CURRICULUM VITAE (CV)

Nama
Tempat/Tanggal Lahir
Institusi
Pangkat
Riwayat Pendidikan
Dokter Umum
Spesialis Anak
Konsultan Endokrin
Doktor

: DR. dr. I Wayan Bikin Suryawan, Sp.A(K)

: Tabanan, 19 September 1960
: RSUD Wangaya, Kota Denpasar
: Pembina Utama Madya / IV d

:
:
:
:

FK UNUD 1986
FK UNDIP 1998
Kolegium IKA Indonesia 2005
Pasca Sarjana UNUD 2011

Jabatan /Pekerjaan
Ketua IDAI Cabang Bali ( 2008 2014)
Ketua UKK Endokrin IDAI ( 2011 - 2017)
Staf Pengajar Endokrinologi Anak FK UNUD

Type II DM: What!s New on

Management
I Wayan Bikin Suryawan

Diabetes is a global disease

Estimated global prevalence of diabetes

171 million1
2000

1.
2.

366 million2
2011
2010

Wild. Diabetes Care. 2004. 27:1047-1053.

International Diabetes Federation. IDF Diabetes Atlas. Fifth Edition. 2011

552 million2
2030

Definition and description of DM

The term diabetes mellitus describes a
complex metabolic disorder characterized by
chronic hyperglycemia resulting from defects
in insulin secretion, insulin action, or both.
Inadequate insulin secretion and/or
diminished tissue responses to insulin, which
leads to abnormalities of carbohydrate, fat,
and protein metabolism.

Diabetes is diagnosed when:

Fasting plasma glucose (FPG) is 7.0
mmol/L(126 mg/dL).
Postchallenge plasma glucose is 11.1
mmol/L(200 mg/dL). 1.75 g/kg (max 75 g)
anhydrous glucose dissolved in water.
Symptoms of diabetes and a casual plasma
glucose 200 mg/dL (11.1 mmol/L).
HbA1c>6.5%.

Childhood T2DM:
disease in the child who typically
is overweight or obese(BMI 85th94th and >95th percentile
for age and gender, respectively)
has a strong family history of T2DM
has substantial residual insulin secretory capacity at diagnosis
has insidious onset of disease
demonstrates insulin resistance (including clinical evidence of
polycystic ovarian syndrome or acanthosis nigricans);
lacks evidence for diabetic autoimmunity (negative for
autoantibodies typically associated with T1DM).
1. Copeland.K.C, at all, Pediatrics 2013, Management of Newly
Diagnosed T2DM in Children and Adolescent
Slide 6

Diabetes is a progressive disease

1.
2.

Type 2 diabetes (T2DM) progression is characterised by decline in

beta-cell function and worsening insulin resistance1

Fonseca VA. Br J Diab Vasc Dis 2008;8:S3

Nathan DM, et al. Diabetes Care 2009;32:193-203

T2DM: Progressive loss of insulin

secretion with increasing insulin resistance1
Impaired
glucose tolerance

Undiagnosed
diabetes

Known
diabetes

Insulin resistance

Insulin secretion
Postprandial glucose

Fasting glucose

Microvascular complications
Macrovascular complications

1.

Adapted from: Ramlo-Halsted BA, Edelman SV. Clincial Diabetes 2000;18(2): http://journal.diabetes.org/clinicaldiabetes/v18n22000/pg80.htm

Prediabetes is diagnosed when:

IFG: FPG is 5.66.9 mmol/L (100125 mg/dL)
IGT: Postchallenge plasma glucose 7.811.1
mmol/L (140199 mg/dL)
HbA1c 5.86.4%

Treatment of youth-onset T2D

1. Management differences between T1D and T2D
2. Management goals
3. Education
4. Behavioral change
5. Dietary management
6. Exercise management
7. Smoking and tobacco use
8. Glycemic monitoring
9. Pharmacologic therapy
10. Gastric surgery

1.Management differences between T1D and T2D

T2D in developed countries

T2D occurs typically in adolescence
T2D more family experience
Prevalence of associated comorbidities and
complications early in the course of disease
Lifestyle education

2.Management goals

Education for diabetes self-management

Normalization of glycemia
Weight loss
Reduction in carbohydrate and calorie intake
Increase in exercise capacity
Control of comorbidities, including
hypertension, dyslipidemia, nephropathy,
sleep disorders, and hepatic steatosis.

3. Education
include a nutritionist, psychologist and/or
social worker, and exercise physiologist
greater emphasis on behavioral, dietary, and
physical activity changes
given by team members with expertise and
knowledge
education of youth and families with T2D.

4. Behavioral Change
The family and child should understand the
medical implications of obesity and T2D.
Clinicians must have an understanding of the
health.
Changes should be made in small achievable
increments and permanent.
The patient and family should be trained to
monitor the quantity and quality.
Any behavioral change, a dynamic and
sustainable reward system is essential for
success.

5. Dietary management
Initial focus on eliminating sugar-containing soft
drinks and juices
Increasing fruit and vegetable intake
Reducing the intake of foods made out of refined
Reducing meals eaten away from home
increased portions of fresh vegetables and
decreased portions of carbohydrate-rich noodles
Changing white rice and white flour to brown rice
and whole grain
Changing family diet behaviors

6. Exercise Management
Exercise is an important part of the diabetes
management plan.
Regular exercise has been shown to improve
blood glucose, reduce cardiovascular risk,
contribute to weight loss, improve well-being.
Youth with T2D should be exercise for at least 60
min daily.
A family or friend should be identified to
participate in physical activity with the patient.

7. Smoking and Tobacco Use

While cigarette smoking is harmful to all
youth, those with special healthcare needs are
especially vulnerable to the negative health
consequences of smoking as a result of their
compromised health status and disease, as
well as treatment-related complications

8. Grycemic Monitoring
SMBG.
Patients on insulin or sulfonylureas need to
monitor for asymptomatic hypoglycemia.
HbA1c concentration should be determined at
least twice a year and quarterly if insulin is
being used or metabolic control is
unsatisfactory.

9. Pharmacologic therapy
Initial treatment of youth with T2D should
include metformin and/or insulin alone or in
combination. The specifics of the initial
treatment modality are determined by
symptoms, severity of hyperglycemia, and
presence or absence of ketosis/ketoacidosis

Diagnosis of diabetes in an
Obese adolescent
Asymptomatic HbA1c < 9%
No acidosis

Acidosis
Symptomatic or HbA1c > 9%
No acidosis
Likely type 2
Basal insulin
Metformin
Lifestyle change

Metformin
Lifestyle change

Insulin as in T1D
until
acidosis resolved
Likely type 1
Initiate MDI insulin
education

Diabetes autoantibodies
(-)

(+)

Continue metformin
Wean insulin
YES

Continue or start MDI insulin

Education
At target
NO

Basal insulin titrate to max 1.2 U/Kg/day

NO
YES

At target

Fig. 1. Approach to initial and subsequent treatment of youth with type 2 diabetes.

Treatment therapies for Type 2 diabetes

Premixed
Insulin
(Twice daily
Treat to target)

Lifestyle +
Metformin

+-other OAD
or GLP-1
agonists

HbA1c 7.0%

Basal Insulin
(Basal + 3
prandial)

Basal Insulin
(Once-daily treatto-target)

Basal Insulin
(Basal + 1 or 2
prandial)

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

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

Insulin remains the most efficacious glucose

lowering agent

HbA1c %

Decrease in HbA1c: Potency of monotherapy

CHOOSING INSULIN EARLIER

FOR BETTER EFFICACY

Nathan et al., Diabetes Care 2009;32:193-203.

Metformin

Hepatic glucose output is reduced by decreased gluconeogenesis.

Insulin stimulated glucose uptake is increased in muscle and fat.
An initial anorexic effect may promote limited weight loss.
There is little to no risk of hypoglycemia with metformin
monotherapy.
Long-term use is associated with a 12% reduction in HbA1c.
Intestinal side effects (transient abdominal pain, diarrhea, nausea)
may occur
The risk of lactic acidosis with metformin is extremely low
Metformin may normalize ovulatory abnormalities in girls with
PCOS, ovarian hyperandrogenism and increase pregnancy risk.
Metformin is now approved for use during pregnancy.

Insulin
Despite hyperinsulinemia and insulin
resistance,supplemental insulin is generally
effective in reducing hyperglycemia and attaining
glycemic targets.
If there is inadequate glycemic control on oral
agents, a long-acting (basal) insulin analog oncedaily NPH may provide satisfactory therapy.
if HbA1c target is not reached and postprandial
hyperglycemia persists, rapid or short acting
insulin can be added.

Physiologic insulin secretion

Analogue insulin mechanisme of action

-------

endogen insulin
Long insulin

Rapid insulin
Mix insulin

Breakfast

Lunch

Dinner

Bed time

Insulin can be initiated at any time in adulth

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

Other available agents

Sulfonylurea and meglitinide/ repaglinide
may not be approved for use in <18 yr in all
countries)
Incretin mimetics [glucagon-like peptide-1
(GLP-1) no published in youth
DPP-IV inhibitors not approved for use in
<18 yr
Sodium-glucose co-transporter-2 (SGLT-2)
inhibitors not approved for use in <18 yr

insulin resistance
Insulin resistance is a physiologic abnormality,
defined as an impaired response to the
physiologic effects of insulin, including effects on
glucose, lipid, protein metabolism, and on
vascular endothelial function.
Insulin resistance can occur in many tissues,
including hepatic, muscle, and adipose tissue,
some areas of the brain.
some tissues continue to respond to
hyperinsulinemia, such as the ovary and the
sympathetic nervous system innervating muscle.

insulin resistance

Dysglycemia
Lipid abnormalities
Endothelial dysfunction
Increased procoagulant factors
Hemodynamic changes
Inflammation
Increased plasma uric acid
Increased hepatic and intramyocellular lipid deposition
Mitochondrial dysfunction
Ovarian hyperandrogenism
Sleep-disordered breathing.

Comorbidities and complications

Obesity
Hypertension
Nephropathy
Dyslipidemia
Polycystic ovarian syndrome
Non-alcoholic fatty liver disease
Systemic inflammation
Obstructive sleep apnea
Depression

Treat T2DM early for long-term benefits1

Long-term benefits in reducing cardiovascular risk can be achieved with

good control from diagnosis1

50% of patients with T2DM with complications

already have them at diagnosis2

Myocardial infarction
Each HbA1c
percentage
point
reduction
counts3

HbA1c

-1%
1.
2.
3.

Holman, et al. NEJM 2008;359:157789

UKPDS 6. Diabetes Res 1990;13(1):1-11
Stratton, et al. BMJ 2000;321(7258):405-12

-14%

Microvascular complications
-37%

Death related to diabetes

-21%

What is the optimal target HbA1c level?

1.
2.
3.

EASD/ADA1

HbA1c
<7.0%

IDF2

HbA1c
<7.0%

EMA3

HbA1c
<7.0%

Goals of optimum HbA1c levels:

Good glycaemic control
Minimise development and progression of microvascular
and macrovascular complications
Inzucchi et al. Diabetes care. Published online 19Apr2012.
IDF Treatment Algorithm. International Diabetes Federation 2011. http://www.idf.org/treatment-algorithm-people-type-2diabetes
EMA Draft guidance on clinical investigation in DM Jan 2010

Initial treatment of T2D

Lifestyle change should be initiated at the
time of diagnosis.
Initial pharmacologic should include
metformin and insulin alone or in
combination.
Determined by symptoms, severity of
hyperglycemia, presence or absence of
ketosis/ketoacidosis.
The goal should be HbA1c<6.5%.

Thank You