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CLASSIFICATION
Diabetes Mellitus
A group of metabolic diseases
Characterized by hyperglycemia
Resulting from defects in insulin secretion , insulin
action, or both
A. Clinical Classification
1. Diabetes Mellitus
IDDM
NIDDM Obese
Non-obese
Secondary Diabetes
MRDM
2. Gestational Diabetes
3. Impaired Glucose Tolerance
B. Statistical Risk Classification
ETIOLOGIC CLASSIFIACTION
I.
II. Type 2
Predominantly insulin resistance + relative insulin
deficiency
Predominantly secretory defect + insulin resistance
III. Other specific types
IV. Gestasional diabetes mellitus
Type 1 + Type 2 = 70 95% of diabetes
The Expert Committee,1997
Controversies in Classification
=
Controversies in Management
Clinical Features
Age at onset
Onset
Weight
Spontaneous ketosis
Chronic complication
Epidemiology
Prevalence
Sex
Insulin (C-petide) level
Genetics
Concordance in twins
HLA asoociation
Pathology
Islet cell mass
Insulitis at onset
Immunology
Associated with other endocrinopathy
Anti-islet ell immunity
Humoral
Cell mediatedl
Type 1
Type 2
Usually < 30
Acute
Non obese
Common
(++)
Usually > 40
Insidious
Obese
Rare
(++)
0,5%
Male prepdominancece
/ (-)
2%
Female predominance
/N/
40%
(+) (DR3/DR4)
70 90%
(-)
Severely reduced
Present
Moderately reduced
?
Frequent
Frequent
60 80% at onset
35 50% at onset
5 20%
< 5%
Type 1 Diabetes
(-cell destruction leading to
absolut deficiency)
100
80
60
40
20
II
III
IV
GAD65 antibodies
ICA antibodies
IAA antibodies
IA2 and IA-2
Abnormal -cell function test
Tolerance reestablished
T-cell tests (+)
T-cell tests ()
Clinical onset
5-10%
(Mehta,1996)
Type 2 Diabetes
Insulin resistance
?
vs
-cell dysfunction
Genetic
Insulin resistance
Obesity (Genetic ?)
Inactivity
Hyperglycemia
Hyperinsulinemia
Drugs
Secondary and
facilitative
Environmental
Insulin Resistance
Normal -cells
Abnormal -cells
Compensatory
Hyperinsulinemia
Inadequate Insulin
Response
Isulin Resistance
Syndrome
Type 2 Diabetes
Hypertension
Dyslipidemia Obesity
CVD
Retinopathy
Neuropathy
Nephropaty
Hyperglycemia
Hypertension
Atherogenic
dyslipidemia
Insulin resistance
+
Hyperinsulinaemia
Abdominal obesity
Impaired
fibrinolysis
Pro-inflammatory
profile
Post-prandial glucose
Fasting glucose
Relative to normal
(%)
Insulin resistance
250
200
150
100
50 At risk for Beta-cell dysfunction
Insulin level
diabetes
0
30
0
5
10 15 20 25
-10 -5
Years
R.M. Bergenstal, International Diabetes Center
Disdorders of Gycemia
Stages Normoglycemia
Types
Type 1
Type 2
Other
types
Gestational
diabetes
Normal glucose
regulation
Diabetes Mellitus
IGT or
Insulin requiring
IFG
No
For control
Insulin requirement
+++
For survival
+++++
F
A
M
I
L
Y
S
T
U
D
Y
F
E
N
O
T
Y
P
E
VS
G
E
N
O
T
Y
P
E
CASE STUDY
A 56 y-old Javanese man presented 7 years
ago with type 2 DM; BMI was 22 kg/m2. He
was taking glybenclamide 2.5 mg b.i.d., with
HbA1c level of 7.8%. Her diet is high in rice
and other complex cbh.
During the subsequent 6 year, his HbA1c
level rose to 10% and body weight decreased
12 kg despite increasing glybenclamide to 10
mg twice daily and combination with
metformin 500 mg three times daily.
CASE
Female 56 y.o, diagnosed as NIDDM 7 years ago, BMI 22
kg/m2, addhere to diet, routine exercise, Tx. Glibenclamide
15 mg/day + metformin 1500 kg, Blood sugar : fasting 230
mg ; 2 h pp 324 mg%
Past medical history : good controlled with 2 mg
glibenclamide but gradually needs higher dose and finally
needs combined oral hypoglycemic drugs
DIAGNOSIS
Prevalence of retinopathy by
deciles of the distribution of FPG,
2-h PG, and HbA1c
126
200
Slama, 2003
DM
ADA, 2004
GESTATIONAL DIABETES
100-g
diagnostic test
Fasting
1-h
2-h
3-h
105
190
165
145
140 mg/dl
-
mg/dl
mg/dl
mg/dl
mg/dl
mmol/l
95
180
155
140
5.3
10.0
8.6
7.8
95
180
155
5.3
10.0
8.6