Insulin Initiation : When We should Start with Basal Insulin?
Dr. Agus Taolin , SpPD, FINASIM | PAPDI CABANG BOGOR
Disampaikan pada acara PIT VI IDI Kota Bogor | 9 Nopember 2013
SGLT2I The paradigm change in diabetes managementPraveen Nagula
Just like ARNI, SGLT2I have changed the face of diabetes management and they have a good profile in multimodality management because of pleiotropic effects
GLP-1 is an incretin (hormone that increases insulin secretion in response to a meal), which is a 30-amino acid peptide secreted in response to the oral ingestion of nutrients by intestinal L cells.
GLP-1 receptors (GLP-1R) are located in islet cells, central nervous system, and other organs. GLP-1 is metabolized by the enzyme dipeptidyl peptidase-4 (DPP-4).
Incretin effect is a phenomenon whereby a glucose load delivered orally produces a much greater insulin secretion than the same glucose load administered intravenously.
This presentation is an overview of the entire GLP-1 system, followed by an introduction to leveraging its therapeutic potential using GLP-1 analogues (Exenatide, Liraglutide, Lixisenatide, Albiglutide, Dulaglutide) and DPP-4 inhibitors (Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin, Anagliptin, Teneligliptin, Alogliptin, Trelagliptin, Omarigliptin).
Shashikiran Umakanth delivered this talk at Manipal on 30th November, 2015
SGLT2I The paradigm change in diabetes managementPraveen Nagula
Just like ARNI, SGLT2I have changed the face of diabetes management and they have a good profile in multimodality management because of pleiotropic effects
GLP-1 is an incretin (hormone that increases insulin secretion in response to a meal), which is a 30-amino acid peptide secreted in response to the oral ingestion of nutrients by intestinal L cells.
GLP-1 receptors (GLP-1R) are located in islet cells, central nervous system, and other organs. GLP-1 is metabolized by the enzyme dipeptidyl peptidase-4 (DPP-4).
Incretin effect is a phenomenon whereby a glucose load delivered orally produces a much greater insulin secretion than the same glucose load administered intravenously.
This presentation is an overview of the entire GLP-1 system, followed by an introduction to leveraging its therapeutic potential using GLP-1 analogues (Exenatide, Liraglutide, Lixisenatide, Albiglutide, Dulaglutide) and DPP-4 inhibitors (Sitagliptin, Vildagliptin, Saxagliptin, Linagliptin, Anagliptin, Teneligliptin, Alogliptin, Trelagliptin, Omarigliptin).
Shashikiran Umakanth delivered this talk at Manipal on 30th November, 2015
Insulin intensification : the usage of premixed insulin after basal fails mataharitimoer MT
Insulin intensification : the usage of premixed insulin after basal fails
EDDY SUPRIADI, MD | MARZOEKI MAHDI , MD. HOSPITAL.BOGOR
Disampaikan pada acara PIT VI IDI Kota Bogor | 9 Nopember 2013
Case studies in the managment of type 2 diabetes NasserAljuhani
Case 1:Poorly controlled type 2 diabetes on triple oral therapies
Case 2:Morning hypoglycemia on premixed InsulinCase 3
Case 3:Newly diagnosed D.M Type1D.M or type 2 D.M ?
All diabetics irrespective of other treatment require some control of their eating and exercise patterns
Dibetics must watch their
- total caloric intake
-types of nutrients and eating schedule
50% of patients may require only diet Another 25% would need to augment their natural insulin with drugs
while the remainder will need insulin
Diet recommendations include
- discouraging fats
encouraging complex carbohydrate and fibre
The recommended diabetic diet except in a few respects is now similar to the normal healthy diet that everyone should eat. i.e regular meals, low in fats, low simple sugars, low in sodium and high in complex carbohydrate (starch) and fibre
Diet recommendations include
- discouraging fats
encouraging complex carbohydrate and fibre
The recommended diabetic diet except in a few respects is now similar to the normal healthy diet that everyone should eat. i.e regular meals, low in fats, low simple sugars, low in sodium and high in complex carbohydrate (starch) and fibre
Diet recommendations include
- discouraging fats
encouraging complex carbohydrate and fibre
The recommended diabetic diet except in a few respects is now similar to the normal healthy diet that everyone should eat. i.e regular meals, low in fats, low simple sugars, low in sodium and high in complex carbohydrate (starch) and fibre Diet recommendations include
- discouraging fats
encouraging complex carbohydrate and fibre
The recommended diabetic diet except in a few respects is now similar to the normal healthy diet that everyone should eat. i.e regular meals, low in fats, low simple sugars, low in sodium and high in complex carbohydrate (starch) and fibre
disampaikan pada sesi husnudzan dalam rangkaian #JamborePelajar #AkuIndonesia Ma'arif Institute, PAUDNI Lembang, 26 Desember 2014.
mohon maaf karena uploading versi PPT gagal terus tersebab koneksi di lokasi, jadi PDFnya dulu ya.
Media Sosial, Manfaat dan Risiko (Presentasi di SMP Sekolah Alam Bogormataharitimoer MT
Disampaikan pada sesi Internet Sehat Festival SALAM
6 Desember 2014.
Presentasi ini diunggah dalam format PDF, jika memiliki bandwidth yang memungkinkan, akan diunggah format PPT-nya agar mudah dimodifikasi oleh siapa saja yang memerlukan.
PENEGAKAN DISIPLIN KEDOKTERAN OLEH MKDKI & CONTOH KASUSmataharitimoer MT
PENEGAKAN DISIPLIN KEDOKTERAN OLEH MKDKI & CONTOH KASUS
Dipresentasikan oleh Dr. SABIR ALWY, SH, MH
Wakil Ketua MKDKI
pada PIT VI IDI Kota Bogor | 10 Nopember 2013
Dr kanadi s penanganan nyeri dismenorea (pit idi bogor) 2013 finalmataharitimoer MT
Dipresentasikan oleh Kanadi Sumapradja
Departemen Obstetri dan Ginekologi Fakultas Kedokteran Universitas Indonesia – RS Dr. Cipto Mangunkusumo
pada PIT VI IDI Kota Bogor | 10 Nopember 2013
Recomendações da OMS sobre cuidados maternos e neonatais para uma experiência pós-natal positiva.
Em consonância com os ODS – Objetivos do Desenvolvimento Sustentável e a Estratégia Global para a Saúde das Mulheres, Crianças e Adolescentes, e aplicando uma abordagem baseada nos direitos humanos, os esforços de cuidados pós-natais devem expandir-se para além da cobertura e da simples sobrevivência, de modo a incluir cuidados de qualidade.
Estas diretrizes visam melhorar a qualidade dos cuidados pós-natais essenciais e de rotina prestados às mulheres e aos recém-nascidos, com o objetivo final de melhorar a saúde e o bem-estar materno e neonatal.
Uma “experiência pós-natal positiva” é um resultado importante para todas as mulheres que dão à luz e para os seus recém-nascidos, estabelecendo as bases para a melhoria da saúde e do bem-estar a curto e longo prazo. Uma experiência pós-natal positiva é definida como aquela em que as mulheres, pessoas que gestam, os recém-nascidos, os casais, os pais, os cuidadores e as famílias recebem informação consistente, garantia e apoio de profissionais de saúde motivados; e onde um sistema de saúde flexível e com recursos reconheça as necessidades das mulheres e dos bebês e respeite o seu contexto cultural.
Estas diretrizes consolidadas apresentam algumas recomendações novas e já bem fundamentadas sobre cuidados pós-natais de rotina para mulheres e neonatos que recebem cuidados no pós-parto em unidades de saúde ou na comunidade, independentemente dos recursos disponíveis.
É fornecido um conjunto abrangente de recomendações para cuidados durante o período puerperal, com ênfase nos cuidados essenciais que todas as mulheres e recém-nascidos devem receber, e com a devida atenção à qualidade dos cuidados; isto é, a entrega e a experiência do cuidado recebido. Estas diretrizes atualizam e ampliam as recomendações da OMS de 2014 sobre cuidados pós-natais da mãe e do recém-nascido e complementam as atuais diretrizes da OMS sobre a gestão de complicações pós-natais.
O estabelecimento da amamentação e o manejo das principais intercorrências é contemplada.
Recomendamos muito.
Vamos discutir essas recomendações no nosso curso de pós-graduação em Aleitamento no Instituto Ciclos.
Esta publicação só está disponível em inglês até o momento.
Prof. Marcus Renato de Carvalho
www.agostodourado.com
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
The Gram stain is a fundamental technique in microbiology used to classify bacteria based on their cell wall structure. It provides a quick and simple method to distinguish between Gram-positive and Gram-negative bacteria, which have different susceptibilities to antibiotics
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
These lecture slides, by Dr Sidra Arshad, offer a quick overview of the physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar lead (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
6. Describe the flow of current around the heart during the cardiac cycle
7. Discuss the placement and polarity of the leads of electrocardiograph
8. Describe the normal electrocardiograms recorded from the limb leads and explain the physiological basis of the different records that are obtained
9. Define mean electrical vector (axis) of the heart and give the normal range
10. Define the mean QRS vector
11. Describe the axes of leads (hexagonal reference system)
12. Comprehend the vectorial analysis of the normal ECG
13. Determine the mean electrical axis of the ventricular QRS and appreciate the mean axis deviation
14. Explain the concepts of current of injury, J point, and their significance
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. Chapter 3, Cardiology Explained, https://www.ncbi.nlm.nih.gov/books/NBK2214/
7. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
Local Advanced Lung Cancer: Artificial Intelligence, Synergetics, Complex Sys...Oleg Kshivets
Overall life span (LS) was 1671.7±1721.6 days and cumulative 5YS reached 62.4%, 10 years – 50.4%, 20 years – 44.6%. 94 LCP lived more than 5 years without cancer (LS=2958.6±1723.6 days), 22 – more than 10 years (LS=5571±1841.8 days). 67 LCP died because of LC (LS=471.9±344 days). AT significantly improved 5YS (68% vs. 53.7%) (P=0.028 by log-rank test). Cox modeling displayed that 5YS of LCP significantly depended on: N0-N12, T3-4, blood cell circuit, cell ratio factors (ratio between cancer cells-CC and blood cells subpopulations), LC cell dynamics, recalcification time, heparin tolerance, prothrombin index, protein, AT, procedure type (P=0.000-0.031). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and N0-12 (rank=1), thrombocytes/CC (rank=2), segmented neutrophils/CC (3), eosinophils/CC (4), erythrocytes/CC (5), healthy cells/CC (6), lymphocytes/CC (7), stick neutrophils/CC (8), leucocytes/CC (9), monocytes/CC (10). Correct prediction of 5YS was 100% by neural networks computing (error=0.000; area under ROC curve=1.0).
6. Diabetes is a progressive disease
• Type 2 diabetes (T2DM) progression is characterised by decline in beta-cell function and
worsening insulin resistance1
• Getting to, or maintaining, target HbA1c levels in T2DM requires intensified treatment
over time2
1.
2.
Fonseca VA. Br J Diab Vasc Dis 2008;8:S3
Nathan DM, et al. Diabetes Care 2009;32:193-203
7. 7
papdi.bogor@ya
hoo.com
Loss of beta cell Pancreas
Apoptosis
induced by
leptin,
Autoimmu
ne
responses
Apoptosis
by:
Sulfonylure
as
Glucocortic
oids
Glucotoxi
city
Oxidative
stress
Proinflam
matory
cytokines
Loss
beta
cell
Lipotoxicit
y: FFA,
LDL-C and
low HDL-C
Wajchenberg BL. Et al.. Endocr. Rev. 28, 187-218 (2007)
9. 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
10. 10
papdi.bogor@ya
hoo.com
Modalities in Diabetes Management
Diet
Management
Physical
Activity
Oral Anti Diabetic
Diabetic
Patients
And or
Insulin
Injection
Education
ADA Consensus statement,2010
11. New position statement of the ADA and EASD on
management of hyperglycemia in type 2 diabetes
Basal
Insulin
Inzucci SE, et al. Diabetologia. 2012
Slide no 11
12. Algoritme Pengelolaan DM Tipe 2 Tanpa Disertai Dekompensasi
DM
Tahap I
GHS
GHS
+
Monoterapi
Catatan
1. Dinyatakan gagal
bila dengan
terapi 2-3 bulan
tidak mencapai
target HbA1c
<7%
2.
Bila tidak ada
pemeriksaan HbA1c
dapat digunakan
pemeriksaan
glukosa darah. Ratarata glukosa darah
sehari dikonversikan
ke HbA1c menurut
kriteria ADA 2010
Jalur alternatif
jika tidak
terdapat
insulin,
menolak dan
target glukosa
belum
optimal
Tahap II
GHS
+
Kombinasi 2 OHO
GHS
+
Kombinasi 2 OHO
+
Basal Insulin
GHS
+
Kombinasi
3 OHO
Tahap III
Insulin
Intensif
12
Konsensus Pengelolaan dan pencegahan Diabetus Melitus, PB Perkeni, 2011
13. Evolving Treatment Paradigm
in T2DM : Delayed Insulin Therapy
- 10
Years
from
Diagnosis
0
-5
+5
+10
13
+15
Amylin ( pramlintide )
Insulin
GLP-1 Analogues and
DPP-IV inhibitor
Oral combination
Oral
monotherapy
Diet management + exercise
Pre-diabetes
Type 2 Diabetes
Joslin Diabetes Centre
14. 14
papdi.bogor@ya
hoo.com
Study to evaluation how many patients move to
next step of therapy when A1c > 8 %
• Sulfonilurea ……..……… 35 % ad second drug
• Metformin ……………... 44 % ad other therapy
• 2 drugs OAD …………….. 18 % ( because the next step is
insulin )
• Spent 5 years duration before decided to give the next
therapy
Keiser Permante Group California
15. 15
papdi.bogor@ya
hoo.com
• Most patients with type 2 diabetes
require insulin therapy when OAD provide
suboptimal glycemic control
• Long-term glycemic improvement reduces the risks of
vascular complications.
• Different insulin regimens have varying effects on
glycemic control, weight gain, and the risk of
hypoglycemia
Holman RR, et al.N Engl J Med 2008;359:1577-89.
2. Turnbull FM, et al. Diabetologia 2009 August 5
3. Lasserson DS, et al. Diabetologiia, 2009;52:1990-2000.
16. 16
papdi.bogor@ya
hoo.com
Intensive diabetes Management
•
•
•
•
•
Mode of treatment for person with Diabetes
Goal : Euglycemic or near normal glycemic
Using all available resources to accomplish this goal
Prevent/ delayed loss beta cell pancreas
Prevent or delayed chronic complication of diabetes
ADA 2011
17. 17
papdi.bogor@ya
hoo.com
Stepwise Intensification of Insulin Therapy
FBG at target
HbA1c above target
FBG above target
HbA1c above target
Basal bolus
Additional prandial
doses as needed
Basal plus
Add prandial insulin at main
meal
HbA1c above
target
Basal
Add basal insulin and titrate
Oral agents
Lifestyle changes
Progressive deterioration of -cell function
Adapted from Raccah D et al. Diabetes Metab Res Rev 2007;23(4):257-64.
18. 18
Insulin
papdi.bogor@ya
hoo.com
• A hormone secreted by the beta cells
• Secreted in response to glucose or other stimuli,
such as amino acids
Insulin
• Normal response characterized by low basal levels of
insulin, with surges of insulin triggered by a rise in
blood glucose
60
40
20
0
Breakfast
Lunch
Supper
19. 19
papdi.bogor@ya
hoo.com
Basal and Prandial Insulin
•Basal insulin
replacement mimics the constant
physiologic release of insulin that regulates metabolism
and hepatic glucose production.
•Prandial insulin
replacement is intended to
mimic the postmeal insulin response to nutrient intake
23. 23
Insulin therapy
• Insulin therapy aims to replicate the normal
physiological insulin response
• Insulin regimens should be individualized
–
type of diabetes
–
willingness to inject
–
lifestyle
–
blood glucose monitoring
–
age
–
dexterity
–
glycaemic targets
papdi.bogor@ya
hoo.com
24. 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.
25. 25
papdi.bogor@ya
hoo.com
Goal Insulin Therapy
• Administration of exogenous insulin to approximate the
normal physiologic patterns of pancreatic insulin
secretion
• Reduce A1c, fasting, and postprandial plasma glucose
concentrations to recommended target level
26. What is the optimal target HbA1c level?
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
1.
2.
3.
Inzucchi et al. Diabetes care. Published online 19Apr2012.
IDF Treatment Algorithm. International Diabetes Federation 2011. http://www.idf.org/treatment-algorithm-people-type-2-diabetes
EMA Draft guidance on clinical investigation in DM Jan 2010
27. 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
Each HbA1c
percentage
point
reduction
counts3
HbA1c
-1%
1.
2.
3.
Holman, et al. NEJM 2008;359:1577–89
UKPDS 6. Diabetes Res 1990;13(1):1-11
Stratton, et al. BMJ 2000;321(7258):405-12
-14%
-37%
-21%
Myocardial infarction
Microvascular complications
Death related to diabetes
28. New ADA/EASD Position on Sequential Insulin
Strategy in Type 2 Diabetes
Non-Insulin
Regimes
Number of
Injections
Regimen
Complexity
Basal Insulin Only
Usually with OAD
1
Low
2
Mod.
+3
High
Basal Insulin + 1 mealtime
rapid-acting injection
Pre-mixed Insulin twice-daily
Basal Insulin + ≥ 2 mealtime
rapid-acting injection
More Flexible
Less Flexible
Less Convenient
More Convenient
Inzucci SE, et al. Diabetologia. 2012. * Gumprecht et al. Intensification to to biphasic insulin
aspart 30/70. Int J Clin Pract 2009
Flexibility
Convenience*
29. Insulin can be initiated at any time
•
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
+ 2 OAD
INITIATE INSULIN
+ 3 OAD
30. How to start Basal Insulin
• Start with basal insulin (Insulin Detemir) 10 U or 0,1-0,2 U per Kg BB
• Once daily injection, anytime injection but in same time per each day
31. Levemir® Dose Titration Guidelines:
3-0-3 Algorithm
Start with Levemir 10 U or 0,1-0,2 U per Kg BB
Simple Dose titration with Levemir
Mean 3-day FPG (mg/dL)
Increase
FPG>90 mg/dl (5.0 mm/L)
FPG target range
70-90 mg/dL
FPG <70 mg/dL (3.8 mmol/L)
3units
units
Maintain
dose
Decrease
3 units
FPG>110 mg/dL (6.1 mmol/L)
FPG target range
80-110 mg/dL
FPG <80 mg/dL (4.4 mmol/L)
Patients who experienced hypoglycemia reduced their daily dose by 3 units
Blonde L et al. Diabetes Obes Metab. 2009; 11(6):623-631.
32. Levemir®/Glargine Head-to-Head:
Similar Profiles in Type 2 Diabetes
Insulin detemir
2.5
(mg/kg/min)
Glucose infusion rate
3.0
0.4 U/kg
0.8 U/kg
Insulin glargine
2.0
1.5
1.0
0.5
0
0
2
4
6
8
10
12
14
16
18
Time (h)
Klein O et al. Diab Obes Metab 2007; 9:290-299
20
22
24
33.
34. Levemir reduces nocturnal hypoglycaemia by up to
65% compared to NPH
NPH vs. glargine
-44%
-53%
-65%
Relative Risk
-29%
NPH vs. detemir
Insulin Determir
Insulin NPH
Insulin glargine
Riddle et al., 2003
Phillis-Tsimikas et al., 2006
Phillis-Tsimikas. Clin Ther 2006;28(10):1569–81; Riddle et al 2003. Diabetes Care; 26 (11): 30806; Asakura T et al, 2008. Expert Opin Pharmacother; 10 (9): 1-5; Hanel H et al 2008. J Diabetes
35. A1chieve study overview and design
• Observational study of people with T2DM in
routine clinical practice
Start a study
insulin
• Biphasic insulin
aspart 30
• Insulin detemir
• Insulin aspart
BASELINE
Week 0
•
INTERIM
Week 12
FINAL
Week 24
Study objectives
•
Primary: number of attributed adverse drug
reactions (includes major hypoglycaemia)
•
Secondary: other safety and effectiveness
measures
47. Conclusion
• Diabetes is a progressive disease that is increasing in prevalence in the world
• Starting with basal insulin detemir is easy way to reach better glycemic control
• In Indonesia, in real life clinical practice (A1chieve study) Levemir show significant
improvements in overall glycaemic control in terms of HbA1c, FPG and PPG.
In the first edition of the IDF Diabetes Atlas, released in 2000, the estimated global diabetes prevalence was 151 million. In the newest 5th edition, the estimated diabetes prevalence for 2011 has risen to 366 million, representing 8.3% of the world’s adult population, with a prediction that by 2030 the number of people with diabetes will have risen to 552 million.
IDF juga memperkirakan bahwa 60% dari kasus diabetes tersebut ada di Asia.
-The prevalence of diabetes varies in different regions of Indonesia – it is higher in urban versus nonurban/outlying provinces and regions-According to the DiabCare Asia 2008 study, the prevalence of diabetes in Jakarta is 3.7%Riskedas 2007 (Cross sectional sampling for a registry conducted across Indonesia)Soewondo et al. DiabCare Asia 2008 Study. Med J Indones 2010.
Penelusuran Litbangkes menunjukkan bahwa prevalensi diabetes tertinggi di daerah di Indonesia adalah sebesar 11,1%, yaitu di Pontianak (Kalimantan Barat) dan Ternate (Maluku Utara).
On this slide we can see the usual pattern of insulin intensification in T2DM, moving from lifestyle interventions, the addition of OADs such as metformin, through to a regimen combining the OAD therapies with basal insulin, which has become a popular way to initiate insulin. When this combined BOT fails to control blood glucose levels, further intensification, to basal–bolus therapy, is recommended.
In the UKPDS study, the incidence of clinical complications was significantly associated with glycaemia3. Each 1% reduction in updated mean HbA1c was associated with reductions in risk of 21% for any end point related to diabetes (95% CI 17% to 24%, P < 0.0001), 21% for deaths related to diabetes (15% to 27%, P < 0.0001), 14% for myocardial infarction (8% to 21%, P < 0.0001), and 37% for microvascular complications (33% to 41%, P < 0.0001). No threshold of risk was observed for any end point.
Speaker Notes:[Click 1]: Detemir OD reduced the risk of hypoglycaemia by 53% versus NPH OD and reduced the risk of nocturnal hypoglycaemia by 65%