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“NISCAYA ALLAH AKAN MENINGGIKAN ORG² YG

BERIMAN DIANTARA KAMU DAN ORG² YG DIBERI


ILMU PENGETAHUAN BEBERAPA DERAJAT “
The diabetes population is increasing rapidly
throughout the world
• In 2000, 171 million people worldwide had diabetes; in 2030, the figure will be 366
million
• In 2030, >82 million people aged over 64 will have diabetes in the developing
countries; the figure for the developed countries is >48 million

79.4

India 42.3

30.3
20.8
17.7 31.7

USA China
18.6 †104%
2000 †71%

7.1 21.3
2030 †151%

†161% 8.4
11.3
4.6 Indonesia
Brazil †154%
†146%
Sub- Saharan
Africa

*Figures are in millions


† Percentage change in number of people with diabetes
Wild S, et al. Diabetes Care 2004; 27: 1047-53.
IFG T2DM METS
25
20.7
20
15.1 15.5

15
12.2
10.1
10 7.8
6.9 6.8 7.5
6.3
5 3.9

0
Pedawa (294) N Ceningan (305) Sangsit (471) Total

Fig. Prevalence of IFG, diabetes, and metabolic syndrome


in adult population of Bali
Diabetics defined by FPG ≥ 126 mg/dl; IFG: >100-125 mg/dl; Mets by IDF 2005

Suastika K, et al. 19th World Diabetes Congress. Cape Town 3-7 December 2006.
Diabetic Medicine 2006; 23 (Supll.4): 185


Criteria for the diagnosis of diabetes

1. Symptoms of diabetes and a casual plasma glucose ≥200


mg/dl (11.1 mmol/l). Casual is defined as any time of day
without regard to time since last meal. The classic
symptoms of diabetes include polyuria, polydipsia, and
unexplained weight loss.

OR
2. FPG ≥ 126 mg/dl (7.0 mmol/l). Fasting is defined as no caloric
intake for at least 8 h.

OR
3. 2-h plasma glucose ≥ 200 mg/dl (11.1 mmol/l) during an
OGTT. The test should be performed as described by the
World Health Organization, using a glucose load containing
the equivalent of 75-g anhydrous glucose dissolved in
water.

ADAPosition Statement. Diabetes Care, 30 (Suppl 1): S5, 2007


DIAGNOSING DIABETES

• Classic complains: polyuria, polidypsia, poliphagia,


loss of body weight
– Diabetes: classical complains (+) RBG ≥200 mg/dl or FBG ≥126
mg/dl
• OGTT ( glucose load 75 g)
– Normoglycemia
• FBG: <100 mg/dl
• 2hppBG: <140 mg/dl
– Impaired fasting glycemia [IFG]
• FBG: 100-125 mg/dl
• 2hppBG: <140 mg/dl
– Impaired glucose tolerance [IGT]
• FBG: <100 mg/dl
• 2hppBG: ≥140-<200 mg/dl
– Diabetes
• FBG: ≥126 mg/dl
• 2hppBG: ≥200 mg/dl
• IFG and IGT are called “prediabetes”
• 8 h fasting
Criteria for testing for diabetes in
asymptomatic adult individuals
1. Testing for diabetes should be considered in all individuals at age 45 years
and above, particularly in those with a BMI 25 kg/m2*, and, if normal, should
be repeated at 3-year intervals.
2. Testing should be considered at a younger age or be carried out more
frequently in individuals who are overweight (BMI 25 kg/m2*) and have
additional risk factors:
are habitually physically inactive
have a first-degree relative with diabetes
are members of a high-risk ethnic population (e.g., African American, Latino,
Native American, Asian American, Pacific Islander)
have delivered a baby weighing 9 lb or have been diagnosed with GDM
are hypertensive (140/90 mmHg)
have an HDL cholesterol level 35 mg/dl (0.90 mmol/l) and/or a triglyceride level
250 mg/dl (2.82 mmol/l)
have PCOS
on previous testing, had IGT or IFG
have other clinical conditions associated with insulin resistance (e.g., PCOS or
acanthosis nigricans)
have a history of vascular disease

*May not be correct for all ethnic groups. PCOS, polycystic ovary syndrome.

ADAPosition Statement. Diabetes Care, 30 (Suppl 1): S5, 2007


Major diabetes prevention studies in
populations with impaired glucose tolerance
Study N Evaluations Diabetes risk
reductions*
Diabetes Prevention study 522 Int. lifestyle - 58%
(Finland)1
STOP-NIDDM 1429 Acarbose - 25%
(international)2
DaQing study (China)3 577 Diet - 31%
Exercise - 46%
Diet + exercise - 42%
XENDOS 4 694 Orlistat - 45%
DPP5 3,234 Lifestyle - 58%
Metformin - 31%
Tripod6 266 Troglitazone - 55%
1Tuomilehto J et al. N EJM 2001;344:1343-50; 2Chiasson J-L et al. Lancet 2002;359:2072-27; 3Pan X et al. Diabetes Care 1997; 20:537-
44;4Torgerson JS et al. Diabetes Care 2004;27:155–61;5Diabetes Prevention Program Research Group. N Engl J Med 2002;346:393-403;
6Buchanan et al. Diabetes 51: 2796-2803, 2002
Pathogenesis and Implications
of Type 2 Diabetes
A progressive disease where uncontrolled
hyperglycemia mirrors beta-cell failure
DIAGNOSTIC
350
300 Post-prandial
(mg/dL)
Glucose

glycemia Major genetic factor:1,2


250
200 Fasting glycemia Insulin deficiency
150 ↓ beta-cell function →
100 ↓ insulin secretion
50
beta-cell function

250 Insulin resistance


Major acquired factor:1,2
Relative

200
(%)

Insulin resistance
150
Insulin level ↑ hepatic glucose production
100
↓ glucose disposal, peripheral tissue
50 Beta-cell failure
0
Obesity IGT Diabetes Uncontrolled hyperglycemia

MACROVASCULAR CHANGES ↑
features
Clinical

MICROVASCULAR CHANGES ↑

-10 -5 0 5 10 15 20 25 30

Years
Adapted from Type 2 Diabetes BASICS. Minneapolis, Minn: International Diabetes Center, 2000 1. Gerich J. Mayo Clin Proc 2003;78:447–56
2. Weyer C, et al. J Clin Invest 1999;104:787–94
MANAGEMENT
Education
Medical nutrition therapy
Exercise
Antidiabetic drugs
Medical nutrition therapy
 Carbohydrates: 45-65%
(mostly starch)
 Dietary fibre: min 20 g/1000
kcal
 Fats: 20-35%
- saturated <10%
- polyunsaturated <10%
- monounsaturated >10%
- cholesterol <300 mg/day
 Protein: 10-20% (0.8 g/kg/day)
 Sodium: <2400 mg/day
 Vitamins and minerals: with a
balanced diet, supplements
not needed

American
Diabetes
Association®
Physical activity recommendations

• Frequency of activity
• Intensity of activity
• Length of time of activity
• Type of activity
•Enjoyment
•Lifestyle
•Time constraints
•Facilities
•Physical ability

Wittert G. Practical Management of Obesity. A guide for a good provider. 2003


Treatment option for T2DM
Inhaled insulin
Dual PPAR DDP-4
GLP-1 CB1 blockade
Detemir
Pramlintide
Exenatide
Aspart
Glargine
Glinides
Glitazones
Lispro
Human insulin
Metformin
Sulfonylurea
Animal insulin

1922 1950s 1982-1985 1995 1996 2001 2003 2005 2006


GB1, cannabinoid-1; DDP-4, dipeptidyl peptidase-4; GLP-1, glucagon-like peptide-1;
PPAR, peroxisome proliferator-activated receptor
Action Profiles of Insulin
Aspart, glulisine, lispro 4–6 hours
Regular 6–8 hours
Plasma
insulin NPH 12–20 hours
levels
Ultralente 18–24 hours

Glargine 24 hours

0 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24
Type and action of insulin
Preparation Action profile, h
Onset Peak Duration
Ultra-rapid- acting
Lispro (Humalog) 0.2 - 0.5 0.5 – 2 3–4
Aspart (Novolog) 0.2 – 0.5 0.5 – 2 3-4
Gluisin (Apidra) 0.2 – 0.5 0.5 - 2
Short-acting
Regular (human) 0.5 - 1 2-3 6–8
Intermediate acting
NPH (human) 1.5 4 10 16 – 24
Lente (human) 1.5 – 3 7 – 15 16 – 24
Detemir (Levemir) 1-3 9 - unknown
Long-acting
Ultralente (human) 3–4 9 – 15 22 – 28
Glargine (Lantus) 4-5 No peak 24

Mixtures (human)
70/30 0.5 - 1 3 – 12 16 – 24
50/50 0.5 – 1 2 – 12 16 – 24
Mixtures (Analog)
75/25 (NPL/lispro, ) 0.2 - 0.5 1–4
70/30 (Protamine aspart/aspart) 0.2 – 0.5 1-4
Normal Insulin Secretion:
The Basal-Bolus Insulin Concept
Endogenous Insulin
Bolus Insulin
Insulin Effect

Basal Insulin

B L D HS
Time of Administration
B, breakfast; L, lunch; D, dinner; HS, bedtime.

Adapted from:
1. Leahy JL. In: Leahy JL, Cefalu WT, eds. Insulin Therapy. New York, NY: Marcel Dekker, Inc.; 2002.
2. Bolli GB et al. Diabetologia. 1999;42:1151-1167.
ADA/EASD algorithm for the management of T2DM (2008)

Tier 1: well-validated therapies


Lifestyle + Metformin Lifestyle + Metformin
+ Basal insulin + Intensive insulin
At diagnosis:
Lifestyle + Metformin
Lifestyle + Metformin
+ Sulfonylureas

STEP 1 STEP 2 STEP 3

Tier 2: Less well validated therapies

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

Lifestyle + metformin Lifestyle + metformin


+ GLP-1 agonist + Basal insulin
No hypoglycaemia
Weight loss
Nausea/vomiting

Nathan D, et al. Diabetes Care 2008;31:1−11.


Treating fasting hyperglycaemia lowers
the entire 24-hour plasma glucose profile

400
20

Plasma glucose (mmol/l)


Plasma glucose (mg/dl)

300 T2DM
15

200 Hyperglycaemia due to an increase in fasting glucose


10

100
5
Normal
Meal Meal Meal
0 0
06.00 10.00 14.00 18.00 22.00 02.00 06.00
Time of day (hours)
Comparison of 24-hour glucose levels in control subjects vs patients with diabetes (p<0.001).
Adapted from Hirsch I, et al. Clin Diabetes 2005;23:78–86.
Summary of glycemic recommendations for
non-pregnant adults with diabetes (ADA, 2009)

A1C <7.0%*
Preprandial capillary plasma glucose 70–130 mg/dl
Peak postprandial capillary plasma glucose <180 mg/dl

Key concepts in setting glycemic goals:


● A1C is the primary target for glycemic control.
● Goals should be individualized based on:
● duration of diabetes
● age/life expectancy
● comorbid conditions
● known CVD or advanced microvascular complications
● hypoglycemia unawareness
● individual patient considerations
● More or less stringent glycemic goals may be appropriate for individual patients.
● Postprandial glucose may be targeted if A1C goals are not met despite reaching
preprandial glucose goals.

*Referenced to a nondiabetic range of 4.0–6.0% using a DCCT-based assay. Postprandial glucose measurements
should be made 1–2 h after the beginning of the meal, generally peak levels in patients with diabetes.
Diabetes is a lifelong condition with
potentially devastating consequences
MACROVASCULAR MICROVASCULAR
COMPLICATIONS COMPLICATIONS

Diabetic retinopathy
Heart disease and stroke causes 12,000 to 24,000
account for ~65% of new cases of blindness each
diabetes-related deaths year, especially in adults
aged 20–74 years

Diabetes is a leading cause


of kidney failure; 44% of
new cases during 2002
Diabetes causes > 60%
of non-traumatic
lower-limb amputations
~60–70% of patients have
mild to severe nervous
system damage

Source: American Diabetes Association, Diabetes statistics


http://www.diabetes.org/diabetes-statistics/complications.jsp. Last accessed 25 January 2007

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