Professional Documents
Culture Documents
592
million
people living
with
diabetes
WORLD
30.0% 30.2% 33.0% 37.8% 32.1%
37.
70.0% 69.8% 67.0% 62.2% 62.2 67.9%
8
Bryant W, et al. MJA. 2006;185:305–9. 2. Kosachunhanun N, et al. J Med Assoc Thai. 2006;89:S66–71. 3. Lee WRW, et al. Singapore Med J. 2001;42:501–7. 4.
Nagpal J & Bhartia A. Diabetes Care. 2006;29:2341–8. 5. Soewondo P, et al. Med J Indoes. 2010;19:235–44. 6. Tong PCY, et al. Diabetes Res Clin Pract.
2008;82:346–52. 7. Pan C, et al. Curr Med Res Opin. 2009;25:39–45. 8. Choi YJ, et al. Diabetes Care. 2009;32:2016–20. 9. Mafauzy M, et al. Med J Malaysia.
2011;66:175–81.
Masalah DM di Indonesia
Tahun 2007 - 2013
3 3
3
2.8
2.7
2.5 2.5
2.5 2.3 2.3 2.3
2.2 2.2
2.1 2.1
2 2
2 1.9 1.9
1.8
1.6 1.6 1.6
1.5
1.5 1.3 1.3
1.2 1.2 1.2
1 1
1
0.8
0.5
• CI, confidence interval; HbA1c, glycated haemoglobin; MI, myocardial infarction; T2DM, type 2 diabetes mellitus
• 1. Stratton IM, et al. Brit Medicine J. 2000; 321:405–12. 2. Colagiuri, et al. National evidence based guideline for blood glucose control in type 2
diabetes. Diabetes Australia and the NHMRC,Canberra 2009.
UKPDS ‘legacy effect’: reductions in relative risk
at 10-year post-study follow-up
0.91
Any diabetes-related endpoint 0.83 0.99 P = 0.04
0.83
Diabetes-related death 0.73 0.96 P = 0.01
Stroke 0.91
1.13 P = 0.39
0.73
0.82
Peripheral vascular disease 0.56 1.19 P = 0.29
0.76
Microvascular disease 0.64 0.89 P = 0.001
-
-
-
Data represent point estimate and 95% CI 0.1 0.5 1 5 10
Intensive better Conventional better
Intensive = Sulfonylurea or insulin in 5-year UKPDS.
Median HbA1c at end of UKPDS 7.9%
Conventional = diet only in 5-year UKPDS.
Median HbA1c at end of UKPDS 8.5%
+ peripheral
hepatic renal glucose
glucose glucose uptake
production excretion
Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011
Multiple, Complex Pathophysiological
Abnormalities in T2DM
GLP-1R Insulin
agonists pancreatic
Glinides S U s insulin
incretin
effect secretion
DPP-4 Amylin pancreatic
inhibitors mimetics glucagon
_ secretion DA
agonists
gut
AGIs
carbohydrate
?
delivery & HYPERGLYCEMIA
absorption
Metformin TZDs
_
Bile acid
sequestrants
+ peripheral
hepatic SGLT2i renal glucose
glucose glucose uptake
production excretion
Adapted from: Inzucchi SE, Sherwin RS in: Cecil Medicine 2011
Patient-Centered Approach
“...providing care that is respectful of and responsive to
individual patient preferences, needs, and values – ensuring
that patient values guide all clinical decisions.”
• Gauge patient’s preferred level of involvement.
Disease duration
newly diagnosed long-standing
Usually not
Life expectancy modifiable
long short
Important comorbidities
absent few / mild severe
Established vascular
complications absent few / mild severe
• Adapted from: Defronzo, RA. Diabetes. 2009;58: 773–95; Erhardt L, et al. Vascular Disease Prevention.
2004; 1:167174.
ADA-EASD Position Statement Update:
Management of Hyperglycemia in T2DM, 2015
3. ANTI-HYPERGLYCEMIC THERAPY
•Glycemic targets
- HbA1c < 7.0% (mean PG 150-160 mg/dl [8.3-8.9 mmol/l])
- Pre-prandial PG <130 mg/dl (7.2 mmol/l)
- Post-prandial PG <180 mg/dl (10.0 mmol/l)
- Individualization is key:
Tighter targets (6.0 - 6.5%) - younger, healthier
Looser targets (7.5 - 8.0%+) - older, comorbidities,
hypoglycemia prone, etc.
- Avoidance of hypoglycemia
PG = plasma glucose
Diabetes Care 2012;35:1364–1379; Diabetologia 2012;55:1577–1596
PILAR PENATALAKSANAAN DM TIPE 2
1. edukasi
Pilar
4. Intervensi penata- 2. Terapi gizi
Farmakologis laksanaan medik
3. Latihan
Jasmani
Safety profiles
Tolerability
Ease of use
Cost
- Agonis GLP1
- DPP4-I - GLP1 agonist
- DPP4-I
- TZD - DPP4-I
- AGI
PERKENI, 2015
Challenges in Achieving Glycemic Goals
in Diabetes
• Less aggressive treat-to-target approach by some
clinicians1
• Suboptimal use of available therapies1
• Inability of any single agent’s MOA to address all core
defects of type 2 diabetes2
• Potential for increased side effects with use of
multiple agents3
• Suboptimal adherence to lifestyle measures1
• Underuse of medications as a result of
– Cost4
– Complexity of therapy5
O’Connor PJ, et al. Agency for Healthcare Research and Quality 2005. Available at:
www.ahrq.gov/downloads/pub/advances/vol2/OConnor.pdf (accessed June 2012).
Conservative vs. proactive management of diabetes
Diet OAD
OAD + multiple
OAD daily insulin
10 monotherapy OAD + basal
monotherapy OAD injections
insulin
uptitration
combination
Conventional 9
HbA1c (%)
management
(traditional stepwise 8
approach)
6
Diet
10 OAD
monotherapy
9 OAD + multiple
HbA1c (%)
6
Duration of diabetes
• 1. Del Prato S, et al. Int J Clin Pract. 2005;59;1345–55. 2. Campbell IW, et al. Br J Cardiol. 2000;7:625–31.
Practical approaches to reducing clinical inertia
Monitoring and
Financial incentives providing feedback on
quality of care
Visit resolution
Reducing
Cognitive interventions
and accountability clinical
targeting specific
tools inertia decision pathologies
Patient initiative
Clinical decision More frequent clinic
visits Physician initiative
support
Healthcare system
initiative
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• O’Connor PJ, et al. Agency for Healthcare Research and Quality 2005. Available at: www.ahrq.gov/downloads/pub/advances/vol2/OConnor.pdf (accessed June 2012).
The diabetes multidisciplinary team
The multidisciplinary team may
include, but is not limited to:
• General practitioners
• Endocrinologists
• Diabetes nurse educators Diabetes
multidisciplinary
• Cardiologists team
• Nephrologists
• Dietitians
• Mental health professionals1
• Pharmacists
• Ophthalmologist/Optometrist
• Podiatrists
| 23
Thank you