yahoo.com

1
Website
06/01/21 : http://dokter-alwi.com
 PATOFISIOLOGI, DIAGNOSIS DAN
PENATALAKSANAAN DIABETES MELITUS

Alwi Shahab
Subbagian Endokrinologi Metabolisme
Bagian Ilmu Penyakit Dalam
FK Unsri/ RSMH Palembang

06/01/21 2
 Diabetes Melitus  penyakit kronis yang
ditandai peningkatan kadar glukosa darah,
akibat gangguan sekresi insulin / kerja insulin
atau keduanya.

Hiperglikemi kronis  gangguan fungsi atau

kerusakan berbagai organ tubuh  retina,
ginjal, syaraf dan meningkatkan risiko
terjadinya penyakit kardiovaskuler.

American Diabetes Association

06/01/21 3
 Klasifikasi Diabetes Melitus
1. Diabetes Tipe-1 (destruksi sel beta)
Autoimun
Idiopatik
2. Diabetes Tipe-2 ( resistensi insulin
disertai defek sekresi insulin atau
sebaliknya)
3. Diabetes Tipe lain
A. Defek genetik fungsi sel beta
MODY 1,2,3. DNA mitokondria
B. Defek genetik kerja insulin
C. Penyakit eksokrin pankreas;
Pankreatitis,tumor pankreas,
pankreatektomi, pankreopati
fibrokalkulus
06/01/21
D. Endokrinopati
Acromegali, sindroma Cushing,
Feokromositoma, hipertiroidisme
E. Karena obat/zat kimia
Vacor, pentamidin,asam
nikotinat
Glukokortikoid, hormontiroid,
tiazid, Dilantin, interferon alfa
F. Infeksi : rubellakongenital, CMV
G. Sebab imunologi yang jarang :
Antibodi anti insulin
H. Sindroma genetik lain:
Sindroma Down, Klinefelter,
Turner dll.
4. Diabetes Gestasional
4
 Global Projections for the
Diabetes Epidemic: 2003-2025
NA EUR
23.0 M EMME
48.4 M WP
36.2 M 58.6 M 19.2 M
↑57.0% ↑21% 39.4 M SEA 43.0 M
↑105% 39.3 75.8 M
M ↑79%
World AFR 81.6
SACA
2003 = 194 M 7.1M M
2025 = 333 M 14.2 M 15.0 M ↑108%
↑ 72% 26.2 M ↑111%
↑85%

URGENT NEED FOR ACTION

2003
2025
M = million, AFR = Africa, NA = North America, EUR = Europe,
SACA = South and Central America, EMME = Eastern Mediterranean and Middle East,
SEA = South-East Asia, WP = Western Pacific
Diabetes Atlas Committee. Diabetes Atlas 2nd Edition: IDF 2003.
06/01/21 5
©2005. American College of Physicians. All Rights Reserved.
 Diabetes in the World

Year
31.7 2000 20.8
China
India 17.7
USA
8.4 6.8
Indonesia millions Japan
Reference: Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes. Diabetes Care. 2004; 27(5): 1047-1053.

06/01/21 6
 Diabetes in the World

Year
79.4 2010 42.3
China
India 30.3
USA
21.3 8.9
Indonesia Japan
millions
Reference: Wild S, Roglic G, Green A, Sicree R, King H. Global prevalence of diabetes. Diabetes Care. 2004; 27(5): 1047-1053 .
06/01/21 7
 Current and Projected Prevalence of Diabetes
in Southeast Asia and the Western Pacific
Region Prevalence of Diabetes*) in
% Increase
2000 2030

Southeast 47 Million 120 255 %

Asia Million

Western Pacific 36 Million 71 199 %

Million

Adapted from : World Health Organization. Retrieved March 14,2007 :

http://www.who.int/diabetes/facts/world_figures/en/index5.html
http://www.who.int/diabetes/facts/world_figures/en/index6.html

06/01/21 8
 Indonesian Diabetes Prevalence
(Guestimate for 2003 / 2005)- BPS& CIA

Tahun
2003 2030
BPS
l Rural 5,548,869 8,076,613
l Urban 8,248.601 12,006,186
l  of DM patients 13,797,470 20,082,799
CIA facts book
l Rural 6,379,735 * 9,031,326
l Urban 9,432,108 * 13,352,348
l  of DM patients 15,881,843 22,383,674
* 2006

- Total population BPS = 214 juta (est.) & Total population  20 years = 133 juta ;
- urban = 56 juta , rural = 77 juta
- Total population CIA = 245 juta (est.) & Total population  20 years = 152juta ;
- 06/01/21
urban = 64 juta, rural = 88 juta 9
 Diabetes in Southeastern Asia
(Extrapolated Statistics)

Countries Population Diabetics

East Timor 1.019,252 59.955
Indonesia 238,452.952 14.026.643
Laos 6.068.172 356.948
Malaysia 23.522482 1.383.675
Philippines 86.241.697 5.073.040
Singapore 4.353.893 256.111
Thailand 64.865.523 3.815.618
• Source: wrong diagnosis website
• US Vietnam 82.662.802
Census Bureau, International Data Base, 2004 4.862.517

06/01/21 10
 Dia
ASKESKIN

bet
Top 10 polyclinic visit (poor people)

es
• 1.Diabetes

is n
• 2.Hypertension
• 3.URI

ot
• 4.Fever
• 5.TBC

a
• 6.Heart Diseases

dis
• 7.General examination-investigation

eas
• 8.Cancer
• 9.Stroke

e
• 10.Epilepsi

of
the
Data: MOH 2006,Mediakom sept-nov 2006

“R
I CH
”
06/01/21 11
 Pre-diabetes in Indonesia

2003 Pre diabetes no. 5 in the world

(12,9 million people)

2025 will increase to no. 3 with 20,9 pre-diabetics

(20,9 million people), behind India and China

i International Diabetes Federation. Did you know? Available at: http://www.idf.org/home/index.cfm?node=37

06/01/21 12
 THE PANCREAS
In the diabetic patients

The β-cells
Disorganized and misshapen
Marked reduction in β-cell number, less insulin secretion

The α-cells
Normal number, normal function, impaired suppression
of glucagon release

The consequence:
less insulin, relative hyperglucagonemia : hyperglycemia
Reduced Incretin Effect in Type 2
Diabetic Patients
Control Subjects Type 2 Diabetic
80 80
Intravenous Glucose Patients
Oral Glucose
60

INSULIN ( mU/L)
INSULIN ( mU/L)

60

40
Incretin 40
effect *
* *
* * 20
20 * * * *
*

0 0
0 30 60 90 120 150 180 0 30 60 90 120 150 180
TIME (min) TIME (min)

Nauck M, et al. Diabetologia. 1986;29:46-52.

 INCRETIN HORMONES

The gut release hormones GLP-1 (glucagon- like

peptide-1) and GIP (glucose - dependent
insulinotropic peptide), so called the incretins, in
response to nutrient intake, especially
carbohydrates
Incretins augment insulin secretion and suppress
glucagon release in a glucose sensitive manner
 Insulin resistance and -cell dysfunction are linked and are
underlying factors in type 2 diabetes

Genetic
+ Increased
Elevated
environtment lipolysis and
release of free circulating FFA
lip
fatty acids ot
o xic
i ty

High insulin demand

Insulin -Cell
resistance dysfunction

t y
x ici
Decreased glucose to
uptake into muscle l uco
g
and adipose tissue Hyperglycemia
and raised hepatic
glucose output

06/01/21 Type 2 diabetes 16

 Major Pathophysiologic Defects in Type 2 Diabetes1,2
Islet-cell dysfunction
Glucagon (alpha cell)

Pancreas

Insulin Insulin
(beta cell) resistance
Hepatic
glucose
output Glucose uptake
Hyperglycemia
Muscle
Liver
Adipose
tissue

Adapted with permission from Kahn CR, Saltiel AR. Joslin’s Diabetes Mellitus. 14th ed.
Lippincott
06/01/21Williams & Wilkins; 2005:145–168. 17
1. Del Prato S, Marchetti P. Horm Metab Res. 2004;36:775–781. 2. Porte D Jr, Kahn SE. Clin Invest Med. 1995;18:247–254.
 Type 2 DM :
 Component of Metabolic Syndrome
The Problem :
Modern Life Has Both Conveniences and Costs

Illustration taken from: Lambert C, Bing C. The Way We Eat Now. Harvard Magazine. May-June, 2004;50.
06/01/21 18
 Metabolic syndrome :
International Diabetes Federation Definition:
Abdominal obesity plus two other components: elevated
BP, low HDL, elevated TG, or impaired fasting glucose

 Obesity- high waist to hip ratio

 Hyperlipidemia
 Hyperinsulinemia
 Hypertension
 Hyperglycemia
 Acanthosis Nigricans
 PCOS
06/01/21 19
 Type 2 diabetes is NOT a mild disease

Stroke
Diabetic 2 to 4 fold increase in
cardiovascular
Retinopathy mortality and stroke3
Leading cause
of blindness
in working age Cardiovascular
adults1
Disease
8/10 diabetic patients
die from CV events4

Diabetic
Nephropathy Diabetic
Leading cause of
Neuropathy
end-stage renal disease2 Leading cause of
non-traumatic lower
extremity amputations5

1
Fong DS, et al. Diabetes Care 2003; 26 (Suppl. 1):S99–S102. 2Molitch ME, et al. Diabetes Care 2003; 26 (Suppl. 1):S94–S98.
06/01/21 3
Kannel WB, et al. Am Heart J 1990; 120:672–676. 4Gray RP & Yudkin JS. In Textbook of Diabetes20 1997.
Mayfield JA, et al. Diabetes Care 2003; 26 (Suppl. 1):S78–S79.
5
 Pathophysiology of Diabetic Complications
Hyperglycemia
Hyperglycemia
AGE
AGEformation
formation Glucose
Glucoseautoxidation
autoxidation Sorbitol
Sorbitolpathway
pathway

Oxidative
Oxidativestress
stress Antioxidants
Antioxidants

leukocyte
leukocyteadhesion
adhesion Endothelial
Endothelialdysfunction:
dysfunction: Hypercoagulability:
lipid Hypercoagulability:
lipidperoxidation
peroxidation NO
NO Fibrinolysis
Fibrinolysis
foam
foamcell
cellformation
formation Endothelin
Endothelin11 platelet
plateletreactivity
reactivity
TNF
TNF
Prostacyclin
Prostacyclin  coagulability
coagulability
Thromboxan
Thromboxan

06/01/21 Vascular
Vascular complications
complications 21
 HYPERGLYCEMIA “PAHA” OXIDATIVE STRESS

CHRONIC HYPERGLYCEMIA
OXIDATIVE STRESS

 PKC  AGE  HEXOSAMINE PATHWAY  AR

GFAT
 ROS
TGF- Sorbitol OH●
TNF
 NFKB 
 NFK-β   MMPs GSH
TNF
 Cell Proliferation  TNF
 NO
P A H A
A.OX A.OX

OXIDATIVE STRESS
INSULIN SENSITIVITY -CELL FUNCTION

ENDOTHELIAL DYSFUNCTION–VASCULAR DAMAGE

The CVDs (MI, STROKE, PAD)

ASK-DNC
 Atherogenic risk markers associated with
Type 2 DM and insulin resistance
Abdominal obesity  WHR,  FFA,  TNF,  resistin,  adiponectin,
 II--hydroxysteroid dehydrogenase type 1

Dyslipidemia  FFA,  TG,  small, dense LDL

 HDL,  large, less dense LDL

Inflammation  CRP,  CD40L,  MMP-9

Oxidative stress  Oxidized LDLs and F2-isoprostanes

Endothelial dysfunction  PAI-1,  cellular adhesion molecules, e.g. e-selectin

Coagulation  Fibrinogen,  PAI-1,  tPA

Hyperglycemia  AGEs,  circulating AGE derivatives

Hyperinsulinemia  Plasma insulin (pre- and early diabetes)

Quinkler M, et al. Eur J Endocrinol. 2001; 144:87-89.

Ross R. N Engl J Med 1999; 340:115–126.
Festa A, et al. Circulation 2000; 102:42–47.
Leinonen E, et al. Atherosclerosis 2003; 166:387–394.
 Kriteria Diagnosis DM :

Tes
Glukosa Glukosa Tes Toleransi
Plasma Plasma Glukosa Oral
Stadium Puasa Sewaktu (TTGO)

Diabetes  126 mg/dl  200 mg/dl + 2 jam PP  200

gejala klasik mg/dl
Gangguan Glukosa Puasa Toleransi Glukosa
Homeostasis Terganggu Terganggu ->
Glukosa  110 dan  126 2 jam PP  140
(PREDIABETES) mg/dl dan  200 mg/dl

Normal < 110 mg/dl < 140 mg/dl

06/01/21 Konsensus Perkeni, 2011 24

Cara pelaksanaan TTGO (WHO 1994) :

- 3 hari sebelumnya makan seperti biasa

- Kegiatan jasmani secukupnya, seperti biasa dilakukan
- Puasa semalam minimal 8 jam, boleh minum air putih
tanpa gula
- Kadar glukosa darah puasa diperiksa
- Diberi beban glukosa 75 gram  larutkan dalam air 250
ml diminum dalam waktu 5 menit
-Puasa kembali sampai pengambilan sampel darah 2 jam
setelah minum larutan glukosa selesai
- Periksa kadar glukosa darah 2 jam sesudah beban
glukosa
- Selama pemeriksaan  tetap istirahat dan tidak merokok

06/01/21 25
Pemeriksaan penyaring perlu dilakukan
pada kelompok risiko tinggi :

 Usia dewasa tua ( > 45 tahun )

 Kegemukan {IMT > 27 (kg/m2)}
 Hipertensi (> 140/90 mmHg)
 Riwayat keluarga DM
 Riwayat persalinan makrosomia (BB lahir
 bayi > 4000 gram
 Riwayat DM pada kehamilan
 Dislipidemia
 Pernah TGT atau GDPT
 PCOS
06/01/21 26
Pengelolaan :
Tujuan :
- Jangka pendek 
- Menghilangkan keluhan / gejala
- Mempertahankan rasa nyaman dan sehat
- Jangka panjang  mencegah penyulit 
menurunkan morbiditas dan mortalitas
Pilar Utama Pengelolaan Diabetes Melitus :
1. Penyuluhan
2. Perencanaan Makan ( Terapi Gizi Medik )
3. Latihan Jasmani (Exercise)
4. Intervensi Farmakologik
06/01/21 Konsensus Perkeni, 2011 27
 Terapi Gizi Medis

Pengintegrasian pelayanan gizi

dengan pelayanan dan
penatalaksanaan diabetes secara total.
 TUJUAN UMUM TGM

Membantu penyandang diabetes memperbaiki

kebiasaan makan dan olahraga untuk
mendapatkan kontrol metabolik yang baik.
 Rekomendasi Gizi Diabetes
(PERKENI 2011)

Total lemak : 20-25 %

• Asam lemak jenuh : <7%
• Pufa : < 10%
• Mufa : selebihnya
 Rekomendasi Gizi Penyandang Diabetes
(PERKENI 2011)

• Kolesterol : < 300 mg

• Protein : 10 - 20 %

• Alkohol : < 30 g pria, <15 g wanita (ADA)

 Peran Aktifitas Fisik
Dalam Manajemen
Diabetes Melitus

06/01/21 32
 THE BENEFIT OF EXERCISE FOR
DIABETIC PATIENTS
• DM TYPE I
• IMPROVE GLYCEMIC CONTROL IN SOME
PATIENTS, MAINLY IN THOSE LESS PRONE TO
HYPOGLYCEMIA
• REDUCE CORONARY ARTERY DISEASE RISK
• REDUCE THE RISK OF CARDIOVASCULAR AND
PERIPHERAL ARTERIAL DISEASES

• DM TYPE II • MAJOR ROLE IN GLYCEMIC CONTROL

• DECREASE INSULIN RESISTANCE AND INCREASE
INSULIN SENSITIVITY (REDUCE INSULIN
DOSAGE)
• REDUCE BODY WEIGHT
GLUCOSE UPTAKE AND EXERCISE
 PHYSIOLOGY OF EXERCISE

Exercise in
Normal Person

HORMONES
Insulin
Cathecolamines
Cortisol Glucose ENERGY
Glucagon FFA
Growth Hormone
EXERCISE
AEROBIC Adr/N-adr Muscle

B cell Pancreas Glycogenolysis ↑

Insulin ↓ Glycolysis ↑

Affinitas/Number Ins Rec ↑ ATP ↑

Glucose uptake ↑
 Intervensi Farmakologik

06/01/21 37
 ADA/EASD: Metabolic
Management of Type 2 Diabetes

01/06/21 Page 38
Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203
 Step One…
Lifestyle intervention and metformin

If HbA1c > 7%*

Add basal insulin Add sulfonylurea Add TZD

(most effective) (least expensive) (no hypoglycemia)

If HbA1c > 7%

Intensify Add basal Add

Add TZD
insulin** insulin** sulfonylurea

If HbA1c > 7%

Add basal or
intensify insulin

Intensive insulin + metformin +/- TZD

* Check HbA1c every 3 months until HbA1c <7%, and then at least every 6 months.
** Preferred based on effectiveness and expense. Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203
 Step One: Lifestyle and Metformin

Lifestyle interventions:
- Weight loss, exercise,
- Diet should be implemented by regis-
tered dieticians

Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203

Step One: Lifestyle and Metformin, cont’d
• Since lifestyle interventions fail in most patients,
initiate metformin at diagnosis
• Metformin is recommended due to its:
Effect on glycemia
Absence of weight gain and hypoglycemia
Generally low level of side effects
High level of acceptance
Relatively low cost

Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203

 Step Two…
Lifestyle intervention and metformin

If HbA1c ≥ 7%*

Add basal insulin Add sulfonylurea Add TZD

(most effective) (least expensive) (no hypoglycemia)

If HbA1c ≥ 7%

Intensify Add basal Add

Add TZD
insulin** insulin** sulfonylurea

If HbA1c ≥ 7%

Add basal or
intensify insulin

Intensive insulin + metformin +/- TZD

* Check HbA1c every 3 months until HbA1c <7%, and then at least every 6 months.
** Preferred based on effectiveness and expense. Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203
-.
 Step Two: Adding a Second Agent
• After 2 - 3 months, if Step 1 fails to achieve glyce-
mic goals, add one of the following:
- Basal insulin (most effective)
- Sulfonylurea (least expensive)
- TZD (no hypoglycemia) - pioglitazone

• Choice of medication depends on HbA1c

Choose insulin for HbA1c level >8.5 or
with symptoms secondary to hypergly-
cemia

Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203

 CONTROLLED AND UNCONTROLLED
DIABETES BASED ON A1C
Data from our Diabetes Clinic :*
791 patients had A1C
A1C < 7,0% = 145 or 18,3%
A1C > 7,0% - < 8,5% = 152 or 19,2%
A1C > 8,5% = 494 or 62,5%
Around 60% of our diabetic patients attending
our Diabetic Clinic needed combination therapy
either two oral agents or oral agent plus insulin
* John MF Adam (Makassar)
 Step Three…
Lifestyle intervention and metformin

If HbA1c ≥ 7%*

Add basal insulin Add sulfonylurea Add TZD

(most effective) (least expensive) (no hypoglycemia)

If HbA1c ≥ 7%

Intensify Add basal Add

Add TZD
insulin** insulin** sulfonylurea

If HbA1c ≥ 7%

Add basal or
intensify insulin

Intensive insulin + metformin +/- TZD

* Check HbA1c every 3 months until HbA1c <7%, and then at least every 6 months.
** Preferred based on effectiveness and expense. Nathan
. DM et al. Diabetes Care 2009; 32(1) : 194-203
-.
 Step Three: Further Adjustments
If Step 2 fails to achieve glycemic goals
after 2 – 3 months …..
• Start or intensify insulin (preferred choice)
- Usually means adding short or rapid acting insu-
lin before selected meals to reduce PPG excur-
sions
- Discontinue use of sulfonylureas or glinides
when short - or rapid - acting insulin injec-
tions are started (not considered synergistic)
• If HbA1c is close to goal (<8.0%) add a third agent
(not the preferred choice due to higher cost and
lower efficacy)
Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203
 Efficacy-Cost Ratio of Adding a Third Oral
Therapy vs. Switching to Insulin + Metformin
HbA1c values at study endpoint (Week 24)
70% p=n.s
HbA1c (%) at study endpoint
Portion of patients achieving

60%
50%
40% p=n.s

30%
20%
10%
0%
HbA1c < 7% HbA1c < 8%
Triple oral therapy ($10.40/day) Insulin + metformin ($3.20/day)

Schwartz S et al. Diabetes Care 2003;26:2238 - 2243

 Considerations for Selecting
Combination Therapy
• Glucose - lowering effect
• Secondary characteristics of the medications
- e.g., weight gain or loss, GI side effects,
injection, frequency, expense, other side effects
• Synergy
- In general, different mechanisms of action will
have the greatest synergy

Nathan DM et al. Diabetes Care 2009; 32(1) : 194-203

 ADA RECOMMENDED COMBINATIONS

• Insulin + metformin
• Insulin + TZD
- However, fluid retention must be considered
• The combination of metformin and TZD has
shown only modest HbA1c reductions (i.e.,
0.3 - 0.8%)

Schwartz S et al. Diabetes Care 2003;26:2238 - 2243

 Insulin + Metformin
12-month reduction in HbA1c for bedtime
Intermediate acting insulin + metformin (2 g)
10
hemoglobin Value (%)

9
Glycosylated

n=19
8

0 3 6 9 12
Time (mo)

Adapted from Yki-Jarvinen H, et al. Ann Intern Med 1999;130(5):389-3 96

 Insulin + TZD
Reduction in HbA1c with dual (Week 0- 16)
and triple (Week 16- 32) therapy
9.0
Insulin + metformin
8.5 (+TZD at Week 16)
n=14
8.0
HbA1c (%)

Insulin + TZD
(+metformin at Week 16)
7.5 n=14
*
7.0

6.5
6.0 †
*‡ †
5.5
Week 0 Week 16 Week 32
* p<0.05 vs. baseline, † p<0.05 vs. week 16, ‡ p<0.05 vs. INS + MET group.

Strowig SM, et al. 2004;27(7):1577- 83.

 Current available drugs for treating DM

• Incretin mimetic :
• Sulfonylureas – GLP-1 Analog :
• Exenatide (Byetta)
• Metformin
– DPP-4 Inhibitor :
• Thiazolidinediones • Sitagliptin
• Alpha-Glucosidase • Vildagliptin
Inhibitors • Amylin Analog
• Meglitinides – Pramlintide
• Insulin
– Injectable
– Inhaled
06/01/21 53
 Sites of Action of Current OAD
GLUCOSE ABSORPTION
INTESTINE

-glucosidase inhibitors
GLUCOSE DPPIV inhibitor
PRODUCTION PERIPHERAL GLUCOSE
UPTAKE & UTILIZATION
LIVER
Glucose
Biguanides MUSCLE
Thiazolidinediones
ADIPOSE TISSUE
Biguanides
INSULIN SECRETION Thiazolidinediones
Sulphonylureas
Meglitinides
06/01/21 DPPIV inhibitor 54
PANCREAS Modified: Ann Intern Med 1999;131:281
 Insulin :
Indications :
- Type 1 DM (absolute)
- Type 2 DM, uncontrolled with maximal doses of OAD
- KAD/ HHS / hyperglycemia with lactic acidosis
- Type 2 DM + Severe metabolic stress :
- Systemic infection
- Surgery
- AMI
- Stroke
- Gestational Diabetes, uncontrolled with diet
- Type 2 DM with impaired liver or kidney function
- Allergy to OAD
06/01/21 55
 Pemantauan hasil pengobatan :
1. Kadar glukosa darah
2. Kadar HbA1c
3. PGDM ( Pemantauan Glukosa Darah Mandiri)
4. Glukosa urin
5. Benda2 keton

Pemantauan komplikasi vaskular/ penyakit penyerta :

1. Mikroalbuminuri
2. D-Dimer
3. CRP
4. Profil lipid
06/01/21 56
 Lowering HbA1c reduces the risk of
complications
Deaths related to
21%
diabetes

HbA1c
Microvascular
37%
1% complications

Myocardial infarction
14%

Stratton IM, et al. BMJ 2000; 321:405–412.

06/01/21 57
 Criteria for Diabetes Control
Good Fair Poor
Fasting blood glucose 80-<100 110-125 ≥126
(mg/dl)
2hpp blood glucose (mg/dl 80-144 145-179 ≥180
A1C (%) <6.5 6.5 - 8 >8
Total- cholesterol (mg/dl) <200 200-239 ≥240
LDL-cholesterol (mg/dl) <100 100-129 >130
HDL-cholesterol (mg/dl) Pria >40
Wanita >50
Triglyceride (mg/dl) <150 150-199 ≥200
Body mass index (kg/m2) 18.5 - 22.9 23-25 >25
Blood pressure (mmHg) <130/80 >130-140/ >140/90
>80-90

06/01/21 Perkeni, 200658

 Simpulan :

 DM = penyakit yang kronik progresif  meningkatkan

morbiditas dan mortalitas kardiovaskular.
 Angka kejadian semakin meningkat  Indonesia peringkat ke 5
 Sasaran pengelolaan DM  kadar glukosa darah senormal
mungkin untuk mencegah komplikasi akut dan kronik.
 DM tipe 1  butuh terapi Insulin seumur hidup
 DM tipe 2  Terapi kombinasi lebih rasional dalam mencapai
kendali glukosa yang optimal.
 Membutuhkan pengelolaan menyeluruh thd faktor risiko
kardiovaskular, terutama pemantauan terhadap Tekanan Darah,
Kadar HbA1C (A1C), Mikroalbuminuri, Profil Lipid, petanda
inflamasi dan hiperkoagulasi.
06/01/21 59
 Type 2 Diabetes &
Metabolic Syndrome

It’s a Nightmare!

Low-grade
Inflammation

NASH
Hypertension Prothrombotic
Endothelial State
Dyslipidemia Dysfunction
Hyperglycemia

Terima Kasih
06/01/21
©2005. American College of Physicians. All Rights Reserved.
60
 Type 2 Diabetes &
Metabolic Syndrome

It’s a Nightmare!

Low-grade
Inflammation

NASH
Hypertension Prothrombotic
Endothelial State
Dyslipidemia Dysfunction
Hyperglycemia

06/01/21 61
©2005. American College of Physicians. All Rights Reserved.