kimia klinik jurnal 2
DESCRIPTION
Role of Glycated Hemoglobin in the Prediction of Future Risk of T2DMTRANSCRIPT
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Henny Elfira Yanti, dr/ Djoko Marsudi, dr SpPKSenin, 21 Oktober 2013
Jurnal Kimia Klinik II
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Selama 2 dekade terakhir , prevalensi diabetesmellitus tipe 2 ( T2DM ) telah meningkat menjadiepidemi
Sifat penyakit yang kronis dan beberapakomplikasi pembuluh darah
Ancaman besar bagi kesehatan masyarakat
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Subyek dengan gangguan glukosa darah puasa( IFG ) dan gangguan toleransi glukosa ( IGT )
berisiko menjadi T2DM
Pencegahan primer dapat membatasi peningkatan prevalensi T2DM
Penelitian hanya sekitar setengah darisubjek dengan IFG dan IGT yang berkembangmenjadi T2DM
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Penelitian sekitar 40 % subjek dengantoleransi glukosa normal berkembangmenjadi T2DM
Banyak yang terlewatkan bila hanyabergantung pada IFG dan / atau IGT untukmengidentifikasi subyek dgn peningkatanresiko T2DM
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American Diabetes Association ( ADA )• Diabetes HbA1c ≥ 6,5 %• Individu yang berisiko tinggi
HbA1c 5,7 - 6,49%
Model prediktif identifikasi subjekumur, jenis kelamin , indeks massa
tubuh ( BMI ) , glukosa plasma puasa( FPG ) , dan profil lipid risk score
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Menilai kekuatan prediksi HbA1c untukmengidentifikasi subjek denganpeningkatan risiko T2DM
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A first degree relative (anak-ortu) FPG ≥ 100 mg / dl Kadar trigliserida plasma ≥ 150 mg / dl High-density lipoprotein ( HDL ) ≤ 50 mg /
dl (wanita) dan ≤ 40 mg / dl (laki-laki)
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DiabetesGangguan fungsi ginjal ( kreatinin > 1,5 ) , Keganasan Terapi dengan obat yang mempengaruhi
toleransi glukosa
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687
•Puasa 10 jam•Tes toleransi glukosa (OGTT)
Glukosa plasma dan konsentrasi insulin diukur • -30 , - 15 , dan 0 menit• 30 , 60 , 90 , dan 120 menit setelah
konsumsi glukosa
Profil lipid dan HbA1c diukur
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Setelah 3,5 ± 0,1 thn , subjek kembali ke pusat penelitian klinis dan OGTT diulang dengan menggunakan protokol yang sama
678
624
63
21
39
Ikut dalam penelitian
Drop Out
Pindah Kota
Tidak ditemukan
3 Meninggal12
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Diagnosis diabetes didasarkan pada kriteriaAmerican Diabetes Asosiasi :
2 -h glukosa plasma ≥ 200 mg / dlGlukosa puasa plasma ≥ 126 mg / dl
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Glukosa plasma Metode heksokinase
Konsentrasi insulin plasma RIA
HbA1c Ionexchange HPLC
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Variabel di sajikan sebagai means ± SEPerbedaan rata-rata diuji dengan Student t testSignifikan P< 0,05 SPSS versi 17
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NGT 286 IFG 201 IGT 137
34 subyek berkembang menjadi DMT2
624
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Cut point HbA1c 5,65 %1-h PG 155 mg/dl
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Tabel 3. T2DM risk in subjects with HbA1c and 1- hPG above and below the cut points.
Condition Total subjects
Subject who developd DM
Risk Odds ratio P
HbA1c<5.65,1-h PG<155 mg/dl
224 0 0 1
HbA1c<5.65,1-h PG>155 mg/dl
181 7 3.87 8.92(1.09-3.18)
0.025
HbA1c>5.65,1-h PG<155 mg/dl
86 3 3.49 7.78(0.99-75.8)
0.07
HbA1c>5.65,1-h PG>155 mg/dl
133 24 18.1 40.24(5.38-00.9)
<0.0001
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HbA1c sebagai prediktor risiko T2DM yangsignifikan, tapi kekuatan prediksinya lebihlemah dibandingkan dengan model lainnya(1-h PG)
Kombinasi HbA1c dan 1-h PG aROCterbesar dibandingkan dengan model prediksilainnya (0,87)
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Cut points 5,65% konsisten dengan penelitianlain dan mendukung rekomendasi klinis ADA
5,7 % untuk subjek dgn peningkatanrisiko diabetes.
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HbA1c memiliki daya prediksi yang lebihrendah dibandingkan dengan 1-h PG (ROC 0,73dan 0,84)
Kombinasi HbA1c dan 1-h PG
Meningkatkan daya prediksi
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Antropometrik, FPG dan profil lipid tidakmemberikan tambahan informasi tentangrisiko T2DM
HbA1c>5.65% sensitivitas 71 %1-h PG>155 mg/dl Spesifisitas 82%
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HbA1c sebesar 5,65 % , seperti yangdisarankan oleh ADA tepat untukmengidentifikasi subjek pada peningkatanrisiko T2DM
Kombinasi HbA1c 5,65 % dan 1 -h PG > 155 mg / dlalat klinis yang berguna untuk identifikasi
subjek dgn peningkatan risiko T2DM di masa depan.
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TERIMA KASIH
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DIABETES CARE, VOLUME 29, NUMBER 8, AUGUST 200628
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Sindroma klinik ditandai dengan hiperglikemia kronik akibat defisiensi Insulin absolut / relatif
Diabetes mellitus merupakan keadaan hiperglikemia dengan gangguan metabolisme karbohidrat, protein & lemakserta penyulit makro/mikrovaskuar
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Sel Beta Pankreas: insulin (kualitas/kuantitas)
Reseptor Insulin: kualitas / kuantitasPasca Reseptor: gangguan sist. Enzim Inhibitor Insulin: antibodi anti insulin
counter regulatory hormones glukagon, epinefrin, kortisol, growth hormone)
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Diagnostic criteria for diabetes :1. A fasting plasma glucose ≥126 mg/dl2. Symptoms of diabetes (polyuria,
polydipsi, loss of BW) plus random blood glucose ≥ 200mg/dl
3. A plasma glucose level ≥ 200 mg/dLafter an oral dose of 75 g of glucose
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A1C ≥6.5%OR
Fasting plasma glucose (FPG)≥126 mg/dL (7.0 mmol/L)
OR
2-h plasma glucose ≥200 mg/dL(11.1 mmol/L) during an OGTT
OR
A random plasma glucose ≥200 mg/dL (11.1mmol/L)
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Categories of increased risk for diabetes (prediabetes)*
FPG 100–125 mg/dL (5.6–6.9 mmol/L): IFGOR
2-h plasma glucose in the 75-g OGTT140–199 mg/dL (7.8–11.0 mmol/L): IGT
OR
A1C 5.7–6.4%
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DM Tipe 1 DM Tipe 21. Mudah ketoasidosis 1. Tidak mudah2. Obat: harus insulin 2. Tidak harus3. Onset akut 3. Onset lambat4. Biasanya kurus 4. Gemuk/tidak gemuk
(obesitas faktor pencetus)
5. Biasanya umur muda 5. Biasanya > 45 tahun
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DM Tipe 1 DM Tipe 26. Berhubungan dengan
HLA DR 3 & DR 46. Tidak
7. Islet Cell Ab (ICA)(proses otoimun)
7.
8. Riwayat kel. DM 8. 30 %9. Kembar identik 30-50
% terkena9. ± 100 %
10. Insulin serum rendah 10. Normal / tinggi
+ -
+
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Consider metformin for prevention of type 2 diabetes if IGT , IFG , or A1C 5.7–6.4% Especially for those with BMI >35 kg/m2,
age <60 years, and women with prior GDM
In those with prediabetes, monitor for development of diabetes annually
ADA. IV. Prevention/Delay of Type 2 Diabetes. Diabetes Care 2013;36(suppl 1):S16.36
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Metabolisme KBH Langsung: Glukosa Darah1. Uptake Glukosa (otot, hati, jar.lemak)2. Sintesa Glikogen (glikogenesis) disimpan
dalam hepar + otot3. Glikogenolisis (pemecahan glikogen )4. Glukoneogenesis (pembentukan glukosa dari as. amino, laktat, piruvat)
Metabolisme Protein :1. Rangsang transport aktif as. amino ke dalam sel2. Rangsang sintesis protein
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Metabolisme Lemak :1. Rangsang lipogenesis (pembentukan
lemak) dalam sel hepar, jar. lemak2. Menghambat lipolisis (pemecahan
lemak)
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Vena DM GDP > 126 mg/dL = 7 mmol/L
2JSM/GDA ≥ 200 mg/dL = 11 mmol/L GTG GDP 100 – 125 mg/dL
2JSB 140 – 199 mg/dLNORMAL GDP < 100 mg/dL
2JSM < 140 mg/dL*) Catatan : - GTG = Gangguan Toleransi Glukosa
- 1 mmol/L glukosa = 18 mg/dL glukosa39
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Metabolic syndrome is defined as the presenceof three of the five following criteria: Increased waist circumference (> 40 inches in
men, >35 inches in women) Plasma triglycerides ≥ 150 mg/dL Plasma high-density lipoprotein cholesterol ,
< 40 mg/dL in men, < 50 mg/dL in women Blood pressure ≥ 130 mm Hg systolic > 85
mm Hg diastolic Fasting plasma glucose ≥ 100 mg/dL
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Sumber :Endocrine secret sixth edition41
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Sumber :Endocrine secret sixth edition42
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Defisiensi Insulin
Glukosa Uptake Proteolisis Lipolisis
As. Amino Nitrogen Loss
Gliserol FFA
Hiperglikemi
Glukoneogenesis
+
Glikogenolisis
Osmotic Diuresis electrolyte depletion
Hyptonic Loss dehydration
Ketogenesis
Ketonemia
Ketonuria
Asidosis
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interpretasi kadar HbA1c
normal : 4,5 – 6 % Hbterkontrol baik : 6 -- 7 % Hb
terkontrol cukup : 7 -- 8 % Hbtidak terkontrol : > 8,2 % Hb
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Nilai Rujukan
Puasa : 70 – 110 mg/dl (3.9 – 6.1 mmol/L)½ jam : 110 – 170 mg/dl (6.1 – 9.4 mmol/L)1 jam : 120 – 170 mg/dl (6.7 – 9.4 mmol/L)1½ jam : 100 – 140 mg/dl (5.6 – 7.8 mmol/L)2 jam : 70 – 120 mg/dl (3.9 – 6.7 mmol/L)
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GDP : 100 – 125 mg/dL 2JSM : < 200 mg/dLDM keluargaGejala DM Hamil : bayi > 4 kg, toksemia, hidramnion
abortus spontan
+
+
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Secondary causes of Diabetes mellitus include:
Acromegaly, Cushing syndrome, Thyrotoxicosis, Pheochromocytoma Chronic pancreatitis, Cancer Drug induced hyperglycemia:
◦ Atypical Antipsychotics - Alter receptor binding characteristics, leading to increased insulin resistance.
◦ Beta-blockers - Inhibit insulin secretion.◦ Calcium Channel Blockers - Inhibits secretion of insulin by interfering with cytosolic calcium
release.◦ Corticosteroids - Cause peripheral insulin resistance and gluconeogensis.◦ Fluoroquinolones - Inhibits insulin secretion by blocking ATP sensitive potassium channels.◦ Naicin - They cause increased insulin resistance due to increased free fatty acid
mobilization.◦ Phenothiazines - Inhibit insulin secretion.◦ Protease Inhibitors - Inhibit the conversion of proinsulin to insulin.◦ Thiazide Diuretics - Inhibit insulin secretion due to hypokalemia. They also cause increased
insulin resistance due to increased free fatty acid mobilization.
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Increasing insulin availability (secretagogues : sulfonyl-
urea) Supressing excessive hepatic glucose
output(biguanide i.e. metformin) Improving insulin sensitivity(thiazolidinediones or
glitazones) Delaying gastrointestinal glucose
absorption(acarbose) Objectives (ADA):FPG 90-130 mg/dL,
postprandial plasma glucose <180 mg/dL,HbA1c < 7%
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HbA1c: Hemoglobin A yang mengalami glikasi non
enzimatik
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Istilah yang mencakup berbagai tipe Hbyang berikatan denganglukosa/karbohidrat pada gugusan amino bebas
HbA1Varian glycated Hb yang berikatan
dengan karbohidrat pada gugusan valindari N – terminal pada rantai beta
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Pada DM/non DM Sebagian HbA mengalami glikasi(HbA1)
Persentasi fraksi HbA1 sebanding dengan rerata konsentrasi glukosa darah
HbA1cHb dengan ikatan spesifik glukosa pada
gugusan valin dari N-terminal pada rantai ß
Normal: 70-90% dari HbA155
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Terdiri dari : Fase Gerak Fase DiamKomponen : Pompa Kolom Injektor Detektor Rekorder
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57Bishop,2005
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Injeksi sampel ke dalam fase gerak
Sampel dialirkan ke dalam kolom denganmenggunakan tekanan tinggi
Komponen larutan berinteraksi dengansenyawa di kolom
Terjadi pemisahan komponen
Deteksi dengan spektofotometer
Hasil berupa kromatogram58
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Kromatografi berdasarkan pertukaranmuatan ion
Muatan ion pada larutan akan bertukardengan muatan ion pada gugus fungsional
Fase diam: resin (polimer besar dan gugusanfungsional yang bermuatan katoda atauanoda)
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HbA1c: +Resin : -
1
Sampel+bufer+cairanelusiPada kolom terjadipertukaran ionHb terglikasidikeluarkan ( muatan <)
2
Bufer keduabermuatan berbedaPada kolom terjadipertukaran ionHemoglobin yang lain dikeluarkan
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Glukosa dengan adanya ATP difoforilasi olehenzim heksokinase menghasilkan glukosa-6-fosfat dan ADP. Selanjutnya glukosa-6-fosfatdengan NADPoleh enzim glukosa-6-fosfatdehidrogenase diubah menjadi 6-fosfoglukonat dan NADPH. NADPH yangterbentuk dapat diukur serapannya dansebanding dengan kadar glukosa darah
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Prinsip reaksinya :
Glukosa + ATP heksokinase glukosa-6-fosfat + ADP
Glukosa-6-fosfat + NADP G-6-DP 6-fosfoglukonat + NADPH
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Radioimmunoassay adalah teknik imunoasaiyang pertama berkembang (1950, oleh Yalow dan Berson).
Label radioisotop yang digunakan adalah 131I, 125I dan 3H. Yang paling banyak adalah 125I karena half life-nya 60 hari
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KELEMAHAN UJI RIA
♦ Butuh alat mahal & tenaga terlatih
♦ Waktu paruh reagens amat pendek ( 1,5 – 2 bln )
♦ Perlu perlindungan khusus pd petugas lab.
♦ Perlu tempat pembuangan reagens yang khusus
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120
160
200
240
30 60 90 120
Glukosa darah (mg/dL)
Waktu (menit)
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Kami sebelumnya telah menunjukkan bahwa 1 -h plasma Konsentrasi glukosa ( 1 -h PG ) selama OGTT adalah prediktor terkuat risiko DMT2 masa depan . konsisten dengan pengamatan kami sebelumnya, aROC untuk 1 -h PG ini kohort adalah 0,84 , dan penambahan 1 -h PG untuk kedua model 1 dan 2 memiliki dampak yang lebih besar pada daya prediksi mereka dibandingkan dengan penambahan HbA1c tersebut
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aROC Model 1 ditambah 1 -h PG dan model 2 ditambah 1 -h PG itu identik , 0.85
Penambahan HbA1c untuk 1 -h PG signifikanmeningkat aROC tersebut 0,84-0,87 ( P < 0,05 )
Model terdiri dari 1-h PG dan HbA1c memilikiterbesar aROC (0.87), menunjukkan bahwa kombinasi 1-h PG dan HbA1c lebih superior dalam memprediksi risiko DMT2
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aROC HbA1c dalam memprediksi resiko diabetes secara signifikan lebih rendah dibandingkan dengan kedua multivariat Model ( model 2 ) dan 1 -h PG , yang sebelumnya memiliki telah terbukti menjadi prediktor kuat risiko DMT2
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