Di Slipid

DISLIPIDEMIA

Krishna W SuciptoDivisi Endokrinologi/MetabolikBgn. Ilmu Penyakit Dalam FK

Unsyiah/RSU Dr. Zainoel Abidin Banda Aceh

Roles of LipidsAdvantageous

•Source of energy•Body protector•Component of cell formation•Synthesis of steroid hormon •Precursor of prostaglandin

Disadvantageous•Atherosclerosis•Xanthomatosis•Pankreatitis

HOHO

HHCHCH33 CHCH33

CCCHCH33

CHCH22CHCH22 CHCH22 CC

CHCH33

CHCH33

HH

KolesterolKolesterol

OO

HH33CC (CH(CH22))77 CCHH

CC (CH(CH22))77 CC

OO

OO CHCH

CHCH22

CHCH22

OO CC (CH(CH22))1414 CHCH33

OO CC

OO(CH(CH22))1616 CHCH33

TrigliseridTrigliserid

Pickup J, Williams G. Lipid Disorders in diabetes mellitus. Text Book of Diabetes. 1997:p. 55.1-31Pickup J, Williams G. Lipid Disorders in diabetes mellitus. Text Book of Diabetes. 1997:p. 55.1-31

FosfolipidFosfolipid

C C HH22.O.CO.R.O.CO.R

R.COOR.COO..CCHH

C C HH22OO PP OCHOCH22.CH.CH22.N.N++

CHCH33CHCH33

CHCH33OO

OO

LIPID PLASMALIPID PLASMA

22

LIPID PLASMA - Trigliserida

- FosfolipidKolesterol

- Bgn Membran sel- Sintesa asam empedu- Steroidogenesis

- 75% sebagai C.E dgn As.Linoleat & Linolenat

Trigliserida- Ester As.Lemak & Gliserol

- Cadangan Energi di adiposa

Fosfolipid - Ikatan Gliserol dgn As Lemak dan Asam Fosfat

- Pembentuk membran sel - Pembentukan Lipoprotein

- Kolesterol

Cholesterol EsterTrigliserida

Tak larut (Hidrofobik)

+ ApoproteinLipoprotein

Larut dalam air(Hidrofilik)

Cholesterol Ester

Trigliserida Fosfolipid

Apoprotein Cholesterol Bebas

= LIPOPROTEIN

Apoprotein + Lipid = Lipoprotein Berfungsi sebagai transportasi lipid

Structure of Lipoprotein

LIPOPROTEIN

JenisLipoprotein

Jenis apoprotein

Lipid, %

Trigliserida Kolesterol Fosfolipid

Kilomikron apo B48 80-95 2-7 3-9

VLDL apo B100 55-80 5-15 10-20

IDL apo B100 20-50 20-40 15-25

LDL apo B100 5-15 40-50 20-25

HDL apo AI & apo AII 5-10 15-25 20-30

Harrison’s Principles of Internal Medicine 14th

Metabolisme Lipoprotein

Jalur Eksogen (Penyerapan lipid dari usus)

Jalur Endogen (Sintesa lipid di hati)

Reverse Cholesterol Transport = Penarikan Cholesterol oleh HDL-Choles terol dari jaringan periferal (makrofag) ke hati untuk di ekskresi

Shepherd J. Eur Heart J Supplements 2001;3(suppl E):E2-E5Shepherd J. Eur Heart J Supplements 2001;3(suppl E):E2-E5

TinjaTinja

remnantsremnants

kilomikronkilomikron

Usus halus

kolesterolkolesterol

KolseterolKolseterolmakananmakanan

HDLHDL

EksogenEksogen

HatiHati

VLDLVLDL

MakrofagMakrofag

VLDLVLDL IDLIDL LDLLDL

EndogenEndogen

METABOLISME LIPOPROTEINMETABOLISME LIPOPROTEIN

RCTPRCTP

RCTP = reverse cholesterolRCTP = reverse cholesterol transport pathwaytransport pathway

1010

Lemak dlm Makanan

TGLIPASE

A.L

Glis +

Trigliserida

sel Enterosit

Cholesterol

Asam Lemak +

Cholesterol Ester

Apoprotein B 48Fosfolipid

ChylomicronUSUS

FL

Kwiterovich PO, Jr. The metabolic pathways of high-density lipoprotein, low-density lipoprotein, and triglycerides: Kwiterovich PO, Jr. The metabolic pathways of high-density lipoprotein, low-density lipoprotein, and triglycerides: A current review. Am J Cardiol 2000;86:5L-10L A current review. Am J Cardiol 2000;86:5L-10L

IDLIDL

LDLDLL

HatiHati

VLDLVLDLVLDLVLDL

MakrofagMakrofag

VLDLVLDL

Timbunan kolesterolTimbunan kolesterol

JALUR METABOLISME ENDOGENJALUR METABOLISME ENDOGENReseptor LDLReseptor LDL

Scavenger receptor-A / CD 36Scavenger receptor-A / CD 36Adenosine triphosphate-binding Adenosine triphosphate-binding cassette transporter-1 (ABC-1)cassette transporter-1 (ABC-1)

Jalur metabolisme HDLUntuk memahami metabolisme HDL, perlu diketahui dulu beberapa hal yang berhubungan dengan reverse cholesterol transport yaitu sumber HDL, reseptor HDL dan protein transporter. Sumber HDL: HDL dibentuk di usus halus dan hati, dikenal sebagai nascent HDL, terutama mengandung fosfolipid dan apo-A1 dengan sedikit sekali kolesterol.Reseptor HDL: Di hati dan jaringan steroidogenik lainnya (ovarium, testis, adrenal) terdapat suatu reseptor HDL yang disebut scavenger receptor class B type 1 (SR-B1). Reseptor ini berfungsi untuk menangkap kolesterol ester yang berada di kolesterol-HDL. Kolesterol ester yang ditangkap akan dihidrolisis dan kolesterol yang terlepas akan digunakan untuk membentuk hormon steroid, dan sebagian akan dimetabolisme sebagai asam empedu ke usus halus.

Protein transporterTerdapat suatu transporter protein, yaitu adenosine-triphosphate-binding cassette transporter-1 (ABC-1), yang bertugas membawa kolesterol yang berada di makrofag ke tepi sel untuk keudian ditangkap oleh HDL.

HDL nascent (Pre-beta HDL) berasal dari usus halus dan hati, berbentuk gepeng dan mengandung apo A1. HDL nascent akan mendekati makrofag untuk mengambil kolesterol yang tersimpan di makrofag. Agar dapat diambil oleh HDL nascent, kol. bebas di bagian dalam makrofag harus dibawa ke permukaan membran sel makrofag oleh suatu transporter yang disebut ABC-1 (ATP -binding cassette transporter-1) Setelah mengambil kol. dari makrofag, HDL nascent berubah menjadi HDL dewasa yang berbentuk bulat.

Kol. bebas yang diambil dari makrofag tsb akan diesterifikasi menjadi kol. ester oleh enzim LCAT (lecithin cholesterol acyl transferase). Selanjutnya kol. ester yang dibawa oleh HDL akan mengambil 2 jalur: Jalur I. ke hati dan ditangkap oleh reseptor SR-B1 (scavenger receptor class B type 1). Jalur II. kol. dalam HDL akan dipertukarkan dengan TG dari VLDL dan IDL dengan bantuan CETP (cholesterol ester transfer protein). Dengan demikian fungsi HDL sebagai “penyerap” kolesterol dari makrofag mempunyai dua jalur yaitu 1. Jalur langsung ke hati yang di tangkap oleh reseptor SRB-1 2. Jalur tidak langsung melalui VLDL dan IDL untuk membawa kolesterol kembali ke hati (titip kolesterol)

Liver LDLR/LRP

SR-BIHDLR?

Adrenal

LDL

VLDL

HDLHDL

HDL

HDL

HDL

Cholesterol

SR-BI

HDL- Bile- Cholesterol- Bile Salts

Cholesterol

CholesterolKidneyPeripheral Tissues

SR-BIABC1

LCAT

CETP

ApoA-IR

ApoA-I

OvaryTestis

1

2

364 7

8

9 HL

HS-PG

5

HDL Metabolism

SS/02

CE = Chol. Ester FC = Free Chol. LCAT =Lecithine:cholesterol acyl transferaseCETP= Cholesterol ester transport protein. HL= Hepatic lipase. ABC1 =ATP binding cassette transporter 1

TG

VLDL IDL LDL

LDL

HDLn

HDL3

Biliary chol.+Bile acids

SRB-1

CE TGCETP

LCAT

Reverse Cholesterol Transport

SRB-1

HL

LDL

HDL2

CEFC

Small dense LDL

FCFC

AB

C1

SRACD36

LDL

NoDown regulation

MACROPHAGE

FC

SS/01 CE = Chol. Ester FC = Free Chol.

LDL metabolism

TG

LDL

MACROPHAGE

VLDL IDL

LDL-RLDL-R

LDL

CEFC

LDL

Biliary chol.+

Bile acids

Down regulation

SRB-1

InsulinInsulin

METABOLISME LIPOPROTEIN PADA RESISTENSI INSULIN METABOLISME LIPOPROTEIN PADA RESISTENSI INSULIN

RIRI****

Sel LemakSel Lemak

ALB*HatiHati

TGTG ApoBApoB VLDLVLDL

VLDLVLDLbesar besar

(CETP)

(CETP)

LDLLDLkecil kecil padatpadat

(lipoprotein atau lipase hati)

ApoA1ApoA1

GinjalGinjal

TGTG

HDLHDL

LDLLDL

TGTG

Kwiterovich PO, Jr. The metabolic pathways of high-density lipoprotein, low-density lipoprotein, Kwiterovich PO, Jr. The metabolic pathways of high-density lipoprotein, low-density lipoprotein, and triglycerides: A current review. Am J Cardiol 2000;86:5L-10L and triglycerides: A current review. Am J Cardiol 2000;86:5L-10L

*Asam lemak bebas

** Resistensi insulin

ElevatedTRL

CHYLOMICRON

VLDL

LPL

LPLHL

Smalldense LDL

Smalldense HDL

Intestine

TRL = Triglyceride rich lipoprotein HL = hepatic lipaseCETP = cholesteryl ester transfer protein

LDL

HDL

CETG

CETG

HL

CE

CETP

TG

CE

TGCETP

FFA

FFA

Formation of Small Dense LDL

SS/01 CE = Chol. Ester FC = Free Chol.

TG

MACROPHAGE

NoDown regulation

IDL LDL

SRACD36

LDL

Scavenger Pathway

LDL

Small dense LDL

VLDLCEFC

FCFC

FC

SRB-1

LDL-R

DISLIPIDEMI DIABETIKDISLIPIDEMI DIABETIK

Trigliserid tinggiTrigliserid tinggi

HDL - kolesterol rendahHDL - kolesterol rendah

LDL kecil padat tinggiLDL kecil padat tinggi

LDL - kolesterol sering normalLDL - kolesterol sering normal

4242

Pathogenesis of Atherosclerotic Plaques

Protective response results in production of cellular adhesion molecules

Monocytes and T lymphocytes attach to ‘sticky’ surface of endothelial cells

Migrate through arterial wall to subendothelial space

Lipid-rich foam cells

Endothelial damage

Macrophages take up oxidised LDL-C

Fatty streak and plaque

The primary event in atherosclerosis is thought to be damage caused to the endothelium of arterial walls, resulting in endothelial dysfunction. This damage may be caused by a variety of factors; haemodynamic forces (shear stress caused by eg. hypertension), a number of vasoactive substances, mediators (cytokines) from blood cells, cigarette smoke, atherogenic diet, elevated glucose levels and oxidised LDL-C.1

Initially, damage causes the endothelial cells to express cellular adhesion molecules such as cytokines (interleukin-1, (IL-1); tumour necrosis factor alpha, (TNF-alpha)), chemokines (monocyte chemoattractant factor 1, (MCP-1; IL-8)) and growth factors (platelet-derived growth factor, (PDGF); basic fibroblast growth factor, (bFGF)).1 This ‘sticky’ surface encourages inflammatory cells such as monocytes and T-lymphocytes to attach to the endothelial surface. Once attached they migrate through the intact endothelium into the subendothelial space. Many of the monocytes differentiate into macrophages and take up oxidised LDL, which is more atherogenic than native LDL; these macrophages then become foam cells.1

Oxidised LDL promotes death of endothelial cells and an inflammatory response resulting in impairmen impairment of normal function of the endothelium. In addition, it modifies the response to angiotensin II, resulting in vasodilatory impairment, and induces a prothrombic state by affecting platelets and coagulation factors.Thus, the endothelium responds to damage by inducing a protective response which will eventually lead to the formation of fibrofatty and fibrous lesions, the atherosclerotic plaque, preceded and accompanied by inflammation.2This schematic linear diagram represents part of a network of complex processes that include various disease (and protecting) mechanisms that occur simultaneously.

(IL-1, TNF a , MCP-1, IL-8)

Permeabel

INTIMA

SS S i iiiiPAI-1

SS

S = selectin i = imunoglobulin ( VCAM dll)

DiabetesShear stress (hypertensio

n),Smoking etc.

HSPG

HSPG

SEL OTOT POLOSMEDIASS

HSPG = heparan sulfate proteogycans

Endothelial Dysfunction in Atherosclerosis

Monocyte

PAI-1

Free radicals.

AGEs

INTIMA

SMCMEDIASS

SS S i iiii

Small dense LDL

HSPG

Macrophage

Foam cell

LDL

LDL ox

Cytokines+ PDGF,FGF

Lipid core

SRACD36


Formation of Lipid Core

PAI-1

Radikal Bebas.AGEs

INTIMA

SEL OTOT POLOSMEDIASS

SS S i iiii

LDL kecil

HSPG

HSPG

Makrofag

SEL BUSA LDL ox

Sitokin+ PDGF,FGF

Lipid core

Plaque

fibrinolisisagregasi tr.

SRACD36


LDL

Formation of Plaque

Adapted from Ross RAdapted from Ross R. N Engl J Med. N Engl J Med 1999; 1999;362362:115–126.:115–126.

Tunica media:Tunica media:Smooth muscle cellSmooth muscle cellMatrix proteinsMatrix proteins

Internal elastic membraneInternal elastic membraneEndotheliumEndothelium

Tunica intima:Tunica intima:

External elastic membraneExternal elastic membrane

LumenLumen

Normal Arterial Wall

The normal artery consists of three distinctive layers: the tunica intima, the innermost layer comprising a single layer of endothelial cells on the luminal surface; the tunica media, a tube of vascular smooth muscle cells (VSMCs) and their extracellular matrix shown in this slide; and the tunica adventitia, (not shown in this slide), the outer protective layer comprising loose connective tissue containing blood vessels and nerves which supply the artery itself.1,2

The endothelial cells of the tunica intima have a number of important functions; forming a non-thrombotic, non-adherent surface, acting as a semi-permeable membrane, synthesising and releasing chemical mediators, maintaining the basement membrane, and modifying lipoproteins as they cross into the artery wall.The VSMCs of the tunica media contract and relax to alter the lumen diameter of the vessel in response to a variety of circulating and local stimuli, regulating vascular tone, blood flow and blood pressure. This is effected through the production of a number of vasoactive substances including prostaglandins, endothelin and nitric oxide (NO).1,2

Upregulation of Upregulation of endothelialendothelialadhesion moleculesadhesion molecules

Increased endothelial Increased endothelial permeabilitypermeability

Migration of Migration of leucocytes into the leucocytes into the artery wallartery wall

Leucocyte adhesionLeucocyte adhesion

Lipoprotein infiltrationLipoprotein infiltration


Endothelial Dysfunction in Atherosclerosis

Endothelial dysfunction in atherosclerosis is characterised by a series of early changes that precede lesion formation. The changes include greater permeability of the endothelium, up-regulation of leucocyte and endothelial adhesion molecules and migration of leucocytes into the artery wall.

Formation of Formation of the fibrous capthe fibrous cap

Accumulation ofAccumulation ofmacrophagesmacrophages

Formation ofFormation ofnecrotic corenecrotic core


Formation of the Complicated Atherosclerotic Plaque

The development of an atherosclerotic plaque indicates an advanced stage in the atherosclerotic process and results from death and rupture of the lipid-laden foam cells in the fatty streak. Migration of vascular smooth muscle cells (VSMCs) to the tunica intima and laying down of collagen fibres results in the formation of a protective fibrous cap over the lipid core. The fibrous cap is a crucial component of the mature atherosclerotic plaque as it separates the highly thrombogenic lipid-rich core from circulating platelets and other coagulation factors. Stable atherosclerotic plaques are characterised by a necrotic lipid core covered by a thick VSM-rich fibrous cap. Lesions expand at the shoulders by continued leucocyte adhesion. 1

Atherosclerotic Plaque Rupture and Thrombus Formation

Adapted from Ross R. N Engl J Med 1999;362:115–126.

Intraluminal thrombusIntraluminal thrombus

Intraplaque thrombusIntraplaque thrombus

Lipid coreLipid core

Pathological studies have shown that rupture of atherosclerotic plaques and subsequent luminal thrombosis underlies the aetiology of acute ischaemic coronary syndromes, including myocardial infarction and unstable angina. A lipid-rich core (particularly in the shoulder regions of lesions), abundance of inflammatory cells, a thin fibrous cap and dysfunctional overlying endothelium characterise morphological features of lesions prone to rupture. Dysfunctional endothelium may contribute to the propensity of plaque rupture owing to its pro-inflammatory, prothrombotic and vasoconstrictive properties that modulate lesion composition, growth responses, vascular tone and local shear stress.

Clinical Manifestations of Atherosclerosis

• Coronary heart disease– Angina pectoris, myocardial infarction,

sudden cardiac death

• Cerebrovascular disease– Transient ischaemic attacks, stroke

• Peripheral vascular disease– Intermittent claudication, gangrene

Coronary heart disease Restriction of blood flow to the myocardium may be caused by an atherosclerotic plaque narrowing the lumen of the coronary arteries. If the diameter of the coronary artery is reduced by more than 50%, ischaemia will develop and the patient will experience tightness or crushing pain in the chest (angina pectoris). However, pain does not always accompany myocardial ischaemia: this is called silent ischaemia.

Coronary plaque rupture and erosion have been shown to result in thrombus formation within coronary arteries. If blood flow is completely obstructed, either due to a thrombus or by a large atherosclerotic plaque, death to part of the myocardium may ensue, resulting in an MI. Depending on the magnitude or site of the damage to the myocardium the pumping action of the heart may be impaired and/or the heart rate and rhythm may become disturbed. These can result in congestive heart failure or, if very severe, sudden cardiac death.1

Cerebrovascular disease Narrowing of the carotid, vertebral and cerebral arteries supplying blood to the brain can cause a brief interruption in the blood supply to the brain resulting in a transient ischaemic attack. This may cause temporary impairment of vision, speech, sensation or movement and may be followed by a stroke. A stroke may also be caused by formation of a thrombus or embolus, arterial rupture or haemorrhage of the cerebral arteries stopping the oxygen supply to parts of the brain. Sudden loss of consciousness often occurs with subsequent paralysis of parts of the body. It can lead to permanent damage and disability and sudden death.

Peripheral vascular disease When the lumen of arteries such as the femoral and iliac arteries supplying blood to the legs has been significantly narrowed, by 60% or more, the symptoms of intermittent claudication become evident. These include an aching or cramping pain, most often in the legs when walking, which occurs when insufficient oxygen is reaching the muscles in the legs. In advanced cases of peripheral vascular disease, blood supply to the legs may become completely blocked, possibly by thrombus formation, and painful leg and foot ulcers may develop. If left untreated gangrene may eventually ensue, requiring amputation of the affected limb.

KLASIFIKASI TOTAL, LDL, HDL-KOLESTEROL, KLASIFIKASI TOTAL, LDL, HDL-KOLESTEROL, DAN TRIGLISERID MENURUT NCEP ATP III DAN TRIGLISERID MENURUT NCEP ATP III

(mg/dl)(mg/dl)LDL kolesterolLDL kolesterol

< 100< 100100 - 129100 - 129130 - 159130 - 159160 - 189160 - 189>> 190 190

Total kolesterolTotal kolesterol< 200< 200200 - 239200 - 239>> 240 240

HDL kolesterolHDL kolesterol< 40< 40>> 60 60

OptimalOptimalMendekati optimalMendekati optimalSedikit tinggi (Borderline) Sedikit tinggi (Borderline) TinggiTinggiSangat tinggiSangat tinggi

DiinginkanDiinginkanSedikit tinggi (Borderline) Sedikit tinggi (Borderline) TinggiTinggi

RendahRendahTinggiTinggi

JAMA 2001;285:24862-497JAMA 2001;285:24862-4971919

TRIGLISERID (NCEP-ATP III)TRIGLISERID (NCEP-ATP III)

OptimalOptimal < 150 mg/dl< 150 mg/dl

Sedikit tinggi (borderline) Sedikit tinggi (borderline) 150 - 199 mg/dl150 - 199 mg/dl

Tinggi Tinggi 200 - 499 mg/dl200 - 499 mg/dl

Sangat tinggi Sangat tinggi > 500 mg/dl > 500 mg/dl

2020

FAKTOR RISIKO PENTING (SELAIN LDL-FAKTOR RISIKO PENTING (SELAIN LDL-KOLESTEROL) YANG MENENTUKAN KOLESTEROL) YANG MENENTUKAN SASARAN LDL-KOLESTEROLSASARAN LDL-KOLESTEROL

• Merokok sigaretMerokok sigaret

• Hipertensi Hipertensi (tekanan darah > 140/90 mmHg, atau (tekanan darah > 140/90 mmHg, atau yang sedang mendapat obat yang sedang mendapat obat antihipertensi)antihipertensi)

•HDL kolesterol rendahHDL kolesterol rendah (< 40 mg/dl)*(< 40 mg/dl)*

• Riwayat keluarga PAK diniRiwayat keluarga PAK dini ayah usia < 55 tahun, ibu < 65 tahunayah usia < 55 tahun, ibu < 65 tahun

• UmurUmur pria > 45 tahun, wanita > 55 tahunpria > 45 tahun, wanita > 55 tahun

JAMA 2001;285:24862-497JAMA 2001;285:24862-497

* HDL kolesterol * HDL kolesterol >> 60 mg/dl mengurangi satu faktor risiko 60 mg/dl mengurangi satu faktor risiko

1111

TIGA KELOMPOK RISIKO YANG TIGA KELOMPOK RISIKO YANG MENENTUKAN SASARAN LDL-KOLESTEROL MENENTUKAN SASARAN LDL-KOLESTEROL

YANG INGIN DICAPAIYANG INGIN DICAPAI

Kelompok risikoKelompok risiko Sasaran LDL (mg/dl)Sasaran LDL (mg/dl)

Mereka dengan PAK atau yang Mereka dengan PAK atau yang disamakandisamakan

Faktor risiko multipel ( Faktor risiko multipel ( >> 2) 2)

0 - 1 faktor risiko0 - 1 faktor risiko

< 100< 100

< 130< 130

< 160< 160

JAMA 2001;285:24862-497JAMA 2001;285:24862-4971313

PENATALAKSANAANPENATALAKSANAAN

Perubahan gaya hidup (therapeutic Perubahan gaya hidup (therapeutic lifestyle changes )lifestyle changes ) Perencanaan makan (diet)Perencanaan makan (diet) Olahraga Olahraga Berhenti merokokBerhenti merokok Batasi alkohol Batasi alkohol

Obat penurun lipidObat penurun lipid

2222

Perubahan gaya hidup terutama diet dan olahraga harus Perubahan gaya hidup terutama diet dan olahraga harus merupakan urutan pertama penatalaksanaan merupakan urutan pertama penatalaksanaan dislipidemi. Pada penderita dislipidemi gemuk, diet dan dislipidemi. Pada penderita dislipidemi gemuk, diet dan olahraga tidak hanya menurunkan berat badan saja olahraga tidak hanya menurunkan berat badan saja tetapi juga memperbaiki kadar trigliserid dan kolesterol tetapi juga memperbaiki kadar trigliserid dan kolesterol penderita. Obat penurun berat badan seperti orlistat penderita. Obat penurun berat badan seperti orlistat (Xenical) dan sibutramin (Reductyl) yang banyak dipakai (Xenical) dan sibutramin (Reductyl) yang banyak dipakai pada saat ini akan membantu menurunkan berat badan pada saat ini akan membantu menurunkan berat badan dan memperbaiki profil lipid penderita. Sibutramin dan memperbaiki profil lipid penderita. Sibutramin sebagai contoh selain menurunkan dan sebagai contoh selain menurunkan dan mempertahankan berat badan yang sudah turun juga mempertahankan berat badan yang sudah turun juga meningkatkan kadar HDL-kolesterol cukup baik.meningkatkan kadar HDL-kolesterol cukup baik.

KETERANGANKETERANGAN

2323

SUSUNAN MAKANAN UNTUK PENDERITA SUSUNAN MAKANAN UNTUK PENDERITA HIPERKOLESTEROLEMIHIPERKOLESTEROLEMI

Jenis makananJenis makanan RekomendasiRekomendasi

Jumlah lemakJumlah lemak

Lemak jenuhLemak jenuh

Polyunsaturated fatPolyunsaturated fat

Monounsaturated fatMonounsaturated fat

KarbohidratKarbohidrat

SeratSerat

ProteinProtein

KolesterolKolesterol

25-30% jumlah kalori25-30% jumlah kalori

< 7% jumlah kalori< 7% jumlah kalori

10% jumlah kalori10% jumlah kalori

10% jumlah kalori10% jumlah kalori

60% jumlah kalori (terutama60% jumlah kalori (terutama

karbohidrat kompleks)karbohidrat kompleks)10 gm/ 1000 kkal per hari10 gm/ 1000 kkal per hari

Sekitar 15% jumlah kaloriSekitar 15% jumlah kalori

< 200 mg / hari< 200 mg / hari

2727

Beberapa hal penting mengenai jenis makanan Beberapa hal penting mengenai jenis makanan yaitu banyak buah, sayur, kacang-kacangan. yaitu banyak buah, sayur, kacang-kacangan. Perlu menghindari kulit ayam atau ikan, dan Perlu menghindari kulit ayam atau ikan, dan untuk mereka yang kadar trilgiserid tinggi untuk mereka yang kadar trilgiserid tinggi sebaiknya menghindari alkohol berlebihan, sebaiknya menghindari alkohol berlebihan, makanan yang kaya karbohidrat seperti kue makanan yang kaya karbohidrat seperti kue manis.manis.

KETERANGANKETERANGAN

2828

OLAHRAGA TERATUROLAHRAGA TERATUR

2424

OBAT PENURUN LIPIDOBAT PENURUN LIPID

DrugDrug LDL-KLDL-K HDL-KHDL-K TGTG

StatinStatin

ResinResin

FibratFibrat

Asam nikotinikAsam nikotinik

18 - 55%18 - 55%

15 - 30%15 - 30%

5 - 25%*5 - 25%*

5 - 25%5 - 25%

5 - 15%5 - 15%

3 - 5%3 - 5%

10 - 20%*10 - 20%*

15 - 35%15 - 35%

7 - 30%7 - 30%

- / - /

20 - 50%*20 - 50%*

20 - 50%20 - 50%

* bezafibrat, cipofibrat dan fenofibrat menurunkan LDL-kolesterol * bezafibrat, cipofibrat dan fenofibrat menurunkan LDL-kolesterol lebih banyak daripada gemfibrozillebih banyak daripada gemfibrozil

Persentasi penurunan LDL-kolesterol dan trigliserid, Persentasi penurunan LDL-kolesterol dan trigliserid, serta kenaikan HDL-kolesterolserta kenaikan HDL-kolesterol

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